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Prioritize lung cancer patients for COVID-19 testing, physicians recommend
Lung cancer patients should be prioritized for COVID-19 testing, according to an editorial published in Annals of Oncology.
In fact, treatment recommendations should call for baseline COVID-19 testing for all patients with lung cancer, Antonio Passaro, MD, PhD, of the European Institute of Oncology in Milan, Italy, and colleagues argued in the editorial.
“While all types of malignancies seem to be associated with high COVID-19 prevalence, morbidity, and mortality, lung cancer represents a specific scenario of cumulative risk factors for COVID-19 complications,” the authors wrote.
“[Lung cancer patients] are at a uniquely escalated risk of complications from COVID-19 due to the common features of smoking history, respiratory and cardiac disease, advanced age, and often predisposing risks from treatment, such as lung surgery and immunosuppressive chemotherapy,” said Howard (Jack) West, MD, of City of Hope Comprehensive Cancer Center in Duarte, Calif., who was not involved in the editorial.
“They also routinely experience a cough as well as chest imaging that may overlap between their underlying lung cancer, possible side effects of treatment, and potential COVID-19, leading to troubling ambiguity that can only be addressed by proactive and widespread testing of patients with lung cancer at the earliest opportunity and as a very high priority,” Dr. West added.
Dr. Passaro and colleagues’ editorial outlined these and other issues that suggest a need to prioritize testing in lung cancer patients.
Disease characteristics, treatment, and imaging
Lung cancer patients may have “defective pulmonary architecture,” such as mechanical obstruction from a tumor or previous lung surgery, that predisposes them to infection and can increase the risk of cytokine release. This is a concern because massive cytokine release during SARS-CoV-2 infection “has been postulated to be the major step in leading to the development of ARDS [acute respiratory distress syndrome],” Dr. Passaro and colleagues wrote.
The authors also argued that similar clinical symptoms among lung cancer patients and those with COVID-19 – such as cough, fever, and dyspnea – underscore the need for an accurate screening model to allow for early COVID-19 detection and potentially improve outcomes.
Similarly, lung cancer patients and COVID-19 patients may have overlapping findings on imaging. The radiologic effects of some common treatments for lung cancer can lead to the same kind of ground glass opacities and other findings seen in COVID-19 patients. Therefore, the authors predict an increase in “COVID-19-suspicious imaging, even in the absence of new symptoms” in the coming weeks.
Another issue to consider is the frequent use of corticosteroids in cancer patients. Corticosteroids may be harmful when used for COVID-19–related acute respiratory distress syndrome and could mask early symptoms of infection. Therefore, routine COVID-19 testing in patients receiving steroids may be warranted, according to Dr. Passaro and colleagues.
In addition, immunosuppression associated with cancer treatment “may impose specific consideration on the schedule and dose of cytotoxic chemotherapy for lung cancer patients in epidemic areas,” the authors wrote.
Increasing awareness: A registry and guidelines
“In the era of COVID-19, the optimal management of patients with lung cancer remains unknown, and the oncology community should have increased awareness to prevent the emergence of an increase in cancer-related and infectious mortality,” Dr. Passaro and colleagues wrote.
To that end, a novel global registry (TERAVOLT) has been launched and is collecting data worldwide with an aim of developing a tailored risk assessment strategy for lung cancer patients. The authors noted that developing international consensus with respect to COVID-19 testing in lung cancer is essential for achieving that goal.
The European Society for Medical Oncology recently released guidelines for treating lung cancer patients during the COVID-19 pandemic, but those guidelines do not include recommendations on COVID-19 testing.
“Baseline SARS-CoV-2 testing for all patients affected by lung cancer should be recommended,” Dr. Passaro and colleagues wrote. “In addition, for those patients with a negative swab test and new ground glass opacities detected on CT scan, with or without new respiratory symptoms, bronchoscopy should be considered to increase testing sensitivity.”
This work was partially supported by the Italian Ministry of Health. The authors reported having no relevant conflicts of interest. Dr. West is a regular correspondent for Medscape, which is owned by the same parent company as MDedge.
SOURCE: Passaro A et al. Annals of Oncology. doi: 10.1016/j.annonc.2020.04.002.
Lung cancer patients should be prioritized for COVID-19 testing, according to an editorial published in Annals of Oncology.
In fact, treatment recommendations should call for baseline COVID-19 testing for all patients with lung cancer, Antonio Passaro, MD, PhD, of the European Institute of Oncology in Milan, Italy, and colleagues argued in the editorial.
“While all types of malignancies seem to be associated with high COVID-19 prevalence, morbidity, and mortality, lung cancer represents a specific scenario of cumulative risk factors for COVID-19 complications,” the authors wrote.
“[Lung cancer patients] are at a uniquely escalated risk of complications from COVID-19 due to the common features of smoking history, respiratory and cardiac disease, advanced age, and often predisposing risks from treatment, such as lung surgery and immunosuppressive chemotherapy,” said Howard (Jack) West, MD, of City of Hope Comprehensive Cancer Center in Duarte, Calif., who was not involved in the editorial.
“They also routinely experience a cough as well as chest imaging that may overlap between their underlying lung cancer, possible side effects of treatment, and potential COVID-19, leading to troubling ambiguity that can only be addressed by proactive and widespread testing of patients with lung cancer at the earliest opportunity and as a very high priority,” Dr. West added.
Dr. Passaro and colleagues’ editorial outlined these and other issues that suggest a need to prioritize testing in lung cancer patients.
Disease characteristics, treatment, and imaging
Lung cancer patients may have “defective pulmonary architecture,” such as mechanical obstruction from a tumor or previous lung surgery, that predisposes them to infection and can increase the risk of cytokine release. This is a concern because massive cytokine release during SARS-CoV-2 infection “has been postulated to be the major step in leading to the development of ARDS [acute respiratory distress syndrome],” Dr. Passaro and colleagues wrote.
The authors also argued that similar clinical symptoms among lung cancer patients and those with COVID-19 – such as cough, fever, and dyspnea – underscore the need for an accurate screening model to allow for early COVID-19 detection and potentially improve outcomes.
Similarly, lung cancer patients and COVID-19 patients may have overlapping findings on imaging. The radiologic effects of some common treatments for lung cancer can lead to the same kind of ground glass opacities and other findings seen in COVID-19 patients. Therefore, the authors predict an increase in “COVID-19-suspicious imaging, even in the absence of new symptoms” in the coming weeks.
Another issue to consider is the frequent use of corticosteroids in cancer patients. Corticosteroids may be harmful when used for COVID-19–related acute respiratory distress syndrome and could mask early symptoms of infection. Therefore, routine COVID-19 testing in patients receiving steroids may be warranted, according to Dr. Passaro and colleagues.
In addition, immunosuppression associated with cancer treatment “may impose specific consideration on the schedule and dose of cytotoxic chemotherapy for lung cancer patients in epidemic areas,” the authors wrote.
Increasing awareness: A registry and guidelines
“In the era of COVID-19, the optimal management of patients with lung cancer remains unknown, and the oncology community should have increased awareness to prevent the emergence of an increase in cancer-related and infectious mortality,” Dr. Passaro and colleagues wrote.
To that end, a novel global registry (TERAVOLT) has been launched and is collecting data worldwide with an aim of developing a tailored risk assessment strategy for lung cancer patients. The authors noted that developing international consensus with respect to COVID-19 testing in lung cancer is essential for achieving that goal.
The European Society for Medical Oncology recently released guidelines for treating lung cancer patients during the COVID-19 pandemic, but those guidelines do not include recommendations on COVID-19 testing.
“Baseline SARS-CoV-2 testing for all patients affected by lung cancer should be recommended,” Dr. Passaro and colleagues wrote. “In addition, for those patients with a negative swab test and new ground glass opacities detected on CT scan, with or without new respiratory symptoms, bronchoscopy should be considered to increase testing sensitivity.”
This work was partially supported by the Italian Ministry of Health. The authors reported having no relevant conflicts of interest. Dr. West is a regular correspondent for Medscape, which is owned by the same parent company as MDedge.
SOURCE: Passaro A et al. Annals of Oncology. doi: 10.1016/j.annonc.2020.04.002.
Lung cancer patients should be prioritized for COVID-19 testing, according to an editorial published in Annals of Oncology.
In fact, treatment recommendations should call for baseline COVID-19 testing for all patients with lung cancer, Antonio Passaro, MD, PhD, of the European Institute of Oncology in Milan, Italy, and colleagues argued in the editorial.
“While all types of malignancies seem to be associated with high COVID-19 prevalence, morbidity, and mortality, lung cancer represents a specific scenario of cumulative risk factors for COVID-19 complications,” the authors wrote.
“[Lung cancer patients] are at a uniquely escalated risk of complications from COVID-19 due to the common features of smoking history, respiratory and cardiac disease, advanced age, and often predisposing risks from treatment, such as lung surgery and immunosuppressive chemotherapy,” said Howard (Jack) West, MD, of City of Hope Comprehensive Cancer Center in Duarte, Calif., who was not involved in the editorial.
“They also routinely experience a cough as well as chest imaging that may overlap between their underlying lung cancer, possible side effects of treatment, and potential COVID-19, leading to troubling ambiguity that can only be addressed by proactive and widespread testing of patients with lung cancer at the earliest opportunity and as a very high priority,” Dr. West added.
Dr. Passaro and colleagues’ editorial outlined these and other issues that suggest a need to prioritize testing in lung cancer patients.
Disease characteristics, treatment, and imaging
Lung cancer patients may have “defective pulmonary architecture,” such as mechanical obstruction from a tumor or previous lung surgery, that predisposes them to infection and can increase the risk of cytokine release. This is a concern because massive cytokine release during SARS-CoV-2 infection “has been postulated to be the major step in leading to the development of ARDS [acute respiratory distress syndrome],” Dr. Passaro and colleagues wrote.
The authors also argued that similar clinical symptoms among lung cancer patients and those with COVID-19 – such as cough, fever, and dyspnea – underscore the need for an accurate screening model to allow for early COVID-19 detection and potentially improve outcomes.
Similarly, lung cancer patients and COVID-19 patients may have overlapping findings on imaging. The radiologic effects of some common treatments for lung cancer can lead to the same kind of ground glass opacities and other findings seen in COVID-19 patients. Therefore, the authors predict an increase in “COVID-19-suspicious imaging, even in the absence of new symptoms” in the coming weeks.
Another issue to consider is the frequent use of corticosteroids in cancer patients. Corticosteroids may be harmful when used for COVID-19–related acute respiratory distress syndrome and could mask early symptoms of infection. Therefore, routine COVID-19 testing in patients receiving steroids may be warranted, according to Dr. Passaro and colleagues.
In addition, immunosuppression associated with cancer treatment “may impose specific consideration on the schedule and dose of cytotoxic chemotherapy for lung cancer patients in epidemic areas,” the authors wrote.
Increasing awareness: A registry and guidelines
“In the era of COVID-19, the optimal management of patients with lung cancer remains unknown, and the oncology community should have increased awareness to prevent the emergence of an increase in cancer-related and infectious mortality,” Dr. Passaro and colleagues wrote.
To that end, a novel global registry (TERAVOLT) has been launched and is collecting data worldwide with an aim of developing a tailored risk assessment strategy for lung cancer patients. The authors noted that developing international consensus with respect to COVID-19 testing in lung cancer is essential for achieving that goal.
The European Society for Medical Oncology recently released guidelines for treating lung cancer patients during the COVID-19 pandemic, but those guidelines do not include recommendations on COVID-19 testing.
“Baseline SARS-CoV-2 testing for all patients affected by lung cancer should be recommended,” Dr. Passaro and colleagues wrote. “In addition, for those patients with a negative swab test and new ground glass opacities detected on CT scan, with or without new respiratory symptoms, bronchoscopy should be considered to increase testing sensitivity.”
This work was partially supported by the Italian Ministry of Health. The authors reported having no relevant conflicts of interest. Dr. West is a regular correspondent for Medscape, which is owned by the same parent company as MDedge.
SOURCE: Passaro A et al. Annals of Oncology. doi: 10.1016/j.annonc.2020.04.002.
FROM ANNALS OF ONCOLOGY
Coping with COVID-19: Things may never be the same
The last few weeks have been confusing and a little overwhelming. A hodgepodge of rapid-fire publications of potential treatments and multiple, sometimes confusing government mandates and initiatives have inundated us. The overriding theme is clear, though: Let’s first concentrate on keeping our civilization intact. State governments have been largely focused on “flattening the curve” of new infections. And the longer we slow this disease down, the better we learn how to treat it.
Multiple existing medications, repurposed from all walks of the pharmacologic world, have been screened and shown to have potential therapeutic benefit, and they are being tested even as I write this column. The nasty form of this disease is a unique form of adult respiratory distress syndrome, and the terminal event appears to be a form of disseminated intravascular coagulation, which may respond to unexpected therapies, such as clot busters (J Thromb Haemost. 2020 Apr 8. doi: 10.1111/jth.14828).
Now, let’s consider the more mundane issue of keeping your medical practice alive.
Some state medical boards have relaxed the rules on licensing, and the federal government on HIPAA compliance, so that telemedicine has finally become practical. Some EHR vendors have even rushed out modules to make it easier to conduct visits with patients through their patient portals. This has all made it almost practical to see, monitor, and treat existing patients with chronic conditions, and even new ones who do not require a biopsy.
But it has also become clear that telemedicine is not a long-term means of keeping your practice viable, at least not in your practice’s current form. It can be difficult to enroll new patients and the process of collecting copays and deductibles can be frustrating and slow. There may also resistance from our patients, who may be used to having this sort of service performed by us free-of-charge. Those selfies that in the past you may have viewed, called the patient to discuss, and then called their medication into the pharmacy – all as a convenience – are coming back to haunt you. It was free before, they say, what has changed?
Another obstacle, as always, is reimbursement. There is an inconsistent patchwork of private insurance coverage that may or may not pay you. The American Academy of Dermatology has put together an excellent resource on its web site on all matters regarding COVID-19 to help you.
But the underlying undeniable reality is that you cannot support your current practice model long term with telemedicine because only about 30% of dermatology reimbursement comes from evaluation and management codes, according to a recently published study – and the rest, procedures, obviously requires patient contact (JAMA Surg. 2020 Apr 15. doi: 10.1001/jamasurg.2020.0422).
The federal government has been economically responsive by injecting money into businesses with less than 500 employees. Most of you will be eligible and probably already have applied for the Paycheck Protection Program. These are small business “loans” that your bank puts the paperwork in for, which can total up to 2.5 times one month’s average payroll. These “loans” may be 100% forgivable (75% must come from two months payroll, another 25% rent and expenses) if you do not lay anyone off.
