What Matters

Chronic cough is defined by the American College of Chest Physicians as a cough lasting longer than 8 weeks. Chronic cough is a troubling disorder, mostly for the patients, who frequently make several outpatient visits to seek help for their symptoms, and whose quality of life can be severely impaired.

An algorithmic approach should be used in the diagnosis of chronic cough. Once we have ruled out the “bad actors” and have run through our nasal sprays, proton pump inhibitors, and antihistamines, it is time to get creative. Don’t neglect to provide lung cancer screening for your smokers – which, in the case of chronic cough, is actually case finding.

Dr. Peter G. Gibson of the University of Newcastle, Australia, and his colleagues published an article presenting some new concepts for chronic cough, an assessment tool, and a literature review on the use of gabapentin for this troubling disorder (Pulm Pharmacol Ther. 2015 Jul 2. pii:S1094-5539[15]00072-3).

The new concepts include laryngeal hypersensitivity, central reflex hypersensitivity, and cough hypersensitivity syndrome. The authors posit that these concepts reformulate into chronic cough as a neuropathic disorder, which may be amenable to treatment with neuromodulatory agents such as gabapentin.

I have several patients in my panel who might benefit from this therapy. But there are a couple of things to remember. First, gabapentin can be taken with food, but antacids decrease the bioavailability by 20% when taken together or up to 2 hours after gabapentin ingestion. Also, gabapentin has a wide therapeutic window, which will make it easier to find an individualized dose for our patients.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Chronic cough is defined by the American College of Chest Physicians as a cough lasting longer than 8 weeks. Chronic cough is a troubling disorder, mostly for the patients, who frequently make several outpatient visits to seek help for their symptoms, and whose quality of life can be severely impaired.

An algorithmic approach should be used in the diagnosis of chronic cough. Once we have ruled out the “bad actors” and have run through our nasal sprays, proton pump inhibitors, and antihistamines, it is time to get creative. Don’t neglect to provide lung cancer screening for your smokers – which, in the case of chronic cough, is actually case finding.

Dr. Peter G. Gibson of the University of Newcastle, Australia, and his colleagues published an article presenting some new concepts for chronic cough, an assessment tool, and a literature review on the use of gabapentin for this troubling disorder (Pulm Pharmacol Ther. 2015 Jul 2. pii:S1094-5539[15]00072-3).

The new concepts include laryngeal hypersensitivity, central reflex hypersensitivity, and cough hypersensitivity syndrome. The authors posit that these concepts reformulate into chronic cough as a neuropathic disorder, which may be amenable to treatment with neuromodulatory agents such as gabapentin.

I have several patients in my panel who might benefit from this therapy. But there are a couple of things to remember. First, gabapentin can be taken with food, but antacids decrease the bioavailability by 20% when taken together or up to 2 hours after gabapentin ingestion. Also, gabapentin has a wide therapeutic window, which will make it easier to find an individualized dose for our patients.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Chronic cough is defined by the American College of Chest Physicians as a cough lasting longer than 8 weeks. Chronic cough is a troubling disorder, mostly for the patients, who frequently make several outpatient visits to seek help for their symptoms, and whose quality of life can be severely impaired.

An algorithmic approach should be used in the diagnosis of chronic cough. Once we have ruled out the “bad actors” and have run through our nasal sprays, proton pump inhibitors, and antihistamines, it is time to get creative. Don’t neglect to provide lung cancer screening for your smokers – which, in the case of chronic cough, is actually case finding.

Dr. Peter G. Gibson of the University of Newcastle, Australia, and his colleagues published an article presenting some new concepts for chronic cough, an assessment tool, and a literature review on the use of gabapentin for this troubling disorder (Pulm Pharmacol Ther. 2015 Jul 2. pii:S1094-5539[15]00072-3).

The new concepts include laryngeal hypersensitivity, central reflex hypersensitivity, and cough hypersensitivity syndrome. The authors posit that these concepts reformulate into chronic cough as a neuropathic disorder, which may be amenable to treatment with neuromodulatory agents such as gabapentin.

I have several patients in my panel who might benefit from this therapy. But there are a couple of things to remember. First, gabapentin can be taken with food, but antacids decrease the bioavailability by 20% when taken together or up to 2 hours after gabapentin ingestion. Also, gabapentin has a wide therapeutic window, which will make it easier to find an individualized dose for our patients.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

What Matters prides itself on reviewing the literature and presenting thoughtful commentary on articles that are relevant and applicable to the practicing clinician. We separate the wheat from the chaff. We are not, however, above taking on attention-grabbing articles.

Over the years, this column has reported on various methods to facilitate the expulsion of kidney stones, including tamsulosin, phosphodiesterase type 5 (PDE5) inhibitors, and steroids. But this one called out for our assessment: sex to expel kidney stones. Erroneously perceived prurient interests must be forgiven.

Dr. Omer Gokhan Doluoglu of the Clinic of Ankara (Turkey) Training and Research Hospital and colleagues conducted a randomized trial evaluating the effectiveness of sexual intercourse, tamsulosin, or standard medical therapy for kidney stone expulsion (Urology. 2015;86[1]:19-24). Potential subjects were eligible for inclusion if they had radiopaque distal ureteral stones. Subjects were excluded if the stones were larger than 6 mm.

Subjects were randomized to encouragement to have sexual intercourse at least three times per week, tamsulosin 0.4 mg/day, or symptomatic therapy alone. All patients received an antispasmodic and an anti-inflammatory, and were told to drink 2 L of water per day. Sexual intercourse and masturbation were prohibited in groups 2 and 3 during the treatment period, which lasted 4 weeks.

Ninety patients were randomized to the three groups. The mean stone size was 4.7-5.0 mm and not significantly different between the groups.

At 2 weeks, 83.9% (26 of 31) of the patients in the intercourse group, 47.6% (10 of 21) in the tamsulosin group, and 34.8% (8 of 23) passed the stones (P = .001). There was no difference between the groups at 4 weeks. Mean expulsion times were 10 days, 16.6 days, and 18 days, respectively (P = .0001).

The study’s authors propose that nitrous oxide is operant here by causing ureteric relaxation when released to create penile tumescence and during sexual activity. Because masturbation could achieve the same effect, patients in the other groups were told they could not. How effective this instruction was in the current study is unknown, because only “sexual intercourses” were collected on follow-up.

The random-envelope method used is less than ideal, and no data were reported on differences in the number of sexual experiences between groups. If we assume for a moment that a real effect exists, one is left wondering if more would be better. Does the requirement of a partner decrease the likelihood of more frequent stone-expelling sexual experiences? If our patients do not have sexual partners, do we not share these data with them?

And if we use PDE5 inhibitors and encourage sexual activity, do we … kill two birds with one stone?

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

What Matters prides itself on reviewing the literature and presenting thoughtful commentary on articles that are relevant and applicable to the practicing clinician. We separate the wheat from the chaff. We are not, however, above taking on attention-grabbing articles.

Over the years, this column has reported on various methods to facilitate the expulsion of kidney stones, including tamsulosin, phosphodiesterase type 5 (PDE5) inhibitors, and steroids. But this one called out for our assessment: sex to expel kidney stones. Erroneously perceived prurient interests must be forgiven.

Dr. Omer Gokhan Doluoglu of the Clinic of Ankara (Turkey) Training and Research Hospital and colleagues conducted a randomized trial evaluating the effectiveness of sexual intercourse, tamsulosin, or standard medical therapy for kidney stone expulsion (Urology. 2015;86[1]:19-24). Potential subjects were eligible for inclusion if they had radiopaque distal ureteral stones. Subjects were excluded if the stones were larger than 6 mm.

Subjects were randomized to encouragement to have sexual intercourse at least three times per week, tamsulosin 0.4 mg/day, or symptomatic therapy alone. All patients received an antispasmodic and an anti-inflammatory, and were told to drink 2 L of water per day. Sexual intercourse and masturbation were prohibited in groups 2 and 3 during the treatment period, which lasted 4 weeks.

