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Delayed prescribing of antibiotics
While not a new phenomenon, antimicrobial resistance is an alarming and, arguably, still underappreciated public health problem. A mere 70 years after the introduction of antibiotics, we face the distinct possibility of a future without effective antibiotics for some infections. Such a reality will render select surgical operations, cancer chemotherapy, and organ transplants exceedingly dangerous.
The scarcity of new antimicrobial agents and the paucity of new agents in the drug development pipeline limit treatment options, particularly for patients with infections caused by multidrug-resistant organisms. Annually, multidrug resistant organisms cause an estimated 25,000 deaths in Europe and 12,000 deaths in the United States. In response to this threat, the Transatlantic Taskforce on Antimicrobial Resistance (TATFAR) was established and published their report with 17 recommendations.
Respiratory tract infections are one of the most common symptoms presenting to primary care. Overprescribing in this setting is rampant, driven largely by patient expectations and clinician need for expediency and desire to receive "high marks" for satisfaction. Available evidence has suggested that delayed antibiotic prescribing is effective. But what is the best method to delay antibiotic prescribing?
Researchers in the United Kingdom evaluated the comparative effectiveness of four different strategies of delayed antibiotic prescribing for patients not needing antibiotics right away:
• Recontact: Patients were asked to contact the office and leave a message for a clinician to prescribe an antibiotic.
• Postdated prescription: The prescription could be filled only after a certain date.
• Wait/Request: Patients were instructed to wait but could request an antibiotic from the front office.
• Delayed use: Patients received antibiotics but were asked to wait to use them.
A "no prescription" arm was added later in the trial. The primary outcome was symptom severity measured at the end of each day during days 2-4 of a two-week symptom diary. Secondary outcomes included antibiotic use and side effects.
No differences were observed between the four strategies with respect to symptom control. Antibiotic use did not differ significantly between strategies and the lowest use was reported in the no prescription arm. No significant differences were observed between groups in patient satisfaction. Complications were slightly higher in the no antibiotic group (2.5%), compared with the delayed groups (1.4%).
Delayed prescribing is associated with less than 40% of patients using an antibiotic. Given the current crisis with multidrug resistance, we should feel obligated to try one of the proposed strategies for delayed antibiotic prescription if patients do not need one right away.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
While not a new phenomenon, antimicrobial resistance is an alarming and, arguably, still underappreciated public health problem. A mere 70 years after the introduction of antibiotics, we face the distinct possibility of a future without effective antibiotics for some infections. Such a reality will render select surgical operations, cancer chemotherapy, and organ transplants exceedingly dangerous.
The scarcity of new antimicrobial agents and the paucity of new agents in the drug development pipeline limit treatment options, particularly for patients with infections caused by multidrug-resistant organisms. Annually, multidrug resistant organisms cause an estimated 25,000 deaths in Europe and 12,000 deaths in the United States. In response to this threat, the Transatlantic Taskforce on Antimicrobial Resistance (TATFAR) was established and published their report with 17 recommendations.
Respiratory tract infections are one of the most common symptoms presenting to primary care. Overprescribing in this setting is rampant, driven largely by patient expectations and clinician need for expediency and desire to receive "high marks" for satisfaction. Available evidence has suggested that delayed antibiotic prescribing is effective. But what is the best method to delay antibiotic prescribing?
Researchers in the United Kingdom evaluated the comparative effectiveness of four different strategies of delayed antibiotic prescribing for patients not needing antibiotics right away:
• Recontact: Patients were asked to contact the office and leave a message for a clinician to prescribe an antibiotic.
• Postdated prescription: The prescription could be filled only after a certain date.
• Wait/Request: Patients were instructed to wait but could request an antibiotic from the front office.
• Delayed use: Patients received antibiotics but were asked to wait to use them.
A "no prescription" arm was added later in the trial. The primary outcome was symptom severity measured at the end of each day during days 2-4 of a two-week symptom diary. Secondary outcomes included antibiotic use and side effects.
No differences were observed between the four strategies with respect to symptom control. Antibiotic use did not differ significantly between strategies and the lowest use was reported in the no prescription arm. No significant differences were observed between groups in patient satisfaction. Complications were slightly higher in the no antibiotic group (2.5%), compared with the delayed groups (1.4%).
Delayed prescribing is associated with less than 40% of patients using an antibiotic. Given the current crisis with multidrug resistance, we should feel obligated to try one of the proposed strategies for delayed antibiotic prescription if patients do not need one right away.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
While not a new phenomenon, antimicrobial resistance is an alarming and, arguably, still underappreciated public health problem. A mere 70 years after the introduction of antibiotics, we face the distinct possibility of a future without effective antibiotics for some infections. Such a reality will render select surgical operations, cancer chemotherapy, and organ transplants exceedingly dangerous.
