What Matters

The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.

Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.

Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).

But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?

In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).

The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.

The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.

Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.

The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.

Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.

Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).

But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?

In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).

The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.

The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.

Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.

The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.

Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.

Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).

But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?

In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).

The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.

The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.

Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.

Although some may perceive that cigarette smoking is the leading cause of statistics, smoking sadly remains the leading cause of preventable death and disability in the United States. Smoking causes one of every five deaths. Tobacco dependence is an addiction, and addiction is hard – really hard. That is why, despite mass casualties from a risk known to arguably all smokers, an estimated 45.3 million U.S. adults (19.3%) currently light up some days or every day.

Because there is no safe level of smoking, abstinence remains the goal. Varenicline, an alpha 4 beta 2 nicotine acetylcholine receptor partial agonist, is one of the most effective treatments we have ever had to combat tobacco dependence. Varenicline is given at a target dose of 1 mg twice per day by mouth. But, as most of us have realized, varenicline does not work for everybody.

New data suggest, however, that for patients who do not respond to the standard dose of varenicline, a higher dose may be helpful (Mayo Clin. Proc. 2013;88:1443-5).

Dr. Carlos A. Jiménez-Ruiz of Spain’s Smoking Cessation Service in the County of Madrid reviewed data from a clinical program consisting of behavioral and pharmacologic components. Patients received varenicline at a target dose of 1 mg twice a day for 8 weeks. After 8 weeks, if patients were still smoking or were smoking abstinent but experienced significant withdrawal, the dose was increased to 3 mg a day (1 mg every 8 hours).

Biochemically confirmed smoking abstinence from week 9 to week 24 was 40% in those who had continued smoking after 8 weeks and 48% in the group abstinent from smoking but experiencing significant withdrawal. In those two groups, 30% of patients had adverse events, which included nausea, vomiting, abnormal dreams, and insomnia.

Smokers receiving varenicline 3 mg per day in this study smoked an average of 36 cigarettes per day. The study authors hypothesized that a higher dose may be required for some smokers, because the standard dose does not saturate enough nicotinic receptors.

We do not know the extent to which this is true, but data suggest that higher doses of other medications, such as nicotine patches, are more effective for smokers than lower doses. Prescribing may work for some smokers, but the higher dose may generate a preauthorization. Let me know if it does.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. Dr. Ebbert has received research funding from Pfizer, manufacturer of varenicline. Contact him at imnews@frontlinemedcom.com.

Although some may perceive that cigarette smoking is the leading cause of statistics, smoking sadly remains the leading cause of preventable death and disability in the United States. Smoking causes one of every five deaths. Tobacco dependence is an addiction, and addiction is hard – really hard. That is why, despite mass casualties from a risk known to arguably all smokers, an estimated 45.3 million U.S. adults (19.3%) currently light up some days or every day.

Because there is no safe level of smoking, abstinence remains the goal. Varenicline, an alpha 4 beta 2 nicotine acetylcholine receptor partial agonist, is one of the most effective treatments we have ever had to combat tobacco dependence. Varenicline is given at a target dose of 1 mg twice per day by mouth. But, as most of us have realized, varenicline does not work for everybody.

New data suggest, however, that for patients who do not respond to the standard dose of varenicline, a higher dose may be helpful (Mayo Clin. Proc. 2013;88:1443-5).

Dr. Carlos A. Jiménez-Ruiz of Spain’s Smoking Cessation Service in the County of Madrid reviewed data from a clinical program consisting of behavioral and pharmacologic components. Patients received varenicline at a target dose of 1 mg twice a day for 8 weeks. After 8 weeks, if patients were still smoking or were smoking abstinent but experienced significant withdrawal, the dose was increased to 3 mg a day (1 mg every 8 hours).

Biochemically confirmed smoking abstinence from week 9 to week 24 was 40% in those who had continued smoking after 8 weeks and 48% in the group abstinent from smoking but experiencing significant withdrawal. In those two groups, 30% of patients had adverse events, which included nausea, vomiting, abnormal dreams, and insomnia.

Smokers receiving varenicline 3 mg per day in this study smoked an average of 36 cigarettes per day. The study authors hypothesized that a higher dose may be required for some smokers, because the standard dose does not saturate enough nicotinic receptors.

We do not know the extent to which this is true, but data suggest that higher doses of other medications, such as nicotine patches, are more effective for smokers than lower doses. Prescribing may work for some smokers, but the higher dose may generate a preauthorization. Let me know if it does.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. Dr. Ebbert has received research funding from Pfizer, manufacturer of varenicline. Contact him at imnews@frontlinemedcom.com.

Although some may perceive that cigarette smoking is the leading cause of statistics, smoking sadly remains the leading cause of preventable death and disability in the United States. Smoking causes one of every five deaths. Tobacco dependence is an addiction, and addiction is hard – really hard. That is why, despite mass casualties from a risk known to arguably all smokers, an estimated 45.3 million U.S. adults (19.3%) currently light up some days or every day.

Because there is no safe level of smoking, abstinence remains the goal. Varenicline, an alpha 4 beta 2 nicotine acetylcholine receptor partial agonist, is one of the most effective treatments we have ever had to combat tobacco dependence. Varenicline is given at a target dose of 1 mg twice per day by mouth. But, as most of us have realized, varenicline does not work for everybody.

New data suggest, however, that for patients who do not respond to the standard dose of varenicline, a higher dose may be helpful (Mayo Clin. Proc. 2013;88:1443-5).

Dr. Carlos A. Jiménez-Ruiz of Spain’s Smoking Cessation Service in the County of Madrid reviewed data from a clinical program consisting of behavioral and pharmacologic components. Patients received varenicline at a target dose of 1 mg twice a day for 8 weeks. After 8 weeks, if patients were still smoking or were smoking abstinent but experienced significant withdrawal, the dose was increased to 3 mg a day (1 mg every 8 hours).

Biochemically confirmed smoking abstinence from week 9 to week 24 was 40% in those who had continued smoking after 8 weeks and 48% in the group abstinent from smoking but experiencing significant withdrawal. In those two groups, 30% of patients had adverse events, which included nausea, vomiting, abnormal dreams, and insomnia.

Smokers receiving varenicline 3 mg per day in this study smoked an average of 36 cigarettes per day. The study authors hypothesized that a higher dose may be required for some smokers, because the standard dose does not saturate enough nicotinic receptors.

We do not know the extent to which this is true, but data suggest that higher doses of other medications, such as nicotine patches, are more effective for smokers than lower doses. Prescribing may work for some smokers, but the higher dose may generate a preauthorization. Let me know if it does.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. Dr. Ebbert has received research funding from Pfizer, manufacturer of varenicline. Contact him at imnews@frontlinemedcom.com.

Many of the patients who seek our help in the midst of the cold and flu season seek what anybody suffering seeks: palliation. But perhaps it is the nature of our times and practice that we find ourselves steeling our nerves for confrontation the moment we mentally conclude that no antibiotic or antiviral is required. Recently, more often than not, I am pleasantly surprised by patient response to this. But perhaps I am more at ease with my position considering the increasing number of patients developing recalcitrant Clostridium difficile colitis from antibiotics.

Some patients may already be fully engaged with products frequenting my laundry list of cold remedies: ibuprofen, acetaminophen, decongestants, guaifenesin, vitamin C, and copious amounts of fluids. For patients who are struggling with the rhinorrhea associated with the common cold, intranasal ipratropium could work as well.

When taken intranasally, ipratropium bromide blocks muscarinic acetylcholine receptors, which, in turn, inhibits mucous secretion. Caution should be exercised in patients with urinary tract obstruction and glaucoma.

But are we prescribing it for the common cold? How effective is it?