Ninety patients were randomized to the three groups. The mean stone size was 4.7-5.0 mm and not significantly different between the groups.

At 2 weeks, 83.9% (26 of 31) of the patients in the intercourse group, 47.6% (10 of 21) in the tamsulosin group, and 34.8% (8 of 23) passed the stones (P = .001). There was no difference between the groups at 4 weeks. Mean expulsion times were 10 days, 16.6 days, and 18 days, respectively (P = .0001).

The study’s authors propose that nitrous oxide is operant here by causing ureteric relaxation when released to create penile tumescence and during sexual activity. Because masturbation could achieve the same effect, patients in the other groups were told they could not. How effective this instruction was in the current study is unknown, because only “sexual intercourses” were collected on follow-up.

The random-envelope method used is less than ideal, and no data were reported on differences in the number of sexual experiences between groups. If we assume for a moment that a real effect exists, one is left wondering if more would be better. Does the requirement of a partner decrease the likelihood of more frequent stone-expelling sexual experiences? If our patients do not have sexual partners, do we not share these data with them?

And if we use PDE5 inhibitors and encourage sexual activity, do we … kill two birds with one stone?

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

What Matters prides itself on reviewing the literature and presenting thoughtful commentary on articles that are relevant and applicable to the practicing clinician. We separate the wheat from the chaff. We are not, however, above taking on attention-grabbing articles.

Over the years, this column has reported on various methods to facilitate the expulsion of kidney stones, including tamsulosin, phosphodiesterase type 5 (PDE5) inhibitors, and steroids. But this one called out for our assessment: sex to expel kidney stones. Erroneously perceived prurient interests must be forgiven.

Dr. Omer Gokhan Doluoglu of the Clinic of Ankara (Turkey) Training and Research Hospital and colleagues conducted a randomized trial evaluating the effectiveness of sexual intercourse, tamsulosin, or standard medical therapy for kidney stone expulsion (Urology. 2015;86[1]:19-24). Potential subjects were eligible for inclusion if they had radiopaque distal ureteral stones. Subjects were excluded if the stones were larger than 6 mm.

Subjects were randomized to encouragement to have sexual intercourse at least three times per week, tamsulosin 0.4 mg/day, or symptomatic therapy alone. All patients received an antispasmodic and an anti-inflammatory, and were told to drink 2 L of water per day. Sexual intercourse and masturbation were prohibited in groups 2 and 3 during the treatment period, which lasted 4 weeks.

Ninety patients were randomized to the three groups. The mean stone size was 4.7-5.0 mm and not significantly different between the groups.

At 2 weeks, 83.9% (26 of 31) of the patients in the intercourse group, 47.6% (10 of 21) in the tamsulosin group, and 34.8% (8 of 23) passed the stones (P = .001). There was no difference between the groups at 4 weeks. Mean expulsion times were 10 days, 16.6 days, and 18 days, respectively (P = .0001).

The study’s authors propose that nitrous oxide is operant here by causing ureteric relaxation when released to create penile tumescence and during sexual activity. Because masturbation could achieve the same effect, patients in the other groups were told they could not. How effective this instruction was in the current study is unknown, because only “sexual intercourses” were collected on follow-up.

The random-envelope method used is less than ideal, and no data were reported on differences in the number of sexual experiences between groups. If we assume for a moment that a real effect exists, one is left wondering if more would be better. Does the requirement of a partner decrease the likelihood of more frequent stone-expelling sexual experiences? If our patients do not have sexual partners, do we not share these data with them?

And if we use PDE5 inhibitors and encourage sexual activity, do we … kill two birds with one stone?

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of fibromyalgia in our clinical practices is about 2%-3%. But it may feel much higher, because some of these patients use a lot of staff and office time. Vacillations in our certainty about the diagnosis, inadequate time to differentiate new problems from the underlying one, failing to engage the patient in disease self-management, and inadequately exhausting the plethora of pharmacologic management options (however weak the data may be for each one) make care of patients with fibromyalgia challenging. Unfortunately, many of these patients are treated with chronic opioids.

So, maybe you have tried every pharmacologic option under the sun. But have you tried memantine?

Dr. Bárbara Olivan-Blázquez of the University of Zaragoza, Spain, and colleagues evaluated the efficacy of memantine for pain symptom control in fibromyalgia (Pain. 2014 Dec;155[12]:2517-25).

In this study, 63 patients with fibromyalgia were randomized to 20 mg/day of memantine or matching placebo for a total of 6 months, including an initial 1-month up-titration period. Follow-up occurred at 3 months and 6 months.

Compared with placebo, memantine decreased pain and depression at 3 months and 6 months. It also increased cognitive function and overall perceptions of function at 3 months and 6 months. More than 80% of patients completed the trial. Dizziness and headaches were the most commonly reported symptoms.

Why does it work? Memantine blocks glutamate, and glutamate may be a player in perpetuating the pain cycle for patients with fibromyalgia. Previously, memantine had been shown to be effective in other pain conditions such as complex regional pain syndrome and phantom limb pain. Memantine is well tolerated and is generically available. In my location, I was able to locate it for less than $1 per day of therapy.

So, before giving up hope or reaching for the opioid du jour, memantine may be worth a trial to decrease pain and improve function in our patients with fibromyalgia.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of fibromyalgia in our clinical practices is about 2%-3%. But it may feel much higher, because some of these patients use a lot of staff and office time. Vacillations in our certainty about the diagnosis, inadequate time to differentiate new problems from the underlying one, failing to engage the patient in disease self-management, and inadequately exhausting the plethora of pharmacologic management options (however weak the data may be for each one) make care of patients with fibromyalgia challenging. Unfortunately, many of these patients are treated with chronic opioids.

So, maybe you have tried every pharmacologic option under the sun. But have you tried memantine?

Dr. Bárbara Olivan-Blázquez of the University of Zaragoza, Spain, and colleagues evaluated the efficacy of memantine for pain symptom control in fibromyalgia (Pain. 2014 Dec;155[12]:2517-25).

In this study, 63 patients with fibromyalgia were randomized to 20 mg/day of memantine or matching placebo for a total of 6 months, including an initial 1-month up-titration period. Follow-up occurred at 3 months and 6 months.

Compared with placebo, memantine decreased pain and depression at 3 months and 6 months. It also increased cognitive function and overall perceptions of function at 3 months and 6 months. More than 80% of patients completed the trial. Dizziness and headaches were the most commonly reported symptoms.

Why does it work? Memantine blocks glutamate, and glutamate may be a player in perpetuating the pain cycle for patients with fibromyalgia. Previously, memantine had been shown to be effective in other pain conditions such as complex regional pain syndrome and phantom limb pain. Memantine is well tolerated and is generically available. In my location, I was able to locate it for less than $1 per day of therapy.

So, before giving up hope or reaching for the opioid du jour, memantine may be worth a trial to decrease pain and improve function in our patients with fibromyalgia.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of fibromyalgia in our clinical practices is about 2%-3%. But it may feel much higher, because some of these patients use a lot of staff and office time. Vacillations in our certainty about the diagnosis, inadequate time to differentiate new problems from the underlying one, failing to engage the patient in disease self-management, and inadequately exhausting the plethora of pharmacologic management options (however weak the data may be for each one) make care of patients with fibromyalgia challenging. Unfortunately, many of these patients are treated with chronic opioids.

So, maybe you have tried every pharmacologic option under the sun. But have you tried memantine?

Dr. Bárbara Olivan-Blázquez of the University of Zaragoza, Spain, and colleagues evaluated the efficacy of memantine for pain symptom control in fibromyalgia (Pain. 2014 Dec;155[12]:2517-25).

In this study, 63 patients with fibromyalgia were randomized to 20 mg/day of memantine or matching placebo for a total of 6 months, including an initial 1-month up-titration period. Follow-up occurred at 3 months and 6 months.

Compared with placebo, memantine decreased pain and depression at 3 months and 6 months. It also increased cognitive function and overall perceptions of function at 3 months and 6 months. More than 80% of patients completed the trial. Dizziness and headaches were the most commonly reported symptoms.