The scarcity of new antimicrobial agents and the paucity of new agents in the drug development pipeline limit treatment options, particularly for patients with infections caused by multidrug-resistant organisms. Annually, multidrug resistant organisms cause an estimated 25,000 deaths in Europe and 12,000 deaths in the United States. In response to this threat, the Transatlantic Taskforce on Antimicrobial Resistance (TATFAR) was established and published their report with 17 recommendations.
Respiratory tract infections are one of the most common symptoms presenting to primary care. Overprescribing in this setting is rampant, driven largely by patient expectations and clinician need for expediency and desire to receive "high marks" for satisfaction. Available evidence has suggested that delayed antibiotic prescribing is effective. But what is the best method to delay antibiotic prescribing?
Researchers in the United Kingdom evaluated the comparative effectiveness of four different strategies of delayed antibiotic prescribing for patients not needing antibiotics right away:
• Recontact: Patients were asked to contact the office and leave a message for a clinician to prescribe an antibiotic.
• Postdated prescription: The prescription could be filled only after a certain date.
• Wait/Request: Patients were instructed to wait but could request an antibiotic from the front office.
• Delayed use: Patients received antibiotics but were asked to wait to use them.
A "no prescription" arm was added later in the trial. The primary outcome was symptom severity measured at the end of each day during days 2-4 of a two-week symptom diary. Secondary outcomes included antibiotic use and side effects.
No differences were observed between the four strategies with respect to symptom control. Antibiotic use did not differ significantly between strategies and the lowest use was reported in the no prescription arm. No significant differences were observed between groups in patient satisfaction. Complications were slightly higher in the no antibiotic group (2.5%), compared with the delayed groups (1.4%).
Delayed prescribing is associated with less than 40% of patients using an antibiotic. Given the current crisis with multidrug resistance, we should feel obligated to try one of the proposed strategies for delayed antibiotic prescription if patients do not need one right away.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Can coffee reduce weight?
Caffeine in the form of tea and coffee is the most widely consumed, socially acceptable stimulant around the globe. More than 150 million people in the United States drink coffee daily, with an average intake of 2 cups (which contains about 280 mg of caffeine).
Caffeine results in the release of excitatory neurotransmitters. Caffeine may increase energy expenditure and has been associated with reduced body mass. Studies have observed lower body mass index (BMI) in coffee consumers, compared with individuals who don’t consume coffee. Coffee may reduce appetite and dietary intake.
Greek researchers at Harokopio University, Athens, conducted a cross-over study to evaluate the effects of caffeinated coffee on appetite and dietary intake (Obesity 2013;21:1127-32). Sixteen normal-weight and 17 overweight/obese habitual coffee consumers (at least 1 cup of coffee/day) were enrolled. Each participant took part in three trials at least 1 week apart. Participants were required to abstain from caffeine for 24 hours and then reported to the lab to consume a breakfast and 200 mL of one of three experimental beverages: instant coffee with 3 mg caffeine/kg body weight (Coffee 3); instant coffee with 6 mg caffeine/kg (Coffee 6); or water. Participants had to consume the breakfast and the beverage within 5 minutes.
During a 3-hour period following beverage consumption, appetite feelings and participants’ dietary intake the day before the experiment were assessed. After this 3-hour period, participants were offered an ad libitum lunch buffet. The following day, participants reported by telephone their food and fluid intake for the rest of the experiment day.
Normal-weight participants consumed comparable energy in the ad libitum meal and in their total daily intake in the three interventions. However, among overweight/obese individuals, Coffee 6 resulted in significantly reduced energy intake during the ad libitum meal, compared with Coffee 3, and in significantly reduced total day energy intake, compared with both water and Coffee 3.
Doses used in this study for participants were somewhat staggering. The average caffeine content of the beverage in the Coffee 6 group was 526 mg. This is the caffeine content of roughly four 8-ounce cups of brewed coffee. The authors acknowledged that the Coffee 6 beverage was not easily consumed by "most of the volunteers."
We need to be cautious about the use of this dosing in the clinical setting. But as part of comprehensive weight-management strategy, caffeinated coffee may be helpful for reducing energy intake.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Caffeine in the form of tea and coffee is the most widely consumed, socially acceptable stimulant around the globe. More than 150 million people in the United States drink coffee daily, with an average intake of 2 cups (which contains about 280 mg of caffeine).
Caffeine results in the release of excitatory neurotransmitters. Caffeine may increase energy expenditure and has been associated with reduced body mass. Studies have observed lower body mass index (BMI) in coffee consumers, compared with individuals who don’t consume coffee. Coffee may reduce appetite and dietary intake.
Greek researchers at Harokopio University, Athens, conducted a cross-over study to evaluate the effects of caffeinated coffee on appetite and dietary intake (Obesity 2013;21:1127-32). Sixteen normal-weight and 17 overweight/obese habitual coffee consumers (at least 1 cup of coffee/day) were enrolled. Each participant took part in three trials at least 1 week apart. Participants were required to abstain from caffeine for 24 hours and then reported to the lab to consume a breakfast and 200 mL of one of three experimental beverages: instant coffee with 3 mg caffeine/kg body weight (Coffee 3); instant coffee with 6 mg caffeine/kg (Coffee 6); or water. Participants had to consume the breakfast and the beverage within 5 minutes.