AlBalawi et al. updated their systematic review on intranasal ipratropium as a treatment for rhinorrhea and nasal congestion associated with the common cold. Investigators searched for randomized controlled trials that compared ipratropium to placebo or to no treatment in children and adults with the common cold (Cochrane Database Syst. Rev. 2013;6:CD008231 [doi: 10.1002/14651858.CD008231.pub3]).

Seven trials were included with a total of 2,144 participants. All studies were consistent in reporting significant benefits of ipratropium. However, ipratropium is associated with side effects (odds ratio, 2.09; 95% confidence interval, 1.40-3.11). The most common side effects include nasal dryness, blood-tinged mucus, and epistaxis.

Nasal ipratropium is expensive, however. The approximate retail price is $130 for a 30 mL bottle at 0.03%. Patients would need to check if their insurance covers it. If not, then patients can decide themselves if it is worth the expense.

We sometimes need to remind ourselves that our job frequently is to reassure. Ipratropium may buy the patient and ourselves some time as we wait for the patient’s immune system to eradicate the problem. Checking with the insurance company on coverage may buy us even a little more time.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

Many of the patients who seek our help in the midst of the cold and flu season seek what anybody suffering seeks: palliation. But perhaps it is the nature of our times and practice that we find ourselves steeling our nerves for confrontation the moment we mentally conclude that no antibiotic or antiviral is required. Recently, more often than not, I am pleasantly surprised by patient response to this. But perhaps I am more at ease with my position considering the increasing number of patients developing recalcitrant Clostridium difficile colitis from antibiotics.

Some patients may already be fully engaged with products frequenting my laundry list of cold remedies: ibuprofen, acetaminophen, decongestants, guaifenesin, vitamin C, and copious amounts of fluids. For patients who are struggling with the rhinorrhea associated with the common cold, intranasal ipratropium could work as well.

When taken intranasally, ipratropium bromide blocks muscarinic acetylcholine receptors, which, in turn, inhibits mucous secretion. Caution should be exercised in patients with urinary tract obstruction and glaucoma.

But are we prescribing it for the common cold? How effective is it?

AlBalawi et al. updated their systematic review on intranasal ipratropium as a treatment for rhinorrhea and nasal congestion associated with the common cold. Investigators searched for randomized controlled trials that compared ipratropium to placebo or to no treatment in children and adults with the common cold (Cochrane Database Syst. Rev. 2013;6:CD008231 [doi: 10.1002/14651858.CD008231.pub3]).

Seven trials were included with a total of 2,144 participants. All studies were consistent in reporting significant benefits of ipratropium. However, ipratropium is associated with side effects (odds ratio, 2.09; 95% confidence interval, 1.40-3.11). The most common side effects include nasal dryness, blood-tinged mucus, and epistaxis.

Nasal ipratropium is expensive, however. The approximate retail price is $130 for a 30 mL bottle at 0.03%. Patients would need to check if their insurance covers it. If not, then patients can decide themselves if it is worth the expense.

We sometimes need to remind ourselves that our job frequently is to reassure. Ipratropium may buy the patient and ourselves some time as we wait for the patient’s immune system to eradicate the problem. Checking with the insurance company on coverage may buy us even a little more time.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

Many of the patients who seek our help in the midst of the cold and flu season seek what anybody suffering seeks: palliation. But perhaps it is the nature of our times and practice that we find ourselves steeling our nerves for confrontation the moment we mentally conclude that no antibiotic or antiviral is required. Recently, more often than not, I am pleasantly surprised by patient response to this. But perhaps I am more at ease with my position considering the increasing number of patients developing recalcitrant Clostridium difficile colitis from antibiotics.

Some patients may already be fully engaged with products frequenting my laundry list of cold remedies: ibuprofen, acetaminophen, decongestants, guaifenesin, vitamin C, and copious amounts of fluids. For patients who are struggling with the rhinorrhea associated with the common cold, intranasal ipratropium could work as well.

When taken intranasally, ipratropium bromide blocks muscarinic acetylcholine receptors, which, in turn, inhibits mucous secretion. Caution should be exercised in patients with urinary tract obstruction and glaucoma.

But are we prescribing it for the common cold? How effective is it?

AlBalawi et al. updated their systematic review on intranasal ipratropium as a treatment for rhinorrhea and nasal congestion associated with the common cold. Investigators searched for randomized controlled trials that compared ipratropium to placebo or to no treatment in children and adults with the common cold (Cochrane Database Syst. Rev. 2013;6:CD008231 [doi: 10.1002/14651858.CD008231.pub3]).

Seven trials were included with a total of 2,144 participants. All studies were consistent in reporting significant benefits of ipratropium. However, ipratropium is associated with side effects (odds ratio, 2.09; 95% confidence interval, 1.40-3.11). The most common side effects include nasal dryness, blood-tinged mucus, and epistaxis.

Nasal ipratropium is expensive, however. The approximate retail price is $130 for a 30 mL bottle at 0.03%. Patients would need to check if their insurance covers it. If not, then patients can decide themselves if it is worth the expense.

We sometimes need to remind ourselves that our job frequently is to reassure. Ipratropium may buy the patient and ourselves some time as we wait for the patient’s immune system to eradicate the problem. Checking with the insurance company on coverage may buy us even a little more time.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

The Internet age has ushered in a dizzying array of new psychoactive substances. Many of these drugs have been marketed as "legal highs," staying ahead of regulatory authority through drug structure modification.

One of these drug classes is synthetic cannabinoids. This class is often referred to using the generic terms "Spice" or "K2." These substances emerged from scientific investigations in the 1980s into novel therapeutics for AIDS, multiple sclerosis, and cancer. They mimic but do not exactly replicate the structure of THC (tetrahydrocannabinol), the principal psychoactive constituent of cannabis. They are high-affinity full agonists at the cannabinoid receptor, which may be responsible for the adverse clinical effects associated with their use.

What are the effects of this class of drugs?

A recent Morbidity and Mortality Weekly Report provides information about a series of 22 patients who had been examined after using synthetic cannabinoids between Aug. 22 and Sept. 9, 2013 (MMWR 2013;62:939). These patients were aged 16-57 years and 82% were male. Patients experienced hyperglycemia, hypokalemia, acidosis, tachycardia, nausea and vomiting, confusion and disorientation, aggression, unresponsiveness, and seizures. Five patients required assisted ventilation but none of them died. The product was sold in a smoke shop in Brunswick, Ga. Previous reports have highlighted the possibility of kidney injury, as well.

The Synthetic Drug Abuse Prevention Act of 2012 was signed into law in July by President Obama. The act banned synthetic compounds commonly found in synthetic cannabinoids, placing them under schedule I status. But, as we see from the report above, these substances are still available.

Many use synthetic cannabinoids to avoid detection because these substances do not show up on routine drug tests – special testing and a high degree of suspicion are needed. Use of these drugs can lead to dependence and withdrawal symptoms when they are discontinued. Referral to drug treatment specialists is the best approach when we suspect patients are struggling with addiction and using synthetic cannabinoids.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported no relevant financial conflicts of interest.

The Internet age has ushered in a dizzying array of new psychoactive substances. Many of these drugs have been marketed as "legal highs," staying ahead of regulatory authority through drug structure modification.

One of these drug classes is synthetic cannabinoids. This class is often referred to using the generic terms "Spice" or "K2." These substances emerged from scientific investigations in the 1980s into novel therapeutics for AIDS, multiple sclerosis, and cancer. They mimic but do not exactly replicate the structure of THC (tetrahydrocannabinol), the principal psychoactive constituent of cannabis. They are high-affinity full agonists at the cannabinoid receptor, which may be responsible for the adverse clinical effects associated with their use.

What are the effects of this class of drugs?