Employees can be kept busy doing other tasks besides directly helping with patients. Like many of you with state-mandated lockdowns, my office has never been so clean, the cabinets so well stocked, and the files so organized. The stock room has been cleaned out, and any extra personal protective gear has been donated to the hospital and emergency medical services. We have landscaped the front of our building and if it warms up, we will seal and remark the parking lot. You get my drift. I have also applied for and received an advance of three months of Medicare payments, which will be automatically paid back as practice resumes. This is in effect an interest-free loan. A few days ago, my business checking account received a deposit from the Department of Health & Human Services for 6.1% of last year’s Medicare billings. This is unexpected, no obligation support to help keep your medical office open in the time of COVID-19. It appears that the office and practice will be able to weather the fire.
Assuming our practices survive more or less intact, there are major social consequences to consider. Society is a conglomeration of individuals, and individuals act on their Maslow’s hierarchy of needs (a concept introduced by psychologist Abraham Maslow, PhD, over 75 years ago). Our society has already slid down several of Maslow’s levels. We have reset to about level two, which is safety, one level above physiologic needs. Recall the grocery store fights. Look at the gun sales. The toilet paper roll has been reset from wheel of fortune spin to safe cracking mode.
This reset of the societal mindset has many ramifications you may not normally consider. For example, who will risk buying up to that dream home or purchasing a second home, if you are being told to shelter in place? Fewer may gamble $300,000 on a college education at a less-than-top-50 school. Who even knows when college will start next year. Who is going to take that promotion to New York City, or even New Jersey, and ride the train and subway to work every day? Who wants to commute through the crowded airport on the jam packed “plane train”?
It is easy to predict we will see a severe recession followed by higher taxes and inflation (stagflation). There is a financial writer I like to read who has been predicting a “great reset” of American society for several years. COVID-19 may have precipitated that reset, and things may never be the same.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com. He has no disclosures.
The last few weeks have been confusing and a little overwhelming. A hodgepodge of rapid-fire publications of potential treatments and multiple, sometimes confusing government mandates and initiatives have inundated us. The overriding theme is clear, though: Let’s first concentrate on keeping our civilization intact. State governments have been largely focused on “flattening the curve” of new infections. And the longer we slow this disease down, the better we learn how to treat it.
Multiple existing medications, repurposed from all walks of the pharmacologic world, have been screened and shown to have potential therapeutic benefit, and they are being tested even as I write this column. The nasty form of this disease is a unique form of adult respiratory distress syndrome, and the terminal event appears to be a form of disseminated intravascular coagulation, which may respond to unexpected therapies, such as clot busters (J Thromb Haemost. 2020 Apr 8. doi: 10.1111/jth.14828).
Now, let’s consider the more mundane issue of keeping your medical practice alive.
Some state medical boards have relaxed the rules on licensing, and the federal government on HIPAA compliance, so that telemedicine has finally become practical. Some EHR vendors have even rushed out modules to make it easier to conduct visits with patients through their patient portals. This has all made it almost practical to see, monitor, and treat existing patients with chronic conditions, and even new ones who do not require a biopsy.
But it has also become clear that telemedicine is not a long-term means of keeping your practice viable, at least not in your practice’s current form. It can be difficult to enroll new patients and the process of collecting copays and deductibles can be frustrating and slow. There may also resistance from our patients, who may be used to having this sort of service performed by us free-of-charge. Those selfies that in the past you may have viewed, called the patient to discuss, and then called their medication into the pharmacy – all as a convenience – are coming back to haunt you. It was free before, they say, what has changed?
Another obstacle, as always, is reimbursement. There is an inconsistent patchwork of private insurance coverage that may or may not pay you. The American Academy of Dermatology has put together an excellent resource on its web site on all matters regarding COVID-19 to help you.
But the underlying undeniable reality is that you cannot support your current practice model long term with telemedicine because only about 30% of dermatology reimbursement comes from evaluation and management codes, according to a recently published study – and the rest, procedures, obviously requires patient contact (JAMA Surg. 2020 Apr 15. doi: 10.1001/jamasurg.2020.0422).
The federal government has been economically responsive by injecting money into businesses with less than 500 employees. Most of you will be eligible and probably already have applied for the Paycheck Protection Program. These are small business “loans” that your bank puts the paperwork in for, which can total up to 2.5 times one month’s average payroll. These “loans” may be 100% forgivable (75% must come from two months payroll, another 25% rent and expenses) if you do not lay anyone off.
Employees can be kept busy doing other tasks besides directly helping with patients. Like many of you with state-mandated lockdowns, my office has never been so clean, the cabinets so well stocked, and the files so organized. The stock room has been cleaned out, and any extra personal protective gear has been donated to the hospital and emergency medical services. We have landscaped the front of our building and if it warms up, we will seal and remark the parking lot. You get my drift. I have also applied for and received an advance of three months of Medicare payments, which will be automatically paid back as practice resumes. This is in effect an interest-free loan. A few days ago, my business checking account received a deposit from the Department of Health & Human Services for 6.1% of last year’s Medicare billings. This is unexpected, no obligation support to help keep your medical office open in the time of COVID-19. It appears that the office and practice will be able to weather the fire.
Assuming our practices survive more or less intact, there are major social consequences to consider. Society is a conglomeration of individuals, and individuals act on their Maslow’s hierarchy of needs (a concept introduced by psychologist Abraham Maslow, PhD, over 75 years ago). Our society has already slid down several of Maslow’s levels. We have reset to about level two, which is safety, one level above physiologic needs. Recall the grocery store fights. Look at the gun sales. The toilet paper roll has been reset from wheel of fortune spin to safe cracking mode.
This reset of the societal mindset has many ramifications you may not normally consider. For example, who will risk buying up to that dream home or purchasing a second home, if you are being told to shelter in place? Fewer may gamble $300,000 on a college education at a less-than-top-50 school. Who even knows when college will start next year. Who is going to take that promotion to New York City, or even New Jersey, and ride the train and subway to work every day? Who wants to commute through the crowded airport on the jam packed “plane train”?
It is easy to predict we will see a severe recession followed by higher taxes and inflation (stagflation). There is a financial writer I like to read who has been predicting a “great reset” of American society for several years. COVID-19 may have precipitated that reset, and things may never be the same.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com. He has no disclosures.
The last few weeks have been confusing and a little overwhelming. A hodgepodge of rapid-fire publications of potential treatments and multiple, sometimes confusing government mandates and initiatives have inundated us. The overriding theme is clear, though: Let’s first concentrate on keeping our civilization intact. State governments have been largely focused on “flattening the curve” of new infections. And the longer we slow this disease down, the better we learn how to treat it.
Multiple existing medications, repurposed from all walks of the pharmacologic world, have been screened and shown to have potential therapeutic benefit, and they are being tested even as I write this column. The nasty form of this disease is a unique form of adult respiratory distress syndrome, and the terminal event appears to be a form of disseminated intravascular coagulation, which may respond to unexpected therapies, such as clot busters (J Thromb Haemost. 2020 Apr 8. doi: 10.1111/jth.14828).
Now, let’s consider the more mundane issue of keeping your medical practice alive.
Some state medical boards have relaxed the rules on licensing, and the federal government on HIPAA compliance, so that telemedicine has finally become practical. Some EHR vendors have even rushed out modules to make it easier to conduct visits with patients through their patient portals. This has all made it almost practical to see, monitor, and treat existing patients with chronic conditions, and even new ones who do not require a biopsy.
But it has also become clear that telemedicine is not a long-term means of keeping your practice viable, at least not in your practice’s current form. It can be difficult to enroll new patients and the process of collecting copays and deductibles can be frustrating and slow. There may also resistance from our patients, who may be used to having this sort of service performed by us free-of-charge. Those selfies that in the past you may have viewed, called the patient to discuss, and then called their medication into the pharmacy – all as a convenience – are coming back to haunt you. It was free before, they say, what has changed?
Another obstacle, as always, is reimbursement. There is an inconsistent patchwork of private insurance coverage that may or may not pay you. The American Academy of Dermatology has put together an excellent resource on its web site on all matters regarding COVID-19 to help you.
But the underlying undeniable reality is that you cannot support your current practice model long term with telemedicine because only about 30% of dermatology reimbursement comes from evaluation and management codes, according to a recently published study – and the rest, procedures, obviously requires patient contact (JAMA Surg. 2020 Apr 15. doi: 10.1001/jamasurg.2020.0422).
The federal government has been economically responsive by injecting money into businesses with less than 500 employees. Most of you will be eligible and probably already have applied for the Paycheck Protection Program. These are small business “loans” that your bank puts the paperwork in for, which can total up to 2.5 times one month’s average payroll. These “loans” may be 100% forgivable (75% must come from two months payroll, another 25% rent and expenses) if you do not lay anyone off.
Employees can be kept busy doing other tasks besides directly helping with patients. Like many of you with state-mandated lockdowns, my office has never been so clean, the cabinets so well stocked, and the files so organized. The stock room has been cleaned out, and any extra personal protective gear has been donated to the hospital and emergency medical services. We have landscaped the front of our building and if it warms up, we will seal and remark the parking lot. You get my drift. I have also applied for and received an advance of three months of Medicare payments, which will be automatically paid back as practice resumes. This is in effect an interest-free loan. A few days ago, my business checking account received a deposit from the Department of Health & Human Services for 6.1% of last year’s Medicare billings. This is unexpected, no obligation support to help keep your medical office open in the time of COVID-19. It appears that the office and practice will be able to weather the fire.
Assuming our practices survive more or less intact, there are major social consequences to consider. Society is a conglomeration of individuals, and individuals act on their Maslow’s hierarchy of needs (a concept introduced by psychologist Abraham Maslow, PhD, over 75 years ago). Our society has already slid down several of Maslow’s levels. We have reset to about level two, which is safety, one level above physiologic needs. Recall the grocery store fights. Look at the gun sales. The toilet paper roll has been reset from wheel of fortune spin to safe cracking mode.
This reset of the societal mindset has many ramifications you may not normally consider. For example, who will risk buying up to that dream home or purchasing a second home, if you are being told to shelter in place? Fewer may gamble $300,000 on a college education at a less-than-top-50 school. Who even knows when college will start next year. Who is going to take that promotion to New York City, or even New Jersey, and ride the train and subway to work every day? Who wants to commute through the crowded airport on the jam packed “plane train”?
It is easy to predict we will see a severe recession followed by higher taxes and inflation (stagflation). There is a financial writer I like to read who has been predicting a “great reset” of American society for several years. COVID-19 may have precipitated that reset, and things may never be the same.
Dr. Coldiron is in private practice but maintains a clinical assistant professorship at the University of Cincinnati. He cares for patients, teaches medical students and residents, and has several active clinical research projects. Dr. Coldiron is the author of more than 80 scientific letters, papers, and several book chapters, and he speaks frequently on a variety of topics. He is a past president of the American Academy of Dermatology. Write to him at dermnews@mdedge.com. He has no disclosures.
Excessive sleepiness linked to heart disease, cancer, and diabetes
, new research suggests. A study of almost 11,000 participants shows those who reported excessive sleepiness were twice as likely as their nonsleepy counterparts to develop these conditions. Hypersomnolence was also linked to development of musculoskeletal and connective tissue conditions.
“Paying attention to sleepiness in older adults could help doctors predict and prevent future medical conditions,” study investigator Maurice M. Ohayon, MD, PhD, Stanford University, California, said in a news release.
The findings were released March 1 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Early warning sign
Prior research has suggested an association between hypersomnolence and several psychiatric disorders, as well as cognitive decline and Alzheimer’s disease. However, its role in the development of other medical conditions is not as well studied.
The current investigation included 10,930 adults who were interviewed by phone on two separate occasions 3 years apart. At the second interview, 3,701 participants were at least 65 years old and 59% were women.
About 23% of the elderly participants reported hypersomnolence in the first interview and 24% reported it in the second interview. Of these individuals, 41% said during the first and second interviews that excessive daytime sleepiness was a chronic problem.
After adjusting for gender and obstructive sleep apnea status, participants who reported hypersomnolence in the first interview had more than a twofold greater risk of developing diabetes (relative risk [RR], 2.3; 95% CI, 1.5 - 3.4) or hypertension (RR, 2.3; 95% CI, 1.5 - 3.4) 3 years later than those who did not report this problem. They were also twice as likely to develop cancer (RR, 2.0; 95% CI, 1.1 - 3.8).
Of the 840 participants who reported hypersomnolence at the first interview, 52 (6.2%) developed diabetes compared with 74 (2.9%) who did not have excessive daytime sleepiness. Twenty (2.4%) individuals who reported hypersomnolence developed cancer compared with 21 (0.8%) who did not have it. Chronic hypersomnolence was associated with a greater than twofold increased risk of developing heart disease (RR, 2.5; 95% CI, 1.8 - 3.4).
Those who reported hypersomnolence at the second interview also were 50% more likely to have diseases of the musculoskeletal system and connective tissue, such as arthritis, tendinitis, and lupus, than their peers who did not have excessive daytime sleepiness.
The findings suggest that hypersomnolence in the elderly “can be an early sign of a developing medical condition,” the investigators wrote.
A limitation of the study is that it relied on participants’ memories rather than monitoring their sleep length and quality and daytime sleepiness in a sleep clinic, they noted.
Sleep as a vital sign?
Commenting on the findings, Harly Greenberg, MD, medical director at the Northwell Health Sleep Disorders Center, New York City, called the study “informative.”
However, because the findings were associations, “the study does not necessarily indicate that hypersomnolence itself is causal for these conditions. Rather excessive sleepiness may be a marker of sleep disorders that can cause sleepiness as well as contribute to the risk of these medical conditions,” said Dr. Greenberg, who was not involved with the research.
“The takeaway point from this study is that excessive sleepiness should not be ignored. Not only does it impair quality of life, daytime function, and vigilance and increase risk of sleepiness-related accidents, it may also be a marker for serious sleep disorders that can increase risk for medical disorders,” he said.
Also commenting on the study, Nathaniel Watson, MD, professor of neurology at the University of Washington (UW) and director of the UW Medicine Sleep Clinic, said it is “not surprising” that excessive daytime sleepiness might contribute to diabetes, hypertension, and other diseases.
“Sleep is something we spend a third of our lives doing. It impacts nearly every aspect of human physiology and we have a lot of basic science and epidemiologic research that shows when sleep is either inadequate or of poor quality or not timed correctly it can be associated with some of these untoward health outcomes,” said Watson, who is a past president of the American Academy of Sleep Medicine.
“This research just provides further evidence in support of the importance of sleep for overall health and well-being,” he added.
Asking patients about sleepiness, sleep, or sleep quality should be a “vital sign just like temperature, blood pressure, weight, and these other measures,” Dr. Watson said.
The study was supported by the Arrillaga Foundation. Drs. Ohayon, Greenberg, and Watson have reported no relevant financial relationships.
This article first appeared on Medscape.com.
, new research suggests. A study of almost 11,000 participants shows those who reported excessive sleepiness were twice as likely as their nonsleepy counterparts to develop these conditions. Hypersomnolence was also linked to development of musculoskeletal and connective tissue conditions.