During a 3-hour period following beverage consumption, appetite feelings and participants’ dietary intake the day before the experiment were assessed. After this 3-hour period, participants were offered an ad libitum lunch buffet. The following day, participants reported by telephone their food and fluid intake for the rest of the experiment day.
Normal-weight participants consumed comparable energy in the ad libitum meal and in their total daily intake in the three interventions. However, among overweight/obese individuals, Coffee 6 resulted in significantly reduced energy intake during the ad libitum meal, compared with Coffee 3, and in significantly reduced total day energy intake, compared with both water and Coffee 3.
Doses used in this study for participants were somewhat staggering. The average caffeine content of the beverage in the Coffee 6 group was 526 mg. This is the caffeine content of roughly four 8-ounce cups of brewed coffee. The authors acknowledged that the Coffee 6 beverage was not easily consumed by "most of the volunteers."
We need to be cautious about the use of this dosing in the clinical setting. But as part of comprehensive weight-management strategy, caffeinated coffee may be helpful for reducing energy intake.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Caffeine in the form of tea and coffee is the most widely consumed, socially acceptable stimulant around the globe. More than 150 million people in the United States drink coffee daily, with an average intake of 2 cups (which contains about 280 mg of caffeine).
Caffeine results in the release of excitatory neurotransmitters. Caffeine may increase energy expenditure and has been associated with reduced body mass. Studies have observed lower body mass index (BMI) in coffee consumers, compared with individuals who don’t consume coffee. Coffee may reduce appetite and dietary intake.
Greek researchers at Harokopio University, Athens, conducted a cross-over study to evaluate the effects of caffeinated coffee on appetite and dietary intake (Obesity 2013;21:1127-32). Sixteen normal-weight and 17 overweight/obese habitual coffee consumers (at least 1 cup of coffee/day) were enrolled. Each participant took part in three trials at least 1 week apart. Participants were required to abstain from caffeine for 24 hours and then reported to the lab to consume a breakfast and 200 mL of one of three experimental beverages: instant coffee with 3 mg caffeine/kg body weight (Coffee 3); instant coffee with 6 mg caffeine/kg (Coffee 6); or water. Participants had to consume the breakfast and the beverage within 5 minutes.
During a 3-hour period following beverage consumption, appetite feelings and participants’ dietary intake the day before the experiment were assessed. After this 3-hour period, participants were offered an ad libitum lunch buffet. The following day, participants reported by telephone their food and fluid intake for the rest of the experiment day.
Normal-weight participants consumed comparable energy in the ad libitum meal and in their total daily intake in the three interventions. However, among overweight/obese individuals, Coffee 6 resulted in significantly reduced energy intake during the ad libitum meal, compared with Coffee 3, and in significantly reduced total day energy intake, compared with both water and Coffee 3.
Doses used in this study for participants were somewhat staggering. The average caffeine content of the beverage in the Coffee 6 group was 526 mg. This is the caffeine content of roughly four 8-ounce cups of brewed coffee. The authors acknowledged that the Coffee 6 beverage was not easily consumed by "most of the volunteers."
We need to be cautious about the use of this dosing in the clinical setting. But as part of comprehensive weight-management strategy, caffeinated coffee may be helpful for reducing energy intake.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Gabapentin for alcohol use disorder
Two-thirds of U.S. adults currently consume alcohol, according to the National Health Interview Survey. While most are infrequent or light drinkers, 8% are problem drinkers (more than 14 drinks per week for men and more than 7 drinks per week for women).
Alcohol consumption is the second-leading cause of preventable death and disability in the United States. Annually, excessive alcohol consumption costs us almost a quarter of a trillion dollars in lost productivity, health care, law enforcement, and motor vehicle collisions.
Alcoholism is a relapsing and remitting disease characterized by psychosocial impairment and drug craving and withdrawal. Challenged by access inequalities to formal treatment services, few alcoholics, when interacting with the medical setting for other reasons, are offered or receive treatment. Some patients may be open to receiving treatment by primary care providers, but few drugs are available (naltrexone, acamprosate, and disulfiram). Clinicians may be unconvinced of their efficacy or uncomfortable with their use.
Gabapentin is an antiepileptic used commonly in primary care settings, mostly for neuropathic pain. Gabapentin is well tolerated, with a favorable pharmacokinetic profile and a broad therapeutic index. Preclinical data suggest that gabapentin normalizes stress-induced GABA (gamma-aminobutyric acid) activation associated with alcohol use disorder. Human data suggest that gabapentin reduces alcohol craving and alcohol-associated sleep and mood problems.