Why does it work? Memantine blocks glutamate, and glutamate may be a player in perpetuating the pain cycle for patients with fibromyalgia. Previously, memantine had been shown to be effective in other pain conditions such as complex regional pain syndrome and phantom limb pain. Memantine is well tolerated and is generically available. In my location, I was able to locate it for less than $1 per day of therapy.

So, before giving up hope or reaching for the opioid du jour, memantine may be worth a trial to decrease pain and improve function in our patients with fibromyalgia.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of diabetes increases as patients age and gain weight. More than one-third of nursing home residents have diabetes. The overall treatment goals for elderly patients with diabetes are similar to those for younger patients, but somehow the stakes feel higher. Polypharmacy, decreased activity, shifting dietary patterns, hyperglycemia, fears of hypoglycemia leading to falls, worsening comorbid conditions, and hospitalization pose great challenges to ideal management.

Because of these concerns, caution is raised about the use of insulin or oral agents that cause hypoglycemia in frail older adults in long-term care facilities. But these agents are used, and perhaps we understand little about their comparative risks.

Dr. Francisco J. Pasquel of Emory University, Atlanta, and his colleagues conducted a randomized clinical trial evaluating the comparative safety and effectiveness of basal insulin or an oral antidiabetic drug (OAD) for 26 weeks (BMJ Open Diab Res Care. 2015;3:e000104).

A total of 150 patients, average age 79 years, with a blood glucose level greater than 180 mg/dL or a hemoglobin A_1c greater than 7.5%, treated with diet or an oral agent, were randomized to either 0.1 U/kg per day of glargine or continuation of oral agents (metformin, insulin secretagogues, thiazolidinediones, or DPP-4 inhibitors). Glargine was adjusted based on blood sugar readings.

In the OAD group, 16% of patients were treated with metformin plus sulfonylurea, 27% with a sulfonylurea alone, and 8% with sulfonylurea and a DPP-4 inhibitor.

There were 62 hypoglycemic events in the OAD group and 43 in the basal insulin group (P = .4). Overall, daily blood glucose levels did not differ between the groups. Rates of cardiovascular events, renal failure, infection, falls, emergency department visits, hospital admissions, and mortality were similar between the two groups.

Although these data are somewhat reassuring, power may have been an issue, and a larger sample size may have resulted in detection of more hypoglycemic events in the OAD group. On the other hand, the data are balanced and resonate with previous data showing that in older adults with diabetes (about 74 years of age), intensive glycemic control is associated with an increased risk of falls in insulin users but not in those treated with OADs. The goal of the current study was not intensive glycemic control.

So, for patients in a long-term care facility, metformin and the DPP-4 inhibitors will be weight neutral without risk of hypoglycemia. Therefore, these may be the “go-to” drugs if the DPP-4 inhibitors are affordable and you do not have a long way to go for control (DPP-4 inhibitors tend to be relatively mild agents, lowering HbA_1c by 0.6%). If a sulfonylurea must be used, glipizide should be chosen, because it has a shorter half-life.

Balance all of this with appropriate HbA_1c goals for your patient adjusted for medical comorbidity, goals of care, and life expectancy.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of diabetes increases as patients age and gain weight. More than one-third of nursing home residents have diabetes. The overall treatment goals for elderly patients with diabetes are similar to those for younger patients, but somehow the stakes feel higher. Polypharmacy, decreased activity, shifting dietary patterns, hyperglycemia, fears of hypoglycemia leading to falls, worsening comorbid conditions, and hospitalization pose great challenges to ideal management.

Because of these concerns, caution is raised about the use of insulin or oral agents that cause hypoglycemia in frail older adults in long-term care facilities. But these agents are used, and perhaps we understand little about their comparative risks.

Dr. Francisco J. Pasquel of Emory University, Atlanta, and his colleagues conducted a randomized clinical trial evaluating the comparative safety and effectiveness of basal insulin or an oral antidiabetic drug (OAD) for 26 weeks (BMJ Open Diab Res Care. 2015;3:e000104).

A total of 150 patients, average age 79 years, with a blood glucose level greater than 180 mg/dL or a hemoglobin A_1c greater than 7.5%, treated with diet or an oral agent, were randomized to either 0.1 U/kg per day of glargine or continuation of oral agents (metformin, insulin secretagogues, thiazolidinediones, or DPP-4 inhibitors). Glargine was adjusted based on blood sugar readings.

In the OAD group, 16% of patients were treated with metformin plus sulfonylurea, 27% with a sulfonylurea alone, and 8% with sulfonylurea and a DPP-4 inhibitor.

There were 62 hypoglycemic events in the OAD group and 43 in the basal insulin group (P = .4). Overall, daily blood glucose levels did not differ between the groups. Rates of cardiovascular events, renal failure, infection, falls, emergency department visits, hospital admissions, and mortality were similar between the two groups.

Although these data are somewhat reassuring, power may have been an issue, and a larger sample size may have resulted in detection of more hypoglycemic events in the OAD group. On the other hand, the data are balanced and resonate with previous data showing that in older adults with diabetes (about 74 years of age), intensive glycemic control is associated with an increased risk of falls in insulin users but not in those treated with OADs. The goal of the current study was not intensive glycemic control.

So, for patients in a long-term care facility, metformin and the DPP-4 inhibitors will be weight neutral without risk of hypoglycemia. Therefore, these may be the “go-to” drugs if the DPP-4 inhibitors are affordable and you do not have a long way to go for control (DPP-4 inhibitors tend to be relatively mild agents, lowering HbA_1c by 0.6%). If a sulfonylurea must be used, glipizide should be chosen, because it has a shorter half-life.

Balance all of this with appropriate HbA_1c goals for your patient adjusted for medical comorbidity, goals of care, and life expectancy.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

The prevalence of diabetes increases as patients age and gain weight. More than one-third of nursing home residents have diabetes. The overall treatment goals for elderly patients with diabetes are similar to those for younger patients, but somehow the stakes feel higher. Polypharmacy, decreased activity, shifting dietary patterns, hyperglycemia, fears of hypoglycemia leading to falls, worsening comorbid conditions, and hospitalization pose great challenges to ideal management.

Because of these concerns, caution is raised about the use of insulin or oral agents that cause hypoglycemia in frail older adults in long-term care facilities. But these agents are used, and perhaps we understand little about their comparative risks.

Dr. Francisco J. Pasquel of Emory University, Atlanta, and his colleagues conducted a randomized clinical trial evaluating the comparative safety and effectiveness of basal insulin or an oral antidiabetic drug (OAD) for 26 weeks (BMJ Open Diab Res Care. 2015;3:e000104).

A total of 150 patients, average age 79 years, with a blood glucose level greater than 180 mg/dL or a hemoglobin A_1c greater than 7.5%, treated with diet or an oral agent, were randomized to either 0.1 U/kg per day of glargine or continuation of oral agents (metformin, insulin secretagogues, thiazolidinediones, or DPP-4 inhibitors). Glargine was adjusted based on blood sugar readings.

In the OAD group, 16% of patients were treated with metformin plus sulfonylurea, 27% with a sulfonylurea alone, and 8% with sulfonylurea and a DPP-4 inhibitor.

There were 62 hypoglycemic events in the OAD group and 43 in the basal insulin group (P = .4). Overall, daily blood glucose levels did not differ between the groups. Rates of cardiovascular events, renal failure, infection, falls, emergency department visits, hospital admissions, and mortality were similar between the two groups.

Although these data are somewhat reassuring, power may have been an issue, and a larger sample size may have resulted in detection of more hypoglycemic events in the OAD group. On the other hand, the data are balanced and resonate with previous data showing that in older adults with diabetes (about 74 years of age), intensive glycemic control is associated with an increased risk of falls in insulin users but not in those treated with OADs. The goal of the current study was not intensive glycemic control.