“Paying attention to sleepiness in older adults could help doctors predict and prevent future medical conditions,” study investigator Maurice M. Ohayon, MD, PhD, Stanford University, California, said in a news release.
The findings were released March 1 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Early warning sign
Prior research has suggested an association between hypersomnolence and several psychiatric disorders, as well as cognitive decline and Alzheimer’s disease. However, its role in the development of other medical conditions is not as well studied.
The current investigation included 10,930 adults who were interviewed by phone on two separate occasions 3 years apart. At the second interview, 3,701 participants were at least 65 years old and 59% were women.
About 23% of the elderly participants reported hypersomnolence in the first interview and 24% reported it in the second interview. Of these individuals, 41% said during the first and second interviews that excessive daytime sleepiness was a chronic problem.
After adjusting for gender and obstructive sleep apnea status, participants who reported hypersomnolence in the first interview had more than a twofold greater risk of developing diabetes (relative risk [RR], 2.3; 95% CI, 1.5 - 3.4) or hypertension (RR, 2.3; 95% CI, 1.5 - 3.4) 3 years later than those who did not report this problem. They were also twice as likely to develop cancer (RR, 2.0; 95% CI, 1.1 - 3.8).
Of the 840 participants who reported hypersomnolence at the first interview, 52 (6.2%) developed diabetes compared with 74 (2.9%) who did not have excessive daytime sleepiness. Twenty (2.4%) individuals who reported hypersomnolence developed cancer compared with 21 (0.8%) who did not have it. Chronic hypersomnolence was associated with a greater than twofold increased risk of developing heart disease (RR, 2.5; 95% CI, 1.8 - 3.4).
Those who reported hypersomnolence at the second interview also were 50% more likely to have diseases of the musculoskeletal system and connective tissue, such as arthritis, tendinitis, and lupus, than their peers who did not have excessive daytime sleepiness.
The findings suggest that hypersomnolence in the elderly “can be an early sign of a developing medical condition,” the investigators wrote.
A limitation of the study is that it relied on participants’ memories rather than monitoring their sleep length and quality and daytime sleepiness in a sleep clinic, they noted.
Sleep as a vital sign?
Commenting on the findings, Harly Greenberg, MD, medical director at the Northwell Health Sleep Disorders Center, New York City, called the study “informative.”
However, because the findings were associations, “the study does not necessarily indicate that hypersomnolence itself is causal for these conditions. Rather excessive sleepiness may be a marker of sleep disorders that can cause sleepiness as well as contribute to the risk of these medical conditions,” said Dr. Greenberg, who was not involved with the research.
“The takeaway point from this study is that excessive sleepiness should not be ignored. Not only does it impair quality of life, daytime function, and vigilance and increase risk of sleepiness-related accidents, it may also be a marker for serious sleep disorders that can increase risk for medical disorders,” he said.
Also commenting on the study, Nathaniel Watson, MD, professor of neurology at the University of Washington (UW) and director of the UW Medicine Sleep Clinic, said it is “not surprising” that excessive daytime sleepiness might contribute to diabetes, hypertension, and other diseases.
“Sleep is something we spend a third of our lives doing. It impacts nearly every aspect of human physiology and we have a lot of basic science and epidemiologic research that shows when sleep is either inadequate or of poor quality or not timed correctly it can be associated with some of these untoward health outcomes,” said Watson, who is a past president of the American Academy of Sleep Medicine.
“This research just provides further evidence in support of the importance of sleep for overall health and well-being,” he added.
Asking patients about sleepiness, sleep, or sleep quality should be a “vital sign just like temperature, blood pressure, weight, and these other measures,” Dr. Watson said.
The study was supported by the Arrillaga Foundation. Drs. Ohayon, Greenberg, and Watson have reported no relevant financial relationships.
This article first appeared on Medscape.com.
, new research suggests. A study of almost 11,000 participants shows those who reported excessive sleepiness were twice as likely as their nonsleepy counterparts to develop these conditions. Hypersomnolence was also linked to development of musculoskeletal and connective tissue conditions.
“Paying attention to sleepiness in older adults could help doctors predict and prevent future medical conditions,” study investigator Maurice M. Ohayon, MD, PhD, Stanford University, California, said in a news release.
The findings were released March 1 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Early warning sign
Prior research has suggested an association between hypersomnolence and several psychiatric disorders, as well as cognitive decline and Alzheimer’s disease. However, its role in the development of other medical conditions is not as well studied.
The current investigation included 10,930 adults who were interviewed by phone on two separate occasions 3 years apart. At the second interview, 3,701 participants were at least 65 years old and 59% were women.
About 23% of the elderly participants reported hypersomnolence in the first interview and 24% reported it in the second interview. Of these individuals, 41% said during the first and second interviews that excessive daytime sleepiness was a chronic problem.
After adjusting for gender and obstructive sleep apnea status, participants who reported hypersomnolence in the first interview had more than a twofold greater risk of developing diabetes (relative risk [RR], 2.3; 95% CI, 1.5 - 3.4) or hypertension (RR, 2.3; 95% CI, 1.5 - 3.4) 3 years later than those who did not report this problem. They were also twice as likely to develop cancer (RR, 2.0; 95% CI, 1.1 - 3.8).
Of the 840 participants who reported hypersomnolence at the first interview, 52 (6.2%) developed diabetes compared with 74 (2.9%) who did not have excessive daytime sleepiness. Twenty (2.4%) individuals who reported hypersomnolence developed cancer compared with 21 (0.8%) who did not have it. Chronic hypersomnolence was associated with a greater than twofold increased risk of developing heart disease (RR, 2.5; 95% CI, 1.8 - 3.4).
Those who reported hypersomnolence at the second interview also were 50% more likely to have diseases of the musculoskeletal system and connective tissue, such as arthritis, tendinitis, and lupus, than their peers who did not have excessive daytime sleepiness.
The findings suggest that hypersomnolence in the elderly “can be an early sign of a developing medical condition,” the investigators wrote.
A limitation of the study is that it relied on participants’ memories rather than monitoring their sleep length and quality and daytime sleepiness in a sleep clinic, they noted.
Sleep as a vital sign?
Commenting on the findings, Harly Greenberg, MD, medical director at the Northwell Health Sleep Disorders Center, New York City, called the study “informative.”
However, because the findings were associations, “the study does not necessarily indicate that hypersomnolence itself is causal for these conditions. Rather excessive sleepiness may be a marker of sleep disorders that can cause sleepiness as well as contribute to the risk of these medical conditions,” said Dr. Greenberg, who was not involved with the research.
“The takeaway point from this study is that excessive sleepiness should not be ignored. Not only does it impair quality of life, daytime function, and vigilance and increase risk of sleepiness-related accidents, it may also be a marker for serious sleep disorders that can increase risk for medical disorders,” he said.
Also commenting on the study, Nathaniel Watson, MD, professor of neurology at the University of Washington (UW) and director of the UW Medicine Sleep Clinic, said it is “not surprising” that excessive daytime sleepiness might contribute to diabetes, hypertension, and other diseases.
“Sleep is something we spend a third of our lives doing. It impacts nearly every aspect of human physiology and we have a lot of basic science and epidemiologic research that shows when sleep is either inadequate or of poor quality or not timed correctly it can be associated with some of these untoward health outcomes,” said Watson, who is a past president of the American Academy of Sleep Medicine.
“This research just provides further evidence in support of the importance of sleep for overall health and well-being,” he added.
Asking patients about sleepiness, sleep, or sleep quality should be a “vital sign just like temperature, blood pressure, weight, and these other measures,” Dr. Watson said.
The study was supported by the Arrillaga Foundation. Drs. Ohayon, Greenberg, and Watson have reported no relevant financial relationships.
This article first appeared on Medscape.com.
Transitions: From editor to president
As I transition out of the role of medical editor for The Hospitalist, and into the role of president of the Society of Hospital Medicine, it is a bittersweet but exciting transition.
In the relatively short time I have served as editor, so much has changed in our hospitalist community! In the last 4 years alone, we have increased:
• Membership from 14,000 to 20,000
• Chapters from 46 to 68
• Special Interest Groups from 8 to 22
• Subscribers to The Hospitalist from 15,000 to 30,000.
This is all a testimony to the engagement of our membership. SHM is clearly no ordinary specialty society; it is full of incredibly intelligent, invested, and talented members, who actively participate in the society for the betterment of their local teams and patients. It is such a privilege to lead this amazing team.
As for The Hospitalist, I would like to warmly welcome Weijen Chang, MD, FACP, SFHM, as the incoming editor. Weijen served as the pediatrics editor for many years and has been extensively involved on The Hospitalist’s editorial advisory board for even longer. He also has a broad track record of experience as a hospitalist in many settings; that combined with an inquisitive mind and curious spirit makes him the ideal editor for The Hospitalist. He brings energy and enthusiasm and will serve us very well.
While I will miss being intimately involved with The Hospitalist, I am very much looking forward to serving in the role of SHM president starting in April. During this pivotal year, SHM will transition from our one-and-only CEO, Larry Wellikson, MD, MHM, to our newly minted CEO Eric Howell, MD, MHM, who will officially transition in July 2020.
This is a very exciting time in the history of SHM, as we refocus on our mission, vision, values, and core activities. As a membership organization, our primary focus has been, and will always be, serving our member’s needs! As a “Big Tent” organization, we have always supported a broad and diverse set of members, ranging far beyond physician hospitalists, to trainees, medical students, nurse practitioners, physician assistants, practice administrators, and other hospital-based specialists. Being in such a dynamic industry, our diverse members needs are constantly and rapidly changing along with the dramatic transformations in the landscape, including profound shifts in care and reimbursement models that could change the very definition of a hospitalist.
While we continuously scour the landscape and anticipate our members’ needs, we will never lose sight of our core mission, which is to promote exceptional care for hospitalized patients. We will continue to do this by supporting all of our members with tools and materials to help them be the very best they can, for all of our patients. As a humble and servant leader, I am prepared to meet the demands and challenges of the year ahead, with energy and focus, and fulfill the needs of our members, so that together, we can make health care better for those we serve.
Thank you in advance for allowing me the great pleasure of serving this amazing and innovative organization!
Dr. Scheurer is chief quality officer and professor of medicine at the Medical University of South Carolina, Charleston. She is the outgoing medical editor of The Hospitalist, and president-elect of SHM.
As I transition out of the role of medical editor for The Hospitalist, and into the role of president of the Society of Hospital Medicine, it is a bittersweet but exciting transition.
In the relatively short time I have served as editor, so much has changed in our hospitalist community! In the last 4 years alone, we have increased:
• Membership from 14,000 to 20,000
• Chapters from 46 to 68
• Special Interest Groups from 8 to 22
• Subscribers to The Hospitalist from 15,000 to 30,000.
This is all a testimony to the engagement of our membership. SHM is clearly no ordinary specialty society; it is full of incredibly intelligent, invested, and talented members, who actively participate in the society for the betterment of their local teams and patients. It is such a privilege to lead this amazing team.
As for The Hospitalist, I would like to warmly welcome Weijen Chang, MD, FACP, SFHM, as the incoming editor. Weijen served as the pediatrics editor for many years and has been extensively involved on The Hospitalist’s editorial advisory board for even longer. He also has a broad track record of experience as a hospitalist in many settings; that combined with an inquisitive mind and curious spirit makes him the ideal editor for The Hospitalist. He brings energy and enthusiasm and will serve us very well.
While I will miss being intimately involved with The Hospitalist, I am very much looking forward to serving in the role of SHM president starting in April. During this pivotal year, SHM will transition from our one-and-only CEO, Larry Wellikson, MD, MHM, to our newly minted CEO Eric Howell, MD, MHM, who will officially transition in July 2020.
This is a very exciting time in the history of SHM, as we refocus on our mission, vision, values, and core activities. As a membership organization, our primary focus has been, and will always be, serving our member’s needs! As a “Big Tent” organization, we have always supported a broad and diverse set of members, ranging far beyond physician hospitalists, to trainees, medical students, nurse practitioners, physician assistants, practice administrators, and other hospital-based specialists. Being in such a dynamic industry, our diverse members needs are constantly and rapidly changing along with the dramatic transformations in the landscape, including profound shifts in care and reimbursement models that could change the very definition of a hospitalist.
While we continuously scour the landscape and anticipate our members’ needs, we will never lose sight of our core mission, which is to promote exceptional care for hospitalized patients. We will continue to do this by supporting all of our members with tools and materials to help them be the very best they can, for all of our patients. As a humble and servant leader, I am prepared to meet the demands and challenges of the year ahead, with energy and focus, and fulfill the needs of our members, so that together, we can make health care better for those we serve.
Thank you in advance for allowing me the great pleasure of serving this amazing and innovative organization!
Dr. Scheurer is chief quality officer and professor of medicine at the Medical University of South Carolina, Charleston. She is the outgoing medical editor of The Hospitalist, and president-elect of SHM.
As I transition out of the role of medical editor for The Hospitalist, and into the role of president of the Society of Hospital Medicine, it is a bittersweet but exciting transition.
In the relatively short time I have served as editor, so much has changed in our hospitalist community! In the last 4 years alone, we have increased:
• Membership from 14,000 to 20,000
• Chapters from 46 to 68
• Special Interest Groups from 8 to 22
• Subscribers to The Hospitalist from 15,000 to 30,000.
This is all a testimony to the engagement of our membership. SHM is clearly no ordinary specialty society; it is full of incredibly intelligent, invested, and talented members, who actively participate in the society for the betterment of their local teams and patients. It is such a privilege to lead this amazing team.
As for The Hospitalist, I would like to warmly welcome Weijen Chang, MD, FACP, SFHM, as the incoming editor. Weijen served as the pediatrics editor for many years and has been extensively involved on The Hospitalist’s editorial advisory board for even longer. He also has a broad track record of experience as a hospitalist in many settings; that combined with an inquisitive mind and curious spirit makes him the ideal editor for The Hospitalist. He brings energy and enthusiasm and will serve us very well.
While I will miss being intimately involved with The Hospitalist, I am very much looking forward to serving in the role of SHM president starting in April. During this pivotal year, SHM will transition from our one-and-only CEO, Larry Wellikson, MD, MHM, to our newly minted CEO Eric Howell, MD, MHM, who will officially transition in July 2020.
This is a very exciting time in the history of SHM, as we refocus on our mission, vision, values, and core activities. As a membership organization, our primary focus has been, and will always be, serving our member’s needs! As a “Big Tent” organization, we have always supported a broad and diverse set of members, ranging far beyond physician hospitalists, to trainees, medical students, nurse practitioners, physician assistants, practice administrators, and other hospital-based specialists. Being in such a dynamic industry, our diverse members needs are constantly and rapidly changing along with the dramatic transformations in the landscape, including profound shifts in care and reimbursement models that could change the very definition of a hospitalist.
