TBD Meeting (5392-19)

SAN DIEGO – Neuropathy can blur the seriousness of injuries, especially in patients with diabetes, and that can lead to severe consequences such as falls, foot ulcers, gangrene, and amputations, said Lucia M. Novak, MSN, ANP-BC, BC-ADM, CDTC, in a presentation on assessing and treating neuropathies at the Metabolic & Endocrine Disease Summit, sponsored by Global Academy for Medical Education.

As many as half of the cases of diabetic neuropathy may have no symptoms, and more than two-thirds of cases of diabetic neuropathy, even some with obvious symptoms, are ignored or missed by clinicians, said Ms. Novak, director of the Riverside Diabetes Center and adjunct assistant professor at the Uniformed Services University of the Health Sciences, both in Bethesda, Md.

At the same time, she said, diabetic neuropathy is very common. It affects an estimated 10%-15% of newly diagnosed patients with type 2 diabetes, 50% of patients with type 2 disease after 10 years, and as many as 30% of patients with prediabetes.

The condition is less common in type 1 diabetes, affecting an estimated 20% of patients after 20 years, she said.

“All we can do in our patients with type 2 diabetes and diabetic neuropathy, is to slow down the progression, although improving glycemic control can prevent it in type 1,” she said, citing findings suggesting that glycemic control could significantly reduce the risk of diabetic neuropathy in type 1 – but not type 2.

A 2012 report analyzed research into the effect of glycemic control on neuropathy in diabetes and found a pair of studies that reported a 60%-70% reduction of risk in patients with type 1 diabetes who received regular insulin dosing. However, the evidence for type 2 diabetes was not as definitive, and analysis of findings from eight randomized, controlled trials in patients with type 2 diabetes supported a relatively small reduction in the development of neuropathy in patients with type 2 diabetes who were receiving enhanced glycemic control (Lancet Neurol. 2012;11[6]:521-34).

Ms. Novak focused mainly on peripheral neuropathy, which is believed to account for 50%-75% of all neuropathy in patients with diabetes. She emphasized the importance of screening because it is crucial for preventing foot ulcers, which affect more than a third of patients with diabetes over their lifetimes.

She recommended following the American Diabetes Association’s 2017 position statement on diabetic neuropathy (Diabetes Care. 2017;40[1]:136-54), beginning with performing a visual examination of the feet at every visit.
 

Comprehensive screening

In patients with type 1 diabetes, there should be an annual comprehensive screening beginning within 5 years of diagnosis. Patients with type 2 disease should be screened at diagnosis and then annually, as outlined in the ADA statement.

The comprehensive exam involves using tools, such as tuning forks and monofilaments, to test sensation. Different tools are required to test both small and large fibers in the foot, Ms. Novak said, and doing both kinds of testing greatly increases the likelihood of detecting neuropathy.
 

Check for pulse, bone deformities, dry skin

In addition, “you’ll be feeling for their pulses, looking for bony deformities, and looking at anything is going on between the toes [to make sure] the skin is intact,” she said.

Patients with diabetic neuropathy often have dry skin, she said, so make sure they’re moisturizing. “Look at the condition of their shoes,” she added, “which will tell you how they walk.”

Ill-fitting shoes are a common cause of foot ulcers, said Ms. Novak, who noted that some patients refuse to wear unattractive diabetic shoes and prefer to wear more fashionable – and dangerous – tight-fitting shoes.
 

Treatment options

Glycemic control makes a difference, especially for patients with type 1, as does control of risk factors, such as obesity. But diabetic neuropathy cannot be reversed.

Pain can be managed with a range of medications. “We can’t cure the neuropathy, we can at least help patients with the symptoms so that they can have a good night’s sleep,” she said.

Ms. Novak also suggested passing on the following snippets of advice to patients:

• Do not walk barefoot.
• Check your feet every day.
• Moisturize your skin, and always dry thoroughly between your toes.
• Seek medical attention if your nails cut into your skin or you develop a callus or areas of redness/warmth.

Global Academy and this news organization are owned by the same parent company. Ms. Novak reported relationships with Nova Nordisk, Sanofi, Janssen, and AstraZeneca.

SAN DIEGO – Neuropathy can blur the seriousness of injuries, especially in patients with diabetes, and that can lead to severe consequences such as falls, foot ulcers, gangrene, and amputations, said Lucia M. Novak, MSN, ANP-BC, BC-ADM, CDTC, in a presentation on assessing and treating neuropathies at the Metabolic & Endocrine Disease Summit, sponsored by Global Academy for Medical Education.

As many as half of the cases of diabetic neuropathy may have no symptoms, and more than two-thirds of cases of diabetic neuropathy, even some with obvious symptoms, are ignored or missed by clinicians, said Ms. Novak, director of the Riverside Diabetes Center and adjunct assistant professor at the Uniformed Services University of the Health Sciences, both in Bethesda, Md.

At the same time, she said, diabetic neuropathy is very common. It affects an estimated 10%-15% of newly diagnosed patients with type 2 diabetes, 50% of patients with type 2 disease after 10 years, and as many as 30% of patients with prediabetes.

The condition is less common in type 1 diabetes, affecting an estimated 20% of patients after 20 years, she said.

“All we can do in our patients with type 2 diabetes and diabetic neuropathy, is to slow down the progression, although improving glycemic control can prevent it in type 1,” she said, citing findings suggesting that glycemic control could significantly reduce the risk of diabetic neuropathy in type 1 – but not type 2.

A 2012 report analyzed research into the effect of glycemic control on neuropathy in diabetes and found a pair of studies that reported a 60%-70% reduction of risk in patients with type 1 diabetes who received regular insulin dosing. However, the evidence for type 2 diabetes was not as definitive, and analysis of findings from eight randomized, controlled trials in patients with type 2 diabetes supported a relatively small reduction in the development of neuropathy in patients with type 2 diabetes who were receiving enhanced glycemic control (Lancet Neurol. 2012;11[6]:521-34).

Ms. Novak focused mainly on peripheral neuropathy, which is believed to account for 50%-75% of all neuropathy in patients with diabetes. She emphasized the importance of screening because it is crucial for preventing foot ulcers, which affect more than a third of patients with diabetes over their lifetimes.

She recommended following the American Diabetes Association’s 2017 position statement on diabetic neuropathy (Diabetes Care. 2017;40[1]:136-54), beginning with performing a visual examination of the feet at every visit.
 

Comprehensive screening

In patients with type 1 diabetes, there should be an annual comprehensive screening beginning within 5 years of diagnosis. Patients with type 2 disease should be screened at diagnosis and then annually, as outlined in the ADA statement.

The comprehensive exam involves using tools, such as tuning forks and monofilaments, to test sensation. Different tools are required to test both small and large fibers in the foot, Ms. Novak said, and doing both kinds of testing greatly increases the likelihood of detecting neuropathy.
 

Check for pulse, bone deformities, dry skin

In addition, “you’ll be feeling for their pulses, looking for bony deformities, and looking at anything is going on between the toes [to make sure] the skin is intact,” she said.

Patients with diabetic neuropathy often have dry skin, she said, so make sure they’re moisturizing. “Look at the condition of their shoes,” she added, “which will tell you how they walk.”

Ill-fitting shoes are a common cause of foot ulcers, said Ms. Novak, who noted that some patients refuse to wear unattractive diabetic shoes and prefer to wear more fashionable – and dangerous – tight-fitting shoes.
 

Treatment options

Glycemic control makes a difference, especially for patients with type 1, as does control of risk factors, such as obesity. But diabetic neuropathy cannot be reversed.

Pain can be managed with a range of medications. “We can’t cure the neuropathy, we can at least help patients with the symptoms so that they can have a good night’s sleep,” she said.

Ms. Novak also suggested passing on the following snippets of advice to patients:

• Do not walk barefoot.
• Check your feet every day.
• Moisturize your skin, and always dry thoroughly between your toes.
• Seek medical attention if your nails cut into your skin or you develop a callus or areas of redness/warmth.

Global Academy and this news organization are owned by the same parent company. Ms. Novak reported relationships with Nova Nordisk, Sanofi, Janssen, and AstraZeneca.

SAN DIEGO – Neuropathy can blur the seriousness of injuries, especially in patients with diabetes, and that can lead to severe consequences such as falls, foot ulcers, gangrene, and amputations, said Lucia M. Novak, MSN, ANP-BC, BC-ADM, CDTC, in a presentation on assessing and treating neuropathies at the Metabolic & Endocrine Disease Summit, sponsored by Global Academy for Medical Education.

As many as half of the cases of diabetic neuropathy may have no symptoms, and more than two-thirds of cases of diabetic neuropathy, even some with obvious symptoms, are ignored or missed by clinicians, said Ms. Novak, director of the Riverside Diabetes Center and adjunct assistant professor at the Uniformed Services University of the Health Sciences, both in Bethesda, Md.