Mason and colleagues published the results from a randomized controlled clinical trial evaluating the efficacy and safety of different doses of gabapentin for increasing alcohol abstinence and reducing heavy drinking, insomnia, dysphoria, and craving. Potential participants were eligible for enrollment if they were aged 18 years or older, met criteria for alcohol dependence, and were recently abstinent from alcohol (at least 3 days). Participants were randomized to gabapentin 900 mg/day, gabapentin 1,800 mg/day, or placebo. Treatment was received for 12 weeks with titration and tapering (JAMA Intern. Med. 2014;174:70-7).
A total of 150 patients were randomized, and the groups were similar at baseline. Abstinence rates were 17%, 11.1%, and 4.1% in the 1,800-mg, 900-mg, and placebo groups (P = .04 for linear dose effect), respectively. The no-heavy-drinking rates were 44.7%, 29.6%, and 22.5% (P = .02 for linear dose effect). A dose effect was also observed for reductions in mood disturbance, sleep problems, and craving. No serious adverse events were reported.
We need to try to meet patients where they are. Patients should be directed to alcohol treatment services if they are willing to go. In my experience, many of them are not. In these cases, recommending an Alcoholics Anonymous group, trying gabapentin, and following them up in a clinic is a harm-reduction strategy worth trying.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Two-thirds of U.S. adults currently consume alcohol, according to the National Health Interview Survey. While most are infrequent or light drinkers, 8% are problem drinkers (more than 14 drinks per week for men and more than 7 drinks per week for women).
Alcohol consumption is the second-leading cause of preventable death and disability in the United States. Annually, excessive alcohol consumption costs us almost a quarter of a trillion dollars in lost productivity, health care, law enforcement, and motor vehicle collisions.
Alcoholism is a relapsing and remitting disease characterized by psychosocial impairment and drug craving and withdrawal. Challenged by access inequalities to formal treatment services, few alcoholics, when interacting with the medical setting for other reasons, are offered or receive treatment. Some patients may be open to receiving treatment by primary care providers, but few drugs are available (naltrexone, acamprosate, and disulfiram). Clinicians may be unconvinced of their efficacy or uncomfortable with their use.
Gabapentin is an antiepileptic used commonly in primary care settings, mostly for neuropathic pain. Gabapentin is well tolerated, with a favorable pharmacokinetic profile and a broad therapeutic index. Preclinical data suggest that gabapentin normalizes stress-induced GABA (gamma-aminobutyric acid) activation associated with alcohol use disorder. Human data suggest that gabapentin reduces alcohol craving and alcohol-associated sleep and mood problems.
Mason and colleagues published the results from a randomized controlled clinical trial evaluating the efficacy and safety of different doses of gabapentin for increasing alcohol abstinence and reducing heavy drinking, insomnia, dysphoria, and craving. Potential participants were eligible for enrollment if they were aged 18 years or older, met criteria for alcohol dependence, and were recently abstinent from alcohol (at least 3 days). Participants were randomized to gabapentin 900 mg/day, gabapentin 1,800 mg/day, or placebo. Treatment was received for 12 weeks with titration and tapering (JAMA Intern. Med. 2014;174:70-7).
A total of 150 patients were randomized, and the groups were similar at baseline. Abstinence rates were 17%, 11.1%, and 4.1% in the 1,800-mg, 900-mg, and placebo groups (P = .04 for linear dose effect), respectively. The no-heavy-drinking rates were 44.7%, 29.6%, and 22.5% (P = .02 for linear dose effect). A dose effect was also observed for reductions in mood disturbance, sleep problems, and craving. No serious adverse events were reported.
We need to try to meet patients where they are. Patients should be directed to alcohol treatment services if they are willing to go. In my experience, many of them are not. In these cases, recommending an Alcoholics Anonymous group, trying gabapentin, and following them up in a clinic is a harm-reduction strategy worth trying.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Two-thirds of U.S. adults currently consume alcohol, according to the National Health Interview Survey. While most are infrequent or light drinkers, 8% are problem drinkers (more than 14 drinks per week for men and more than 7 drinks per week for women).
Alcohol consumption is the second-leading cause of preventable death and disability in the United States. Annually, excessive alcohol consumption costs us almost a quarter of a trillion dollars in lost productivity, health care, law enforcement, and motor vehicle collisions.
Alcoholism is a relapsing and remitting disease characterized by psychosocial impairment and drug craving and withdrawal. Challenged by access inequalities to formal treatment services, few alcoholics, when interacting with the medical setting for other reasons, are offered or receive treatment. Some patients may be open to receiving treatment by primary care providers, but few drugs are available (naltrexone, acamprosate, and disulfiram). Clinicians may be unconvinced of their efficacy or uncomfortable with their use.
Gabapentin is an antiepileptic used commonly in primary care settings, mostly for neuropathic pain. Gabapentin is well tolerated, with a favorable pharmacokinetic profile and a broad therapeutic index. Preclinical data suggest that gabapentin normalizes stress-induced GABA (gamma-aminobutyric acid) activation associated with alcohol use disorder. Human data suggest that gabapentin reduces alcohol craving and alcohol-associated sleep and mood problems.