While we continuously scour the landscape and anticipate our members’ needs, we will never lose sight of our core mission, which is to promote exceptional care for hospitalized patients. We will continue to do this by supporting all of our members with tools and materials to help them be the very best they can, for all of our patients. As a humble and servant leader, I am prepared to meet the demands and challenges of the year ahead, with energy and focus, and fulfill the needs of our members, so that together, we can make health care better for those we serve.
Thank you in advance for allowing me the great pleasure of serving this amazing and innovative organization!
Dr. Scheurer is chief quality officer and professor of medicine at the Medical University of South Carolina, Charleston. She is the outgoing medical editor of The Hospitalist, and president-elect of SHM.
A healthy heart in youth protects the brain later on
, new research suggests. New findings from the Coronary Artery Risk Development in Young Adults (CARDIA) study show that individuals who had better cardiovascular health in their 20s scored higher on tests of thinking and memory 30 years later than their peers who had poorer cardiovascular health as young adults.
“We have learned that midlife vascular risk factors, rather than risk factors in older age, are particularly associated with cognition in older age,” study author Farzaneh Sorond, MD, PhD, Northwestern University Feinberg School of Medicine, Chicago, Illinois, told Medscape Medical News
“Our findings from the CARDIA study expand this knowledge and show that vascular health during young adulthood, rather than midlife, is also specifically associated with brain vascular health and cognitive function” in later life, Dr. Sorond said.
“These results indicate that people need to pay close attention to their health even in their early 20s,” she added in a statement.
The findings were released February 26 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Early prevention key
The analysis examined data from 189 participants (45% women, 45% black) in the CARDIA study who were followed for 30 years. The mean age at baseline was 24 years.
Vascular risk factors were assessed eight times during the 30-year study period. A cardiovascular health score (range, 0 – 10) was calculated on the basis of smoking status, body mass index, blood pressure, total cholesterol level, and fasting glucose level.
At the final assessment, which was conducted 30 years after baseline, dynamic cerebral autoregulation was calculated as the transfer function phase of the spontaneous oscillations in blood pressure and flow velocity in the middle cerebral artery using transcranial Doppler ultrasound.
Cognition was assessed using a series of standard neuropsychological tests. Multivariate linear regression models were used to assess the association of heart health at each visit with cerebral autoregulation and cognition.
Results showed that the participants with better cardiovascular health at the beginning of the study were more likely to have higher cognitive test scores 30 years later in comparison with those with worse cardiovascular health.
For example, on a test of attention skills in which scores ranged from 7 to 103, each point higher on the cardiovascular health score was associated with a 2.2-point higher score in attention skills. These results held up after adjustment for other factors that could affect cognitive test scores, such as education level.
Better cardiovascular health at baseline and at 7 years was also associated with significantly better dynamic cerebral autoregulation.
“Our findings suggest that the earlier vascular risk factors are modified and addressed, the more likely that they will impact brain health across life span,” Dr. Sorond said.
“Moreover, these findings underscore the importance of primordial prevention and addressing the significant knowledge gap that currently exist in this domain,” she added.
Good for the heart, good for the brain
Commenting on the findings, Rebecca Edelmayer, PhD, director of scientific engagement for the Alzheimer’s Association, said that the longitudinal study adds to the growing body of research showing that “what is good for the heart is also good for the brain.”
“This is still a relatively small study, and larger studies have been published that show similar results,” said Dr. Edelmayer, who was not involved with the research.
She noted that results of the large SPRINT-MIND trial, published last year in JAMA and reported by Medscape Medical News, “provided the strongest evidence to date about reducing risk of mild cognitive impairment through the management of high blood pressure.”
The Alzheimer’s Association has provided seed funding for SPRINT-MIND 2.0, a 2-year extension of the study to evaluate whether intensive blood pressure management reduces risk for all-cause dementia.
Support for the current study was provided by the National Institutes of Health, the National Heart, Lung, and Blood Institute, the University of Alabama at Birmingham, Northwestern University, the University of Minnesota, and the Kaiser Foundation Research Institute. Drs. Sorond and Edelmayer have reported no relevant financial relationships.
This article first appeared on Medscape.com.
, new research suggests. New findings from the Coronary Artery Risk Development in Young Adults (CARDIA) study show that individuals who had better cardiovascular health in their 20s scored higher on tests of thinking and memory 30 years later than their peers who had poorer cardiovascular health as young adults.
“We have learned that midlife vascular risk factors, rather than risk factors in older age, are particularly associated with cognition in older age,” study author Farzaneh Sorond, MD, PhD, Northwestern University Feinberg School of Medicine, Chicago, Illinois, told Medscape Medical News
“Our findings from the CARDIA study expand this knowledge and show that vascular health during young adulthood, rather than midlife, is also specifically associated with brain vascular health and cognitive function” in later life, Dr. Sorond said.
“These results indicate that people need to pay close attention to their health even in their early 20s,” she added in a statement.
The findings were released February 26 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Early prevention key
The analysis examined data from 189 participants (45% women, 45% black) in the CARDIA study who were followed for 30 years. The mean age at baseline was 24 years.
Vascular risk factors were assessed eight times during the 30-year study period. A cardiovascular health score (range, 0 – 10) was calculated on the basis of smoking status, body mass index, blood pressure, total cholesterol level, and fasting glucose level.
At the final assessment, which was conducted 30 years after baseline, dynamic cerebral autoregulation was calculated as the transfer function phase of the spontaneous oscillations in blood pressure and flow velocity in the middle cerebral artery using transcranial Doppler ultrasound.
Cognition was assessed using a series of standard neuropsychological tests. Multivariate linear regression models were used to assess the association of heart health at each visit with cerebral autoregulation and cognition.
Results showed that the participants with better cardiovascular health at the beginning of the study were more likely to have higher cognitive test scores 30 years later in comparison with those with worse cardiovascular health.
For example, on a test of attention skills in which scores ranged from 7 to 103, each point higher on the cardiovascular health score was associated with a 2.2-point higher score in attention skills. These results held up after adjustment for other factors that could affect cognitive test scores, such as education level.
Better cardiovascular health at baseline and at 7 years was also associated with significantly better dynamic cerebral autoregulation.
“Our findings suggest that the earlier vascular risk factors are modified and addressed, the more likely that they will impact brain health across life span,” Dr. Sorond said.
“Moreover, these findings underscore the importance of primordial prevention and addressing the significant knowledge gap that currently exist in this domain,” she added.
Good for the heart, good for the brain
Commenting on the findings, Rebecca Edelmayer, PhD, director of scientific engagement for the Alzheimer’s Association, said that the longitudinal study adds to the growing body of research showing that “what is good for the heart is also good for the brain.”
“This is still a relatively small study, and larger studies have been published that show similar results,” said Dr. Edelmayer, who was not involved with the research.
She noted that results of the large SPRINT-MIND trial, published last year in JAMA and reported by Medscape Medical News, “provided the strongest evidence to date about reducing risk of mild cognitive impairment through the management of high blood pressure.”
The Alzheimer’s Association has provided seed funding for SPRINT-MIND 2.0, a 2-year extension of the study to evaluate whether intensive blood pressure management reduces risk for all-cause dementia.
Support for the current study was provided by the National Institutes of Health, the National Heart, Lung, and Blood Institute, the University of Alabama at Birmingham, Northwestern University, the University of Minnesota, and the Kaiser Foundation Research Institute. Drs. Sorond and Edelmayer have reported no relevant financial relationships.
This article first appeared on Medscape.com.
, new research suggests. New findings from the Coronary Artery Risk Development in Young Adults (CARDIA) study show that individuals who had better cardiovascular health in their 20s scored higher on tests of thinking and memory 30 years later than their peers who had poorer cardiovascular health as young adults.
“We have learned that midlife vascular risk factors, rather than risk factors in older age, are particularly associated with cognition in older age,” study author Farzaneh Sorond, MD, PhD, Northwestern University Feinberg School of Medicine, Chicago, Illinois, told Medscape Medical News
“Our findings from the CARDIA study expand this knowledge and show that vascular health during young adulthood, rather than midlife, is also specifically associated with brain vascular health and cognitive function” in later life, Dr. Sorond said.
“These results indicate that people need to pay close attention to their health even in their early 20s,” she added in a statement.
The findings were released February 26 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Early prevention key
The analysis examined data from 189 participants (45% women, 45% black) in the CARDIA study who were followed for 30 years. The mean age at baseline was 24 years.
Vascular risk factors were assessed eight times during the 30-year study period. A cardiovascular health score (range, 0 – 10) was calculated on the basis of smoking status, body mass index, blood pressure, total cholesterol level, and fasting glucose level.
At the final assessment, which was conducted 30 years after baseline, dynamic cerebral autoregulation was calculated as the transfer function phase of the spontaneous oscillations in blood pressure and flow velocity in the middle cerebral artery using transcranial Doppler ultrasound.
Cognition was assessed using a series of standard neuropsychological tests. Multivariate linear regression models were used to assess the association of heart health at each visit with cerebral autoregulation and cognition.
Results showed that the participants with better cardiovascular health at the beginning of the study were more likely to have higher cognitive test scores 30 years later in comparison with those with worse cardiovascular health.
For example, on a test of attention skills in which scores ranged from 7 to 103, each point higher on the cardiovascular health score was associated with a 2.2-point higher score in attention skills. These results held up after adjustment for other factors that could affect cognitive test scores, such as education level.
Better cardiovascular health at baseline and at 7 years was also associated with significantly better dynamic cerebral autoregulation.
“Our findings suggest that the earlier vascular risk factors are modified and addressed, the more likely that they will impact brain health across life span,” Dr. Sorond said.
“Moreover, these findings underscore the importance of primordial prevention and addressing the significant knowledge gap that currently exist in this domain,” she added.
Good for the heart, good for the brain
Commenting on the findings, Rebecca Edelmayer, PhD, director of scientific engagement for the Alzheimer’s Association, said that the longitudinal study adds to the growing body of research showing that “what is good for the heart is also good for the brain.”
“This is still a relatively small study, and larger studies have been published that show similar results,” said Dr. Edelmayer, who was not involved with the research.
She noted that results of the large SPRINT-MIND trial, published last year in JAMA and reported by Medscape Medical News, “provided the strongest evidence to date about reducing risk of mild cognitive impairment through the management of high blood pressure.”
The Alzheimer’s Association has provided seed funding for SPRINT-MIND 2.0, a 2-year extension of the study to evaluate whether intensive blood pressure management reduces risk for all-cause dementia.
Support for the current study was provided by the National Institutes of Health, the National Heart, Lung, and Blood Institute, the University of Alabama at Birmingham, Northwestern University, the University of Minnesota, and the Kaiser Foundation Research Institute. Drs. Sorond and Edelmayer have reported no relevant financial relationships.
This article first appeared on Medscape.com.
COVID-19 strikes hard at state-run veterans nursing homes
In early March, 35 residents in the Life Care Center in Kirkland, Washington, died due to complications associated with COVID-19. And that facility thus became the first example of how extremely vulnerable nursing home residents are to COVID-19. Since then, around the US, thousands of nursing home residents have died from complications of the virus. US Department of Veterans Affairs (VA) nursing homes, while rated high in VA health inspection reports, have not been exempt.
As of April 21, the VA had confirmed > 5,500 coronavirus cases in 50 states, the District of Columbia, and Puerto Rico. More than 350 veterans have died of COVID-19, according to VA data. The VA calculates its rates by health care system or VA medical center and does not provide separate data for the community living centers (CLCs).
The VA initiated an isolation strategy on March 10 that suspended most new admissions and barred outsiders from all of its 134 nursing homes. The only exception to the rule was when a patient was expected to die soon. The VA has taken other precautions as well, including extra screening and directing patients to use telehealth where possible.
State-run long-term care facilities for veterans have been hard hit across the country. At the Soldiers’ Home in Holyoke, Massachusetts, which is run by the state of Massachusetts, 5 of 11 veterans who died recently tested positive for COVID-19. At the 4 state-run nursing homes in Alabama, as of April 14, 45 people were confirmed positive and 2 residents had died. The largest outbreak was in the Bill Nichols State Veterans Home in Alexander City. Alabama State Rep. Ed Oliver and Commissioner Kent Davis, of the Alabama Department of Veterans Affairs (ADVA), are looking into how the outbreak started and whether it could have been prevented. “We have reports of lack of hand sanitizers, and those are the things we’re looking at right now,” Rep. Oliver said. The ADVA says residents who test positive are isolated for treatment, and infected employees are prohibited from entering the homes.
States have deployed National Guard troops to facilities following large scale outbreaks and multiple deaths. Pennsylvania deployed 30 National Guard troops to its Southeastern Veterans Center facility in Spring City after at least 10 veterans had died and at least 19 health care workers had tested positive for the virus. The facility is 1 of 6 extended-care facilities run by the Pennsylvania Department of Military and Veterans Affairs. In New Jersey, 40 National Guard troops, 25 New Jersey Department of Health nurses, and 90 VA nurses were deployed to 2 of its veterans facilities amid worsening outbreaks. At the Paramus facility, 155 residents had tested positive and 39 had died, and at the home in Edison, 86 veterans had tested positive and 25 died; 6 more died at a third state facility.
However, reporting remains inconsistent across many states and facilities. Only on April 19 did the Centers for Medicare and Medicaid Services (CMS) order nursing home facilities to inform residents and families about COVID-19 cases inside. This followed similar orders in New Jersey, New York, California, Washington, and other states.
“Nursing homes have been ground zero for COVID-19,” said CMS Administrator Seema Verma in a written statement. “Nursing home reporting to the [Centers for Disease Control and Prevention] is a critical component of the go-forward national COVID-19 surveillance system and to efforts to reopen America.”
In early March, 35 residents in the Life Care Center in Kirkland, Washington, died due to complications associated with COVID-19. And that facility thus became the first example of how extremely vulnerable nursing home residents are to COVID-19. Since then, around the US, thousands of nursing home residents have died from complications of the virus. US Department of Veterans Affairs (VA) nursing homes, while rated high in VA health inspection reports, have not been exempt.
As of April 21, the VA had confirmed > 5,500 coronavirus cases in 50 states, the District of Columbia, and Puerto Rico. More than 350 veterans have died of COVID-19, according to VA data. The VA calculates its rates by health care system or VA medical center and does not provide separate data for the community living centers (CLCs).
The VA initiated an isolation strategy on March 10 that suspended most new admissions and barred outsiders from all of its 134 nursing homes. The only exception to the rule was when a patient was expected to die soon. The VA has taken other precautions as well, including extra screening and directing patients to use telehealth where possible.
State-run long-term care facilities for veterans have been hard hit across the country. At the Soldiers’ Home in Holyoke, Massachusetts, which is run by the state of Massachusetts, 5 of 11 veterans who died recently tested positive for COVID-19. At the 4 state-run nursing homes in Alabama, as of April 14, 45 people were confirmed positive and 2 residents had died. The largest outbreak was in the Bill Nichols State Veterans Home in Alexander City. Alabama State Rep. Ed Oliver and Commissioner Kent Davis, of the Alabama Department of Veterans Affairs (ADVA), are looking into how the outbreak started and whether it could have been prevented. “We have reports of lack of hand sanitizers, and those are the things we’re looking at right now,” Rep. Oliver said. The ADVA says residents who test positive are isolated for treatment, and infected employees are prohibited from entering the homes.