At the same time, she said, diabetic neuropathy is very common. It affects an estimated 10%-15% of newly diagnosed patients with type 2 diabetes, 50% of patients with type 2 disease after 10 years, and as many as 30% of patients with prediabetes.

The condition is less common in type 1 diabetes, affecting an estimated 20% of patients after 20 years, she said.

“All we can do in our patients with type 2 diabetes and diabetic neuropathy, is to slow down the progression, although improving glycemic control can prevent it in type 1,” she said, citing findings suggesting that glycemic control could significantly reduce the risk of diabetic neuropathy in type 1 – but not type 2.

A 2012 report analyzed research into the effect of glycemic control on neuropathy in diabetes and found a pair of studies that reported a 60%-70% reduction of risk in patients with type 1 diabetes who received regular insulin dosing. However, the evidence for type 2 diabetes was not as definitive, and analysis of findings from eight randomized, controlled trials in patients with type 2 diabetes supported a relatively small reduction in the development of neuropathy in patients with type 2 diabetes who were receiving enhanced glycemic control (Lancet Neurol. 2012;11[6]:521-34).

Ms. Novak focused mainly on peripheral neuropathy, which is believed to account for 50%-75% of all neuropathy in patients with diabetes. She emphasized the importance of screening because it is crucial for preventing foot ulcers, which affect more than a third of patients with diabetes over their lifetimes.

She recommended following the American Diabetes Association’s 2017 position statement on diabetic neuropathy (Diabetes Care. 2017;40[1]:136-54), beginning with performing a visual examination of the feet at every visit.
 

Comprehensive screening

In patients with type 1 diabetes, there should be an annual comprehensive screening beginning within 5 years of diagnosis. Patients with type 2 disease should be screened at diagnosis and then annually, as outlined in the ADA statement.

The comprehensive exam involves using tools, such as tuning forks and monofilaments, to test sensation. Different tools are required to test both small and large fibers in the foot, Ms. Novak said, and doing both kinds of testing greatly increases the likelihood of detecting neuropathy.
 

Check for pulse, bone deformities, dry skin

In addition, “you’ll be feeling for their pulses, looking for bony deformities, and looking at anything is going on between the toes [to make sure] the skin is intact,” she said.

Patients with diabetic neuropathy often have dry skin, she said, so make sure they’re moisturizing. “Look at the condition of their shoes,” she added, “which will tell you how they walk.”

Ill-fitting shoes are a common cause of foot ulcers, said Ms. Novak, who noted that some patients refuse to wear unattractive diabetic shoes and prefer to wear more fashionable – and dangerous – tight-fitting shoes.
 

Treatment options

Glycemic control makes a difference, especially for patients with type 1, as does control of risk factors, such as obesity. But diabetic neuropathy cannot be reversed.

Pain can be managed with a range of medications. “We can’t cure the neuropathy, we can at least help patients with the symptoms so that they can have a good night’s sleep,” she said.

Ms. Novak also suggested passing on the following snippets of advice to patients:

• Do not walk barefoot.
• Check your feet every day.
• Moisturize your skin, and always dry thoroughly between your toes.
• Seek medical attention if your nails cut into your skin or you develop a callus or areas of redness/warmth.

Global Academy and this news organization are owned by the same parent company. Ms. Novak reported relationships with Nova Nordisk, Sanofi, Janssen, and AstraZeneca.

SAN DIEGO – Nearly 350 years ago, British physician Thomas Willis wrote that diabetes seemed often to occur in patients who were experiencing “significant life stress, sadness, or long sorrow.” That, according to Ellen D. Mandel, DMH, MPA, MS, PA-C, RDN, CDE, a clinical professor at Pace University in New York City, was an important insight into the link between mind and body in patients with diabetes.

“As clinicians, we should be worried about mental illness in our patients with diabetes,” Dr. Mandel, a physician assistant educator, said during a presentation at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

In particular, she said, medical professionals should consider how diabetes might contribute to depression – and vice versa.

Dr. Mandel pointed to findings suggesting that 11% of patients with diabetes show signs of clinical depression, which is higher than in the general population, with many more believed to have subclinical depression (Diabetes Care. 2015;38[4]:551-60).

Anxiety can be a key factor in trying to understand how diabetes might contribute to depression. “Diabetes is a very stressful condition ... [and patients] may be fatigued and exhausted.” On top of that, they have to make nutrition changes, or at least pay attention to their diet and overall care, all of which can have a cumulatively negative impact on patient well-being.

Conversely, depression can contribute to diabetes. “They kind of go hand in hand,” she said, pointing to depression’s ability to disrupt appetite, diminish energy, and boost levels of cortisol.

Among the findings that provide evidence of a link between diabetes and depression are those from a study in which investigators estimated that for every 1-point increase in depression symptoms, the risk of diabetes will go up by as much as 5% (Clin Diabetes Endocrinol. 2018 Jan 4. doi: 10.1186/s40842-017-0052-1). Moreover, a 2013 review linked the combination of diabetes and depression to an adjusted 1.5-fold increase in risk of all-cause death (PLoS One. 2013 Mar 5. doi: 10.1371/journal.pone.0057058).

Dr. Mandel offered these tips about diagnosing depression in patients with diabetes and helping them feel comfortable:

• Put yourself in the patient’s shoes. “One of the biggest barriers to referring patients to diabetic education is that they don’t want to have to admit to a group that they have diabetes. They keep it to themselves, to their own detriment. In addition, there’s a lot of worry about insurance.” Patients with diabetes often have self-esteem issues and financial or insurance challenges, all of which need to be factored in when working with them, Dr. Mandel said.
• Ask questions and use screening tools. Two simple questions are helpful in starting a conversation and gathering useful information: Over the past 2 weeks, have you often been bothered by [having] little interest or pleasure in doing things? What about being bothered by feeling down, depressed, or hopeless? If the patient answers “yes” to either of these questions, it will be a positive screen, and two “no” answers will be a negative screen. With the “yes” responses, one should follow-up with a screening tool – typically, the one approved by your institution. Dr. Mandel also highlighted the Patient Health Questionnaire depression scale (PHQ-9), which is available online, or the brief, two-item Diabetes Distress Scale (DDS2) questionnaire.
• Keep your own language in mind. “The way you communicate with your patients can elevate their feeling about themselves or destroy how they feel about themselves,” Dr. Mandel said. “We’re trying to stop calling people with diabetes ‘diabetics.’ People don’t want to be labeled like that. Don’t blame yourself if you use this language, but work to make the changes,” Dr. Mandel suggested.
• Watch out for other forms of bias. Beware of unconsciously stereotyping your patients. “It affects how people relate to you, how they adhere to your suggestions, and how much they’ll trust [and confide in] you, which can have clinical implications,” Dr. Mandel said.

Global Academy and this news organization are owned by the same parent company. Dr. Mandel has no disclosures.

SAN DIEGO – Nearly 350 years ago, British physician Thomas Willis wrote that diabetes seemed often to occur in patients who were experiencing “significant life stress, sadness, or long sorrow.” That, according to Ellen D. Mandel, DMH, MPA, MS, PA-C, RDN, CDE, a clinical professor at Pace University in New York City, was an important insight into the link between mind and body in patients with diabetes.

“As clinicians, we should be worried about mental illness in our patients with diabetes,” Dr. Mandel, a physician assistant educator, said during a presentation at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

In particular, she said, medical professionals should consider how diabetes might contribute to depression – and vice versa.

Dr. Mandel pointed to findings suggesting that 11% of patients with diabetes show signs of clinical depression, which is higher than in the general population, with many more believed to have subclinical depression (Diabetes Care. 2015;38[4]:551-60).

Anxiety can be a key factor in trying to understand how diabetes might contribute to depression. “Diabetes is a very stressful condition ... [and patients] may be fatigued and exhausted.” On top of that, they have to make nutrition changes, or at least pay attention to their diet and overall care, all of which can have a cumulatively negative impact on patient well-being.

Conversely, depression can contribute to diabetes. “They kind of go hand in hand,” she said, pointing to depression’s ability to disrupt appetite, diminish energy, and boost levels of cortisol.

Among the findings that provide evidence of a link between diabetes and depression are those from a study in which investigators estimated that for every 1-point increase in depression symptoms, the risk of diabetes will go up by as much as 5% (Clin Diabetes Endocrinol. 2018 Jan 4. doi: 10.1186/s40842-017-0052-1). Moreover, a 2013 review linked the combination of diabetes and depression to an adjusted 1.5-fold increase in risk of all-cause death (PLoS One. 2013 Mar 5. doi: 10.1371/journal.pone.0057058).