So, for patients in a long-term care facility, metformin and the DPP-4 inhibitors will be weight neutral without risk of hypoglycemia. Therefore, these may be the “go-to” drugs if the DPP-4 inhibitors are affordable and you do not have a long way to go for control (DPP-4 inhibitors tend to be relatively mild agents, lowering HbA_1c by 0.6%). If a sulfonylurea must be used, glipizide should be chosen, because it has a shorter half-life.

Balance all of this with appropriate HbA_1c goals for your patient adjusted for medical comorbidity, goals of care, and life expectancy.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

As we head into influenza season, we are likely steeling our nerves for the inevitable debate with some of our patients about receiving the influenza vaccination.

We are used to hearing patients say, “I have never had it, and I have never gotten the flu,” or (my favorite), “Last time I got the shot, I got the flu.” Arguments that – while defying chance, logic, and science in general – keep us rooted in the daily joys of clinical practice.

Some handy influenza facts:

1. In well-matched years, the number needed to treat (NNT) to prevent one flu-like illness is 33.

2. In unmatched years, the NNT is 100.

We should be adding to this discussion some information about the observed association between the influenza vaccine and acute myocardial infarction (AMI). If compelling arguments about preventing flu-like symptoms don’t carry the day, maybe preventing heart attack will.

Dr. Michelle Barnes and her colleagues at UNSW Australia, Sydney, published the results of a systematic review of case-control studies evaluating the association between the influenza vaccine and AMI (Heart, 2015 Aug. 26. doi:10.1136/heartjnl-2015-307691). In this study, the investigators identified 16 studies on AMI and influenza vaccination or influenza infection.

The odds of influenza infection, influenza-like illness, or respiratory infection were significantly greater in patients with AMI (odds ratio, 2.01; 95% confidence interval: 1.47-2.76). Influenza vaccine was associated with a lower risk of AMI (OR, 0.71; 95% CI: 0.56-0.91).

This is the first meta-analysis compiling all case-control data on the relationship between AMI and the influenza vaccine. Overall, cases had double the risk of influenza or respiratory tract infection, compared with controls.

Influenza has been hypothesized to cause coronary artery occlusion through stenosis of subcritical atherosclerotic plaque, and it has been shown to promote atherogenesis in animal models. The connection between AMI and influenza was first observed in the 1930s during the flu season.

But medicine has a short memory, and our patients sometimes do as well. So, it is time we remind them about this link and encourage them to get their flu shots.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

As we head into influenza season, we are likely steeling our nerves for the inevitable debate with some of our patients about receiving the influenza vaccination.

We are used to hearing patients say, “I have never had it, and I have never gotten the flu,” or (my favorite), “Last time I got the shot, I got the flu.” Arguments that – while defying chance, logic, and science in general – keep us rooted in the daily joys of clinical practice.

Some handy influenza facts:

1. In well-matched years, the number needed to treat (NNT) to prevent one flu-like illness is 33.

2. In unmatched years, the NNT is 100.

We should be adding to this discussion some information about the observed association between the influenza vaccine and acute myocardial infarction (AMI). If compelling arguments about preventing flu-like symptoms don’t carry the day, maybe preventing heart attack will.

Dr. Michelle Barnes and her colleagues at UNSW Australia, Sydney, published the results of a systematic review of case-control studies evaluating the association between the influenza vaccine and AMI (Heart, 2015 Aug. 26. doi:10.1136/heartjnl-2015-307691). In this study, the investigators identified 16 studies on AMI and influenza vaccination or influenza infection.

The odds of influenza infection, influenza-like illness, or respiratory infection were significantly greater in patients with AMI (odds ratio, 2.01; 95% confidence interval: 1.47-2.76). Influenza vaccine was associated with a lower risk of AMI (OR, 0.71; 95% CI: 0.56-0.91).

This is the first meta-analysis compiling all case-control data on the relationship between AMI and the influenza vaccine. Overall, cases had double the risk of influenza or respiratory tract infection, compared with controls.

Influenza has been hypothesized to cause coronary artery occlusion through stenosis of subcritical atherosclerotic plaque, and it has been shown to promote atherogenesis in animal models. The connection between AMI and influenza was first observed in the 1930s during the flu season.

But medicine has a short memory, and our patients sometimes do as well. So, it is time we remind them about this link and encourage them to get their flu shots.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

As we head into influenza season, we are likely steeling our nerves for the inevitable debate with some of our patients about receiving the influenza vaccination.

We are used to hearing patients say, “I have never had it, and I have never gotten the flu,” or (my favorite), “Last time I got the shot, I got the flu.” Arguments that – while defying chance, logic, and science in general – keep us rooted in the daily joys of clinical practice.

Some handy influenza facts:

1. In well-matched years, the number needed to treat (NNT) to prevent one flu-like illness is 33.

2. In unmatched years, the NNT is 100.

We should be adding to this discussion some information about the observed association between the influenza vaccine and acute myocardial infarction (AMI). If compelling arguments about preventing flu-like symptoms don’t carry the day, maybe preventing heart attack will.

Dr. Michelle Barnes and her colleagues at UNSW Australia, Sydney, published the results of a systematic review of case-control studies evaluating the association between the influenza vaccine and AMI (Heart, 2015 Aug. 26. doi:10.1136/heartjnl-2015-307691). In this study, the investigators identified 16 studies on AMI and influenza vaccination or influenza infection.

The odds of influenza infection, influenza-like illness, or respiratory infection were significantly greater in patients with AMI (odds ratio, 2.01; 95% confidence interval: 1.47-2.76). Influenza vaccine was associated with a lower risk of AMI (OR, 0.71; 95% CI: 0.56-0.91).

This is the first meta-analysis compiling all case-control data on the relationship between AMI and the influenza vaccine. Overall, cases had double the risk of influenza or respiratory tract infection, compared with controls.

Influenza has been hypothesized to cause coronary artery occlusion through stenosis of subcritical atherosclerotic plaque, and it has been shown to promote atherogenesis in animal models. The connection between AMI and influenza was first observed in the 1930s during the flu season.

But medicine has a short memory, and our patients sometimes do as well. So, it is time we remind them about this link and encourage them to get their flu shots.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

At one time or another, insomnia afflicts nearly one-half of U.S. adults, half of whom have a clinically diagnosable disorder. This presents perpetual challenges in the face of patient populations that have been told to “ask your doctor about” sleeping medications or have received them already.

We know that the Z-drugs (zolpidem, zaleplon, and eszopiclone), some of the most widely used pharmacologics for insomnia, are benzodiazepine receptor agonists. As such, tolerance develops, and this tolerance leads to escalating doses, increased side effects, and sleepier patients.

Cognitive-behavioral therapy has been shown to be effective for insomnia, but this clinical service is not widely available. For busy clinicians trying to help these patients, we need a simple tool that can be easily explained to patients, giving them a project on which to work.

This tool is sleep restriction. The goal of sleep restriction is to consolidate fragmented sleep to increase the intrinsic sleep drive.

You might have heard your patients describe their bedroom as a “torture chamber.” Some of this torture relates to sleepless staring at the ceiling for hours on end. Sleep restriction gets them out of the chamber.

Karen Falloon, Ph.D., of the University of Auckland (New Zealand), and her colleagues conducted a randomized trial in New Zealand investigating the impact of simplified sleep restriction (SSR) for patients with primary insomnia (Br J Gen Pract. 2015 Aug;65(637):e508-15).

A total of 97 patients were randomized. All patients received sleep hygiene advice, including avoiding caffeine and developing a consistent bedtime routine. Patients in the SSR arm received a verbal and written sleep prescription establishing bedtime and wake-up times informed by a baseline 2-week daily sleep diary.

The sleep prescription was average total sleep duration plus 50% of the total time spent awake in bed. The minimum time in bed was 5 hours. If participants were sleeping less than 85% of the time in bed, the time allowed in bed was reduced to total sleep time plus 30 minutes. Sleepy patients could spend 30 more minutes in bed. All changes were made at bedtime, with wake-up time held constant.

At 6 months, the SSR group had improved perceived sleep quality and fatigue, and improved sleep efficiency as measured by actigraphy. A total of 67% of patients responded to SSR, compared with 41% of controls (number needed to treat = 4).