States have deployed National Guard troops to facilities following large scale outbreaks and multiple deaths. Pennsylvania deployed 30 National Guard troops to its Southeastern Veterans Center facility in Spring City after at least 10 veterans had died and at least 19 health care workers had tested positive for the virus. The facility is 1 of 6 extended-care facilities run by the Pennsylvania Department of Military and Veterans Affairs. In New Jersey, 40 National Guard troops, 25 New Jersey Department of Health nurses, and 90 VA nurses were deployed to 2 of its veterans facilities amid worsening outbreaks. At the Paramus facility, 155 residents had tested positive and 39 had died, and at the home in Edison, 86 veterans had tested positive and 25 died; 6 more died at a third state facility.
However, reporting remains inconsistent across many states and facilities. Only on April 19 did the Centers for Medicare and Medicaid Services (CMS) order nursing home facilities to inform residents and families about COVID-19 cases inside. This followed similar orders in New Jersey, New York, California, Washington, and other states.
“Nursing homes have been ground zero for COVID-19,” said CMS Administrator Seema Verma in a written statement. “Nursing home reporting to the [Centers for Disease Control and Prevention] is a critical component of the go-forward national COVID-19 surveillance system and to efforts to reopen America.”
In early March, 35 residents in the Life Care Center in Kirkland, Washington, died due to complications associated with COVID-19. And that facility thus became the first example of how extremely vulnerable nursing home residents are to COVID-19. Since then, around the US, thousands of nursing home residents have died from complications of the virus. US Department of Veterans Affairs (VA) nursing homes, while rated high in VA health inspection reports, have not been exempt.
As of April 21, the VA had confirmed > 5,500 coronavirus cases in 50 states, the District of Columbia, and Puerto Rico. More than 350 veterans have died of COVID-19, according to VA data. The VA calculates its rates by health care system or VA medical center and does not provide separate data for the community living centers (CLCs).
The VA initiated an isolation strategy on March 10 that suspended most new admissions and barred outsiders from all of its 134 nursing homes. The only exception to the rule was when a patient was expected to die soon. The VA has taken other precautions as well, including extra screening and directing patients to use telehealth where possible.
State-run long-term care facilities for veterans have been hard hit across the country. At the Soldiers’ Home in Holyoke, Massachusetts, which is run by the state of Massachusetts, 5 of 11 veterans who died recently tested positive for COVID-19. At the 4 state-run nursing homes in Alabama, as of April 14, 45 people were confirmed positive and 2 residents had died. The largest outbreak was in the Bill Nichols State Veterans Home in Alexander City. Alabama State Rep. Ed Oliver and Commissioner Kent Davis, of the Alabama Department of Veterans Affairs (ADVA), are looking into how the outbreak started and whether it could have been prevented. “We have reports of lack of hand sanitizers, and those are the things we’re looking at right now,” Rep. Oliver said. The ADVA says residents who test positive are isolated for treatment, and infected employees are prohibited from entering the homes.
States have deployed National Guard troops to facilities following large scale outbreaks and multiple deaths. Pennsylvania deployed 30 National Guard troops to its Southeastern Veterans Center facility in Spring City after at least 10 veterans had died and at least 19 health care workers had tested positive for the virus. The facility is 1 of 6 extended-care facilities run by the Pennsylvania Department of Military and Veterans Affairs. In New Jersey, 40 National Guard troops, 25 New Jersey Department of Health nurses, and 90 VA nurses were deployed to 2 of its veterans facilities amid worsening outbreaks. At the Paramus facility, 155 residents had tested positive and 39 had died, and at the home in Edison, 86 veterans had tested positive and 25 died; 6 more died at a third state facility.
However, reporting remains inconsistent across many states and facilities. Only on April 19 did the Centers for Medicare and Medicaid Services (CMS) order nursing home facilities to inform residents and families about COVID-19 cases inside. This followed similar orders in New Jersey, New York, California, Washington, and other states.
“Nursing homes have been ground zero for COVID-19,” said CMS Administrator Seema Verma in a written statement. “Nursing home reporting to the [Centers for Disease Control and Prevention] is a critical component of the go-forward national COVID-19 surveillance system and to efforts to reopen America.”
Mislabeled clopidogrel lot recalled, may contain simvastatin
International Laboratories has initiated a voluntary recall to the consumer level in the United States of a single lot of the antiplatelet clopidogrel because it is mislabeled and may contain simvastatin, a cholesterol-lowering drug, instead of clopidogrel.
The recalled product ― lot number 117099A of clopidogrel tablets (USP 75 mg) packaged in bottles of 30 tablets ― may contain clopidogrel 75 mg tablets or it could contain simvastatin tablets (USP 10 mg), according to a company announcement posted on the US Food and Drug Administration (FDA) website.
“Missed doses of clopidogrel increases the risk of heart attack and stroke which can be life threatening. Additionally, unintentional consumption of simvastatin could include the common side effects associated with its use and may cause fetal harm when administered to a pregnant woman,” the company cautions.
To date, the company has not received any reports of harm arising from the problem that prompted the recall.
The recalled product was distributed nationwide and was delivered to distribution centers in Arkansas, Georgia, Indiana, California, and Maryland and to retail stores in all US states.
International Laboratories is notifying distributors and customers by letter and is arranging for the return of all recalled products.
For questions regarding this recall, contact Inmar by phone 855-258-7280 (weekdays between 9:00 AM and 5:00 PM EST) or by email at internationallabs@inmar.com.
Adverse reactions or quality problems experienced with the use of this product should be reported to the FDA’s MedWatch adverse event reporting program.
This article first appeared on Medscape.com.
International Laboratories has initiated a voluntary recall to the consumer level in the United States of a single lot of the antiplatelet clopidogrel because it is mislabeled and may contain simvastatin, a cholesterol-lowering drug, instead of clopidogrel.
The recalled product ― lot number 117099A of clopidogrel tablets (USP 75 mg) packaged in bottles of 30 tablets ― may contain clopidogrel 75 mg tablets or it could contain simvastatin tablets (USP 10 mg), according to a company announcement posted on the US Food and Drug Administration (FDA) website.
“Missed doses of clopidogrel increases the risk of heart attack and stroke which can be life threatening. Additionally, unintentional consumption of simvastatin could include the common side effects associated with its use and may cause fetal harm when administered to a pregnant woman,” the company cautions.
To date, the company has not received any reports of harm arising from the problem that prompted the recall.
The recalled product was distributed nationwide and was delivered to distribution centers in Arkansas, Georgia, Indiana, California, and Maryland and to retail stores in all US states.
International Laboratories is notifying distributors and customers by letter and is arranging for the return of all recalled products.
For questions regarding this recall, contact Inmar by phone 855-258-7280 (weekdays between 9:00 AM and 5:00 PM EST) or by email at internationallabs@inmar.com.
Adverse reactions or quality problems experienced with the use of this product should be reported to the FDA’s MedWatch adverse event reporting program.
This article first appeared on Medscape.com.
International Laboratories has initiated a voluntary recall to the consumer level in the United States of a single lot of the antiplatelet clopidogrel because it is mislabeled and may contain simvastatin, a cholesterol-lowering drug, instead of clopidogrel.
The recalled product ― lot number 117099A of clopidogrel tablets (USP 75 mg) packaged in bottles of 30 tablets ― may contain clopidogrel 75 mg tablets or it could contain simvastatin tablets (USP 10 mg), according to a company announcement posted on the US Food and Drug Administration (FDA) website.
“Missed doses of clopidogrel increases the risk of heart attack and stroke which can be life threatening. Additionally, unintentional consumption of simvastatin could include the common side effects associated with its use and may cause fetal harm when administered to a pregnant woman,” the company cautions.
To date, the company has not received any reports of harm arising from the problem that prompted the recall.
The recalled product was distributed nationwide and was delivered to distribution centers in Arkansas, Georgia, Indiana, California, and Maryland and to retail stores in all US states.
International Laboratories is notifying distributors and customers by letter and is arranging for the return of all recalled products.
For questions regarding this recall, contact Inmar by phone 855-258-7280 (weekdays between 9:00 AM and 5:00 PM EST) or by email at internationallabs@inmar.com.
Adverse reactions or quality problems experienced with the use of this product should be reported to the FDA’s MedWatch adverse event reporting program.
This article first appeared on Medscape.com.
New gene variants linked to tau deposits in Alzheimer’s disease
Investigator Vijay Ramanan, MD, PhD, behavioral neurology fellow, Mayo Clinic, Rochester, Minnesota, noted that this is the first genome-wide study of tau positron-emission tomography (PET) and that it identifies variations in DNA profiles associated with tau load in the brain.
“These early results represent an important step to better understanding why some individuals have a greater susceptibility to tau accumulation while others are more resistant,” Dr. Ramanan told Medscape Medical News.
“As we learn more about that process, the longer-term hope would be to use that information to better predict who may become symptomatic from the disease and to develop targets for treatment based on those individualized profiles,” he added.
The findings were released March 9 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Genome-wide associations
The researchers assessed genetic profile and regional tau-PET data for 754 participants (mean age, 72.4 years; 54.6% men; 87% cognitively unimpaired) in the Mayo Clinic Study of Aging.
They found that individuals with novel genetic variants on chromosomes 1 and 5 had a higher amount of tau in their brains, compared with their counterparts who had more typical gene sequences in those regions.
The genetic variants were found in 2% to 3% of the group, and those individuals had about 10% higher tau levels than patients who did not have the variants.
Specifically, investigators identified genome-wide significant associations with higher tau for rs76752255 in protein phosphatase 2 regulatory subunit B (PPP2R2B), an enzyme of the PPP2R2B gene on chromosome 5, and for rs115862481 in an intergenic region on chromosome 1. Each minor allele had a stronger association in amyloid-positive than in amyloid-negative individuals.
In addition, three single-nucleotide polymorphisms (SNPs) within microtubule-associated protein tau (MAPT) genes displayed nominal associations to tau burden. These included rs3785883, which previously was found to be associated with higher levels of cerebrospinal fluid tau in an independent cohort.
However, no associations with tau burden were identified for the SNPs defining apolipoprotein E (APOE) e4 or for genotyped SNPs previously associated with Alzheimer’s disease in large case-control studies.
“The fact that these variants are new, coupled with the lack of strong signal for tau in APOE, reinforces the concept that Alzheimer’s disease is complex and that across patients, different sets of genes may be involved in entering into the Alzheimer’s disease pathway versus modifying its course or symptomatic expression,” Dr. Ramanan said.
“Lots of exciting work is ongoing to try to disentangle those issues, and this study is a valuable step on that path,” he added.
Dr. Ramanan said there is a great need for a better understanding of the factors that influence tau deposition, particularly since the burden and location of tau buildup in the brain are closely related to cognitive symptoms of Alzheimer’s disease.
He noted that the approach of “imaging genetics”—using brain scans that capture disease biomarkers and connecting those with data on the genome to improve knowledge about risk and treatment targeting—has been growing. However, only recently has it become possible to apply that framework to tau.
Dr, Ramanan emphasized that replication studies and functional characterization of these novel genetic findings are needed.
“Distant” clinical implications
Commenting on the study, Howard Fillit, MD, founding executive director and chief science officer of the Alzheimer’s Drug Discovery Foundation, said that there is currently “a fair amount of this kind of work going on” in assessing polygenetic risk in Alzheimer’s disease. This includes examining APOE as well as “a whole bunch of other genes” associated with the disease.
“Far and away, the APOE genetic association with Alzheimer’s disease risk is the most powerful one. In and of themselves, none of these other risk genes cause Alzheimer’s disease, they only contribute to risk,” Dr. Fillit noted.
“This study found some new genes that were associated with susceptibility to tau deposition, but at the end of the day, they are just associations. They don’t prove causality,” he added.
“It’s interesting, but really hard to know what to conclude from it; and the clinical implications, I think, are rather distant,” Dr. Fillit concluded.
The study was supported by the National Institutes of Health; the Gerald and Henrietta Rauenhorst Foundation; the Alexander Family Alzheimer’s Disease Research Professorship of Mayo Clinic; the Mayo Foundation for Medical Education and Research; a Liston Award; the Elsie and Marvin Dekelboum Family Foundation; the Schuler Foundation; and Avid Radiopharmaceuticals, which supplied the imaging agent used by researchers to detect tau in the brain. Ramanan and Fillit have reported no relevant financial relationships.
This article first appeared on Medscape.com.
Investigator Vijay Ramanan, MD, PhD, behavioral neurology fellow, Mayo Clinic, Rochester, Minnesota, noted that this is the first genome-wide study of tau positron-emission tomography (PET) and that it identifies variations in DNA profiles associated with tau load in the brain.
“These early results represent an important step to better understanding why some individuals have a greater susceptibility to tau accumulation while others are more resistant,” Dr. Ramanan told Medscape Medical News.
“As we learn more about that process, the longer-term hope would be to use that information to better predict who may become symptomatic from the disease and to develop targets for treatment based on those individualized profiles,” he added.
The findings were released March 9 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Genome-wide associations
The researchers assessed genetic profile and regional tau-PET data for 754 participants (mean age, 72.4 years; 54.6% men; 87% cognitively unimpaired) in the Mayo Clinic Study of Aging.
They found that individuals with novel genetic variants on chromosomes 1 and 5 had a higher amount of tau in their brains, compared with their counterparts who had more typical gene sequences in those regions.
The genetic variants were found in 2% to 3% of the group, and those individuals had about 10% higher tau levels than patients who did not have the variants.
Specifically, investigators identified genome-wide significant associations with higher tau for rs76752255 in protein phosphatase 2 regulatory subunit B (PPP2R2B), an enzyme of the PPP2R2B gene on chromosome 5, and for rs115862481 in an intergenic region on chromosome 1. Each minor allele had a stronger association in amyloid-positive than in amyloid-negative individuals.
In addition, three single-nucleotide polymorphisms (SNPs) within microtubule-associated protein tau (MAPT) genes displayed nominal associations to tau burden. These included rs3785883, which previously was found to be associated with higher levels of cerebrospinal fluid tau in an independent cohort.
However, no associations with tau burden were identified for the SNPs defining apolipoprotein E (APOE) e4 or for genotyped SNPs previously associated with Alzheimer’s disease in large case-control studies.
“The fact that these variants are new, coupled with the lack of strong signal for tau in APOE, reinforces the concept that Alzheimer’s disease is complex and that across patients, different sets of genes may be involved in entering into the Alzheimer’s disease pathway versus modifying its course or symptomatic expression,” Dr. Ramanan said.