Dr. Mandel offered these tips about diagnosing depression in patients with diabetes and helping them feel comfortable:

• Put yourself in the patient’s shoes. “One of the biggest barriers to referring patients to diabetic education is that they don’t want to have to admit to a group that they have diabetes. They keep it to themselves, to their own detriment. In addition, there’s a lot of worry about insurance.” Patients with diabetes often have self-esteem issues and financial or insurance challenges, all of which need to be factored in when working with them, Dr. Mandel said.
• Ask questions and use screening tools. Two simple questions are helpful in starting a conversation and gathering useful information: Over the past 2 weeks, have you often been bothered by [having] little interest or pleasure in doing things? What about being bothered by feeling down, depressed, or hopeless? If the patient answers “yes” to either of these questions, it will be a positive screen, and two “no” answers will be a negative screen. With the “yes” responses, one should follow-up with a screening tool – typically, the one approved by your institution. Dr. Mandel also highlighted the Patient Health Questionnaire depression scale (PHQ-9), which is available online, or the brief, two-item Diabetes Distress Scale (DDS2) questionnaire.
• Keep your own language in mind. “The way you communicate with your patients can elevate their feeling about themselves or destroy how they feel about themselves,” Dr. Mandel said. “We’re trying to stop calling people with diabetes ‘diabetics.’ People don’t want to be labeled like that. Don’t blame yourself if you use this language, but work to make the changes,” Dr. Mandel suggested.
• Watch out for other forms of bias. Beware of unconsciously stereotyping your patients. “It affects how people relate to you, how they adhere to your suggestions, and how much they’ll trust [and confide in] you, which can have clinical implications,” Dr. Mandel said.

Global Academy and this news organization are owned by the same parent company. Dr. Mandel has no disclosures.

SAN DIEGO – Nearly 350 years ago, British physician Thomas Willis wrote that diabetes seemed often to occur in patients who were experiencing “significant life stress, sadness, or long sorrow.” That, according to Ellen D. Mandel, DMH, MPA, MS, PA-C, RDN, CDE, a clinical professor at Pace University in New York City, was an important insight into the link between mind and body in patients with diabetes.

“As clinicians, we should be worried about mental illness in our patients with diabetes,” Dr. Mandel, a physician assistant educator, said during a presentation at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

In particular, she said, medical professionals should consider how diabetes might contribute to depression – and vice versa.

Dr. Mandel pointed to findings suggesting that 11% of patients with diabetes show signs of clinical depression, which is higher than in the general population, with many more believed to have subclinical depression (Diabetes Care. 2015;38[4]:551-60).

Anxiety can be a key factor in trying to understand how diabetes might contribute to depression. “Diabetes is a very stressful condition ... [and patients] may be fatigued and exhausted.” On top of that, they have to make nutrition changes, or at least pay attention to their diet and overall care, all of which can have a cumulatively negative impact on patient well-being.

Conversely, depression can contribute to diabetes. “They kind of go hand in hand,” she said, pointing to depression’s ability to disrupt appetite, diminish energy, and boost levels of cortisol.

Among the findings that provide evidence of a link between diabetes and depression are those from a study in which investigators estimated that for every 1-point increase in depression symptoms, the risk of diabetes will go up by as much as 5% (Clin Diabetes Endocrinol. 2018 Jan 4. doi: 10.1186/s40842-017-0052-1). Moreover, a 2013 review linked the combination of diabetes and depression to an adjusted 1.5-fold increase in risk of all-cause death (PLoS One. 2013 Mar 5. doi: 10.1371/journal.pone.0057058).

Dr. Mandel offered these tips about diagnosing depression in patients with diabetes and helping them feel comfortable:

• Put yourself in the patient’s shoes. “One of the biggest barriers to referring patients to diabetic education is that they don’t want to have to admit to a group that they have diabetes. They keep it to themselves, to their own detriment. In addition, there’s a lot of worry about insurance.” Patients with diabetes often have self-esteem issues and financial or insurance challenges, all of which need to be factored in when working with them, Dr. Mandel said.
• Ask questions and use screening tools. Two simple questions are helpful in starting a conversation and gathering useful information: Over the past 2 weeks, have you often been bothered by [having] little interest or pleasure in doing things? What about being bothered by feeling down, depressed, or hopeless? If the patient answers “yes” to either of these questions, it will be a positive screen, and two “no” answers will be a negative screen. With the “yes” responses, one should follow-up with a screening tool – typically, the one approved by your institution. Dr. Mandel also highlighted the Patient Health Questionnaire depression scale (PHQ-9), which is available online, or the brief, two-item Diabetes Distress Scale (DDS2) questionnaire.
• Keep your own language in mind. “The way you communicate with your patients can elevate their feeling about themselves or destroy how they feel about themselves,” Dr. Mandel said. “We’re trying to stop calling people with diabetes ‘diabetics.’ People don’t want to be labeled like that. Don’t blame yourself if you use this language, but work to make the changes,” Dr. Mandel suggested.
• Watch out for other forms of bias. Beware of unconsciously stereotyping your patients. “It affects how people relate to you, how they adhere to your suggestions, and how much they’ll trust [and confide in] you, which can have clinical implications,” Dr. Mandel said.

Global Academy and this news organization are owned by the same parent company. Dr. Mandel has no disclosures.

SAN DIEGO – The incidence of polycystic ovary syndrome (PCOS) is on the rise, and a nurse practitioner urged her colleagues to give it full attention because of the danger it poses to patients.

“Underdiagnosed and undermanaged, it’s complex and a more serious condition than ever before because of the complications that can occur,” said R. Mimi Secor, DNP, FNP-BC, FAANP, FAAN, who spoke at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

PCOS is the most common reproductive endocrine disorder in the United States, affecting more than 5 million women, or an estimated 6%-10% of the population. Obesity is a risk factor, although lean women account for 10% of cases for reasons that are not understood, according to Dr. Secor, a senior lecturer at Advanced Practice Education Associates in Onset, Mass. In addition, the condition is linked to many sequelae, including multiple sclerosis, diabetes, cardiovascular disease, infertility, mental health problems, and cancer, she said.

Dr. Secor offered these pearls about PCOS:

• Understand the predictive value of oligomenorrhea (infrequent menstrual periods) as a sign of PCOS. “If you’re working in a low-income clinic, you can do well to make a diagnosis without a lot of expensive tests,” she said.
• Urge women with PCOS to get pregnant early if they want to have children. “Infertility is a big problem [among these women],” she said. “They shouldn’t wait until they’re 35 to have babies. They should have them in their 20s.”
• Use insulin control as a tool. “Insulin stimulates ovarian production of testosterone. If we can manage patients around insulin, that can be very helpful.” Losing just 5% of body weight can make a difference in insulin control, Dr. Secor said. “Go for a small change, and help [the patient] maintain that.”
• Monitor patients carefully for cancer. Women who don’t ovulate regularly on a monthly basis face a higher risk of uterine cancer, compared with women who ovulate monthly, she said, and tumors can develop with few symptoms. “If [there is] one drop of bleeding more than a year after menopause,” you need to get a mandatory workup to make sure the patient doesn’t have uterine cancer. Biopsy remains the “gold standard” as a diagnostic tool, she reminded attendees.
• Watch for mental health conditions, especially anxiety, in patients with PCOS. “They seem to be wired for anxiety, and they need a lot of emotional support,” Dr. Secor said.
• Hormonal contraceptives can be safe and effective as a treatment for PCOS in women who don’t wish to become pregnant, she said. But be aware that combination contraceptive drugs can affect women emotionally.

Global Academy and this news organization are owned by the same parent company. Dr. Secor disclosed speaker relationships with Duchesnay and Osphena.

SAN DIEGO – The incidence of polycystic ovary syndrome (PCOS) is on the rise, and a nurse practitioner urged her colleagues to give it full attention because of the danger it poses to patients.

“Underdiagnosed and undermanaged, it’s complex and a more serious condition than ever before because of the complications that can occur,” said R. Mimi Secor, DNP, FNP-BC, FAANP, FAAN, who spoke at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

PCOS is the most common reproductive endocrine disorder in the United States, affecting more than 5 million women, or an estimated 6%-10% of the population. Obesity is a risk factor, although lean women account for 10% of cases for reasons that are not understood, according to Dr. Secor, a senior lecturer at Advanced Practice Education Associates in Onset, Mass. In addition, the condition is linked to many sequelae, including multiple sclerosis, diabetes, cardiovascular disease, infertility, mental health problems, and cancer, she said.