A recent Morbidity and Mortality Weekly Report provides information about a series of 22 patients who had been examined after using synthetic cannabinoids between Aug. 22 and Sept. 9, 2013 (MMWR 2013;62:939). These patients were aged 16-57 years and 82% were male. Patients experienced hyperglycemia, hypokalemia, acidosis, tachycardia, nausea and vomiting, confusion and disorientation, aggression, unresponsiveness, and seizures. Five patients required assisted ventilation but none of them died. The product was sold in a smoke shop in Brunswick, Ga. Previous reports have highlighted the possibility of kidney injury, as well.

The Synthetic Drug Abuse Prevention Act of 2012 was signed into law in July by President Obama. The act banned synthetic compounds commonly found in synthetic cannabinoids, placing them under schedule I status. But, as we see from the report above, these substances are still available.

Many use synthetic cannabinoids to avoid detection because these substances do not show up on routine drug tests – special testing and a high degree of suspicion are needed. Use of these drugs can lead to dependence and withdrawal symptoms when they are discontinued. Referral to drug treatment specialists is the best approach when we suspect patients are struggling with addiction and using synthetic cannabinoids.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported no relevant financial conflicts of interest.

The Internet age has ushered in a dizzying array of new psychoactive substances. Many of these drugs have been marketed as "legal highs," staying ahead of regulatory authority through drug structure modification.

One of these drug classes is synthetic cannabinoids. This class is often referred to using the generic terms "Spice" or "K2." These substances emerged from scientific investigations in the 1980s into novel therapeutics for AIDS, multiple sclerosis, and cancer. They mimic but do not exactly replicate the structure of THC (tetrahydrocannabinol), the principal psychoactive constituent of cannabis. They are high-affinity full agonists at the cannabinoid receptor, which may be responsible for the adverse clinical effects associated with their use.

What are the effects of this class of drugs?

A recent Morbidity and Mortality Weekly Report provides information about a series of 22 patients who had been examined after using synthetic cannabinoids between Aug. 22 and Sept. 9, 2013 (MMWR 2013;62:939). These patients were aged 16-57 years and 82% were male. Patients experienced hyperglycemia, hypokalemia, acidosis, tachycardia, nausea and vomiting, confusion and disorientation, aggression, unresponsiveness, and seizures. Five patients required assisted ventilation but none of them died. The product was sold in a smoke shop in Brunswick, Ga. Previous reports have highlighted the possibility of kidney injury, as well.

The Synthetic Drug Abuse Prevention Act of 2012 was signed into law in July by President Obama. The act banned synthetic compounds commonly found in synthetic cannabinoids, placing them under schedule I status. But, as we see from the report above, these substances are still available.

Many use synthetic cannabinoids to avoid detection because these substances do not show up on routine drug tests – special testing and a high degree of suspicion are needed. Use of these drugs can lead to dependence and withdrawal symptoms when they are discontinued. Referral to drug treatment specialists is the best approach when we suspect patients are struggling with addiction and using synthetic cannabinoids.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported no relevant financial conflicts of interest.

Benign prostatic hyperplasia is a common condition. An estimated 50% of men over the age of 50 years have BPH. Presenting symptoms include urinary hesitancy, urgency, decreased strength of stream, and double-voiding. In my practice, nocturia is usually what starts the conversation.

First-line therapies include alpha-1 adrenergic receptor antagonists ("alpha-blockers") and 5-alpha-reductase inhibitors ("5-ARIs"). Alpha-blockers are effective, but are associated with orthostasis and syncopal events. Orthostasis has been more commonly associated with medications such as doxazosin and terazosin (in other words, "first-dose phenomenon"). Tamsulosin, a uroselective agent, is supposedly less likely to cause decreases in blood pressure.

But is tamsulosin associated with clinically important dips in blood pressure?

Steven T. Bird, Pharm.D., of the Food and Drug Administration’s Center for Drug Evaluation and Research, and his colleagues published the results from a retrospective, population-based cohort study examining whether tamsulosin is associated with hypotension and hospitalization (i.e., "severe hypotension"). Using information from a database of paid claims from more than 102 health care plans, the authors identified men aged 40-85 years who received alpha-blockers and 5-ARIs. In total, 297,596 new users of tamsulosin and 85,971 new users of 5-ARIs were identified. Median duration of use was 14 weeks for tamsulosin and 34 weeks for 5-ARIs (BMJ 2013;347:f6320).

Patients who took tamsulosin were 2.12 times more likely to experience severe hypotension during the first 4 weeks of therapy (95% confidence interval: 1.29-3.04). During weeks 5-8, severe hypotension was 1.51 times more likely in those who used tamsulosin (95% CI: 1.04-2.18). No significantly increased risk of hypotension was noted during weeks 9-12. Drug restarting (after a 4-week gap) was associated with a significantly increased risk of severe hypotension through 8 weeks of therapy, but not during weeks 9-12. Patients also were at an increased risk of hypotension during maintenance therapy.

In clinical trials of tamsulosin, patients were retained at research sites for 8 hours after the first dose and counseled on the effects of orthostatic hypotension – an environment that "may not apply to treatment practice in the real world," the authors cautioned. The incidence of hypotension in those studies was 12%, compared with 6% for placebo.

We should remind our patients that tamsulosin can cause clinically important dips in blood pressure. Simple instructions about sitting on the edge of the bed when going from supine to standing could make the difference between a better night’s sleep and a worse one in the hospital.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

Benign prostatic hyperplasia is a common condition. An estimated 50% of men over the age of 50 years have BPH. Presenting symptoms include urinary hesitancy, urgency, decreased strength of stream, and double-voiding. In my practice, nocturia is usually what starts the conversation.

First-line therapies include alpha-1 adrenergic receptor antagonists ("alpha-blockers") and 5-alpha-reductase inhibitors ("5-ARIs"). Alpha-blockers are effective, but are associated with orthostasis and syncopal events. Orthostasis has been more commonly associated with medications such as doxazosin and terazosin (in other words, "first-dose phenomenon"). Tamsulosin, a uroselective agent, is supposedly less likely to cause decreases in blood pressure.

But is tamsulosin associated with clinically important dips in blood pressure?

Steven T. Bird, Pharm.D., of the Food and Drug Administration’s Center for Drug Evaluation and Research, and his colleagues published the results from a retrospective, population-based cohort study examining whether tamsulosin is associated with hypotension and hospitalization (i.e., "severe hypotension"). Using information from a database of paid claims from more than 102 health care plans, the authors identified men aged 40-85 years who received alpha-blockers and 5-ARIs. In total, 297,596 new users of tamsulosin and 85,971 new users of 5-ARIs were identified. Median duration of use was 14 weeks for tamsulosin and 34 weeks for 5-ARIs (BMJ 2013;347:f6320).

Patients who took tamsulosin were 2.12 times more likely to experience severe hypotension during the first 4 weeks of therapy (95% confidence interval: 1.29-3.04). During weeks 5-8, severe hypotension was 1.51 times more likely in those who used tamsulosin (95% CI: 1.04-2.18). No significantly increased risk of hypotension was noted during weeks 9-12. Drug restarting (after a 4-week gap) was associated with a significantly increased risk of severe hypotension through 8 weeks of therapy, but not during weeks 9-12. Patients also were at an increased risk of hypotension during maintenance therapy.

In clinical trials of tamsulosin, patients were retained at research sites for 8 hours after the first dose and counseled on the effects of orthostatic hypotension – an environment that "may not apply to treatment practice in the real world," the authors cautioned. The incidence of hypotension in those studies was 12%, compared with 6% for placebo.

We should remind our patients that tamsulosin can cause clinically important dips in blood pressure. Simple instructions about sitting on the edge of the bed when going from supine to standing could make the difference between a better night’s sleep and a worse one in the hospital.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

Benign prostatic hyperplasia is a common condition. An estimated 50% of men over the age of 50 years have BPH. Presenting symptoms include urinary hesitancy, urgency, decreased strength of stream, and double-voiding. In my practice, nocturia is usually what starts the conversation.