Mason and colleagues published the results from a randomized controlled clinical trial evaluating the efficacy and safety of different doses of gabapentin for increasing alcohol abstinence and reducing heavy drinking, insomnia, dysphoria, and craving. Potential participants were eligible for enrollment if they were aged 18 years or older, met criteria for alcohol dependence, and were recently abstinent from alcohol (at least 3 days). Participants were randomized to gabapentin 900 mg/day, gabapentin 1,800 mg/day, or placebo. Treatment was received for 12 weeks with titration and tapering (JAMA Intern. Med. 2014;174:70-7).
A total of 150 patients were randomized, and the groups were similar at baseline. Abstinence rates were 17%, 11.1%, and 4.1% in the 1,800-mg, 900-mg, and placebo groups (P = .04 for linear dose effect), respectively. The no-heavy-drinking rates were 44.7%, 29.6%, and 22.5% (P = .02 for linear dose effect). A dose effect was also observed for reductions in mood disturbance, sleep problems, and craving. No serious adverse events were reported.
We need to try to meet patients where they are. Patients should be directed to alcohol treatment services if they are willing to go. In my experience, many of them are not. In these cases, recommending an Alcoholics Anonymous group, trying gabapentin, and following them up in a clinic is a harm-reduction strategy worth trying.
Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Treating female pattern hair loss
Female pattern hair loss, which affects over 21 million women in the United States, is a nonscarring hair loss primarily involving the frontal and vertex scalp. FPHS causes women significant emotional and psychological distress. We see, and will continue to see, a lot of these cases in primary care. If left untreated or unaddressed, FPHL results in a slow, progressive decline in the density of scalp hair.
FPHL is characterized by the production of shorter and finer hairs and shortening of the growth phase of hair follicles. One may find it important to rule out secondary causes of hair loss, such as hyperandrogenism. So after excluding secondary causes, what are the best treatment options for treatment?
Researchers conducted a systematic review (Cochrane Database Syst. Rev. 2012 May, CD007628 [doi:10.1002/14651858.CD007628.pub3]) assessing the effectiveness of interventions for female pattern hair loss. Studies were included if they compared any type of monotherapy or combination therapy to treat FPHL. Studies evaluating treatments in women with increased circulating androgens (such as polycystic ovarian syndrome) were included. Primary outcomes included self-reported hair regrowth, quality of life, and adverse effects.
The Cochrane review included 22 studies that enrolled a total of 2,349 subjects. Ten studies evaluated minoxidil, four evaluated finasteride, two cyproterone acetate, and two flutamide. A variety of other exotic interventions was evaluated, including topical melatonin-alcohol solution, adenosine lotion, and pulsed electrostatic field.
The best data continue to exist for minoxidil. "Pooled data from 4 studies indicated that a greater proportion of participants (121/488) treated with minoxidil reported a moderate increase in their hair regrowth when compared with placebo (64/476) (risk ratio, 1.86; 95% confidence interval [CI], 1.42 to 2.43). In 7 studies, there was an important increase of 13.28 in total hair count per cm² in the minoxidil group compared to the placebo group (95% CI, 10.89 to 15.68). There was no difference in the number of adverse events in the twice daily minoxidil and placebo intervention groups, with the exception of a reported increase of adverse events (additional hair growth on areas other than the scalp) with minoxidil (5%) twice daily," according to the Cochrane report.
Other promising agents might be octyl nicotinate (0.5%), myristyl nicotinate (5%), and flutamide. Fulvestrant, adenosine, pulsed electrostatic field, and estradiol valerate are ineffective.
Minoxidil it is. It may be important to remind patients that 2% twice daily may be as effective and safe as 5% once a day.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Female pattern hair loss, which affects over 21 million women in the United States, is a nonscarring hair loss primarily involving the frontal and vertex scalp. FPHS causes women significant emotional and psychological distress. We see, and will continue to see, a lot of these cases in primary care. If left untreated or unaddressed, FPHL results in a slow, progressive decline in the density of scalp hair.
FPHL is characterized by the production of shorter and finer hairs and shortening of the growth phase of hair follicles. One may find it important to rule out secondary causes of hair loss, such as hyperandrogenism. So after excluding secondary causes, what are the best treatment options for treatment?
Researchers conducted a systematic review (Cochrane Database Syst. Rev. 2012 May, CD007628 [doi:10.1002/14651858.CD007628.pub3]) assessing the effectiveness of interventions for female pattern hair loss. Studies were included if they compared any type of monotherapy or combination therapy to treat FPHL. Studies evaluating treatments in women with increased circulating androgens (such as polycystic ovarian syndrome) were included. Primary outcomes included self-reported hair regrowth, quality of life, and adverse effects.