Dr. Secor offered these pearls about PCOS:

• Understand the predictive value of oligomenorrhea (infrequent menstrual periods) as a sign of PCOS. “If you’re working in a low-income clinic, you can do well to make a diagnosis without a lot of expensive tests,” she said.
• Urge women with PCOS to get pregnant early if they want to have children. “Infertility is a big problem [among these women],” she said. “They shouldn’t wait until they’re 35 to have babies. They should have them in their 20s.”
• Use insulin control as a tool. “Insulin stimulates ovarian production of testosterone. If we can manage patients around insulin, that can be very helpful.” Losing just 5% of body weight can make a difference in insulin control, Dr. Secor said. “Go for a small change, and help [the patient] maintain that.”
• Monitor patients carefully for cancer. Women who don’t ovulate regularly on a monthly basis face a higher risk of uterine cancer, compared with women who ovulate monthly, she said, and tumors can develop with few symptoms. “If [there is] one drop of bleeding more than a year after menopause,” you need to get a mandatory workup to make sure the patient doesn’t have uterine cancer. Biopsy remains the “gold standard” as a diagnostic tool, she reminded attendees.
• Watch for mental health conditions, especially anxiety, in patients with PCOS. “They seem to be wired for anxiety, and they need a lot of emotional support,” Dr. Secor said.
• Hormonal contraceptives can be safe and effective as a treatment for PCOS in women who don’t wish to become pregnant, she said. But be aware that combination contraceptive drugs can affect women emotionally.

Global Academy and this news organization are owned by the same parent company. Dr. Secor disclosed speaker relationships with Duchesnay and Osphena.

SAN DIEGO – The incidence of polycystic ovary syndrome (PCOS) is on the rise, and a nurse practitioner urged her colleagues to give it full attention because of the danger it poses to patients.

“Underdiagnosed and undermanaged, it’s complex and a more serious condition than ever before because of the complications that can occur,” said R. Mimi Secor, DNP, FNP-BC, FAANP, FAAN, who spoke at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

PCOS is the most common reproductive endocrine disorder in the United States, affecting more than 5 million women, or an estimated 6%-10% of the population. Obesity is a risk factor, although lean women account for 10% of cases for reasons that are not understood, according to Dr. Secor, a senior lecturer at Advanced Practice Education Associates in Onset, Mass. In addition, the condition is linked to many sequelae, including multiple sclerosis, diabetes, cardiovascular disease, infertility, mental health problems, and cancer, she said.

Dr. Secor offered these pearls about PCOS:

• Understand the predictive value of oligomenorrhea (infrequent menstrual periods) as a sign of PCOS. “If you’re working in a low-income clinic, you can do well to make a diagnosis without a lot of expensive tests,” she said.
• Urge women with PCOS to get pregnant early if they want to have children. “Infertility is a big problem [among these women],” she said. “They shouldn’t wait until they’re 35 to have babies. They should have them in their 20s.”
• Use insulin control as a tool. “Insulin stimulates ovarian production of testosterone. If we can manage patients around insulin, that can be very helpful.” Losing just 5% of body weight can make a difference in insulin control, Dr. Secor said. “Go for a small change, and help [the patient] maintain that.”
• Monitor patients carefully for cancer. Women who don’t ovulate regularly on a monthly basis face a higher risk of uterine cancer, compared with women who ovulate monthly, she said, and tumors can develop with few symptoms. “If [there is] one drop of bleeding more than a year after menopause,” you need to get a mandatory workup to make sure the patient doesn’t have uterine cancer. Biopsy remains the “gold standard” as a diagnostic tool, she reminded attendees.
• Watch for mental health conditions, especially anxiety, in patients with PCOS. “They seem to be wired for anxiety, and they need a lot of emotional support,” Dr. Secor said.
• Hormonal contraceptives can be safe and effective as a treatment for PCOS in women who don’t wish to become pregnant, she said. But be aware that combination contraceptive drugs can affect women emotionally.

Global Academy and this news organization are owned by the same parent company. Dr. Secor disclosed speaker relationships with Duchesnay and Osphena.

SAN DIEGO – We all know about type 1 and type 2 diabetes. But when an adult patient comes in with symptoms suggestive of diabetes, it is never a good idea to assume it’s either one or the other. In fact, said physician assistant Ji Hyun “CJ” Chun, PA-C, MPAS, BC-ADM, there are plenty of other possibilities from cancer, to monogenetic diabetes, to a condition informally known as type 1.5.

“In most cases, it will be type 1 or type 2, but don’t default everything,” Mr. Chun said at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

He offered the following advice on the diagnosis of adult-onset diabetes:

• Don’t forget the 5% ... and the other 5%. In adults, an estimated 90% of cases of diabetes are type 2, but 5% are type 1 and another 5% are secondary to other conditions, said Mr. Chun, who is based at OptumCare Medical Group, Laguna Niguel, Calif., and has served as president of the American Society of Endocrine PAs. In the past, age seemed to be an important tool for diagnosis, because younger patients typically had type 1 diabetes and older patients typically had type 2, he said. But age alone is no longer useful for diagnosis. Cases of type 2 diabetes are much more common in children these days because of the prevalence of obesity in that population, and an estimated 60% of cases of type 1 disease are diagnosed after the age of 20. In fact, patients may develop type 1 into their 30s, 40s, or 50s, he said, depending on the severity of their autoimmunity.
• Keep ‘type 1.5’ in mind. Latent autoimmune diabetes in adults (LADA), also known as type 1.5, is a slowly developing subtype of type 1 diabetes, Mr. Chun said. There is reason to suspect LADA in lean patients, those younger than 50, and those with personal or family histories of autoimmunity, Mr. Chun said.
• Consider monogenetic diabetes. Many conditions can cause secondary diabetes, among them, monogenetic diabetes, which is caused by a single genetic mutation, whereas type 1 and type 2 diabetes are caused by multiple mutations. Monogenetic diabetes causes an estimated 1%-2% of diabetes cases, said Mr. Chun. Research findings have suggested that it is most likely to be misdiagnosed in younger adults, and that patients may go many years without receiving a correct diagnosis. Maturity-onset diabetes of the young (MODY) is a kind of monogenetic diabetes and typically occurs before the age of 25. There are many subtypes, of which one – MODY 2 – requires no treatment at all. In those patients, said Mr. Chun, “you do nothing. You leave them alone.” It is important to keep in mind that the genetic testing for MODY is expensive, Mr Chun cautioned. Some labs charge between $5,000 and $7,000 for panels, so “look for labs that perform cheaper tests,” he advised, adding that he has found a lab that charges just $250.
• Watch out for cancer. There is a long list of other possible causes of secondary diabetes, including Cushing’s syndrome, hyperthyroidism, hemochromatosis (iron overload), and pancreatic cancer. Mr. Chun said he has lost three patients to pancreatic cancer, while two other patients did well. “Keep in mind that these cases aren’t that common, but they’re there.” He suggested that pancreatic cancer should be considered in patients with rapid onset or worsening of diabetes without known cause, abnormal weight loss, abnormal liver/biliary studies, and jaundice.

Global Academy and this news organization are owned by the same parent company. Mr. Chun disclosed that he is on the AstraZeneca speakers bureau and the Sanofi advisory board.

SAN DIEGO – We all know about type 1 and type 2 diabetes. But when an adult patient comes in with symptoms suggestive of diabetes, it is never a good idea to assume it’s either one or the other. In fact, said physician assistant Ji Hyun “CJ” Chun, PA-C, MPAS, BC-ADM, there are plenty of other possibilities from cancer, to monogenetic diabetes, to a condition informally known as type 1.5.

“In most cases, it will be type 1 or type 2, but don’t default everything,” Mr. Chun said at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

He offered the following advice on the diagnosis of adult-onset diabetes:

• Don’t forget the 5% ... and the other 5%. In adults, an estimated 90% of cases of diabetes are type 2, but 5% are type 1 and another 5% are secondary to other conditions, said Mr. Chun, who is based at OptumCare Medical Group, Laguna Niguel, Calif., and has served as president of the American Society of Endocrine PAs. In the past, age seemed to be an important tool for diagnosis, because younger patients typically had type 1 diabetes and older patients typically had type 2, he said. But age alone is no longer useful for diagnosis. Cases of type 2 diabetes are much more common in children these days because of the prevalence of obesity in that population, and an estimated 60% of cases of type 1 disease are diagnosed after the age of 20. In fact, patients may develop type 1 into their 30s, 40s, or 50s, he said, depending on the severity of their autoimmunity.
• Keep ‘type 1.5’ in mind. Latent autoimmune diabetes in adults (LADA), also known as type 1.5, is a slowly developing subtype of type 1 diabetes, Mr. Chun said. There is reason to suspect LADA in lean patients, those younger than 50, and those with personal or family histories of autoimmunity, Mr. Chun said.
• Consider monogenetic diabetes. Many conditions can cause secondary diabetes, among them, monogenetic diabetes, which is caused by a single genetic mutation, whereas type 1 and type 2 diabetes are caused by multiple mutations. Monogenetic diabetes causes an estimated 1%-2% of diabetes cases, said Mr. Chun. Research findings have suggested that it is most likely to be misdiagnosed in younger adults, and that patients may go many years without receiving a correct diagnosis. Maturity-onset diabetes of the young (MODY) is a kind of monogenetic diabetes and typically occurs before the age of 25. There are many subtypes, of which one – MODY 2 – requires no treatment at all. In those patients, said Mr. Chun, “you do nothing. You leave them alone.” It is important to keep in mind that the genetic testing for MODY is expensive, Mr Chun cautioned. Some labs charge between $5,000 and $7,000 for panels, so “look for labs that perform cheaper tests,” he advised, adding that he has found a lab that charges just $250.
• Watch out for cancer. There is a long list of other possible causes of secondary diabetes, including Cushing’s syndrome, hyperthyroidism, hemochromatosis (iron overload), and pancreatic cancer. Mr. Chun said he has lost three patients to pancreatic cancer, while two other patients did well. “Keep in mind that these cases aren’t that common, but they’re there.” He suggested that pancreatic cancer should be considered in patients with rapid onset or worsening of diabetes without known cause, abnormal weight loss, abnormal liver/biliary studies, and jaundice.