First-line therapies include alpha-1 adrenergic receptor antagonists ("alpha-blockers") and 5-alpha-reductase inhibitors ("5-ARIs"). Alpha-blockers are effective, but are associated with orthostasis and syncopal events. Orthostasis has been more commonly associated with medications such as doxazosin and terazosin (in other words, "first-dose phenomenon"). Tamsulosin, a uroselective agent, is supposedly less likely to cause decreases in blood pressure.

But is tamsulosin associated with clinically important dips in blood pressure?

Steven T. Bird, Pharm.D., of the Food and Drug Administration’s Center for Drug Evaluation and Research, and his colleagues published the results from a retrospective, population-based cohort study examining whether tamsulosin is associated with hypotension and hospitalization (i.e., "severe hypotension"). Using information from a database of paid claims from more than 102 health care plans, the authors identified men aged 40-85 years who received alpha-blockers and 5-ARIs. In total, 297,596 new users of tamsulosin and 85,971 new users of 5-ARIs were identified. Median duration of use was 14 weeks for tamsulosin and 34 weeks for 5-ARIs (BMJ 2013;347:f6320).

Patients who took tamsulosin were 2.12 times more likely to experience severe hypotension during the first 4 weeks of therapy (95% confidence interval: 1.29-3.04). During weeks 5-8, severe hypotension was 1.51 times more likely in those who used tamsulosin (95% CI: 1.04-2.18). No significantly increased risk of hypotension was noted during weeks 9-12. Drug restarting (after a 4-week gap) was associated with a significantly increased risk of severe hypotension through 8 weeks of therapy, but not during weeks 9-12. Patients also were at an increased risk of hypotension during maintenance therapy.

In clinical trials of tamsulosin, patients were retained at research sites for 8 hours after the first dose and counseled on the effects of orthostatic hypotension – an environment that "may not apply to treatment practice in the real world," the authors cautioned. The incidence of hypotension in those studies was 12%, compared with 6% for placebo.

We should remind our patients that tamsulosin can cause clinically important dips in blood pressure. Simple instructions about sitting on the edge of the bed when going from supine to standing could make the difference between a better night’s sleep and a worse one in the hospital.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.

Prescription opioids remain a profound clinical challenge, and we as prescribing practitioners have a significant amount of control over this epidemic. About 14,000 people die from prescription opioid overdoses each year in the United States. Our good intentions to alleviate patient suffering are inextricably bound to the reality of potential iatrogenic harm.

As the corpus of knowledge around best practices for safe prescribing has evolved, hopefully we are evolving our practice for our own patients. But for patients whom we inherit from other practitioners or for those who have been in our practice for years on high doses of opioid analgesics, we need to become comfortable telling them, "Things are different now." In order for us to feel comfortable saying this, though, we have to know what best practices are and how they are different from our current practices.

So what are best practices?

For opioid prescribing, best practices reduce the risk of overdose and misuse. Dr. Teryl Nuckols of the University of California, Los Angeles, and her colleagues published a systematic review of guideline recommendations related to mitigating the risk for accidental overdose and misuse (Ann. Intern. Med. 2013 Nov. 12 [doi: 10.7326/0003-4819-160-1-201401070-00732]). Thirteen guidelines informed the major conclusions, and all were published after 2009.

One risk mitigation strategy is having an upper dosing threshold that we do not violate. Evidence suggests that the risk for accidental overdose increases an estimated 1.9- to 3.1-fold with doses of 50- to 100-mg morphine equivalents, and even more dramatically with doses above 200 mg. Another strategy is to avoid prescribing methadone unless you are extremely comfortable with this medication, and to be careful with fentanyl because of unpredictable absorption with fever, exercise, or heat exposure.

Telling our patients that they can "have opioids or benzodiazepines, but not both" (especially if they are on more than 100 mg of morphine equivalents per day) can reduce risk, because 50% of accidental overdoses involve both. When switching opioids, reducing the dose of the equivalent opioids by 25%-50% is a safe practice, and free apps are available that can do this conversion for us.

Opioid contracts also may be helpful, and the use of screening tools (Current Opioid Misuse Measure) may inform our practice. Urine drug testing for the presence of the medication may be helpful to ensure adherence; the differential for a true negative is diversion, hoarding, or self-dosing leading to running out prematurely.

Concern about abuse is high, but data suggest that the absolute prevalence of this is low. Abuse occurs among 0.43%-3.27% of patients on chronic opioids, and addiction affects less than 0.05% (J. Pain Symptom Manage. 2008;35:214-28). Some experts suggest that trying to decipher abuse in the setting of chronic pain management with opioids is a "distinction without a difference."

Our main focus needs to remain on patient safety. We need to have honest conversations with our patients about mutual concerns and goals, and change discussions around appropriate dose reductions from "You want me to be in pain!" to "We need you to be safe."

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reports no conflicts of interest.

Prescription opioids remain a profound clinical challenge, and we as prescribing practitioners have a significant amount of control over this epidemic. About 14,000 people die from prescription opioid overdoses each year in the United States. Our good intentions to alleviate patient suffering are inextricably bound to the reality of potential iatrogenic harm.

As the corpus of knowledge around best practices for safe prescribing has evolved, hopefully we are evolving our practice for our own patients. But for patients whom we inherit from other practitioners or for those who have been in our practice for years on high doses of opioid analgesics, we need to become comfortable telling them, "Things are different now." In order for us to feel comfortable saying this, though, we have to know what best practices are and how they are different from our current practices.

So what are best practices?

For opioid prescribing, best practices reduce the risk of overdose and misuse. Dr. Teryl Nuckols of the University of California, Los Angeles, and her colleagues published a systematic review of guideline recommendations related to mitigating the risk for accidental overdose and misuse (Ann. Intern. Med. 2013 Nov. 12 [doi: 10.7326/0003-4819-160-1-201401070-00732]). Thirteen guidelines informed the major conclusions, and all were published after 2009.

One risk mitigation strategy is having an upper dosing threshold that we do not violate. Evidence suggests that the risk for accidental overdose increases an estimated 1.9- to 3.1-fold with doses of 50- to 100-mg morphine equivalents, and even more dramatically with doses above 200 mg. Another strategy is to avoid prescribing methadone unless you are extremely comfortable with this medication, and to be careful with fentanyl because of unpredictable absorption with fever, exercise, or heat exposure.

Telling our patients that they can "have opioids or benzodiazepines, but not both" (especially if they are on more than 100 mg of morphine equivalents per day) can reduce risk, because 50% of accidental overdoses involve both. When switching opioids, reducing the dose of the equivalent opioids by 25%-50% is a safe practice, and free apps are available that can do this conversion for us.

Opioid contracts also may be helpful, and the use of screening tools (Current Opioid Misuse Measure) may inform our practice. Urine drug testing for the presence of the medication may be helpful to ensure adherence; the differential for a true negative is diversion, hoarding, or self-dosing leading to running out prematurely.

Concern about abuse is high, but data suggest that the absolute prevalence of this is low. Abuse occurs among 0.43%-3.27% of patients on chronic opioids, and addiction affects less than 0.05% (J. Pain Symptom Manage. 2008;35:214-28). Some experts suggest that trying to decipher abuse in the setting of chronic pain management with opioids is a "distinction without a difference."

Our main focus needs to remain on patient safety. We need to have honest conversations with our patients about mutual concerns and goals, and change discussions around appropriate dose reductions from "You want me to be in pain!" to "We need you to be safe."

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reports no conflicts of interest.

Prescription opioids remain a profound clinical challenge, and we as prescribing practitioners have a significant amount of control over this epidemic. About 14,000 people die from prescription opioid overdoses each year in the United States. Our good intentions to alleviate patient suffering are inextricably bound to the reality of potential iatrogenic harm.