The efficacy of this intervention is extremely impressive. Importantly, it was delivered by a general practitioner without specialized training during two “slightly extended” visits.

Potential participants were excluded if they were on a sleeping medication, which does not imply that this would not work in a population already on Z-drugs. Consideration should to be given to possible risks when implementing sleep restriction with patients taking Z-drugs with longer half-lives (for example, eszopiclone is 6 hours, zolpidem is 3 hours, and zaleplon is 1 hour), because of higher serum concentrations upon waking.

But when these medications fail, or you have Z-drug–naive patients with insomnia, have this intervention ready.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

At one time or another, insomnia afflicts nearly one-half of U.S. adults, half of whom have a clinically diagnosable disorder. This presents perpetual challenges in the face of patient populations that have been told to “ask your doctor about” sleeping medications or have received them already.

We know that the Z-drugs (zolpidem, zaleplon, and eszopiclone), some of the most widely used pharmacologics for insomnia, are benzodiazepine receptor agonists. As such, tolerance develops, and this tolerance leads to escalating doses, increased side effects, and sleepier patients.

Cognitive-behavioral therapy has been shown to be effective for insomnia, but this clinical service is not widely available. For busy clinicians trying to help these patients, we need a simple tool that can be easily explained to patients, giving them a project on which to work.

This tool is sleep restriction. The goal of sleep restriction is to consolidate fragmented sleep to increase the intrinsic sleep drive.

You might have heard your patients describe their bedroom as a “torture chamber.” Some of this torture relates to sleepless staring at the ceiling for hours on end. Sleep restriction gets them out of the chamber.

Karen Falloon, Ph.D., of the University of Auckland (New Zealand), and her colleagues conducted a randomized trial in New Zealand investigating the impact of simplified sleep restriction (SSR) for patients with primary insomnia (Br J Gen Pract. 2015 Aug;65(637):e508-15).

A total of 97 patients were randomized. All patients received sleep hygiene advice, including avoiding caffeine and developing a consistent bedtime routine. Patients in the SSR arm received a verbal and written sleep prescription establishing bedtime and wake-up times informed by a baseline 2-week daily sleep diary.

The sleep prescription was average total sleep duration plus 50% of the total time spent awake in bed. The minimum time in bed was 5 hours. If participants were sleeping less than 85% of the time in bed, the time allowed in bed was reduced to total sleep time plus 30 minutes. Sleepy patients could spend 30 more minutes in bed. All changes were made at bedtime, with wake-up time held constant.

At 6 months, the SSR group had improved perceived sleep quality and fatigue, and improved sleep efficiency as measured by actigraphy. A total of 67% of patients responded to SSR, compared with 41% of controls (number needed to treat = 4).

The efficacy of this intervention is extremely impressive. Importantly, it was delivered by a general practitioner without specialized training during two “slightly extended” visits.

Potential participants were excluded if they were on a sleeping medication, which does not imply that this would not work in a population already on Z-drugs. Consideration should to be given to possible risks when implementing sleep restriction with patients taking Z-drugs with longer half-lives (for example, eszopiclone is 6 hours, zolpidem is 3 hours, and zaleplon is 1 hour), because of higher serum concentrations upon waking.

But when these medications fail, or you have Z-drug–naive patients with insomnia, have this intervention ready.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

At one time or another, insomnia afflicts nearly one-half of U.S. adults, half of whom have a clinically diagnosable disorder. This presents perpetual challenges in the face of patient populations that have been told to “ask your doctor about” sleeping medications or have received them already.

We know that the Z-drugs (zolpidem, zaleplon, and eszopiclone), some of the most widely used pharmacologics for insomnia, are benzodiazepine receptor agonists. As such, tolerance develops, and this tolerance leads to escalating doses, increased side effects, and sleepier patients.

Cognitive-behavioral therapy has been shown to be effective for insomnia, but this clinical service is not widely available. For busy clinicians trying to help these patients, we need a simple tool that can be easily explained to patients, giving them a project on which to work.

This tool is sleep restriction. The goal of sleep restriction is to consolidate fragmented sleep to increase the intrinsic sleep drive.

You might have heard your patients describe their bedroom as a “torture chamber.” Some of this torture relates to sleepless staring at the ceiling for hours on end. Sleep restriction gets them out of the chamber.

Karen Falloon, Ph.D., of the University of Auckland (New Zealand), and her colleagues conducted a randomized trial in New Zealand investigating the impact of simplified sleep restriction (SSR) for patients with primary insomnia (Br J Gen Pract. 2015 Aug;65(637):e508-15).

A total of 97 patients were randomized. All patients received sleep hygiene advice, including avoiding caffeine and developing a consistent bedtime routine. Patients in the SSR arm received a verbal and written sleep prescription establishing bedtime and wake-up times informed by a baseline 2-week daily sleep diary.

The sleep prescription was average total sleep duration plus 50% of the total time spent awake in bed. The minimum time in bed was 5 hours. If participants were sleeping less than 85% of the time in bed, the time allowed in bed was reduced to total sleep time plus 30 minutes. Sleepy patients could spend 30 more minutes in bed. All changes were made at bedtime, with wake-up time held constant.

At 6 months, the SSR group had improved perceived sleep quality and fatigue, and improved sleep efficiency as measured by actigraphy. A total of 67% of patients responded to SSR, compared with 41% of controls (number needed to treat = 4).

The efficacy of this intervention is extremely impressive. Importantly, it was delivered by a general practitioner without specialized training during two “slightly extended” visits.

Potential participants were excluded if they were on a sleeping medication, which does not imply that this would not work in a population already on Z-drugs. Consideration should to be given to possible risks when implementing sleep restriction with patients taking Z-drugs with longer half-lives (for example, eszopiclone is 6 hours, zolpidem is 3 hours, and zaleplon is 1 hour), because of higher serum concentrations upon waking.

But when these medications fail, or you have Z-drug–naive patients with insomnia, have this intervention ready.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

My 27-year-old patient with a body mass index of 64 kg/m² presented to my clinic with back and leg pain. Unfortunately, I was not the least bit surprised.

When bending over, he developed acute onset of back pain, with radiating pain down the lateral side of his right leg to his foot. Exam and history were consistent with lumbar radiculopathy.

©Ingram Publishing/Thinkstock.com

Over the next several months, the patient had intractable pain in the presence of escalating opioids. The neurosurgeons said that his weight created too high a risk for intraoperative and postoperative complications, with which I agreed.

And so began the work of titrating his pain-modulating agents, along with the significantly less glamorous and substantially more challenging task of helping him lose weight.

He was staunchly opposed to bariatric surgery and could not afford weight loss medications, presenting a bit of an impasse. To me, the fact that his insurance company would have covered his spinal surgery but not his FDA-approved weight loss medications embodies one of the great medical mysteries of modern times.

His mother accompanied him on one of his several visits and chimed in, “He needs to eat bread, doesn’t he?”

One of my common weight loss counseling mantras is “no whites for breakfast, lunch, or dinner.” These whites would include rice, bread, pasta, and potatoes. The airwaves have been crackling for a while with calls to decrease carbohydrate consumption to combat the obesity epidemic and to eat bread only if you’re a duck. As a result, bread consumption has declined worldwide.

So how bad is bread? Are all breads the same?

Luis Serra-Majem and Inmaculada Bautista-Castano of the University of Las Palmas de Gran Canaria, Spain, conducted a systematic review of the impact of bread consumption on obesity and abdominal adiposity (Br. J. Nutr. 2015;113:S29-S35). The authors concluded that white (refined grain) bread, but not whole-grain bread, may be associated with excess abdominal fat.

Proposed hypotheses for how breads impact adiposity differently are:

1. Whole-grain bread increases satiety more than white bread;

2. Whole-grain bread results in lower plasma glucose and insulin responses than white bread;

3. Higher fiber content of whole-grain bread limits glucose absorption more than white bread; and

4. Whole-grain bread may positively influence gut microbiota through a probiotic effect.

My advice to the patient was to restrict calories, avoid carbohydrates, and if bread must be consumed, then it must be whole grain. Baby steps.