Global Academy and this news organization are owned by the same parent company. Mr. Chun disclosed that he is on the AstraZeneca speakers bureau and the Sanofi advisory board.

SAN DIEGO – We all know about type 1 and type 2 diabetes. But when an adult patient comes in with symptoms suggestive of diabetes, it is never a good idea to assume it’s either one or the other. In fact, said physician assistant Ji Hyun “CJ” Chun, PA-C, MPAS, BC-ADM, there are plenty of other possibilities from cancer, to monogenetic diabetes, to a condition informally known as type 1.5.

“In most cases, it will be type 1 or type 2, but don’t default everything,” Mr. Chun said at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

He offered the following advice on the diagnosis of adult-onset diabetes:

• Don’t forget the 5% ... and the other 5%. In adults, an estimated 90% of cases of diabetes are type 2, but 5% are type 1 and another 5% are secondary to other conditions, said Mr. Chun, who is based at OptumCare Medical Group, Laguna Niguel, Calif., and has served as president of the American Society of Endocrine PAs. In the past, age seemed to be an important tool for diagnosis, because younger patients typically had type 1 diabetes and older patients typically had type 2, he said. But age alone is no longer useful for diagnosis. Cases of type 2 diabetes are much more common in children these days because of the prevalence of obesity in that population, and an estimated 60% of cases of type 1 disease are diagnosed after the age of 20. In fact, patients may develop type 1 into their 30s, 40s, or 50s, he said, depending on the severity of their autoimmunity.
• Keep ‘type 1.5’ in mind. Latent autoimmune diabetes in adults (LADA), also known as type 1.5, is a slowly developing subtype of type 1 diabetes, Mr. Chun said. There is reason to suspect LADA in lean patients, those younger than 50, and those with personal or family histories of autoimmunity, Mr. Chun said.
• Consider monogenetic diabetes. Many conditions can cause secondary diabetes, among them, monogenetic diabetes, which is caused by a single genetic mutation, whereas type 1 and type 2 diabetes are caused by multiple mutations. Monogenetic diabetes causes an estimated 1%-2% of diabetes cases, said Mr. Chun. Research findings have suggested that it is most likely to be misdiagnosed in younger adults, and that patients may go many years without receiving a correct diagnosis. Maturity-onset diabetes of the young (MODY) is a kind of monogenetic diabetes and typically occurs before the age of 25. There are many subtypes, of which one – MODY 2 – requires no treatment at all. In those patients, said Mr. Chun, “you do nothing. You leave them alone.” It is important to keep in mind that the genetic testing for MODY is expensive, Mr Chun cautioned. Some labs charge between $5,000 and $7,000 for panels, so “look for labs that perform cheaper tests,” he advised, adding that he has found a lab that charges just $250.
• Watch out for cancer. There is a long list of other possible causes of secondary diabetes, including Cushing’s syndrome, hyperthyroidism, hemochromatosis (iron overload), and pancreatic cancer. Mr. Chun said he has lost three patients to pancreatic cancer, while two other patients did well. “Keep in mind that these cases aren’t that common, but they’re there.” He suggested that pancreatic cancer should be considered in patients with rapid onset or worsening of diabetes without known cause, abnormal weight loss, abnormal liver/biliary studies, and jaundice.

Global Academy and this news organization are owned by the same parent company. Mr. Chun disclosed that he is on the AstraZeneca speakers bureau and the Sanofi advisory board.

SAN DIEGO – A physician assistant urged colleagues to cast a skeptical eye on male patients who try to jump on board the testosterone therapy train.

“I see many patients getting onto testosterone without having had an adequate evaluation. And I see many patients who might not need testosterone replacement,” Ji Hyun “CJ” Chun, PA-C, MPAS, BC-ADM, said at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

Mr. Chun, who is based at OptumCare Medical Group, Laguna Niguel, Calif., and has served as president of the American Society of Endocrine PAs, offered this advice on evaluating male patients for testosterone therapy:

• Pinpoint the type of hypogonadism. After hypogonadism has been confirmed with lab tests, additional testing should be done to distinguish primary from secondary hypogonadism. Primary hypogonadism refers to the failure of the testes to properly produce testosterone and sperm and is indicated by elevated levels of LH and FSH. Secondary hypogonadism is caused by failures of the hypothalamus, the pituitary, or both, to stimulate the testes to produce testosterone and sperm. It is indicated by low or low-normal levels of LH and FSH.
• Determine the cause of hypogonadism. Cases of hypogonadism are either organic or functional. Diagnostic guidelines provided by the Endocrine Society are helpful in determining the proper category, Mr. Chun said (J Clin Endocrinol Metab. 2018;103[5]:1715-44). Functional hypogonadism is caused by some medications; opioids; abuse of steroids, alcohol, or marijuana; and obesity, which also greatly increases the risk of secondary hypogonadism. These factors – and functional hypogonadism itself – can conceivably be stopped and/or reversed. This form of hypogonadism tends to be mild, compared with organic or “classic” hypogonadism, which is permanent and caused by factors such as advanced age, some types of chemotherapy, and testicle removal. “Organic male hypogonadism mimics female menopause,” Mr. Chun said, in areas such as rate of hormonal decline, which is typically rapid, and hormone deficiency, which is profound. When it comes to treatment, “the benefits far outweigh the risks in organic hypogonadism. But if [a patient has] late-onset [functional] hypogonadism, it gets more complicated.”
• Late-onset hypogonadism treatment. What should be done for patients who have late-onset, organic hypogonadism? According to Mr. Chun, the data regarding testosterone therapy in this population are mixed. The Food and Drug Administration has approved testosterone therapy only for men with organic hypogonadism, he said, noting that “none of the FDA-approved testosterone products are approved for use in men with low testosterone levels who lack an associated medical condition.” However, the Endocrine Society guidelines are less restrictive. In its 2018 guidelines, the society frowned on testosterone therapy for men younger than 65 years with age-related hypogonadism. As for older men, it said that for those “who have symptoms or conditions suggestive of testosterone deficiency (such as low libido or unexplained anemia) and consistently and unequivocally low morning testosterone concentrations, we suggest that clinicians offer testosterone therapy on an individualized basis after explicit discussion of the potential risks and benefits.”
• Don’t push for high testosterone levels. When treating patients, “you want to restore the testosterone to an adequate level,” Mr. Chun said. “What’s an adequate level? We don’t know.” He urged colleagues to not overdo it and to consider aiming for a testosterone level ranging between 350 ng/dL and 700 ng/dL. “I get [the levels] to the lowest level at which the patient is symptomatically fine.”

Global Academy and this news organization are owned by the same parent company. Mr. Chun disclosed that he is on the AstraZeneca speakers bureau and the Sanofi advisory board.

SAN DIEGO – A physician assistant urged colleagues to cast a skeptical eye on male patients who try to jump on board the testosterone therapy train.