As the corpus of knowledge around best practices for safe prescribing has evolved, hopefully we are evolving our practice for our own patients. But for patients whom we inherit from other practitioners or for those who have been in our practice for years on high doses of opioid analgesics, we need to become comfortable telling them, "Things are different now." In order for us to feel comfortable saying this, though, we have to know what best practices are and how they are different from our current practices.

So what are best practices?

For opioid prescribing, best practices reduce the risk of overdose and misuse. Dr. Teryl Nuckols of the University of California, Los Angeles, and her colleagues published a systematic review of guideline recommendations related to mitigating the risk for accidental overdose and misuse (Ann. Intern. Med. 2013 Nov. 12 [doi: 10.7326/0003-4819-160-1-201401070-00732]). Thirteen guidelines informed the major conclusions, and all were published after 2009.

One risk mitigation strategy is having an upper dosing threshold that we do not violate. Evidence suggests that the risk for accidental overdose increases an estimated 1.9- to 3.1-fold with doses of 50- to 100-mg morphine equivalents, and even more dramatically with doses above 200 mg. Another strategy is to avoid prescribing methadone unless you are extremely comfortable with this medication, and to be careful with fentanyl because of unpredictable absorption with fever, exercise, or heat exposure.

Telling our patients that they can "have opioids or benzodiazepines, but not both" (especially if they are on more than 100 mg of morphine equivalents per day) can reduce risk, because 50% of accidental overdoses involve both. When switching opioids, reducing the dose of the equivalent opioids by 25%-50% is a safe practice, and free apps are available that can do this conversion for us.

Opioid contracts also may be helpful, and the use of screening tools (Current Opioid Misuse Measure) may inform our practice. Urine drug testing for the presence of the medication may be helpful to ensure adherence; the differential for a true negative is diversion, hoarding, or self-dosing leading to running out prematurely.

Concern about abuse is high, but data suggest that the absolute prevalence of this is low. Abuse occurs among 0.43%-3.27% of patients on chronic opioids, and addiction affects less than 0.05% (J. Pain Symptom Manage. 2008;35:214-28). Some experts suggest that trying to decipher abuse in the setting of chronic pain management with opioids is a "distinction without a difference."

Our main focus needs to remain on patient safety. We need to have honest conversations with our patients about mutual concerns and goals, and change discussions around appropriate dose reductions from "You want me to be in pain!" to "We need you to be safe."

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reports no conflicts of interest.

The prevalence of dry eye increases with age and may be as high as 30% of the population age 50 years or older. Women are more likely to have it than men. Other common risk factors include contact lens use, medications (e.g., antihistamines, SSRIs, anticholinergics), tobacco use, diabetes, and ophthalmic surgery.

Patients will present with eye irritation, a foreign body sensation, excessive tearing, and altered vision. If you are like me, you will do a general nondilated ophthalmologic exam and, seeing nothing grossly abnormal, recommend artificial tears in disposable-unit–dose aliquots. But before recommending a subspecialty consult, is there anything else that we can do?

Recall that the tear film of the eye is made up of aqueous, mucous, and lipid components. Some of us might be aware of the literature suggesting patients with high intake of n-3 (or "omega-3") polyunsaturated fatty acids (i.e., fish oil) have lower rates of dry eyes. Fish oil may enhance the tear lipid layer and increase tear stability.

So, does giving fish oil supplementation to patients decrease dry eye symptoms?

Dr. Tetsuya Kawakita of Keio University, Tokyo, and his colleagues conducted a randomized trial of the effectiveness of fish oil capsules containing EPA (eicosapentaenoic acid) 1,245 mg/day and DHA (docosahexaenoic acid) 540 mg/day for the relief of dry eye symptoms (Biomed. Res. 2013;34:215-20).

Patients were eligible for enrollment if they were at least 40 years of age and had dry eye symptoms, abnormal tear production (Schirmer test), or presence of tear film instability (tear break-up time) and positive ocular rose bengal staining or fluorescein vital staining. Patients took five fish oil capsules at breakfast, lunch, and dinner (15 capsules per day) or matching placebo for 12 weeks, with a 4-week wash out period. Objective and subjective measures of dry eye were used as outcomes.

A total of 27 patients were randomized, and data from 26 were used (15 fish oil patients, 11 placebo patients).

Fish oil was associated with significantly reduced eye pain, compared with placebo, as well as significant prolongation of tear-film break-up time. There were no significant differences in the two groups’ Schirmer test results, rose bengal staining scores, or fluorescein vital staining scores.

Thus, fish oil supplementation may be helpful for the treatment of dry eyes. However, 15 pills a day seems like a lot. We could seek to find the lowest effective dose that our patients can tolerate. For patients who have gastrointestinal distress (i.e., "fish burps") from fish oil tablets, I have learned that keeping them in the freezer and swallowing the pills frozen helps. For patients who do not tolerate the nausea that occasionally accompanies high fish oil doses, new preparations of fish oil are available.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author. He reports no conflicts of interest.

The prevalence of dry eye increases with age and may be as high as 30% of the population age 50 years or older. Women are more likely to have it than men. Other common risk factors include contact lens use, medications (e.g., antihistamines, SSRIs, anticholinergics), tobacco use, diabetes, and ophthalmic surgery.

Patients will present with eye irritation, a foreign body sensation, excessive tearing, and altered vision. If you are like me, you will do a general nondilated ophthalmologic exam and, seeing nothing grossly abnormal, recommend artificial tears in disposable-unit–dose aliquots. But before recommending a subspecialty consult, is there anything else that we can do?

Recall that the tear film of the eye is made up of aqueous, mucous, and lipid components. Some of us might be aware of the literature suggesting patients with high intake of n-3 (or "omega-3") polyunsaturated fatty acids (i.e., fish oil) have lower rates of dry eyes. Fish oil may enhance the tear lipid layer and increase tear stability.

So, does giving fish oil supplementation to patients decrease dry eye symptoms?

Dr. Tetsuya Kawakita of Keio University, Tokyo, and his colleagues conducted a randomized trial of the effectiveness of fish oil capsules containing EPA (eicosapentaenoic acid) 1,245 mg/day and DHA (docosahexaenoic acid) 540 mg/day for the relief of dry eye symptoms (Biomed. Res. 2013;34:215-20).

Patients were eligible for enrollment if they were at least 40 years of age and had dry eye symptoms, abnormal tear production (Schirmer test), or presence of tear film instability (tear break-up time) and positive ocular rose bengal staining or fluorescein vital staining. Patients took five fish oil capsules at breakfast, lunch, and dinner (15 capsules per day) or matching placebo for 12 weeks, with a 4-week wash out period. Objective and subjective measures of dry eye were used as outcomes.

A total of 27 patients were randomized, and data from 26 were used (15 fish oil patients, 11 placebo patients).

Fish oil was associated with significantly reduced eye pain, compared with placebo, as well as significant prolongation of tear-film break-up time. There were no significant differences in the two groups’ Schirmer test results, rose bengal staining scores, or fluorescein vital staining scores.

Thus, fish oil supplementation may be helpful for the treatment of dry eyes. However, 15 pills a day seems like a lot. We could seek to find the lowest effective dose that our patients can tolerate. For patients who have gastrointestinal distress (i.e., "fish burps") from fish oil tablets, I have learned that keeping them in the freezer and swallowing the pills frozen helps. For patients who do not tolerate the nausea that occasionally accompanies high fish oil doses, new preparations of fish oil are available.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author. He reports no conflicts of interest.

The prevalence of dry eye increases with age and may be as high as 30% of the population age 50 years or older. Women are more likely to have it than men. Other common risk factors include contact lens use, medications (e.g., antihistamines, SSRIs, anticholinergics), tobacco use, diabetes, and ophthalmic surgery.