But he found religion in this (and in walking) and lost 200 pounds over the next 5 years. Miracles are still possible.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

My 27-year-old patient with a body mass index of 64 kg/m² presented to my clinic with back and leg pain. Unfortunately, I was not the least bit surprised.

When bending over, he developed acute onset of back pain, with radiating pain down the lateral side of his right leg to his foot. Exam and history were consistent with lumbar radiculopathy.

©Ingram Publishing/Thinkstock.com

Over the next several months, the patient had intractable pain in the presence of escalating opioids. The neurosurgeons said that his weight created too high a risk for intraoperative and postoperative complications, with which I agreed.

And so began the work of titrating his pain-modulating agents, along with the significantly less glamorous and substantially more challenging task of helping him lose weight.

He was staunchly opposed to bariatric surgery and could not afford weight loss medications, presenting a bit of an impasse. To me, the fact that his insurance company would have covered his spinal surgery but not his FDA-approved weight loss medications embodies one of the great medical mysteries of modern times.

His mother accompanied him on one of his several visits and chimed in, “He needs to eat bread, doesn’t he?”

One of my common weight loss counseling mantras is “no whites for breakfast, lunch, or dinner.” These whites would include rice, bread, pasta, and potatoes. The airwaves have been crackling for a while with calls to decrease carbohydrate consumption to combat the obesity epidemic and to eat bread only if you’re a duck. As a result, bread consumption has declined worldwide.

So how bad is bread? Are all breads the same?

Luis Serra-Majem and Inmaculada Bautista-Castano of the University of Las Palmas de Gran Canaria, Spain, conducted a systematic review of the impact of bread consumption on obesity and abdominal adiposity (Br. J. Nutr. 2015;113:S29-S35). The authors concluded that white (refined grain) bread, but not whole-grain bread, may be associated with excess abdominal fat.

Proposed hypotheses for how breads impact adiposity differently are:

1. Whole-grain bread increases satiety more than white bread;

2. Whole-grain bread results in lower plasma glucose and insulin responses than white bread;

3. Higher fiber content of whole-grain bread limits glucose absorption more than white bread; and

4. Whole-grain bread may positively influence gut microbiota through a probiotic effect.

My advice to the patient was to restrict calories, avoid carbohydrates, and if bread must be consumed, then it must be whole grain. Baby steps.

But he found religion in this (and in walking) and lost 200 pounds over the next 5 years. Miracles are still possible.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

My 27-year-old patient with a body mass index of 64 kg/m² presented to my clinic with back and leg pain. Unfortunately, I was not the least bit surprised.

When bending over, he developed acute onset of back pain, with radiating pain down the lateral side of his right leg to his foot. Exam and history were consistent with lumbar radiculopathy.

©Ingram Publishing/Thinkstock.com

Over the next several months, the patient had intractable pain in the presence of escalating opioids. The neurosurgeons said that his weight created too high a risk for intraoperative and postoperative complications, with which I agreed.

And so began the work of titrating his pain-modulating agents, along with the significantly less glamorous and substantially more challenging task of helping him lose weight.

He was staunchly opposed to bariatric surgery and could not afford weight loss medications, presenting a bit of an impasse. To me, the fact that his insurance company would have covered his spinal surgery but not his FDA-approved weight loss medications embodies one of the great medical mysteries of modern times.

His mother accompanied him on one of his several visits and chimed in, “He needs to eat bread, doesn’t he?”

One of my common weight loss counseling mantras is “no whites for breakfast, lunch, or dinner.” These whites would include rice, bread, pasta, and potatoes. The airwaves have been crackling for a while with calls to decrease carbohydrate consumption to combat the obesity epidemic and to eat bread only if you’re a duck. As a result, bread consumption has declined worldwide.

So how bad is bread? Are all breads the same?

Luis Serra-Majem and Inmaculada Bautista-Castano of the University of Las Palmas de Gran Canaria, Spain, conducted a systematic review of the impact of bread consumption on obesity and abdominal adiposity (Br. J. Nutr. 2015;113:S29-S35). The authors concluded that white (refined grain) bread, but not whole-grain bread, may be associated with excess abdominal fat.

Proposed hypotheses for how breads impact adiposity differently are:

1. Whole-grain bread increases satiety more than white bread;

2. Whole-grain bread results in lower plasma glucose and insulin responses than white bread;

3. Higher fiber content of whole-grain bread limits glucose absorption more than white bread; and

4. Whole-grain bread may positively influence gut microbiota through a probiotic effect.

My advice to the patient was to restrict calories, avoid carbohydrates, and if bread must be consumed, then it must be whole grain. Baby steps.

But he found religion in this (and in walking) and lost 200 pounds over the next 5 years. Miracles are still possible.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter @jonebbert.

Last week, one of my patients presented with a BMI of 49 and two canes. Knee x-ray shows marked medial compartment narrowing bilaterally. We will inject her knees with steroids, but this will be temporary.

As the obesity epidemic continues to rage, native joints are rapidly being replaced with metal ones. Our pitiful homegrown joints were not designed to carry all this human weight. Joint forces in the hip and knee have been estimated to be 3 times body weight when walking on level ground and 6-10 times body weight when stooping or bending. Combine this with all the ‘screen time’ (average 8 hours a day for U.S. adults) and all the trips to the bathroom from the poorly controlled diabetes, and we are set up for needing a lot more orthopedic surgeons.

So should we push for surgery?

I am reluctant to immediately and eagerly pursue surgery based upon data from Ward et al. elucidating the increased risk for complications after joint surgery among patients with a BMI > 40 (J.Arthroplasty. 2015 Jun 3. pii: S0883-5403(15)00474-X. doi: 10.1016/j.arth.2015.03.045. [Epub ahead of print]). Data from the bariatric literature suggest that the risk of complications following joint replacement is lower if bariatric surgery is performed first. Weight loss as we look toward joint replacement is a good idea for both our orthopedic colleagues and our patients.

So we will work on weight loss first

In patients with osteoarthritis, a moderate amount of weight loss can significantly improve knee function. The short term efficacy of weight loss is comparable to joint replacement. But clinicians need to be wary of the “pain-exercise block”: patients telling us they cannot lose weight because the pain prevents them from exercising. I tell my patients that weight loss and weight maintenance can be managed effectively through dietary modification and that they do not have to run a marathon, they just need to walk if they can. But patients do not always want to hear this. Caloric restriction is psychologically painful for many. I remind them that 30 minutes of exercise can be undone in 30 seconds with a bar of chocolate, so we need to skip the chocolate bar if we do light exercise or forgo exercise altogether. Exercise is important for a million other reasons, but many of our patients can’t engage, especially when presenting with gait assist devices.

My patient and I started the discussion of bariatric surgery. In the meantime, we are going to try a trial of lorcaserin and hope the knees hold out. We are likely going to need more steroids.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter: @jonebbert.

Last week, one of my patients presented with a BMI of 49 and two canes. Knee x-ray shows marked medial compartment narrowing bilaterally. We will inject her knees with steroids, but this will be temporary.

As the obesity epidemic continues to rage, native joints are rapidly being replaced with metal ones. Our pitiful homegrown joints were not designed to carry all this human weight. Joint forces in the hip and knee have been estimated to be 3 times body weight when walking on level ground and 6-10 times body weight when stooping or bending. Combine this with all the ‘screen time’ (average 8 hours a day for U.S. adults) and all the trips to the bathroom from the poorly controlled diabetes, and we are set up for needing a lot more orthopedic surgeons.

So should we push for surgery?

I am reluctant to immediately and eagerly pursue surgery based upon data from Ward et al. elucidating the increased risk for complications after joint surgery among patients with a BMI > 40 (J.Arthroplasty. 2015 Jun 3. pii: S0883-5403(15)00474-X. doi: 10.1016/j.arth.2015.03.045. [Epub ahead of print]). Data from the bariatric literature suggest that the risk of complications following joint replacement is lower if bariatric surgery is performed first. Weight loss as we look toward joint replacement is a good idea for both our orthopedic colleagues and our patients.