“Lots of exciting work is ongoing to try to disentangle those issues, and this study is a valuable step on that path,” he added.
Dr. Ramanan said there is a great need for a better understanding of the factors that influence tau deposition, particularly since the burden and location of tau buildup in the brain are closely related to cognitive symptoms of Alzheimer’s disease.
He noted that the approach of “imaging genetics”—using brain scans that capture disease biomarkers and connecting those with data on the genome to improve knowledge about risk and treatment targeting—has been growing. However, only recently has it become possible to apply that framework to tau.
Dr, Ramanan emphasized that replication studies and functional characterization of these novel genetic findings are needed.
“Distant” clinical implications
Commenting on the study, Howard Fillit, MD, founding executive director and chief science officer of the Alzheimer’s Drug Discovery Foundation, said that there is currently “a fair amount of this kind of work going on” in assessing polygenetic risk in Alzheimer’s disease. This includes examining APOE as well as “a whole bunch of other genes” associated with the disease.
“Far and away, the APOE genetic association with Alzheimer’s disease risk is the most powerful one. In and of themselves, none of these other risk genes cause Alzheimer’s disease, they only contribute to risk,” Dr. Fillit noted.
“This study found some new genes that were associated with susceptibility to tau deposition, but at the end of the day, they are just associations. They don’t prove causality,” he added.
“It’s interesting, but really hard to know what to conclude from it; and the clinical implications, I think, are rather distant,” Dr. Fillit concluded.
The study was supported by the National Institutes of Health; the Gerald and Henrietta Rauenhorst Foundation; the Alexander Family Alzheimer’s Disease Research Professorship of Mayo Clinic; the Mayo Foundation for Medical Education and Research; a Liston Award; the Elsie and Marvin Dekelboum Family Foundation; the Schuler Foundation; and Avid Radiopharmaceuticals, which supplied the imaging agent used by researchers to detect tau in the brain. Ramanan and Fillit have reported no relevant financial relationships.
This article first appeared on Medscape.com.
Investigator Vijay Ramanan, MD, PhD, behavioral neurology fellow, Mayo Clinic, Rochester, Minnesota, noted that this is the first genome-wide study of tau positron-emission tomography (PET) and that it identifies variations in DNA profiles associated with tau load in the brain.
“These early results represent an important step to better understanding why some individuals have a greater susceptibility to tau accumulation while others are more resistant,” Dr. Ramanan told Medscape Medical News.
“As we learn more about that process, the longer-term hope would be to use that information to better predict who may become symptomatic from the disease and to develop targets for treatment based on those individualized profiles,” he added.
The findings were released March 9 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
Genome-wide associations
The researchers assessed genetic profile and regional tau-PET data for 754 participants (mean age, 72.4 years; 54.6% men; 87% cognitively unimpaired) in the Mayo Clinic Study of Aging.
They found that individuals with novel genetic variants on chromosomes 1 and 5 had a higher amount of tau in their brains, compared with their counterparts who had more typical gene sequences in those regions.
The genetic variants were found in 2% to 3% of the group, and those individuals had about 10% higher tau levels than patients who did not have the variants.
Specifically, investigators identified genome-wide significant associations with higher tau for rs76752255 in protein phosphatase 2 regulatory subunit B (PPP2R2B), an enzyme of the PPP2R2B gene on chromosome 5, and for rs115862481 in an intergenic region on chromosome 1. Each minor allele had a stronger association in amyloid-positive than in amyloid-negative individuals.
In addition, three single-nucleotide polymorphisms (SNPs) within microtubule-associated protein tau (MAPT) genes displayed nominal associations to tau burden. These included rs3785883, which previously was found to be associated with higher levels of cerebrospinal fluid tau in an independent cohort.
However, no associations with tau burden were identified for the SNPs defining apolipoprotein E (APOE) e4 or for genotyped SNPs previously associated with Alzheimer’s disease in large case-control studies.
“The fact that these variants are new, coupled with the lack of strong signal for tau in APOE, reinforces the concept that Alzheimer’s disease is complex and that across patients, different sets of genes may be involved in entering into the Alzheimer’s disease pathway versus modifying its course or symptomatic expression,” Dr. Ramanan said.
“Lots of exciting work is ongoing to try to disentangle those issues, and this study is a valuable step on that path,” he added.
Dr. Ramanan said there is a great need for a better understanding of the factors that influence tau deposition, particularly since the burden and location of tau buildup in the brain are closely related to cognitive symptoms of Alzheimer’s disease.
He noted that the approach of “imaging genetics”—using brain scans that capture disease biomarkers and connecting those with data on the genome to improve knowledge about risk and treatment targeting—has been growing. However, only recently has it become possible to apply that framework to tau.
Dr, Ramanan emphasized that replication studies and functional characterization of these novel genetic findings are needed.
“Distant” clinical implications
Commenting on the study, Howard Fillit, MD, founding executive director and chief science officer of the Alzheimer’s Drug Discovery Foundation, said that there is currently “a fair amount of this kind of work going on” in assessing polygenetic risk in Alzheimer’s disease. This includes examining APOE as well as “a whole bunch of other genes” associated with the disease.
“Far and away, the APOE genetic association with Alzheimer’s disease risk is the most powerful one. In and of themselves, none of these other risk genes cause Alzheimer’s disease, they only contribute to risk,” Dr. Fillit noted.
“This study found some new genes that were associated with susceptibility to tau deposition, but at the end of the day, they are just associations. They don’t prove causality,” he added.
“It’s interesting, but really hard to know what to conclude from it; and the clinical implications, I think, are rather distant,” Dr. Fillit concluded.
The study was supported by the National Institutes of Health; the Gerald and Henrietta Rauenhorst Foundation; the Alexander Family Alzheimer’s Disease Research Professorship of Mayo Clinic; the Mayo Foundation for Medical Education and Research; a Liston Award; the Elsie and Marvin Dekelboum Family Foundation; the Schuler Foundation; and Avid Radiopharmaceuticals, which supplied the imaging agent used by researchers to detect tau in the brain. Ramanan and Fillit have reported no relevant financial relationships.
This article first appeared on Medscape.com.
Do I Have Coronavirus?
“To journey for the sake of saving our own lives is little by little to cease to live in any sense that really matters, even to ourselves, because it is only by journeying for the world’s sake—even when the world bores and sickens and scares you half to death—that little by little we start to come alive.”
—Frederick Buechner
On February 29, 2020, I find out by text from my intern when the first patient at our hospital in Seattle tests positive for COVID-19. He learns of it from his fellow intern who is caring for the patient. The news quickly spreads through the hospital like the virus itself, going from person to person while official communication channels remain initially silent. The news comes on the heels of a friend’s text that her daughter’s high school is closing for disinfection after a classmate also tested positive for COVID-19. I know the cataclysmic significance of these two events: Public health efforts to contain the SARS-CoV-2 coronavirus have failed, and there is ongoing community spread of the infection in Washington state. I text my intern back with the emoji of The Scream by Edvard Munch.
Could I be asymptomatically infected with the coronavirus? I work in close quarters with my colleagues who cared for the COVID-19–positive patient before he was placed in infection precautions. Social distancing has yet to enter our lexicon and our lives. In our crowded office, shared surfaces abound. Suddenly, every hard surface seems suspect—chairs, phones, dictaphone handsets, code pagers, printers, keypads, and door handles. All can be vectors of viral transmission. Normally insouciant about cleanliness, my coworkers and I start swabbing down every surface with disinfectant wipes. I ponder my likelihood of infection and decide it is possible but not probable.
In the next few days, I have a trip to Sedona, Arizona, planned with my extended family. Originally conceived as a celebration for my mom’s 80th birthday, we repurposed it as a time to grieve together after she unexpectedly passed away. I debate back and forth whether to go on the trip. If there is a chance I am infected with the coronavirus, it feels irresponsible to board an airplane with hundreds of other people. Yet the trip carries such high value for me. My family holds out hope I can get tested for the coronavirus, but I know just how limited testing capability is. It cuts me to the heart, but I cancel my flight. The deciding factor is that my sister has an autoimmune disease and is immunosuppressed. I don’t want to jeopardize her health. The world has truly gone topsy-turvy when the greatest thoughtfulness you can show to someone you love is to stay the hell away from her.
AM I A HYPOCHONDRIAC?
After my work stretch, I hunker down at home to monitor myself. I have a mild sore throat but convince myself it is psychosomatic. My plausible deniability of illness dies when I develop a cough and fatigue. Based on my symptoms, it is impossible to tell if I have the coronavirus or a common cold. I place myself on home quarantine. I don’t pursue coronavirus testing because there are hospitalized patients who need it much more than I do. I diligently monitor my temperature twice daily and it remains normal. My sore throat and fatigue go away, but my cough and some mild shortness of breath persists. I attribute it to my asthma, but the possibility of COVID-19 always lurks in the back of my mind. COVID-19 patients often don’t worsen until their second week of infection. Ordinarily, I would start using my steroid inhaler, but I hold off since steroids are thought to prolong viral replication.
When I tire of staying in the house, I go outside to work in the yard. I get on a low ladder to pull down the English ivy climbing up and smothering a tree. The ivy strand I’m tugging on suddenly breaks and I fall hard onto my back. Like a slap in the face, the accident shocks me into a new state of mental clarity. As a hospitalist, I’m a precious resource to my community right now. I can’t knock myself out of commission for dumb reasons. I ban myself from climbing any more ladders.
WHY CAN’T I GET TESTED?
As my time in quarantine draws to a close, I put my legal and financial affairs in order and pack a just-in-case backpack. The emergency room doctor hospitalized at a nearby hospital with severe COVID-19 is about my age. I am still coughing so I check in with the head of Infection Control to see if I need to be tested before returning to work. He tells me no. As I start working, I realize that coughing is the new leprosy. Even though I wear a mask, I get tense looks from others who carefully keep their distance from me. I tell everyone I have cough variant asthma, but what they all want to know is if I have been tested for the coronavirus. I haven’t been.
When my hospital sets up a new dedicated Employee Health screening phone line, I call right away. The nurse tells me I don’t meet criteria for coronavirus testing even though I am working on the COVID-19 rule-out unit with patients who have tested positive. While I agree with her from a medical standpoint, I don’t from a social or psychological perspective. This is a particularly unpropitious time in history to be a Chinese American doctor who can’t stop coughing. A negative test will reassure my patients and coworkers I am not a risk to them. A positive test, which is a possibility because of known prolonged viral shedding of the coronavirus, will reassure me I’m likely on my way to developing serologic immunity. I don’t get a test. When I tell my colleague, he suggests I resort to lying, but I won’t do it. As I’ve watched how power, wealth, and privilege play out in access to testing, I refuse to manipulate the system. But my experience is pointed commentary on the abysmal failure of testing in the United States when a frontline symptomatic doctor taking care of COVID-19 patients in one of the epicenters of the pandemic can’t get a coronavirus test. During a meeting, the head of Infection Control bluntly states he hopes we know that all of us are going to get the coronavirus at some point, but hopefully it won’t take us out of commission all at once. I feel better hearing him acknowledge that because it confirms my own sense of reality.
ARE WE RUNNING OUT OF PERSONAL PROTECTIVE EQUIPMENT?
While the ongoing pandemic definitely increases stress and anxiety levels in the hospital, there also continues to be caring and kindness. As I don my personal protective equipment (PPE), a nurse notices an exposed gap in the back of my gown and fixes it for me. He has my back, literally and figuratively. Our unit clerk, hearing my persistent cough, braves the 6-foot danger zone to hand me cough drops. Another nurse asks when the last time was I drank anything, and I give her a blank look because I can’t remember. I’m trying to minimize my use of masks, so I have kept my current one on all day. The front of the mask may be contaminated, but as long as I don’t touch that surface, it is still protecting me. She hands me a cup of water and I consider the benefit of staying hydrated versus using up another mask. Having previously landed in the emergency room with a kidney stone from not properly hydrating, I take off the mask, throw it away, wash my hands, and drink the water. But in my mind, I’m acutely aware of our shrinking supply of PPE.
On our time off work, my coworkers and I reach out to everyone we know to ask for mask donations. One friend tells me her husband is fashioning a mask for her from their furnace filter. She considers it the most romantic thing he’s ever done for her. The two of us agree that if we run out of PPE, we will go on caring for our patients anyway. We are doctors and caring for others is not only what we do, but an intrinsic part of who we are. Our journey amid the coronavirus pandemic may at times scare us half to death, but in caring for others “little by little we start to come alive.”
“To journey for the sake of saving our own lives is little by little to cease to live in any sense that really matters, even to ourselves, because it is only by journeying for the world’s sake—even when the world bores and sickens and scares you half to death—that little by little we start to come alive.”
—Frederick Buechner
On February 29, 2020, I find out by text from my intern when the first patient at our hospital in Seattle tests positive for COVID-19. He learns of it from his fellow intern who is caring for the patient. The news quickly spreads through the hospital like the virus itself, going from person to person while official communication channels remain initially silent. The news comes on the heels of a friend’s text that her daughter’s high school is closing for disinfection after a classmate also tested positive for COVID-19. I know the cataclysmic significance of these two events: Public health efforts to contain the SARS-CoV-2 coronavirus have failed, and there is ongoing community spread of the infection in Washington state. I text my intern back with the emoji of The Scream by Edvard Munch.
Could I be asymptomatically infected with the coronavirus? I work in close quarters with my colleagues who cared for the COVID-19–positive patient before he was placed in infection precautions. Social distancing has yet to enter our lexicon and our lives. In our crowded office, shared surfaces abound. Suddenly, every hard surface seems suspect—chairs, phones, dictaphone handsets, code pagers, printers, keypads, and door handles. All can be vectors of viral transmission. Normally insouciant about cleanliness, my coworkers and I start swabbing down every surface with disinfectant wipes. I ponder my likelihood of infection and decide it is possible but not probable.
In the next few days, I have a trip to Sedona, Arizona, planned with my extended family. Originally conceived as a celebration for my mom’s 80th birthday, we repurposed it as a time to grieve together after she unexpectedly passed away. I debate back and forth whether to go on the trip. If there is a chance I am infected with the coronavirus, it feels irresponsible to board an airplane with hundreds of other people. Yet the trip carries such high value for me. My family holds out hope I can get tested for the coronavirus, but I know just how limited testing capability is. It cuts me to the heart, but I cancel my flight. The deciding factor is that my sister has an autoimmune disease and is immunosuppressed. I don’t want to jeopardize her health. The world has truly gone topsy-turvy when the greatest thoughtfulness you can show to someone you love is to stay the hell away from her.
AM I A HYPOCHONDRIAC?