The Cochrane review included 22 studies that enrolled a total of 2,349 subjects. Ten studies evaluated minoxidil, four evaluated finasteride, two cyproterone acetate, and two flutamide. A variety of other exotic interventions was evaluated, including topical melatonin-alcohol solution, adenosine lotion, and pulsed electrostatic field.
The best data continue to exist for minoxidil. "Pooled data from 4 studies indicated that a greater proportion of participants (121/488) treated with minoxidil reported a moderate increase in their hair regrowth when compared with placebo (64/476) (risk ratio, 1.86; 95% confidence interval [CI], 1.42 to 2.43). In 7 studies, there was an important increase of 13.28 in total hair count per cm² in the minoxidil group compared to the placebo group (95% CI, 10.89 to 15.68). There was no difference in the number of adverse events in the twice daily minoxidil and placebo intervention groups, with the exception of a reported increase of adverse events (additional hair growth on areas other than the scalp) with minoxidil (5%) twice daily," according to the Cochrane report.
Other promising agents might be octyl nicotinate (0.5%), myristyl nicotinate (5%), and flutamide. Fulvestrant, adenosine, pulsed electrostatic field, and estradiol valerate are ineffective.
Minoxidil it is. It may be important to remind patients that 2% twice daily may be as effective and safe as 5% once a day.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Female pattern hair loss, which affects over 21 million women in the United States, is a nonscarring hair loss primarily involving the frontal and vertex scalp. FPHS causes women significant emotional and psychological distress. We see, and will continue to see, a lot of these cases in primary care. If left untreated or unaddressed, FPHL results in a slow, progressive decline in the density of scalp hair.
FPHL is characterized by the production of shorter and finer hairs and shortening of the growth phase of hair follicles. One may find it important to rule out secondary causes of hair loss, such as hyperandrogenism. So after excluding secondary causes, what are the best treatment options for treatment?
Researchers conducted a systematic review (Cochrane Database Syst. Rev. 2012 May, CD007628 [doi:10.1002/14651858.CD007628.pub3]) assessing the effectiveness of interventions for female pattern hair loss. Studies were included if they compared any type of monotherapy or combination therapy to treat FPHL. Studies evaluating treatments in women with increased circulating androgens (such as polycystic ovarian syndrome) were included. Primary outcomes included self-reported hair regrowth, quality of life, and adverse effects.
The Cochrane review included 22 studies that enrolled a total of 2,349 subjects. Ten studies evaluated minoxidil, four evaluated finasteride, two cyproterone acetate, and two flutamide. A variety of other exotic interventions was evaluated, including topical melatonin-alcohol solution, adenosine lotion, and pulsed electrostatic field.
The best data continue to exist for minoxidil. "Pooled data from 4 studies indicated that a greater proportion of participants (121/488) treated with minoxidil reported a moderate increase in their hair regrowth when compared with placebo (64/476) (risk ratio, 1.86; 95% confidence interval [CI], 1.42 to 2.43). In 7 studies, there was an important increase of 13.28 in total hair count per cm² in the minoxidil group compared to the placebo group (95% CI, 10.89 to 15.68). There was no difference in the number of adverse events in the twice daily minoxidil and placebo intervention groups, with the exception of a reported increase of adverse events (additional hair growth on areas other than the scalp) with minoxidil (5%) twice daily," according to the Cochrane report.
Other promising agents might be octyl nicotinate (0.5%), myristyl nicotinate (5%), and flutamide. Fulvestrant, adenosine, pulsed electrostatic field, and estradiol valerate are ineffective.
Minoxidil it is. It may be important to remind patients that 2% twice daily may be as effective and safe as 5% once a day.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Actinic keratoses: The cold truth
Actinic keratosis, or solar keratosis, results from the proliferation of atypical epidermal keratinocytes. When we can take the time to do a skin examination, we all see a lot of them especially among our older and middle-aged sun worshippers and sunscreen agnostics. My traditional approach, for better or for worse, has been to acquire the liquid nitrogen bottle on the floor and go to work. But my recent review of guidelines prepared on behalf of the British Association of Dermatologists and published several years ago have prompted me to open my eyes a bit more to other possible approaches.
Reassuringly, the likelihood of progression of an AK to squamous cell carcinoma (SCC) is low. Estimates from a large U.S. cohort revealed a rate of transformation to invasive or in situ SCC of 0.6% after 1 year and 2.6 % after 4 years. But we have to remember that although the progression rate is low, 60% of SCC arise from AKs.
The AK guideline authors synthesized and graded published evidence. Topical therapies receiving an "A grade" (i.e., good evidence) included no therapy or emollients for mild AKs and 5-fluorouracil. Therapies with a "B grade" (i.e., fair evidence) include diclofenac gel and imiquimod.
Other treatments include cryosurgery (A grade) and photodynamic therapy (B grade). We do a lot of cryotherapy in our practice but patients need to be informed of the scarring and possible hyper- or hypopigmentation that can occur with treatment. Photodynamic therapy will, in most cases, be administered by dermatologists.