So we will work on weight loss first

In patients with osteoarthritis, a moderate amount of weight loss can significantly improve knee function. The short term efficacy of weight loss is comparable to joint replacement. But clinicians need to be wary of the “pain-exercise block”: patients telling us they cannot lose weight because the pain prevents them from exercising. I tell my patients that weight loss and weight maintenance can be managed effectively through dietary modification and that they do not have to run a marathon, they just need to walk if they can. But patients do not always want to hear this. Caloric restriction is psychologically painful for many. I remind them that 30 minutes of exercise can be undone in 30 seconds with a bar of chocolate, so we need to skip the chocolate bar if we do light exercise or forgo exercise altogether. Exercise is important for a million other reasons, but many of our patients can’t engage, especially when presenting with gait assist devices.

My patient and I started the discussion of bariatric surgery. In the meantime, we are going to try a trial of lorcaserin and hope the knees hold out. We are likely going to need more steroids.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter: @jonebbert.

Last week, one of my patients presented with a BMI of 49 and two canes. Knee x-ray shows marked medial compartment narrowing bilaterally. We will inject her knees with steroids, but this will be temporary.

As the obesity epidemic continues to rage, native joints are rapidly being replaced with metal ones. Our pitiful homegrown joints were not designed to carry all this human weight. Joint forces in the hip and knee have been estimated to be 3 times body weight when walking on level ground and 6-10 times body weight when stooping or bending. Combine this with all the ‘screen time’ (average 8 hours a day for U.S. adults) and all the trips to the bathroom from the poorly controlled diabetes, and we are set up for needing a lot more orthopedic surgeons.

So should we push for surgery?

I am reluctant to immediately and eagerly pursue surgery based upon data from Ward et al. elucidating the increased risk for complications after joint surgery among patients with a BMI > 40 (J.Arthroplasty. 2015 Jun 3. pii: S0883-5403(15)00474-X. doi: 10.1016/j.arth.2015.03.045. [Epub ahead of print]). Data from the bariatric literature suggest that the risk of complications following joint replacement is lower if bariatric surgery is performed first. Weight loss as we look toward joint replacement is a good idea for both our orthopedic colleagues and our patients.

So we will work on weight loss first

In patients with osteoarthritis, a moderate amount of weight loss can significantly improve knee function. The short term efficacy of weight loss is comparable to joint replacement. But clinicians need to be wary of the “pain-exercise block”: patients telling us they cannot lose weight because the pain prevents them from exercising. I tell my patients that weight loss and weight maintenance can be managed effectively through dietary modification and that they do not have to run a marathon, they just need to walk if they can. But patients do not always want to hear this. Caloric restriction is psychologically painful for many. I remind them that 30 minutes of exercise can be undone in 30 seconds with a bar of chocolate, so we need to skip the chocolate bar if we do light exercise or forgo exercise altogether. Exercise is important for a million other reasons, but many of our patients can’t engage, especially when presenting with gait assist devices.

My patient and I started the discussion of bariatric surgery. In the meantime, we are going to try a trial of lorcaserin and hope the knees hold out. We are likely going to need more steroids.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow him on Twitter: @jonebbert.

Despite all its glamour and opportunities to write columns like this one, primary care does not attract as many clinicians as it needs to provide for the aging population. Some have proposed that this is because when learners rotate with us, they witness frustration with preauthorizations and physician-patient relationships poisoned by opioid addiction – not the intangible spiritual fulfillment of long-term relationships with people who share their lives with us.

In addition, many primary care providers have other competing interests that take them away from practice. This trend will likely increase as practitioners work beyond the age of 65 years but at reduced hours. These demands naturally decrease patient access and can theoretically lead to dissatisfaction, which is potentially devastating if we are reimbursed based upon satisfaction scores.

So, do reduced hours frustrate patients?

Laura Panattoni, Ph.D., and her colleagues at the Palo Alto Medical Foundation Research Institute, Mountain View, Calif., evaluated the relationship between physicians’ clinical time, continuity of care, access to care, and patient satisfaction with the physician (J. Gen. Intern. Med. 2015;30:327-33). The study was a cross-section survey of physicians in family and internal medicine and their patients.

The investigators found that greater office time was directly associated with increased continuity and access but with lower patient satisfaction scores. Restated, reduced clinical hours were associated with improved patient satisfaction.

These findings are interesting and important at many levels. First, they suggest that clinicians who choose less than a full-time clinical obligation can keep their patients happy. Second, we can hypothesize that what is lost in continuity and access is made up for in effective communication delivered by clinicians who are happy themselves. Third, practice redesign should not require full-time commitment to deliver on the satisfaction side of the equation. The world is clamoring for alternative care models where electronic “touches” alleviate the pressure for “patients in rooms.” Studies have shown that up to 93% of patients would select a physician who allows them to communicate with them electronically. About 450,000 patients will see a doctor through the Internet this year. UnitedHealth Group started covering telemedicine and plans to expand this to 20 million customers next year.

I personally spend one-third of my time seeing patients in rooms, but I am electronically and telephonically accessible to them every day at all times. Maybe this helps keep my patients happy, despite me not being in the office every day.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified, practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow Dr. Ebbert on Twitter @jonebbert.

Despite all its glamour and opportunities to write columns like this one, primary care does not attract as many clinicians as it needs to provide for the aging population. Some have proposed that this is because when learners rotate with us, they witness frustration with preauthorizations and physician-patient relationships poisoned by opioid addiction – not the intangible spiritual fulfillment of long-term relationships with people who share their lives with us.

In addition, many primary care providers have other competing interests that take them away from practice. This trend will likely increase as practitioners work beyond the age of 65 years but at reduced hours. These demands naturally decrease patient access and can theoretically lead to dissatisfaction, which is potentially devastating if we are reimbursed based upon satisfaction scores.

So, do reduced hours frustrate patients?

Laura Panattoni, Ph.D., and her colleagues at the Palo Alto Medical Foundation Research Institute, Mountain View, Calif., evaluated the relationship between physicians’ clinical time, continuity of care, access to care, and patient satisfaction with the physician (J. Gen. Intern. Med. 2015;30:327-33). The study was a cross-section survey of physicians in family and internal medicine and their patients.

The investigators found that greater office time was directly associated with increased continuity and access but with lower patient satisfaction scores. Restated, reduced clinical hours were associated with improved patient satisfaction.

These findings are interesting and important at many levels. First, they suggest that clinicians who choose less than a full-time clinical obligation can keep their patients happy. Second, we can hypothesize that what is lost in continuity and access is made up for in effective communication delivered by clinicians who are happy themselves. Third, practice redesign should not require full-time commitment to deliver on the satisfaction side of the equation. The world is clamoring for alternative care models where electronic “touches” alleviate the pressure for “patients in rooms.” Studies have shown that up to 93% of patients would select a physician who allows them to communicate with them electronically. About 450,000 patients will see a doctor through the Internet this year. UnitedHealth Group started covering telemedicine and plans to expand this to 20 million customers next year.

I personally spend one-third of my time seeing patients in rooms, but I am electronically and telephonically accessible to them every day at all times. Maybe this helps keep my patients happy, despite me not being in the office every day.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified, practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow Dr. Ebbert on Twitter @jonebbert.

Despite all its glamour and opportunities to write columns like this one, primary care does not attract as many clinicians as it needs to provide for the aging population. Some have proposed that this is because when learners rotate with us, they witness frustration with preauthorizations and physician-patient relationships poisoned by opioid addiction – not the intangible spiritual fulfillment of long-term relationships with people who share their lives with us.

In addition, many primary care providers have other competing interests that take them away from practice. This trend will likely increase as practitioners work beyond the age of 65 years but at reduced hours. These demands naturally decrease patient access and can theoretically lead to dissatisfaction, which is potentially devastating if we are reimbursed based upon satisfaction scores.

So, do reduced hours frustrate patients?