Patients will present with eye irritation, a foreign body sensation, excessive tearing, and altered vision. If you are like me, you will do a general nondilated ophthalmologic exam and, seeing nothing grossly abnormal, recommend artificial tears in disposable-unit–dose aliquots. But before recommending a subspecialty consult, is there anything else that we can do?

Recall that the tear film of the eye is made up of aqueous, mucous, and lipid components. Some of us might be aware of the literature suggesting patients with high intake of n-3 (or "omega-3") polyunsaturated fatty acids (i.e., fish oil) have lower rates of dry eyes. Fish oil may enhance the tear lipid layer and increase tear stability.

So, does giving fish oil supplementation to patients decrease dry eye symptoms?

Dr. Tetsuya Kawakita of Keio University, Tokyo, and his colleagues conducted a randomized trial of the effectiveness of fish oil capsules containing EPA (eicosapentaenoic acid) 1,245 mg/day and DHA (docosahexaenoic acid) 540 mg/day for the relief of dry eye symptoms (Biomed. Res. 2013;34:215-20).

Patients were eligible for enrollment if they were at least 40 years of age and had dry eye symptoms, abnormal tear production (Schirmer test), or presence of tear film instability (tear break-up time) and positive ocular rose bengal staining or fluorescein vital staining. Patients took five fish oil capsules at breakfast, lunch, and dinner (15 capsules per day) or matching placebo for 12 weeks, with a 4-week wash out period. Objective and subjective measures of dry eye were used as outcomes.

A total of 27 patients were randomized, and data from 26 were used (15 fish oil patients, 11 placebo patients).

Fish oil was associated with significantly reduced eye pain, compared with placebo, as well as significant prolongation of tear-film break-up time. There were no significant differences in the two groups’ Schirmer test results, rose bengal staining scores, or fluorescein vital staining scores.

Thus, fish oil supplementation may be helpful for the treatment of dry eyes. However, 15 pills a day seems like a lot. We could seek to find the lowest effective dose that our patients can tolerate. For patients who have gastrointestinal distress (i.e., "fish burps") from fish oil tablets, I have learned that keeping them in the freezer and swallowing the pills frozen helps. For patients who do not tolerate the nausea that occasionally accompanies high fish oil doses, new preparations of fish oil are available.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author. He reports no conflicts of interest.

So that we all may learn, I offer myself as an example. I freely admit that I have been following yearly urinary microalbumin in my patients with diabetes who are already on an ACE inhibitor or an angiotensin receptor blocker. Somewhere along the line, I learned that we were "supposed to" do this. Weak justification for clinical behavior, I know, but I also know I am not the only one doing this.

Further complicating this behavior is my lack of understanding about what to do with the results when I receive them.

Typical scenario: A patient has diabetes and is on an ACE inhibitor with persistent microalbuminuria. ... Now what? I have traditionally increased the dose to the highest tolerable level or planned to recheck the following year, hoping it will go away. Somewhere along the line, an annual microalbumin has been incorporated into performance measures and clinical algorithms. ACP to the rescue.

The American College of Physicians just published a clinical guideline on the "Screening, Monitoring, and Treatment of Stage 1 to 3 Chronic Kidney Disease" (Ann. Intern. Med. 2013 Oct. 22 [doi:10.7326/0003-4819-159-12-201312170-00726]).

One of the four guideline recommendations speaking to this issue is that the ACP "recommends against testing for proteinuria in adults with or without diabetes who are currently taking an angiotensin-converting enzyme inhibitor or an angiotensin II–receptor blocker." Reviewed evidence suggests that ACE inhibitors or ARBs reduce the risk for end-stage renal disease (ESRD) and that there is no evidence that monitoring for proteinuria in patients on these medications improves outcomes for patients with chronic kidney disease (CKD).

The other guideline recommendations are to not screen for CKD in asymptomatic adults without risk factors for it, to select an ACE inhibitor or ARB in patients with hypertension and stage 1-3 CKD, and to select a statin to manage elevated low-density lipoprotein cholesterol in patients with stage 1-3 CKD.

How long it will take for clinical practice to catch up and remove this as a performance measure remains to be seen.

Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

So that we all may learn, I offer myself as an example. I freely admit that I have been following yearly urinary microalbumin in my patients with diabetes who are already on an ACE inhibitor or an angiotensin receptor blocker. Somewhere along the line, I learned that we were "supposed to" do this. Weak justification for clinical behavior, I know, but I also know I am not the only one doing this.

Further complicating this behavior is my lack of understanding about what to do with the results when I receive them.

Typical scenario: A patient has diabetes and is on an ACE inhibitor with persistent microalbuminuria. ... Now what? I have traditionally increased the dose to the highest tolerable level or planned to recheck the following year, hoping it will go away. Somewhere along the line, an annual microalbumin has been incorporated into performance measures and clinical algorithms. ACP to the rescue.

The American College of Physicians just published a clinical guideline on the "Screening, Monitoring, and Treatment of Stage 1 to 3 Chronic Kidney Disease" (Ann. Intern. Med. 2013 Oct. 22 [doi:10.7326/0003-4819-159-12-201312170-00726]).

One of the four guideline recommendations speaking to this issue is that the ACP "recommends against testing for proteinuria in adults with or without diabetes who are currently taking an angiotensin-converting enzyme inhibitor or an angiotensin II–receptor blocker." Reviewed evidence suggests that ACE inhibitors or ARBs reduce the risk for end-stage renal disease (ESRD) and that there is no evidence that monitoring for proteinuria in patients on these medications improves outcomes for patients with chronic kidney disease (CKD).

The other guideline recommendations are to not screen for CKD in asymptomatic adults without risk factors for it, to select an ACE inhibitor or ARB in patients with hypertension and stage 1-3 CKD, and to select a statin to manage elevated low-density lipoprotein cholesterol in patients with stage 1-3 CKD.

How long it will take for clinical practice to catch up and remove this as a performance measure remains to be seen.

Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

So that we all may learn, I offer myself as an example. I freely admit that I have been following yearly urinary microalbumin in my patients with diabetes who are already on an ACE inhibitor or an angiotensin receptor blocker. Somewhere along the line, I learned that we were "supposed to" do this. Weak justification for clinical behavior, I know, but I also know I am not the only one doing this.

Further complicating this behavior is my lack of understanding about what to do with the results when I receive them.

Typical scenario: A patient has diabetes and is on an ACE inhibitor with persistent microalbuminuria. ... Now what? I have traditionally increased the dose to the highest tolerable level or planned to recheck the following year, hoping it will go away. Somewhere along the line, an annual microalbumin has been incorporated into performance measures and clinical algorithms. ACP to the rescue.

The American College of Physicians just published a clinical guideline on the "Screening, Monitoring, and Treatment of Stage 1 to 3 Chronic Kidney Disease" (Ann. Intern. Med. 2013 Oct. 22 [doi:10.7326/0003-4819-159-12-201312170-00726]).

One of the four guideline recommendations speaking to this issue is that the ACP "recommends against testing for proteinuria in adults with or without diabetes who are currently taking an angiotensin-converting enzyme inhibitor or an angiotensin II–receptor blocker." Reviewed evidence suggests that ACE inhibitors or ARBs reduce the risk for end-stage renal disease (ESRD) and that there is no evidence that monitoring for proteinuria in patients on these medications improves outcomes for patients with chronic kidney disease (CKD).

The other guideline recommendations are to not screen for CKD in asymptomatic adults without risk factors for it, to select an ACE inhibitor or ARB in patients with hypertension and stage 1-3 CKD, and to select a statin to manage elevated low-density lipoprotein cholesterol in patients with stage 1-3 CKD.

How long it will take for clinical practice to catch up and remove this as a performance measure remains to be seen.

Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

Shame is not an effective way to change behavior. In the face of shame, one may emotionally shut down or become angry and defensive. We need to start this discussion by believing that we do a fantastic job every day for our patients, and that we went into medicine because we are compassionate and empathic people. We are enough just by showing up at work and doing what we do.

But we can always improve.

Starting from here, we need to remind ourselves that viruses are the cause of 90% of sore throats. The prevalence of group A Streptococcus (GAS) infection is approximately 10%. GAS would be the only cause of sore throat requiring antibiotics.

The antibiotic prescribing rate for adults with sore throat was 70% in 1993. Using national survey data, Dr. Michael Barnett and Dr. Jeffrey Linder reported that physicians prescribed antibiotics for sore throat at 60% of primary care and emergency department visits (95% CI: 57%-63%). The use of broad-spectrum antibiotics such as azithromycin was common despite the fact that GAS is universally susceptible to penicillin. Penicillin was given in only 9% of visits (JAMA Internal Medicine 2013 [doi:10.1001/jamainternmed.2013.11673]).

Adverse consequences of antibiotic prescribing are not uncommon. The Clostridium difficile diarrhea and colitis that we are seeing in our practice is not only becoming more prevalent, but much more difficult to treat. Telling patients that they can develop C. difficile colitis should become a routine part of side effect discussions when prescribing antibiotics.

And, although we may recommend the use of probiotics for patients to prevent both antibiotic-associated and C. difficile diarrhea (CDD), a large study of adults aged 65 and older suggested that a multistrain preparation of lactobacilli and bifidobacteria was not effective in the prevention of antibiotic-associated diarrhea or C. difficile diarrhea (Lancet 2013;382:1249-57).

So, our challenge is that patients come in and demand antibiotics. But most do not have a real understanding of the risks to them personally and to the population at large through the indiscriminate use of antibiotics.

In a non-shame–based manner, we need to teach them.

Telling them that symptoms resolve in 40% of patients within 3 days and 80% of patients within 1 week, irrespective of whether the cause was viral or streptococcal, may be helpful. The use of a clinical decision aid for sore throat may also be helpful.

Many may be familiar with the clinical scoring algorithm known as the "Centor Criteria." The criteria consist of four findings that are each assigned one point: history of fever, absence of cough, tender or swollen lymph glands in the neck, and red and tonsillar exduates.* Patients with zero or one finding do not require testing or antibiotics. Patients with two or three findings should have a rapid strep test performed, and the results should guide antibiotic treatment. Patients with four findings should receive antibiotics.

This algorithm is available in the incredibly useful MedCalc medical calculator app in the iTunes store.

We need to keep telling ourselves that we have nothing to be ashamed about by currently prescribing too many antibiotics for adults with sore throat – and that we can and will do better.

Dr. Ebbert is professor of medicine, a general internist, and a diplomate of the American Board of Addiction Medicine who works at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

*Correction, 1/3/2014: An earlier version of this story misstated the Centor Criteria.

Shame is not an effective way to change behavior. In the face of shame, one may emotionally shut down or become angry and defensive. We need to start this discussion by believing that we do a fantastic job every day for our patients, and that we went into medicine because we are compassionate and empathic people. We are enough just by showing up at work and doing what we do.

But we can always improve.

Starting from here, we need to remind ourselves that viruses are the cause of 90% of sore throats. The prevalence of group A Streptococcus (GAS) infection is approximately 10%. GAS would be the only cause of sore throat requiring antibiotics.

The antibiotic prescribing rate for adults with sore throat was 70% in 1993. Using national survey data, Dr. Michael Barnett and Dr. Jeffrey Linder reported that physicians prescribed antibiotics for sore throat at 60% of primary care and emergency department visits (95% CI: 57%-63%). The use of broad-spectrum antibiotics such as azithromycin was common despite the fact that GAS is universally susceptible to penicillin. Penicillin was given in only 9% of visits (JAMA Internal Medicine 2013 [doi:10.1001/jamainternmed.2013.11673]).

Adverse consequences of antibiotic prescribing are not uncommon. The Clostridium difficile diarrhea and colitis that we are seeing in our practice is not only becoming more prevalent, but much more difficult to treat. Telling patients that they can develop C. difficile colitis should become a routine part of side effect discussions when prescribing antibiotics.

And, although we may recommend the use of probiotics for patients to prevent both antibiotic-associated and C. difficile diarrhea (CDD), a large study of adults aged 65 and older suggested that a multistrain preparation of lactobacilli and bifidobacteria was not effective in the prevention of antibiotic-associated diarrhea or C. difficile diarrhea (Lancet 2013;382:1249-57).

So, our challenge is that patients come in and demand antibiotics. But most do not have a real understanding of the risks to them personally and to the population at large through the indiscriminate use of antibiotics.

In a non-shame–based manner, we need to teach them.

Telling them that symptoms resolve in 40% of patients within 3 days and 80% of patients within 1 week, irrespective of whether the cause was viral or streptococcal, may be helpful. The use of a clinical decision aid for sore throat may also be helpful.

Many may be familiar with the clinical scoring algorithm known as the "Centor Criteria." The criteria consist of four findings that are each assigned one point: history of fever, absence of cough, tender or swollen lymph glands in the neck, and red and tonsillar exduates.* Patients with zero or one finding do not require testing or antibiotics. Patients with two or three findings should have a rapid strep test performed, and the results should guide antibiotic treatment. Patients with four findings should receive antibiotics.

This algorithm is available in the incredibly useful MedCalc medical calculator app in the iTunes store.

We need to keep telling ourselves that we have nothing to be ashamed about by currently prescribing too many antibiotics for adults with sore throat – and that we can and will do better.

Dr. Ebbert is professor of medicine, a general internist, and a diplomate of the American Board of Addiction Medicine who works at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

*Correction, 1/3/2014: An earlier version of this story misstated the Centor Criteria.

Shame is not an effective way to change behavior. In the face of shame, one may emotionally shut down or become angry and defensive. We need to start this discussion by believing that we do a fantastic job every day for our patients, and that we went into medicine because we are compassionate and empathic people. We are enough just by showing up at work and doing what we do.

But we can always improve.

Starting from here, we need to remind ourselves that viruses are the cause of 90% of sore throats. The prevalence of group A Streptococcus (GAS) infection is approximately 10%. GAS would be the only cause of sore throat requiring antibiotics.

The antibiotic prescribing rate for adults with sore throat was 70% in 1993. Using national survey data, Dr. Michael Barnett and Dr. Jeffrey Linder reported that physicians prescribed antibiotics for sore throat at 60% of primary care and emergency department visits (95% CI: 57%-63%). The use of broad-spectrum antibiotics such as azithromycin was common despite the fact that GAS is universally susceptible to penicillin. Penicillin was given in only 9% of visits (JAMA Internal Medicine 2013 [doi:10.1001/jamainternmed.2013.11673]).

Adverse consequences of antibiotic prescribing are not uncommon. The Clostridium difficile diarrhea and colitis that we are seeing in our practice is not only becoming more prevalent, but much more difficult to treat. Telling patients that they can develop C. difficile colitis should become a routine part of side effect discussions when prescribing antibiotics.

And, although we may recommend the use of probiotics for patients to prevent both antibiotic-associated and C. difficile diarrhea (CDD), a large study of adults aged 65 and older suggested that a multistrain preparation of lactobacilli and bifidobacteria was not effective in the prevention of antibiotic-associated diarrhea or C. difficile diarrhea (Lancet 2013;382:1249-57).

So, our challenge is that patients come in and demand antibiotics. But most do not have a real understanding of the risks to them personally and to the population at large through the indiscriminate use of antibiotics.

In a non-shame–based manner, we need to teach them.

Telling them that symptoms resolve in 40% of patients within 3 days and 80% of patients within 1 week, irrespective of whether the cause was viral or streptococcal, may be helpful. The use of a clinical decision aid for sore throat may also be helpful.