According to a recent paper in the Drugs and Therapeutic Bulletin, patients should be referred to a dermatologist if there is diagnostic uncertainty, concerns about malignancy, treatment failure or management concerns, or if the patient is at high risk (e.g., organ transplant recipients, multiple large lesions, or previous SCC).
The guideline authors suggest that most patients can be evaluated and treated in the primary care setting. They go on to say that there is inadequate evidence to justify treatment of all AKs in an attempt to prevent malignant transformation. While reassuring, this requires us to consider all possible treatment approaches. One liquid nitrogen bottle does not fit all.
Dr. Ebbert is professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Actinic keratosis, or solar keratosis, results from the proliferation of atypical epidermal keratinocytes. When we can take the time to do a skin examination, we all see a lot of them especially among our older and middle-aged sun worshippers and sunscreen agnostics. My traditional approach, for better or for worse, has been to acquire the liquid nitrogen bottle on the floor and go to work. But my recent review of guidelines prepared on behalf of the British Association of Dermatologists and published several years ago have prompted me to open my eyes a bit more to other possible approaches.
Reassuringly, the likelihood of progression of an AK to squamous cell carcinoma (SCC) is low. Estimates from a large U.S. cohort revealed a rate of transformation to invasive or in situ SCC of 0.6% after 1 year and 2.6 % after 4 years. But we have to remember that although the progression rate is low, 60% of SCC arise from AKs.
The AK guideline authors synthesized and graded published evidence. Topical therapies receiving an "A grade" (i.e., good evidence) included no therapy or emollients for mild AKs and 5-fluorouracil. Therapies with a "B grade" (i.e., fair evidence) include diclofenac gel and imiquimod.
Other treatments include cryosurgery (A grade) and photodynamic therapy (B grade). We do a lot of cryotherapy in our practice but patients need to be informed of the scarring and possible hyper- or hypopigmentation that can occur with treatment. Photodynamic therapy will, in most cases, be administered by dermatologists.
According to a recent paper in the Drugs and Therapeutic Bulletin, patients should be referred to a dermatologist if there is diagnostic uncertainty, concerns about malignancy, treatment failure or management concerns, or if the patient is at high risk (e.g., organ transplant recipients, multiple large lesions, or previous SCC).
The guideline authors suggest that most patients can be evaluated and treated in the primary care setting. They go on to say that there is inadequate evidence to justify treatment of all AKs in an attempt to prevent malignant transformation. While reassuring, this requires us to consider all possible treatment approaches. One liquid nitrogen bottle does not fit all.
Dr. Ebbert is professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Actinic keratosis, or solar keratosis, results from the proliferation of atypical epidermal keratinocytes. When we can take the time to do a skin examination, we all see a lot of them especially among our older and middle-aged sun worshippers and sunscreen agnostics. My traditional approach, for better or for worse, has been to acquire the liquid nitrogen bottle on the floor and go to work. But my recent review of guidelines prepared on behalf of the British Association of Dermatologists and published several years ago have prompted me to open my eyes a bit more to other possible approaches.
Reassuringly, the likelihood of progression of an AK to squamous cell carcinoma (SCC) is low. Estimates from a large U.S. cohort revealed a rate of transformation to invasive or in situ SCC of 0.6% after 1 year and 2.6 % after 4 years. But we have to remember that although the progression rate is low, 60% of SCC arise from AKs.
The AK guideline authors synthesized and graded published evidence. Topical therapies receiving an "A grade" (i.e., good evidence) included no therapy or emollients for mild AKs and 5-fluorouracil. Therapies with a "B grade" (i.e., fair evidence) include diclofenac gel and imiquimod.
Other treatments include cryosurgery (A grade) and photodynamic therapy (B grade). We do a lot of cryotherapy in our practice but patients need to be informed of the scarring and possible hyper- or hypopigmentation that can occur with treatment. Photodynamic therapy will, in most cases, be administered by dermatologists.
According to a recent paper in the Drugs and Therapeutic Bulletin, patients should be referred to a dermatologist if there is diagnostic uncertainty, concerns about malignancy, treatment failure or management concerns, or if the patient is at high risk (e.g., organ transplant recipients, multiple large lesions, or previous SCC).
The guideline authors suggest that most patients can be evaluated and treated in the primary care setting. They go on to say that there is inadequate evidence to justify treatment of all AKs in an attempt to prevent malignant transformation. While reassuring, this requires us to consider all possible treatment approaches. One liquid nitrogen bottle does not fit all.
Dr. Ebbert is professor of medicine and general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
CVS takes health care seriously
CVS Pharmacy, the nation’s second largest pharmacy and 13th largest company in the world, threw down the gauntlet today to other pharmacy chains and vowed to stop selling tobacco products by Oct. 1, 2014.