Laura Panattoni, Ph.D., and her colleagues at the Palo Alto Medical Foundation Research Institute, Mountain View, Calif., evaluated the relationship between physicians’ clinical time, continuity of care, access to care, and patient satisfaction with the physician (J. Gen. Intern. Med. 2015;30:327-33). The study was a cross-section survey of physicians in family and internal medicine and their patients.

The investigators found that greater office time was directly associated with increased continuity and access but with lower patient satisfaction scores. Restated, reduced clinical hours were associated with improved patient satisfaction.

These findings are interesting and important at many levels. First, they suggest that clinicians who choose less than a full-time clinical obligation can keep their patients happy. Second, we can hypothesize that what is lost in continuity and access is made up for in effective communication delivered by clinicians who are happy themselves. Third, practice redesign should not require full-time commitment to deliver on the satisfaction side of the equation. The world is clamoring for alternative care models where electronic “touches” alleviate the pressure for “patients in rooms.” Studies have shown that up to 93% of patients would select a physician who allows them to communicate with them electronically. About 450,000 patients will see a doctor through the Internet this year. UnitedHealth Group started covering telemedicine and plans to expand this to 20 million customers next year.

I personally spend one-third of my time seeing patients in rooms, but I am electronically and telephonically accessible to them every day at all times. Maybe this helps keep my patients happy, despite me not being in the office every day.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition, nor should they be used as a substitute for medical advice from a qualified, board-certified, practicing clinician. Dr. Ebbert has no relevant financial disclosures about this article. Follow Dr. Ebbert on Twitter @jonebbert.

The other day, I received an electronic message that my patient presented to the emergency department following his attempt at lifting a relatively immovable object. The only thing apparently moved by this activity was his intervertebral disk – outward from its usual place and onto a nerve. He was quickly diagnosed with acute sciatica and treated with a healthy dose of steroids.

I enjoyed the subsequent soliloquy of the brilliance and outstanding clinical skill of our emergency department clinicians (which is true, by the way) when I saw him for follow-up. He was markedly improved.

In a moment of introspection, I questioned why we do not tend to use this strategy more in my practice, especially because it worked so well for my patient.

Perhaps it is because we are so used to dealing with medication side effects and the downstream consequences of insulin resistance in primary care that steroids make us squeamish. Perhaps it is also because we tend to see patients later in the course of their disease and think that it is too late for steroids to be beneficial. Maybe we are uncertain of their benefits.

So, how well do they work?

Dr. Harley Goldberg and colleagues recently published data from a randomized clinical trial exploring the efficacy of oral steroids for the treatment of acute sciatica (JAMA 2015;313:1915-23). A total of 269 adults with radicular pain for 3 months or less, an Oswestry Disability Index (ODI) of at least 30, and a herniated disk confirmed on MRI were randomized to prednisone or placebo. The prednisone dose was 60 mg for 5 days, then 40 mg for 5 days, and finally 20 mg for 5 days.

The prednisone group demonstrated significant reduction in the ODI at 3 weeks and 12 months, compared with placebo. No differences in pain or in rates of surgery were observed.

Adverse events were more common with prednisone, the most common being insomnia, increased appetite, and nervousness. No serious adverse events occurred related to treatment, and no differences were observed at 1 year.

The authors point out that the observation of a reduction in disability but no reduction in pain may be related to the fact that as patients improve functionally, they increase activity and experience more pain. Although analyses did not demonstrate a relationship between time until starting the steroids and identified effects of prednisone, clinical sense may press us to want to start them earlier in the course of disease.

Steroids might be a reasonable option in this setting, and combining them with other modalities (e.g., gabapentin) might further improve patients’ functional status and pain. As always, engaging patients in the shared decision making may help manage expectations.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no disclosures about this article.

The other day, I received an electronic message that my patient presented to the emergency department following his attempt at lifting a relatively immovable object. The only thing apparently moved by this activity was his intervertebral disk – outward from its usual place and onto a nerve. He was quickly diagnosed with acute sciatica and treated with a healthy dose of steroids.

I enjoyed the subsequent soliloquy of the brilliance and outstanding clinical skill of our emergency department clinicians (which is true, by the way) when I saw him for follow-up. He was markedly improved.

In a moment of introspection, I questioned why we do not tend to use this strategy more in my practice, especially because it worked so well for my patient.

Perhaps it is because we are so used to dealing with medication side effects and the downstream consequences of insulin resistance in primary care that steroids make us squeamish. Perhaps it is also because we tend to see patients later in the course of their disease and think that it is too late for steroids to be beneficial. Maybe we are uncertain of their benefits.

So, how well do they work?

Dr. Harley Goldberg and colleagues recently published data from a randomized clinical trial exploring the efficacy of oral steroids for the treatment of acute sciatica (JAMA 2015;313:1915-23). A total of 269 adults with radicular pain for 3 months or less, an Oswestry Disability Index (ODI) of at least 30, and a herniated disk confirmed on MRI were randomized to prednisone or placebo. The prednisone dose was 60 mg for 5 days, then 40 mg for 5 days, and finally 20 mg for 5 days.

The prednisone group demonstrated significant reduction in the ODI at 3 weeks and 12 months, compared with placebo. No differences in pain or in rates of surgery were observed.

Adverse events were more common with prednisone, the most common being insomnia, increased appetite, and nervousness. No serious adverse events occurred related to treatment, and no differences were observed at 1 year.

The authors point out that the observation of a reduction in disability but no reduction in pain may be related to the fact that as patients improve functionally, they increase activity and experience more pain. Although analyses did not demonstrate a relationship between time until starting the steroids and identified effects of prednisone, clinical sense may press us to want to start them earlier in the course of disease.

Steroids might be a reasonable option in this setting, and combining them with other modalities (e.g., gabapentin) might further improve patients’ functional status and pain. As always, engaging patients in the shared decision making may help manage expectations.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no disclosures about this article.

The other day, I received an electronic message that my patient presented to the emergency department following his attempt at lifting a relatively immovable object. The only thing apparently moved by this activity was his intervertebral disk – outward from its usual place and onto a nerve. He was quickly diagnosed with acute sciatica and treated with a healthy dose of steroids.

I enjoyed the subsequent soliloquy of the brilliance and outstanding clinical skill of our emergency department clinicians (which is true, by the way) when I saw him for follow-up. He was markedly improved.

In a moment of introspection, I questioned why we do not tend to use this strategy more in my practice, especially because it worked so well for my patient.

Perhaps it is because we are so used to dealing with medication side effects and the downstream consequences of insulin resistance in primary care that steroids make us squeamish. Perhaps it is also because we tend to see patients later in the course of their disease and think that it is too late for steroids to be beneficial. Maybe we are uncertain of their benefits.

So, how well do they work?

Dr. Harley Goldberg and colleagues recently published data from a randomized clinical trial exploring the efficacy of oral steroids for the treatment of acute sciatica (JAMA 2015;313:1915-23). A total of 269 adults with radicular pain for 3 months or less, an Oswestry Disability Index (ODI) of at least 30, and a herniated disk confirmed on MRI were randomized to prednisone or placebo. The prednisone dose was 60 mg for 5 days, then 40 mg for 5 days, and finally 20 mg for 5 days.

The prednisone group demonstrated significant reduction in the ODI at 3 weeks and 12 months, compared with placebo. No differences in pain or in rates of surgery were observed.

Adverse events were more common with prednisone, the most common being insomnia, increased appetite, and nervousness. No serious adverse events occurred related to treatment, and no differences were observed at 1 year.

The authors point out that the observation of a reduction in disability but no reduction in pain may be related to the fact that as patients improve functionally, they increase activity and experience more pain. Although analyses did not demonstrate a relationship between time until starting the steroids and identified effects of prednisone, clinical sense may press us to want to start them earlier in the course of disease.

Steroids might be a reasonable option in this setting, and combining them with other modalities (e.g., gabapentin) might further improve patients’ functional status and pain. As always, engaging patients in the shared decision making may help manage expectations.

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 and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician. Dr. Ebbert has no disclosures about this article.