After my work stretch, I hunker down at home to monitor myself. I have a mild sore throat but convince myself it is psychosomatic. My plausible deniability of illness dies when I develop a cough and fatigue. Based on my symptoms, it is impossible to tell if I have the coronavirus or a common cold. I place myself on home quarantine. I don’t pursue coronavirus testing because there are hospitalized patients who need it much more than I do. I diligently monitor my temperature twice daily and it remains normal. My sore throat and fatigue go away, but my cough and some mild shortness of breath persists. I attribute it to my asthma, but the possibility of COVID-19 always lurks in the back of my mind. COVID-19 patients often don’t worsen until their second week of infection. Ordinarily, I would start using my steroid inhaler, but I hold off since steroids are thought to prolong viral replication.
When I tire of staying in the house, I go outside to work in the yard. I get on a low ladder to pull down the English ivy climbing up and smothering a tree. The ivy strand I’m tugging on suddenly breaks and I fall hard onto my back. Like a slap in the face, the accident shocks me into a new state of mental clarity. As a hospitalist, I’m a precious resource to my community right now. I can’t knock myself out of commission for dumb reasons. I ban myself from climbing any more ladders.
WHY CAN’T I GET TESTED?
As my time in quarantine draws to a close, I put my legal and financial affairs in order and pack a just-in-case backpack. The emergency room doctor hospitalized at a nearby hospital with severe COVID-19 is about my age. I am still coughing so I check in with the head of Infection Control to see if I need to be tested before returning to work. He tells me no. As I start working, I realize that coughing is the new leprosy. Even though I wear a mask, I get tense looks from others who carefully keep their distance from me. I tell everyone I have cough variant asthma, but what they all want to know is if I have been tested for the coronavirus. I haven’t been.
When my hospital sets up a new dedicated Employee Health screening phone line, I call right away. The nurse tells me I don’t meet criteria for coronavirus testing even though I am working on the COVID-19 rule-out unit with patients who have tested positive. While I agree with her from a medical standpoint, I don’t from a social or psychological perspective. This is a particularly unpropitious time in history to be a Chinese American doctor who can’t stop coughing. A negative test will reassure my patients and coworkers I am not a risk to them. A positive test, which is a possibility because of known prolonged viral shedding of the coronavirus, will reassure me I’m likely on my way to developing serologic immunity. I don’t get a test. When I tell my colleague, he suggests I resort to lying, but I won’t do it. As I’ve watched how power, wealth, and privilege play out in access to testing, I refuse to manipulate the system. But my experience is pointed commentary on the abysmal failure of testing in the United States when a frontline symptomatic doctor taking care of COVID-19 patients in one of the epicenters of the pandemic can’t get a coronavirus test. During a meeting, the head of Infection Control bluntly states he hopes we know that all of us are going to get the coronavirus at some point, but hopefully it won’t take us out of commission all at once. I feel better hearing him acknowledge that because it confirms my own sense of reality.
ARE WE RUNNING OUT OF PERSONAL PROTECTIVE EQUIPMENT?
While the ongoing pandemic definitely increases stress and anxiety levels in the hospital, there also continues to be caring and kindness. As I don my personal protective equipment (PPE), a nurse notices an exposed gap in the back of my gown and fixes it for me. He has my back, literally and figuratively. Our unit clerk, hearing my persistent cough, braves the 6-foot danger zone to hand me cough drops. Another nurse asks when the last time was I drank anything, and I give her a blank look because I can’t remember. I’m trying to minimize my use of masks, so I have kept my current one on all day. The front of the mask may be contaminated, but as long as I don’t touch that surface, it is still protecting me. She hands me a cup of water and I consider the benefit of staying hydrated versus using up another mask. Having previously landed in the emergency room with a kidney stone from not properly hydrating, I take off the mask, throw it away, wash my hands, and drink the water. But in my mind, I’m acutely aware of our shrinking supply of PPE.
On our time off work, my coworkers and I reach out to everyone we know to ask for mask donations. One friend tells me her husband is fashioning a mask for her from their furnace filter. She considers it the most romantic thing he’s ever done for her. The two of us agree that if we run out of PPE, we will go on caring for our patients anyway. We are doctors and caring for others is not only what we do, but an intrinsic part of who we are. Our journey amid the coronavirus pandemic may at times scare us half to death, but in caring for others “little by little we start to come alive.”
“To journey for the sake of saving our own lives is little by little to cease to live in any sense that really matters, even to ourselves, because it is only by journeying for the world’s sake—even when the world bores and sickens and scares you half to death—that little by little we start to come alive.”
—Frederick Buechner
On February 29, 2020, I find out by text from my intern when the first patient at our hospital in Seattle tests positive for COVID-19. He learns of it from his fellow intern who is caring for the patient. The news quickly spreads through the hospital like the virus itself, going from person to person while official communication channels remain initially silent. The news comes on the heels of a friend’s text that her daughter’s high school is closing for disinfection after a classmate also tested positive for COVID-19. I know the cataclysmic significance of these two events: Public health efforts to contain the SARS-CoV-2 coronavirus have failed, and there is ongoing community spread of the infection in Washington state. I text my intern back with the emoji of The Scream by Edvard Munch.
Could I be asymptomatically infected with the coronavirus? I work in close quarters with my colleagues who cared for the COVID-19–positive patient before he was placed in infection precautions. Social distancing has yet to enter our lexicon and our lives. In our crowded office, shared surfaces abound. Suddenly, every hard surface seems suspect—chairs, phones, dictaphone handsets, code pagers, printers, keypads, and door handles. All can be vectors of viral transmission. Normally insouciant about cleanliness, my coworkers and I start swabbing down every surface with disinfectant wipes. I ponder my likelihood of infection and decide it is possible but not probable.
In the next few days, I have a trip to Sedona, Arizona, planned with my extended family. Originally conceived as a celebration for my mom’s 80th birthday, we repurposed it as a time to grieve together after she unexpectedly passed away. I debate back and forth whether to go on the trip. If there is a chance I am infected with the coronavirus, it feels irresponsible to board an airplane with hundreds of other people. Yet the trip carries such high value for me. My family holds out hope I can get tested for the coronavirus, but I know just how limited testing capability is. It cuts me to the heart, but I cancel my flight. The deciding factor is that my sister has an autoimmune disease and is immunosuppressed. I don’t want to jeopardize her health. The world has truly gone topsy-turvy when the greatest thoughtfulness you can show to someone you love is to stay the hell away from her.
AM I A HYPOCHONDRIAC?
After my work stretch, I hunker down at home to monitor myself. I have a mild sore throat but convince myself it is psychosomatic. My plausible deniability of illness dies when I develop a cough and fatigue. Based on my symptoms, it is impossible to tell if I have the coronavirus or a common cold. I place myself on home quarantine. I don’t pursue coronavirus testing because there are hospitalized patients who need it much more than I do. I diligently monitor my temperature twice daily and it remains normal. My sore throat and fatigue go away, but my cough and some mild shortness of breath persists. I attribute it to my asthma, but the possibility of COVID-19 always lurks in the back of my mind. COVID-19 patients often don’t worsen until their second week of infection. Ordinarily, I would start using my steroid inhaler, but I hold off since steroids are thought to prolong viral replication.
When I tire of staying in the house, I go outside to work in the yard. I get on a low ladder to pull down the English ivy climbing up and smothering a tree. The ivy strand I’m tugging on suddenly breaks and I fall hard onto my back. Like a slap in the face, the accident shocks me into a new state of mental clarity. As a hospitalist, I’m a precious resource to my community right now. I can’t knock myself out of commission for dumb reasons. I ban myself from climbing any more ladders.
WHY CAN’T I GET TESTED?
As my time in quarantine draws to a close, I put my legal and financial affairs in order and pack a just-in-case backpack. The emergency room doctor hospitalized at a nearby hospital with severe COVID-19 is about my age. I am still coughing so I check in with the head of Infection Control to see if I need to be tested before returning to work. He tells me no. As I start working, I realize that coughing is the new leprosy. Even though I wear a mask, I get tense looks from others who carefully keep their distance from me. I tell everyone I have cough variant asthma, but what they all want to know is if I have been tested for the coronavirus. I haven’t been.
When my hospital sets up a new dedicated Employee Health screening phone line, I call right away. The nurse tells me I don’t meet criteria for coronavirus testing even though I am working on the COVID-19 rule-out unit with patients who have tested positive. While I agree with her from a medical standpoint, I don’t from a social or psychological perspective. This is a particularly unpropitious time in history to be a Chinese American doctor who can’t stop coughing. A negative test will reassure my patients and coworkers I am not a risk to them. A positive test, which is a possibility because of known prolonged viral shedding of the coronavirus, will reassure me I’m likely on my way to developing serologic immunity. I don’t get a test. When I tell my colleague, he suggests I resort to lying, but I won’t do it. As I’ve watched how power, wealth, and privilege play out in access to testing, I refuse to manipulate the system. But my experience is pointed commentary on the abysmal failure of testing in the United States when a frontline symptomatic doctor taking care of COVID-19 patients in one of the epicenters of the pandemic can’t get a coronavirus test. During a meeting, the head of Infection Control bluntly states he hopes we know that all of us are going to get the coronavirus at some point, but hopefully it won’t take us out of commission all at once. I feel better hearing him acknowledge that because it confirms my own sense of reality.
ARE WE RUNNING OUT OF PERSONAL PROTECTIVE EQUIPMENT?
While the ongoing pandemic definitely increases stress and anxiety levels in the hospital, there also continues to be caring and kindness. As I don my personal protective equipment (PPE), a nurse notices an exposed gap in the back of my gown and fixes it for me. He has my back, literally and figuratively. Our unit clerk, hearing my persistent cough, braves the 6-foot danger zone to hand me cough drops. Another nurse asks when the last time was I drank anything, and I give her a blank look because I can’t remember. I’m trying to minimize my use of masks, so I have kept my current one on all day. The front of the mask may be contaminated, but as long as I don’t touch that surface, it is still protecting me. She hands me a cup of water and I consider the benefit of staying hydrated versus using up another mask. Having previously landed in the emergency room with a kidney stone from not properly hydrating, I take off the mask, throw it away, wash my hands, and drink the water. But in my mind, I’m acutely aware of our shrinking supply of PPE.
On our time off work, my coworkers and I reach out to everyone we know to ask for mask donations. One friend tells me her husband is fashioning a mask for her from their furnace filter. She considers it the most romantic thing he’s ever done for her. The two of us agree that if we run out of PPE, we will go on caring for our patients anyway. We are doctors and caring for others is not only what we do, but an intrinsic part of who we are. Our journey amid the coronavirus pandemic may at times scare us half to death, but in caring for others “little by little we start to come alive.”
© 2020 Society of Hospital Medicine
Doctors push back on treating COVID-19 as HAPE
For Luanne Freer, MD, an expert in high-altitude pulmonary edema (HAPE) and founder and director of Everest ER, a nonprofit seasonal clinic at the Mt. Everest base camp in Nepal (elevation, 17,600 ft), a sudden flurry of messages and questions she received about a possible COVID-19/HAPE link was startling.
“That’s why it kind of poked me in the eye,” she said, referencing her extensive experience treating HAPE, which she described as a pressure-related phenomenon. “My goodness, they are so completely different.”
Dr. Freer, an emergency physician, reached out to several pulmonary intensivists with experience treating both HAPE and COVID-19 to gauge their reactions, and within 36 hours, they had drafted their response. In the commentary, published in High Altitude Medicine & Biology, the clinicians note that the comparison between HAPE and COVID-19 is potentially risky.
“As a group of physicians who have in some cases cared for patients with COVID-19 and in all cases cared for patients with HAPE and studied its pathophysiology and management, we feel it important to correct this misconception, as continued amplification of this message could have adverse effects on management of these patients,” they wrote.
The suggestion that COVID-19 lung injury sometimes looks more like HAPE than like acute respiratory distress syndrome (ARDS) appeared in a journal review article in late March and was put forth by medical professionals on social media where it gained traction in recent weeks and was amplified in multiple media outlets, including this one.
“With COVID, we don’t understand everything that’s going on, but we know for sure it’s an inflammatory process – not a pressure-related problem,” Dr. Freer said. “I thought ... this could be so dangerous to load the medicines that we use when we’re treating HAPE onto patients with COVID-19.”
The pathophysiological mechanisms in HAPE are different than those in other respiratory syndromes, including those associated with COVID-19, said Andrew M. Luks, MD, of the UW Medicine, Seattle, and the first author on the commentary.
“HAPE is a noncardiogenic form of pulmonary edema, as are ARDS due to bacteria or viral pneumonia, re-expansion pulmonary edema, immersion pulmonary edema, negative pressure pulmonary edema, and neurogenic pulmonary edema,” Dr. Luks, Dr. Freer, and colleagues wrote in the commentary, explaining that all of these entities cause varying degrees of hypoxemia and diffuse bilateral opacities on chest imaging. “Importantly, in all of these cases, edema accumulates in the interstitial and alveolar spaces of the lung as a result of imbalance in Starling forces.”
A difference between these entities, however, is “the mechanism by which that imbalance develops,” they noted.
The excessive and uneven hypoxic pulmonary vasoconstriction that leads to a marked increase in pulmonary artery pressure, subsequent lung overperfusion, increased pulmonary capillary hydrostatic pressure, and leakage of fluid from the vascular space into the alveolar space as seen in HAPE, is a “fundamentally different phenomenon than what is seen in COVID-19-related ARDS, which involves viral-mediated inflammatory responses as the primary pathophysiological mechanism,” they added.
The authors described several other differences between the conditions, ultimately noting that “understanding the distinction between the pathophysiological mechanisms of these entities is critical for patient management.”
In HAPE, supplemental oxygen alone may be sufficient; in COVID-19, it may improve hypoxemia but won’t resolve the underlying inflammation or injury, they explained, adding that “only good supportive care including mechanical ventilation, quite often for long periods of time, allows some patients to survive until their disease resolves.”
Further, HAPE can be prevented or treated with pulmonary vasodilators such a nifedipine or sildenafil, which decrease pulmonary artery pressure and, as a result lower pulmonary capillary hydrostatic pressure, they said.
Use of such medications for COVID-19 might decrease pulmonary artery pressure and improve right ventricular function in COVID-19, but “by releasing hypoxic pulmonary vasoconstriction and increasing perfusion to nonventilated regions of the lung, they could also worsen ventilation-perfusion mismatch” and thereby worsen hypoxemia, they explained, adding that the treatments can also cause or worsen hypotension.
Efforts to share observations and experience are important in medicine, but sometimes, as in this circumstance, “they get out there, spread around – like a brushfire almost – and get [unwarranted] face validity,” Dr. Luks said, noting that in response to information circulating about COVID-19 and HAPE, he has already heard medical professionals floating the idea of treating COVID-19 with treatments used for HAPE.
It’s true that some COVID-19 lung injury cases are behaving differently than typical ARDS, he said, adding that presentation can vary.
“But trying to equate HAPE and COVID-19 is just wrong,” he said. “HAPE and COVID-19 may share several features ...but those are features that are shared by a lot of different forms of respiratory failure.”