“I see many patients getting onto testosterone without having had an adequate evaluation. And I see many patients who might not need testosterone replacement,” Ji Hyun “CJ” Chun, PA-C, MPAS, BC-ADM, said at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

Mr. Chun, who is based at OptumCare Medical Group, Laguna Niguel, Calif., and has served as president of the American Society of Endocrine PAs, offered this advice on evaluating male patients for testosterone therapy:

• Pinpoint the type of hypogonadism. After hypogonadism has been confirmed with lab tests, additional testing should be done to distinguish primary from secondary hypogonadism. Primary hypogonadism refers to the failure of the testes to properly produce testosterone and sperm and is indicated by elevated levels of LH and FSH. Secondary hypogonadism is caused by failures of the hypothalamus, the pituitary, or both, to stimulate the testes to produce testosterone and sperm. It is indicated by low or low-normal levels of LH and FSH.
• Determine the cause of hypogonadism. Cases of hypogonadism are either organic or functional. Diagnostic guidelines provided by the Endocrine Society are helpful in determining the proper category, Mr. Chun said (J Clin Endocrinol Metab. 2018;103[5]:1715-44). Functional hypogonadism is caused by some medications; opioids; abuse of steroids, alcohol, or marijuana; and obesity, which also greatly increases the risk of secondary hypogonadism. These factors – and functional hypogonadism itself – can conceivably be stopped and/or reversed. This form of hypogonadism tends to be mild, compared with organic or “classic” hypogonadism, which is permanent and caused by factors such as advanced age, some types of chemotherapy, and testicle removal. “Organic male hypogonadism mimics female menopause,” Mr. Chun said, in areas such as rate of hormonal decline, which is typically rapid, and hormone deficiency, which is profound. When it comes to treatment, “the benefits far outweigh the risks in organic hypogonadism. But if [a patient has] late-onset [functional] hypogonadism, it gets more complicated.”
• Late-onset hypogonadism treatment. What should be done for patients who have late-onset, organic hypogonadism? According to Mr. Chun, the data regarding testosterone therapy in this population are mixed. The Food and Drug Administration has approved testosterone therapy only for men with organic hypogonadism, he said, noting that “none of the FDA-approved testosterone products are approved for use in men with low testosterone levels who lack an associated medical condition.” However, the Endocrine Society guidelines are less restrictive. In its 2018 guidelines, the society frowned on testosterone therapy for men younger than 65 years with age-related hypogonadism. As for older men, it said that for those “who have symptoms or conditions suggestive of testosterone deficiency (such as low libido or unexplained anemia) and consistently and unequivocally low morning testosterone concentrations, we suggest that clinicians offer testosterone therapy on an individualized basis after explicit discussion of the potential risks and benefits.”
• Don’t push for high testosterone levels. When treating patients, “you want to restore the testosterone to an adequate level,” Mr. Chun said. “What’s an adequate level? We don’t know.” He urged colleagues to not overdo it and to consider aiming for a testosterone level ranging between 350 ng/dL and 700 ng/dL. “I get [the levels] to the lowest level at which the patient is symptomatically fine.”

Global Academy and this news organization are owned by the same parent company. Mr. Chun disclosed that he is on the AstraZeneca speakers bureau and the Sanofi advisory board.

SAN DIEGO – A physician assistant urged colleagues to cast a skeptical eye on male patients who try to jump on board the testosterone therapy train.

“I see many patients getting onto testosterone without having had an adequate evaluation. And I see many patients who might not need testosterone replacement,” Ji Hyun “CJ” Chun, PA-C, MPAS, BC-ADM, said at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education.

Mr. Chun, who is based at OptumCare Medical Group, Laguna Niguel, Calif., and has served as president of the American Society of Endocrine PAs, offered this advice on evaluating male patients for testosterone therapy:

• Pinpoint the type of hypogonadism. After hypogonadism has been confirmed with lab tests, additional testing should be done to distinguish primary from secondary hypogonadism. Primary hypogonadism refers to the failure of the testes to properly produce testosterone and sperm and is indicated by elevated levels of LH and FSH. Secondary hypogonadism is caused by failures of the hypothalamus, the pituitary, or both, to stimulate the testes to produce testosterone and sperm. It is indicated by low or low-normal levels of LH and FSH.
• Determine the cause of hypogonadism. Cases of hypogonadism are either organic or functional. Diagnostic guidelines provided by the Endocrine Society are helpful in determining the proper category, Mr. Chun said (J Clin Endocrinol Metab. 2018;103[5]:1715-44). Functional hypogonadism is caused by some medications; opioids; abuse of steroids, alcohol, or marijuana; and obesity, which also greatly increases the risk of secondary hypogonadism. These factors – and functional hypogonadism itself – can conceivably be stopped and/or reversed. This form of hypogonadism tends to be mild, compared with organic or “classic” hypogonadism, which is permanent and caused by factors such as advanced age, some types of chemotherapy, and testicle removal. “Organic male hypogonadism mimics female menopause,” Mr. Chun said, in areas such as rate of hormonal decline, which is typically rapid, and hormone deficiency, which is profound. When it comes to treatment, “the benefits far outweigh the risks in organic hypogonadism. But if [a patient has] late-onset [functional] hypogonadism, it gets more complicated.”
• Late-onset hypogonadism treatment. What should be done for patients who have late-onset, organic hypogonadism? According to Mr. Chun, the data regarding testosterone therapy in this population are mixed. The Food and Drug Administration has approved testosterone therapy only for men with organic hypogonadism, he said, noting that “none of the FDA-approved testosterone products are approved for use in men with low testosterone levels who lack an associated medical condition.” However, the Endocrine Society guidelines are less restrictive. In its 2018 guidelines, the society frowned on testosterone therapy for men younger than 65 years with age-related hypogonadism. As for older men, it said that for those “who have symptoms or conditions suggestive of testosterone deficiency (such as low libido or unexplained anemia) and consistently and unequivocally low morning testosterone concentrations, we suggest that clinicians offer testosterone therapy on an individualized basis after explicit discussion of the potential risks and benefits.”
• Don’t push for high testosterone levels. When treating patients, “you want to restore the testosterone to an adequate level,” Mr. Chun said. “What’s an adequate level? We don’t know.” He urged colleagues to not overdo it and to consider aiming for a testosterone level ranging between 350 ng/dL and 700 ng/dL. “I get [the levels] to the lowest level at which the patient is symptomatically fine.”

Global Academy and this news organization are owned by the same parent company. Mr. Chun disclosed that he is on the AstraZeneca speakers bureau and the Sanofi advisory board.

SAN DIEGO – When it comes to metabolic and endocrine health, nonalcoholic fatty liver disease (NAFLD) is the furthest thing from a nonissue – it’s “a harbinger of deadly dysmetabolism,” said Christine Kessler, MN, ANP-BC, CNS, BC-ADM, FAANP, a nurse practitioner and founder of Metabolic Medicine Associates, King George, Va.

“I chase it, I follow it, I worry about it. Never look at it again as a benign thing,” Ms. Kessler said in a presentation at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education. “It’s the most common chronic liver disease in the United States – move over, hep C ... and it’ll be the number one cause of liver transplant within 20 years.”

But the news isn’t all grim: NAFLD can be reversible, because the liver is one organ that can “take a licking and keep on ticking,” she said.

An estimated 30%-40% of adults in the United States have NAFLD, according to the National Institute of Diabetes and Digestive and Kidney Diseases. The most severe form of the disease, nonalcoholic steatohepatitis (NASH), causes liver cell damage and affects an estimated 3%-12% of adults.

Why worry about NAFLD? Because it can boost cardiovascular risk (especially in conjunction with metabolic syndrome) and the risk for liver cancer, said Ms. Kessler.

Among the risk factors for NAFLD are obesity, type 2 diabetes, metabolic syndrome, polycystic ovary syndrome, and many others, including medications such as methotrexate, corticosteroids, and tetracyclines. Men, and Latino and Asian individuals are especially vulnerable, whereas black individuals may have protection against it.

Researchers are exploring the possibility that NAFLD is a “multihit” condition that is linked to multiple causes, possibly including overgrowth of bacteria in the gut, Ms. Kessler noted. It is not clear, however, whether regulation of gut microbiota would be helpful in preventing the condition.

Ms. Kessler urged her colleagues to consider workups in the following situations: when an incidental finding is noticed during imaging, when liver enzymes are abnormal (although they can misleadingly appear normal), and when there are overt symptoms of liver diseases. Causes such as alcohol use, medications, and hepatitis must first be ruled out, she said, and patients should be referred to a gastroenterologist if NAFLD is confirmed.

In regard to treatment, weight and diet control are crucial because they can have a significant impact in a patient with NAFLD. “You don’t come down with NAFLD, and then NASH, and then cirrhosis,” she explained. “It goes back and forth. You can go from normal liver to fatty liver, and back to normal. We’ve all seen it.”

Reduce weight, blood pressure, and blood sugar, she said, “and you’ll see NASH go to fatty liver, and fatty liver go over to normal. If you can have someone lose between 9% and 10% of their weight, you can turn around NASH. This is huge.”

As for medications, she said, “there is no one drug for fatty liver disease.” No medication has been approved by the Food and Drug Administration for the treatment of NAFLD or NASH, but there are several treatments that seem to be helpful, she said.

They include statins, though not for patients with decompensated cirrhosis, and some of the diabetes drugs – pioglitazone (Actos; to treat steatohepatitis in patients with or without type 2 diabetes who have biopsy-proven NASH); metformin (only in patients with diabetes); and the glucagon-like peptide-1 receptor agonists.

Also included among the therapies are vitamin E 800 IU/day and omega-3 fatty acids for patients who have a high levels of triglycerides, as well as lower-dose vitamin E (600 IU/day) and vitamin C (500 mg/day), which are best when used with lifestyle changes; increased choline intake – which supports liver health in menopausal women – from foods such as eggs; and milk thistle, which helps decrease liver inflammation.

Patients without chronic liver disease may find another helpful preventive tool on the shelves of their local liquor store: red wine, but with moderation, Ms. Kessler cautioned.