Many may be familiar with the clinical scoring algorithm known as the "Centor Criteria." The criteria consist of four findings that are each assigned one point: history of fever, absence of cough, tender or swollen lymph glands in the neck, and red and tonsillar exduates.* Patients with zero or one finding do not require testing or antibiotics. Patients with two or three findings should have a rapid strep test performed, and the results should guide antibiotic treatment. Patients with four findings should receive antibiotics.

This algorithm is available in the incredibly useful MedCalc medical calculator app in the iTunes store.

We need to keep telling ourselves that we have nothing to be ashamed about by currently prescribing too many antibiotics for adults with sore throat – and that we can and will do better.

Dr. Ebbert is professor of medicine, a general internist, and a diplomate of the American Board of Addiction Medicine who works at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

*Correction, 1/3/2014: An earlier version of this story misstated the Centor Criteria.

’Tis the season to be coughing.

The most common condition we are seeing and will be seeing in the coming months is bronchitis. Bronchitis is a self-limited inflammation of the bronchi due to upper airway infection (i.e., cough without pneumonia), which is most commonly viral in etiology. Antibiotics are not recommended for treatment.

Many of our patients will be making appointments to see us when they hit 10-14 days without improvement. But remember that the cough from bronchitis can last up to 4 weeks or more. Reports indicate that more than 60%-90% percent of patients with acute bronchitis who seek care receive antibiotics. Furthermore, 75% of all antibiotic prescriptions are written for upper respiratory infections – yet most patients, if not all, do not need them.

Many of our patients will say that they have tried the usual over-the-counter remedies, which can ruin the best-laid plans for conservative management. But have they tried ibuprofen? (Assuming there is no contraindication, of course.)

Dr. Carl Llor and his colleagues recently published a randomized, blinded clinical trial evaluating the comparative efficacy of an anti-inflammatory, antibiotic, or placebo in the resolution of cough in patients with bronchitis (BMJ 2013 Oct. 4;347:f5762).

Adults aged 18-70 years were eligible to be randomized if they were presenting with a respiratory tract infection less than 1 week in duration and had cough, discolored sputum, and at least one of three symptoms: dyspnea, wheezing, or chest discomfort or chest pain. Subjects were randomized to ibuprofen 600 mg three times a day, amoxicillin-clavulanic acid 500 mg/125 mg three times a day, or placebo three times a day. Treatment was given for 10 days.

The median number of days with frequent cough was numerically lower, but not statistically significantly lower, in the ibuprofen group (9 days; 95% CI: 8-10 days), compared with participants receiving antibiotics (11 days; 95% CI: 10-12 days) or placebo (11 days; 95% CI: 8-14 days). Adverse events were more common in the antibiotic arm (12%), compared with ibuprofen or placebo (5% and 3%, respectively, P = .008).

Other nonantibiotic cough remedies have been evaluated in the treatment of patients presenting with cough. Inhaled fluticasone may be effective, but the cost might be prohibitive for many patients.

For ibuprofen, the price is right – and it may buy us some time before we feel compelled to prescribe antibiotics.

Dr. Ebbert is a professor of medicine, a general internist, and a diplomate of the American Board of Addiction Medicine who works at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

’Tis the season to be coughing.

The most common condition we are seeing and will be seeing in the coming months is bronchitis. Bronchitis is a self-limited inflammation of the bronchi due to upper airway infection (i.e., cough without pneumonia), which is most commonly viral in etiology. Antibiotics are not recommended for treatment.

Many of our patients will be making appointments to see us when they hit 10-14 days without improvement. But remember that the cough from bronchitis can last up to 4 weeks or more. Reports indicate that more than 60%-90% percent of patients with acute bronchitis who seek care receive antibiotics. Furthermore, 75% of all antibiotic prescriptions are written for upper respiratory infections – yet most patients, if not all, do not need them.

Many of our patients will say that they have tried the usual over-the-counter remedies, which can ruin the best-laid plans for conservative management. But have they tried ibuprofen? (Assuming there is no contraindication, of course.)

Dr. Carl Llor and his colleagues recently published a randomized, blinded clinical trial evaluating the comparative efficacy of an anti-inflammatory, antibiotic, or placebo in the resolution of cough in patients with bronchitis (BMJ 2013 Oct. 4;347:f5762).

Adults aged 18-70 years were eligible to be randomized if they were presenting with a respiratory tract infection less than 1 week in duration and had cough, discolored sputum, and at least one of three symptoms: dyspnea, wheezing, or chest discomfort or chest pain. Subjects were randomized to ibuprofen 600 mg three times a day, amoxicillin-clavulanic acid 500 mg/125 mg three times a day, or placebo three times a day. Treatment was given for 10 days.

The median number of days with frequent cough was numerically lower, but not statistically significantly lower, in the ibuprofen group (9 days; 95% CI: 8-10 days), compared with participants receiving antibiotics (11 days; 95% CI: 10-12 days) or placebo (11 days; 95% CI: 8-14 days). Adverse events were more common in the antibiotic arm (12%), compared with ibuprofen or placebo (5% and 3%, respectively, P = .008).

Other nonantibiotic cough remedies have been evaluated in the treatment of patients presenting with cough. Inhaled fluticasone may be effective, but the cost might be prohibitive for many patients.

For ibuprofen, the price is right – and it may buy us some time before we feel compelled to prescribe antibiotics.

Dr. Ebbert is a professor of medicine, a general internist, and a diplomate of the American Board of Addiction Medicine who works at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.

’Tis the season to be coughing.

The most common condition we are seeing and will be seeing in the coming months is bronchitis. Bronchitis is a self-limited inflammation of the bronchi due to upper airway infection (i.e., cough without pneumonia), which is most commonly viral in etiology. Antibiotics are not recommended for treatment.

Many of our patients will be making appointments to see us when they hit 10-14 days without improvement. But remember that the cough from bronchitis can last up to 4 weeks or more. Reports indicate that more than 60%-90% percent of patients with acute bronchitis who seek care receive antibiotics. Furthermore, 75% of all antibiotic prescriptions are written for upper respiratory infections – yet most patients, if not all, do not need them.

Many of our patients will say that they have tried the usual over-the-counter remedies, which can ruin the best-laid plans for conservative management. But have they tried ibuprofen? (Assuming there is no contraindication, of course.)

Dr. Carl Llor and his colleagues recently published a randomized, blinded clinical trial evaluating the comparative efficacy of an anti-inflammatory, antibiotic, or placebo in the resolution of cough in patients with bronchitis (BMJ 2013 Oct. 4;347:f5762).

Adults aged 18-70 years were eligible to be randomized if they were presenting with a respiratory tract infection less than 1 week in duration and had cough, discolored sputum, and at least one of three symptoms: dyspnea, wheezing, or chest discomfort or chest pain. Subjects were randomized to ibuprofen 600 mg three times a day, amoxicillin-clavulanic acid 500 mg/125 mg three times a day, or placebo three times a day. Treatment was given for 10 days.

The median number of days with frequent cough was numerically lower, but not statistically significantly lower, in the ibuprofen group (9 days; 95% CI: 8-10 days), compared with participants receiving antibiotics (11 days; 95% CI: 10-12 days) or placebo (11 days; 95% CI: 8-14 days). Adverse events were more common in the antibiotic arm (12%), compared with ibuprofen or placebo (5% and 3%, respectively, P = .008).

Other nonantibiotic cough remedies have been evaluated in the treatment of patients presenting with cough. Inhaled fluticasone may be effective, but the cost might be prohibitive for many patients.

For ibuprofen, the price is right – and it may buy us some time before we feel compelled to prescribe antibiotics.

Dr. Ebbert is a professor of medicine, a general internist, and a diplomate of the American Board of Addiction Medicine who works at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.