In a recent video interview, WebMD’s chief medical officer John Whyte, MD, spoke with a New York City physician trained in critical care and emergency medicine, Cameron Kyle-Sidell, MD, who raised the need to consider different respiratory protocols for COVID-19, noting that standard protocols were falling short in many cases.
“What we’re seeing ... is something unusual, it’s something that we are not used to,” Dr. Kyle-Sidell of Maimonides Medical Center said in that interview, stressing that the presentation differed from that seen in typical ARDS. “The patterns I was seeing did not make sense.”
Like others, he noted that COVID-19 patients were presenting with illness that clinically looked more like HAPE, but that the pathophysiology is not necessary similar to HAPE.
At around the same time, Luciano Gattinoni, MD, of the Medical University of Göttingen in Germany and colleagues, published a letter to the editor in the American Journal of Respiratory and Critical Care Medicine stressing that the ARDS presentation in COVID-19 patients is atypical and requires a patient physiology–driven treatment approach, rather than a standard protocol–driven approach. Dr. Gattinoni and colleagues suggested that instead of high positive end-expiratory pressure (PEEP), physicians should consider the lowest possible PEEP and gentle ventilation.
Dr. Luks agreed that “some patients with COVID-19 do not have the same physiologic derangements that we see in a lot of other people with ARDS.”
“[Dr. Gattinoni] is making the point that we need to treat these people differently ... and I think that’s a valid point, and honestly, that’s a point that applied even before COVID-19,” he said. “Most of the things that we see in clinical practice – there’s a lot of heterogeneity between patients, and you have to be prepared to tailor your therapy in light of the differences that you’re picking up from your observations at the bedside and other data that you’re getting on the patient.”
The main concern Dr. Luks and his coauthors wanted to convey, they said, is making sure that the anecdotal experiences and observations of clinicians struggling to find answers don’t spiral out of control without proper vetting, thereby leading to patient harm.
“In this challenging time, we must identify the best means to care for these critically ill patients. That approach should be grounded in sound pulmonary physiology, clinical experience and, when available, evidence from clinical studies,” they concluded.
Dr. Luks and Dr. Freer reported having no financial disclosures.
For Luanne Freer, MD, an expert in high-altitude pulmonary edema (HAPE) and founder and director of Everest ER, a nonprofit seasonal clinic at the Mt. Everest base camp in Nepal (elevation, 17,600 ft), a sudden flurry of messages and questions she received about a possible COVID-19/HAPE link was startling.
“That’s why it kind of poked me in the eye,” she said, referencing her extensive experience treating HAPE, which she described as a pressure-related phenomenon. “My goodness, they are so completely different.”
Dr. Freer, an emergency physician, reached out to several pulmonary intensivists with experience treating both HAPE and COVID-19 to gauge their reactions, and within 36 hours, they had drafted their response. In the commentary, published in High Altitude Medicine & Biology, the clinicians note that the comparison between HAPE and COVID-19 is potentially risky.
“As a group of physicians who have in some cases cared for patients with COVID-19 and in all cases cared for patients with HAPE and studied its pathophysiology and management, we feel it important to correct this misconception, as continued amplification of this message could have adverse effects on management of these patients,” they wrote.
The suggestion that COVID-19 lung injury sometimes looks more like HAPE than like acute respiratory distress syndrome (ARDS) appeared in a journal review article in late March and was put forth by medical professionals on social media where it gained traction in recent weeks and was amplified in multiple media outlets, including this one.
“With COVID, we don’t understand everything that’s going on, but we know for sure it’s an inflammatory process – not a pressure-related problem,” Dr. Freer said. “I thought ... this could be so dangerous to load the medicines that we use when we’re treating HAPE onto patients with COVID-19.”
The pathophysiological mechanisms in HAPE are different than those in other respiratory syndromes, including those associated with COVID-19, said Andrew M. Luks, MD, of the UW Medicine, Seattle, and the first author on the commentary.
“HAPE is a noncardiogenic form of pulmonary edema, as are ARDS due to bacteria or viral pneumonia, re-expansion pulmonary edema, immersion pulmonary edema, negative pressure pulmonary edema, and neurogenic pulmonary edema,” Dr. Luks, Dr. Freer, and colleagues wrote in the commentary, explaining that all of these entities cause varying degrees of hypoxemia and diffuse bilateral opacities on chest imaging. “Importantly, in all of these cases, edema accumulates in the interstitial and alveolar spaces of the lung as a result of imbalance in Starling forces.”
A difference between these entities, however, is “the mechanism by which that imbalance develops,” they noted.
The excessive and uneven hypoxic pulmonary vasoconstriction that leads to a marked increase in pulmonary artery pressure, subsequent lung overperfusion, increased pulmonary capillary hydrostatic pressure, and leakage of fluid from the vascular space into the alveolar space as seen in HAPE, is a “fundamentally different phenomenon than what is seen in COVID-19-related ARDS, which involves viral-mediated inflammatory responses as the primary pathophysiological mechanism,” they added.
The authors described several other differences between the conditions, ultimately noting that “understanding the distinction between the pathophysiological mechanisms of these entities is critical for patient management.”
In HAPE, supplemental oxygen alone may be sufficient; in COVID-19, it may improve hypoxemia but won’t resolve the underlying inflammation or injury, they explained, adding that “only good supportive care including mechanical ventilation, quite often for long periods of time, allows some patients to survive until their disease resolves.”
Further, HAPE can be prevented or treated with pulmonary vasodilators such a nifedipine or sildenafil, which decrease pulmonary artery pressure and, as a result lower pulmonary capillary hydrostatic pressure, they said.
Use of such medications for COVID-19 might decrease pulmonary artery pressure and improve right ventricular function in COVID-19, but “by releasing hypoxic pulmonary vasoconstriction and increasing perfusion to nonventilated regions of the lung, they could also worsen ventilation-perfusion mismatch” and thereby worsen hypoxemia, they explained, adding that the treatments can also cause or worsen hypotension.
Efforts to share observations and experience are important in medicine, but sometimes, as in this circumstance, “they get out there, spread around – like a brushfire almost – and get [unwarranted] face validity,” Dr. Luks said, noting that in response to information circulating about COVID-19 and HAPE, he has already heard medical professionals floating the idea of treating COVID-19 with treatments used for HAPE.
It’s true that some COVID-19 lung injury cases are behaving differently than typical ARDS, he said, adding that presentation can vary.
“But trying to equate HAPE and COVID-19 is just wrong,” he said. “HAPE and COVID-19 may share several features ...but those are features that are shared by a lot of different forms of respiratory failure.”
In a recent video interview, WebMD’s chief medical officer John Whyte, MD, spoke with a New York City physician trained in critical care and emergency medicine, Cameron Kyle-Sidell, MD, who raised the need to consider different respiratory protocols for COVID-19, noting that standard protocols were falling short in many cases.
“What we’re seeing ... is something unusual, it’s something that we are not used to,” Dr. Kyle-Sidell of Maimonides Medical Center said in that interview, stressing that the presentation differed from that seen in typical ARDS. “The patterns I was seeing did not make sense.”
Like others, he noted that COVID-19 patients were presenting with illness that clinically looked more like HAPE, but that the pathophysiology is not necessary similar to HAPE.
At around the same time, Luciano Gattinoni, MD, of the Medical University of Göttingen in Germany and colleagues, published a letter to the editor in the American Journal of Respiratory and Critical Care Medicine stressing that the ARDS presentation in COVID-19 patients is atypical and requires a patient physiology–driven treatment approach, rather than a standard protocol–driven approach. Dr. Gattinoni and colleagues suggested that instead of high positive end-expiratory pressure (PEEP), physicians should consider the lowest possible PEEP and gentle ventilation.
Dr. Luks agreed that “some patients with COVID-19 do not have the same physiologic derangements that we see in a lot of other people with ARDS.”
“[Dr. Gattinoni] is making the point that we need to treat these people differently ... and I think that’s a valid point, and honestly, that’s a point that applied even before COVID-19,” he said. “Most of the things that we see in clinical practice – there’s a lot of heterogeneity between patients, and you have to be prepared to tailor your therapy in light of the differences that you’re picking up from your observations at the bedside and other data that you’re getting on the patient.”
The main concern Dr. Luks and his coauthors wanted to convey, they said, is making sure that the anecdotal experiences and observations of clinicians struggling to find answers don’t spiral out of control without proper vetting, thereby leading to patient harm.
“In this challenging time, we must identify the best means to care for these critically ill patients. That approach should be grounded in sound pulmonary physiology, clinical experience and, when available, evidence from clinical studies,” they concluded.
Dr. Luks and Dr. Freer reported having no financial disclosures.
For Luanne Freer, MD, an expert in high-altitude pulmonary edema (HAPE) and founder and director of Everest ER, a nonprofit seasonal clinic at the Mt. Everest base camp in Nepal (elevation, 17,600 ft), a sudden flurry of messages and questions she received about a possible COVID-19/HAPE link was startling.
“That’s why it kind of poked me in the eye,” she said, referencing her extensive experience treating HAPE, which she described as a pressure-related phenomenon. “My goodness, they are so completely different.”
Dr. Freer, an emergency physician, reached out to several pulmonary intensivists with experience treating both HAPE and COVID-19 to gauge their reactions, and within 36 hours, they had drafted their response. In the commentary, published in High Altitude Medicine & Biology, the clinicians note that the comparison between HAPE and COVID-19 is potentially risky.
“As a group of physicians who have in some cases cared for patients with COVID-19 and in all cases cared for patients with HAPE and studied its pathophysiology and management, we feel it important to correct this misconception, as continued amplification of this message could have adverse effects on management of these patients,” they wrote.
The suggestion that COVID-19 lung injury sometimes looks more like HAPE than like acute respiratory distress syndrome (ARDS) appeared in a journal review article in late March and was put forth by medical professionals on social media where it gained traction in recent weeks and was amplified in multiple media outlets, including this one.
“With COVID, we don’t understand everything that’s going on, but we know for sure it’s an inflammatory process – not a pressure-related problem,” Dr. Freer said. “I thought ... this could be so dangerous to load the medicines that we use when we’re treating HAPE onto patients with COVID-19.”
The pathophysiological mechanisms in HAPE are different than those in other respiratory syndromes, including those associated with COVID-19, said Andrew M. Luks, MD, of the UW Medicine, Seattle, and the first author on the commentary.
“HAPE is a noncardiogenic form of pulmonary edema, as are ARDS due to bacteria or viral pneumonia, re-expansion pulmonary edema, immersion pulmonary edema, negative pressure pulmonary edema, and neurogenic pulmonary edema,” Dr. Luks, Dr. Freer, and colleagues wrote in the commentary, explaining that all of these entities cause varying degrees of hypoxemia and diffuse bilateral opacities on chest imaging. “Importantly, in all of these cases, edema accumulates in the interstitial and alveolar spaces of the lung as a result of imbalance in Starling forces.”
A difference between these entities, however, is “the mechanism by which that imbalance develops,” they noted.
The excessive and uneven hypoxic pulmonary vasoconstriction that leads to a marked increase in pulmonary artery pressure, subsequent lung overperfusion, increased pulmonary capillary hydrostatic pressure, and leakage of fluid from the vascular space into the alveolar space as seen in HAPE, is a “fundamentally different phenomenon than what is seen in COVID-19-related ARDS, which involves viral-mediated inflammatory responses as the primary pathophysiological mechanism,” they added.
The authors described several other differences between the conditions, ultimately noting that “understanding the distinction between the pathophysiological mechanisms of these entities is critical for patient management.”
In HAPE, supplemental oxygen alone may be sufficient; in COVID-19, it may improve hypoxemia but won’t resolve the underlying inflammation or injury, they explained, adding that “only good supportive care including mechanical ventilation, quite often for long periods of time, allows some patients to survive until their disease resolves.”
Further, HAPE can be prevented or treated with pulmonary vasodilators such a nifedipine or sildenafil, which decrease pulmonary artery pressure and, as a result lower pulmonary capillary hydrostatic pressure, they said.
Use of such medications for COVID-19 might decrease pulmonary artery pressure and improve right ventricular function in COVID-19, but “by releasing hypoxic pulmonary vasoconstriction and increasing perfusion to nonventilated regions of the lung, they could also worsen ventilation-perfusion mismatch” and thereby worsen hypoxemia, they explained, adding that the treatments can also cause or worsen hypotension.
Efforts to share observations and experience are important in medicine, but sometimes, as in this circumstance, “they get out there, spread around – like a brushfire almost – and get [unwarranted] face validity,” Dr. Luks said, noting that in response to information circulating about COVID-19 and HAPE, he has already heard medical professionals floating the idea of treating COVID-19 with treatments used for HAPE.
It’s true that some COVID-19 lung injury cases are behaving differently than typical ARDS, he said, adding that presentation can vary.
“But trying to equate HAPE and COVID-19 is just wrong,” he said. “HAPE and COVID-19 may share several features ...but those are features that are shared by a lot of different forms of respiratory failure.”
In a recent video interview, WebMD’s chief medical officer John Whyte, MD, spoke with a New York City physician trained in critical care and emergency medicine, Cameron Kyle-Sidell, MD, who raised the need to consider different respiratory protocols for COVID-19, noting that standard protocols were falling short in many cases.
“What we’re seeing ... is something unusual, it’s something that we are not used to,” Dr. Kyle-Sidell of Maimonides Medical Center said in that interview, stressing that the presentation differed from that seen in typical ARDS. “The patterns I was seeing did not make sense.”
Like others, he noted that COVID-19 patients were presenting with illness that clinically looked more like HAPE, but that the pathophysiology is not necessary similar to HAPE.
At around the same time, Luciano Gattinoni, MD, of the Medical University of Göttingen in Germany and colleagues, published a letter to the editor in the American Journal of Respiratory and Critical Care Medicine stressing that the ARDS presentation in COVID-19 patients is atypical and requires a patient physiology–driven treatment approach, rather than a standard protocol–driven approach. Dr. Gattinoni and colleagues suggested that instead of high positive end-expiratory pressure (PEEP), physicians should consider the lowest possible PEEP and gentle ventilation.
Dr. Luks agreed that “some patients with COVID-19 do not have the same physiologic derangements that we see in a lot of other people with ARDS.”
“[Dr. Gattinoni] is making the point that we need to treat these people differently ... and I think that’s a valid point, and honestly, that’s a point that applied even before COVID-19,” he said. “Most of the things that we see in clinical practice – there’s a lot of heterogeneity between patients, and you have to be prepared to tailor your therapy in light of the differences that you’re picking up from your observations at the bedside and other data that you’re getting on the patient.”
The main concern Dr. Luks and his coauthors wanted to convey, they said, is making sure that the anecdotal experiences and observations of clinicians struggling to find answers don’t spiral out of control without proper vetting, thereby leading to patient harm.
“In this challenging time, we must identify the best means to care for these critically ill patients. That approach should be grounded in sound pulmonary physiology, clinical experience and, when available, evidence from clinical studies,” they concluded.
Dr. Luks and Dr. Freer reported having no financial disclosures.