Global Academy and this news organization are owned by the same parent company. Ms. Kessler disclosed relationships as an adviser and speaker with Novo Nordisk, and with Clarion Brands.

SAN DIEGO – When it comes to metabolic and endocrine health, nonalcoholic fatty liver disease (NAFLD) is the furthest thing from a nonissue – it’s “a harbinger of deadly dysmetabolism,” said Christine Kessler, MN, ANP-BC, CNS, BC-ADM, FAANP, a nurse practitioner and founder of Metabolic Medicine Associates, King George, Va.

“I chase it, I follow it, I worry about it. Never look at it again as a benign thing,” Ms. Kessler said in a presentation at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education. “It’s the most common chronic liver disease in the United States – move over, hep C ... and it’ll be the number one cause of liver transplant within 20 years.”

But the news isn’t all grim: NAFLD can be reversible, because the liver is one organ that can “take a licking and keep on ticking,” she said.

An estimated 30%-40% of adults in the United States have NAFLD, according to the National Institute of Diabetes and Digestive and Kidney Diseases. The most severe form of the disease, nonalcoholic steatohepatitis (NASH), causes liver cell damage and affects an estimated 3%-12% of adults.

Why worry about NAFLD? Because it can boost cardiovascular risk (especially in conjunction with metabolic syndrome) and the risk for liver cancer, said Ms. Kessler.

Among the risk factors for NAFLD are obesity, type 2 diabetes, metabolic syndrome, polycystic ovary syndrome, and many others, including medications such as methotrexate, corticosteroids, and tetracyclines. Men, and Latino and Asian individuals are especially vulnerable, whereas black individuals may have protection against it.

Researchers are exploring the possibility that NAFLD is a “multihit” condition that is linked to multiple causes, possibly including overgrowth of bacteria in the gut, Ms. Kessler noted. It is not clear, however, whether regulation of gut microbiota would be helpful in preventing the condition.

Ms. Kessler urged her colleagues to consider workups in the following situations: when an incidental finding is noticed during imaging, when liver enzymes are abnormal (although they can misleadingly appear normal), and when there are overt symptoms of liver diseases. Causes such as alcohol use, medications, and hepatitis must first be ruled out, she said, and patients should be referred to a gastroenterologist if NAFLD is confirmed.

In regard to treatment, weight and diet control are crucial because they can have a significant impact in a patient with NAFLD. “You don’t come down with NAFLD, and then NASH, and then cirrhosis,” she explained. “It goes back and forth. You can go from normal liver to fatty liver, and back to normal. We’ve all seen it.”

Reduce weight, blood pressure, and blood sugar, she said, “and you’ll see NASH go to fatty liver, and fatty liver go over to normal. If you can have someone lose between 9% and 10% of their weight, you can turn around NASH. This is huge.”

As for medications, she said, “there is no one drug for fatty liver disease.” No medication has been approved by the Food and Drug Administration for the treatment of NAFLD or NASH, but there are several treatments that seem to be helpful, she said.

They include statins, though not for patients with decompensated cirrhosis, and some of the diabetes drugs – pioglitazone (Actos; to treat steatohepatitis in patients with or without type 2 diabetes who have biopsy-proven NASH); metformin (only in patients with diabetes); and the glucagon-like peptide-1 receptor agonists.

Also included among the therapies are vitamin E 800 IU/day and omega-3 fatty acids for patients who have a high levels of triglycerides, as well as lower-dose vitamin E (600 IU/day) and vitamin C (500 mg/day), which are best when used with lifestyle changes; increased choline intake – which supports liver health in menopausal women – from foods such as eggs; and milk thistle, which helps decrease liver inflammation.

Patients without chronic liver disease may find another helpful preventive tool on the shelves of their local liquor store: red wine, but with moderation, Ms. Kessler cautioned.

Global Academy and this news organization are owned by the same parent company. Ms. Kessler disclosed relationships as an adviser and speaker with Novo Nordisk, and with Clarion Brands.

SAN DIEGO – When it comes to metabolic and endocrine health, nonalcoholic fatty liver disease (NAFLD) is the furthest thing from a nonissue – it’s “a harbinger of deadly dysmetabolism,” said Christine Kessler, MN, ANP-BC, CNS, BC-ADM, FAANP, a nurse practitioner and founder of Metabolic Medicine Associates, King George, Va.

“I chase it, I follow it, I worry about it. Never look at it again as a benign thing,” Ms. Kessler said in a presentation at the Metabolic & Endocrine Disease Summit by Global Academy for Medical Education. “It’s the most common chronic liver disease in the United States – move over, hep C ... and it’ll be the number one cause of liver transplant within 20 years.”

But the news isn’t all grim: NAFLD can be reversible, because the liver is one organ that can “take a licking and keep on ticking,” she said.

An estimated 30%-40% of adults in the United States have NAFLD, according to the National Institute of Diabetes and Digestive and Kidney Diseases. The most severe form of the disease, nonalcoholic steatohepatitis (NASH), causes liver cell damage and affects an estimated 3%-12% of adults.

Why worry about NAFLD? Because it can boost cardiovascular risk (especially in conjunction with metabolic syndrome) and the risk for liver cancer, said Ms. Kessler.

Among the risk factors for NAFLD are obesity, type 2 diabetes, metabolic syndrome, polycystic ovary syndrome, and many others, including medications such as methotrexate, corticosteroids, and tetracyclines. Men, and Latino and Asian individuals are especially vulnerable, whereas black individuals may have protection against it.

Researchers are exploring the possibility that NAFLD is a “multihit” condition that is linked to multiple causes, possibly including overgrowth of bacteria in the gut, Ms. Kessler noted. It is not clear, however, whether regulation of gut microbiota would be helpful in preventing the condition.

Ms. Kessler urged her colleagues to consider workups in the following situations: when an incidental finding is noticed during imaging, when liver enzymes are abnormal (although they can misleadingly appear normal), and when there are overt symptoms of liver diseases. Causes such as alcohol use, medications, and hepatitis must first be ruled out, she said, and patients should be referred to a gastroenterologist if NAFLD is confirmed.

In regard to treatment, weight and diet control are crucial because they can have a significant impact in a patient with NAFLD. “You don’t come down with NAFLD, and then NASH, and then cirrhosis,” she explained. “It goes back and forth. You can go from normal liver to fatty liver, and back to normal. We’ve all seen it.”

Reduce weight, blood pressure, and blood sugar, she said, “and you’ll see NASH go to fatty liver, and fatty liver go over to normal. If you can have someone lose between 9% and 10% of their weight, you can turn around NASH. This is huge.”

As for medications, she said, “there is no one drug for fatty liver disease.” No medication has been approved by the Food and Drug Administration for the treatment of NAFLD or NASH, but there are several treatments that seem to be helpful, she said.

They include statins, though not for patients with decompensated cirrhosis, and some of the diabetes drugs – pioglitazone (Actos; to treat steatohepatitis in patients with or without type 2 diabetes who have biopsy-proven NASH); metformin (only in patients with diabetes); and the glucagon-like peptide-1 receptor agonists.

Also included among the therapies are vitamin E 800 IU/day and omega-3 fatty acids for patients who have a high levels of triglycerides, as well as lower-dose vitamin E (600 IU/day) and vitamin C (500 mg/day), which are best when used with lifestyle changes; increased choline intake – which supports liver health in menopausal women – from foods such as eggs; and milk thistle, which helps decrease liver inflammation.

Patients without chronic liver disease may find another helpful preventive tool on the shelves of their local liquor store: red wine, but with moderation, Ms. Kessler cautioned.

Global Academy and this news organization are owned by the same parent company. Ms. Kessler disclosed relationships as an adviser and speaker with Novo Nordisk, and with Clarion Brands.

SAN DIEGO – Whatever you do, don’t order a 24-hour urine test. Do encourage “pork holidays.” And choose between an ACE inhibitor and an ARB – don’t give them both to a single patient, according to Kim Zuber, PA-C, MS, a nephrology physician assistant from St. Petersburg, Fla., in a presentation about kidney disease, hypertension, and diabetes at the Metabolic & Endocrine Disease Summit, sponsored by Global Academy for Medical Education.

Ms. Zuber, who is the executive director of the American Academy of Nephrology PAs and the outreach chair of the National Kidney Foundation, outlined some approaches for the diagnosis, management, and treatment of chronic kidney disease (CKD) with comorbid hypertension and diabetes.

• Use the right urine test. Urine albumin testing, which detects albuminuria, is vital in patients who are at risk of chronic kidney disease, Ms. Zuber said, although it’s often not performed. In fact, research suggests that most Medicare patients with diabetes, hypertension, or both do not have this test, she said. Order a urine albumin-to-creatinine ratio (UACR) test at least once a year in at-risk patients, she recommended, and more frequently if they show signs of abnormal values. But be aware, she said, some labs might refer to the test as microalbuminuria instead of UACR, and be prepared to calculate the UACR yourself if your institution provides only albumin and creatinine levels. Also watch out for mix-ups regarding UACR measurements. Nephrotic-range proteinuria starts at 3 g/dL or 3,000 mg/dL, she said, and residents often confuse those two sets of units. “Many have gotten in trouble with that,” she said.
• Don’t go near a 24-hour urine test. Thinking about ordering a 24-hour urine test that requires a patients to collect all their urine for a day? Think again. “We’ve been telling you almost 20 years not to do this,” Ms. Zuber said. These tests “are unreliable, and they don’t work.”
• Don’t focus on tight blood pressure control. Studies provide little insight into the ideal blood pressure readings for patients with diabetes and CKD, according to Ms. Zuber, but some findings suggest that tight control can be harmful to the kidneys. She urges her patients to treat hypertension in part by embracing lifestyle change. “I tell them that if you improve your lifestyle, you can give up one of your drugs. When they average 15 drugs a day, that becomes popular.” Physical activity, the DASH diet, salt restriction, moderate alcohol consumption, weight loss, stress reduction, and smoking cessation can all lower blood pressure, she added.
• Talk up the “pork holiday.” For patients with hypertension, “sodium restriction is huge,” Ms. Zuber said, especially among black patients. She urges her patients to take “pork holidays”, that is, eat pork only four times a year, on holidays such as the Fourth of July. She also urges them to prepare food in ways that begin with B, as in bake, boil, and barbecue. “You’ll notice that ‘fry’ doesn’t start with a B.”
• Try an ACE inhibitor or an ARB, but not both. In patients with hypertension plus diabetes and/or CKD, Ms. Zuber suggests using an angiotensin-converting enzyme inhibitor or angiotensin receptor blockers, but not both. One or the other can improve albuminuria, she said, but together they can boost risk of CKD, hyperkalemia, and hypotension.

Consider factors such as formularies and personal experience when trying to decide which drug to use, she said. If a patient still has hypertension, consider a diuretic and then move to a calcium channel or beta blocker. However, she cautioned, although beta blockers, they can cause erectile dysfunction.

Global Academy for Medical Education and this news organization are owned by the same parent company. Ms. Zuber reported no disclosures.

SAN DIEGO – Whatever you do, don’t order a 24-hour urine test. Do encourage “pork holidays.” And choose between an ACE inhibitor and an ARB – don’t give them both to a single patient, according to Kim Zuber, PA-C, MS, a nephrology physician assistant from St. Petersburg, Fla., in a presentation about kidney disease, hypertension, and diabetes at the Metabolic & Endocrine Disease Summit, sponsored by Global Academy for Medical Education.

Ms. Zuber, who is the executive director of the American Academy of Nephrology PAs and the outreach chair of the National Kidney Foundation, outlined some approaches for the diagnosis, management, and treatment of chronic kidney disease (CKD) with comorbid hypertension and diabetes.

• Use the right urine test. Urine albumin testing, which detects albuminuria, is vital in patients who are at risk of chronic kidney disease, Ms. Zuber said, although it’s often not performed. In fact, research suggests that most Medicare patients with diabetes, hypertension, or both do not have this test, she said. Order a urine albumin-to-creatinine ratio (UACR) test at least once a year in at-risk patients, she recommended, and more frequently if they show signs of abnormal values. But be aware, she said, some labs might refer to the test as microalbuminuria instead of UACR, and be prepared to calculate the UACR yourself if your institution provides only albumin and creatinine levels. Also watch out for mix-ups regarding UACR measurements. Nephrotic-range proteinuria starts at 3 g/dL or 3,000 mg/dL, she said, and residents often confuse those two sets of units. “Many have gotten in trouble with that,” she said.
• Don’t go near a 24-hour urine test. Thinking about ordering a 24-hour urine test that requires a patients to collect all their urine for a day? Think again. “We’ve been telling you almost 20 years not to do this,” Ms. Zuber said. These tests “are unreliable, and they don’t work.”
• Don’t focus on tight blood pressure control. Studies provide little insight into the ideal blood pressure readings for patients with diabetes and CKD, according to Ms. Zuber, but some findings suggest that tight control can be harmful to the kidneys. She urges her patients to treat hypertension in part by embracing lifestyle change. “I tell them that if you improve your lifestyle, you can give up one of your drugs. When they average 15 drugs a day, that becomes popular.” Physical activity, the DASH diet, salt restriction, moderate alcohol consumption, weight loss, stress reduction, and smoking cessation can all lower blood pressure, she added.
• Talk up the “pork holiday.” For patients with hypertension, “sodium restriction is huge,” Ms. Zuber said, especially among black patients. She urges her patients to take “pork holidays”, that is, eat pork only four times a year, on holidays such as the Fourth of July. She also urges them to prepare food in ways that begin with B, as in bake, boil, and barbecue. “You’ll notice that ‘fry’ doesn’t start with a B.”
• Try an ACE inhibitor or an ARB, but not both. In patients with hypertension plus diabetes and/or CKD, Ms. Zuber suggests using an angiotensin-converting enzyme inhibitor or angiotensin receptor blockers, but not both. One or the other can improve albuminuria, she said, but together they can boost risk of CKD, hyperkalemia, and hypotension.

Consider factors such as formularies and personal experience when trying to decide which drug to use, she said. If a patient still has hypertension, consider a diuretic and then move to a calcium channel or beta blocker. However, she cautioned, although beta blockers, they can cause erectile dysfunction.

Global Academy for Medical Education and this news organization are owned by the same parent company. Ms. Zuber reported no disclosures.

SAN DIEGO – Whatever you do, don’t order a 24-hour urine test. Do encourage “pork holidays.” And choose between an ACE inhibitor and an ARB – don’t give them both to a single patient, according to Kim Zuber, PA-C, MS, a nephrology physician assistant from St. Petersburg, Fla., in a presentation about kidney disease, hypertension, and diabetes at the Metabolic & Endocrine Disease Summit, sponsored by Global Academy for Medical Education.

Ms. Zuber, who is the executive director of the American Academy of Nephrology PAs and the outreach chair of the National Kidney Foundation, outlined some approaches for the diagnosis, management, and treatment of chronic kidney disease (CKD) with comorbid hypertension and diabetes.

• Use the right urine test. Urine albumin testing, which detects albuminuria, is vital in patients who are at risk of chronic kidney disease, Ms. Zuber said, although it’s often not performed. In fact, research suggests that most Medicare patients with diabetes, hypertension, or both do not have this test, she said. Order a urine albumin-to-creatinine ratio (UACR) test at least once a year in at-risk patients, she recommended, and more frequently if they show signs of abnormal values. But be aware, she said, some labs might refer to the test as microalbuminuria instead of UACR, and be prepared to calculate the UACR yourself if your institution provides only albumin and creatinine levels. Also watch out for mix-ups regarding UACR measurements. Nephrotic-range proteinuria starts at 3 g/dL or 3,000 mg/dL, she said, and residents often confuse those two sets of units. “Many have gotten in trouble with that,” she said.
• Don’t go near a 24-hour urine test. Thinking about ordering a 24-hour urine test that requires a patients to collect all their urine for a day? Think again. “We’ve been telling you almost 20 years not to do this,” Ms. Zuber said. These tests “are unreliable, and they don’t work.”
• Don’t focus on tight blood pressure control. Studies provide little insight into the ideal blood pressure readings for patients with diabetes and CKD, according to Ms. Zuber, but some findings suggest that tight control can be harmful to the kidneys. She urges her patients to treat hypertension in part by embracing lifestyle change. “I tell them that if you improve your lifestyle, you can give up one of your drugs. When they average 15 drugs a day, that becomes popular.” Physical activity, the DASH diet, salt restriction, moderate alcohol consumption, weight loss, stress reduction, and smoking cessation can all lower blood pressure, she added.
• Talk up the “pork holiday.” For patients with hypertension, “sodium restriction is huge,” Ms. Zuber said, especially among black patients. She urges her patients to take “pork holidays”, that is, eat pork only four times a year, on holidays such as the Fourth of July. She also urges them to prepare food in ways that begin with B, as in bake, boil, and barbecue. “You’ll notice that ‘fry’ doesn’t start with a B.”
• Try an ACE inhibitor or an ARB, but not both. In patients with hypertension plus diabetes and/or CKD, Ms. Zuber suggests using an angiotensin-converting enzyme inhibitor or angiotensin receptor blockers, but not both. One or the other can improve albuminuria, she said, but together they can boost risk of CKD, hyperkalemia, and hypotension.

Consider factors such as formularies and personal experience when trying to decide which drug to use, she said. If a patient still has hypertension, consider a diuretic and then move to a calcium channel or beta blocker. However, she cautioned, although beta blockers, they can cause erectile dysfunction.

Global Academy for Medical Education and this news organization are owned by the same parent company. Ms. Zuber reported no disclosures.