As a retail pharmacy division of CVS Caremark, CVS Pharmacy is a drug store chain, a pharmacy benefit manager, and a leading retail health care provider. They have the "MinuteClinic" retail health clinics and can provide assistance with blood pressure and blood sugar management. In this sense, eliminating the sale of cigarettes is akin to removing cigarettes from the gift shops of hospitals and medical clinics. The major difference is that hospitals and clinics carried cigarettes as convenience items; for a company such as CVS Pharmacy, tobacco provided more than $1.5 billion in annual sales.
This is no small gamble. But it’s one that will hopefully pay off.
First of all, it’s the right thing to do in the interest of public health; 480,000 Americans still die of tobacco-related diseases annually. Second, the media attention and accolades received from President Obama, the American Medical Association, the Robert Wood Johnson Foundation, and the Campaign for Tobacco-Free Kids will, however short lived, bring recognition to the brand. CVS Pharmacy will now be identified as being concerned not only about patients who fill their prescriptions there, but also about the health and well-being of the communities in which the pharmacies operate. If another pharmacy chain follows suit, great, but CVS was first.
This attention will also garner attention to the other health care services that the retail chain provides, and it will increase the likelihood that hospitals, clinics, and ACOs will partner with the company.
Retail pharmacies will undoubtedly be a significant player in the delivery of health care, and medical organizations should be partnering with these companies. Unlike large medical institutions, which may be slow to action, a company like CVS could be more nimble and able to implement models of care in many of its more than 7,600 stores.
This could have a true population impact – arguably, more of an impact than training more physicians to provide care using traditional models. CVS’s announcement demonstrates that they are a willing and able partner in improving public health and engaging in health care delivery.
Dr. Ebbert is a professor of medicine at the Mayo Clinic, Rochester, Minn. He disclosed having financial relationships with Pfizer and GlaxoSmithKline, manufacturers of tobacco-dependence treatments.
CVS Pharmacy, the nation’s second largest pharmacy and 13th largest company in the world, threw down the gauntlet today to other pharmacy chains and vowed to stop selling tobacco products by Oct. 1, 2014.
As a retail pharmacy division of CVS Caremark, CVS Pharmacy is a drug store chain, a pharmacy benefit manager, and a leading retail health care provider. They have the "MinuteClinic" retail health clinics and can provide assistance with blood pressure and blood sugar management. In this sense, eliminating the sale of cigarettes is akin to removing cigarettes from the gift shops of hospitals and medical clinics. The major difference is that hospitals and clinics carried cigarettes as convenience items; for a company such as CVS Pharmacy, tobacco provided more than $1.5 billion in annual sales.
This is no small gamble. But it’s one that will hopefully pay off.
First of all, it’s the right thing to do in the interest of public health; 480,000 Americans still die of tobacco-related diseases annually. Second, the media attention and accolades received from President Obama, the American Medical Association, the Robert Wood Johnson Foundation, and the Campaign for Tobacco-Free Kids will, however short lived, bring recognition to the brand. CVS Pharmacy will now be identified as being concerned not only about patients who fill their prescriptions there, but also about the health and well-being of the communities in which the pharmacies operate. If another pharmacy chain follows suit, great, but CVS was first.
This attention will also garner attention to the other health care services that the retail chain provides, and it will increase the likelihood that hospitals, clinics, and ACOs will partner with the company.
Retail pharmacies will undoubtedly be a significant player in the delivery of health care, and medical organizations should be partnering with these companies. Unlike large medical institutions, which may be slow to action, a company like CVS could be more nimble and able to implement models of care in many of its more than 7,600 stores.
This could have a true population impact – arguably, more of an impact than training more physicians to provide care using traditional models. CVS’s announcement demonstrates that they are a willing and able partner in improving public health and engaging in health care delivery.
Dr. Ebbert is a professor of medicine at the Mayo Clinic, Rochester, Minn. He disclosed having financial relationships with Pfizer and GlaxoSmithKline, manufacturers of tobacco-dependence treatments.
CVS Pharmacy, the nation’s second largest pharmacy and 13th largest company in the world, threw down the gauntlet today to other pharmacy chains and vowed to stop selling tobacco products by Oct. 1, 2014.
As a retail pharmacy division of CVS Caremark, CVS Pharmacy is a drug store chain, a pharmacy benefit manager, and a leading retail health care provider. They have the "MinuteClinic" retail health clinics and can provide assistance with blood pressure and blood sugar management. In this sense, eliminating the sale of cigarettes is akin to removing cigarettes from the gift shops of hospitals and medical clinics. The major difference is that hospitals and clinics carried cigarettes as convenience items; for a company such as CVS Pharmacy, tobacco provided more than $1.5 billion in annual sales.
This is no small gamble. But it’s one that will hopefully pay off.
First of all, it’s the right thing to do in the interest of public health; 480,000 Americans still die of tobacco-related diseases annually. Second, the media attention and accolades received from President Obama, the American Medical Association, the Robert Wood Johnson Foundation, and the Campaign for Tobacco-Free Kids will, however short lived, bring recognition to the brand. CVS Pharmacy will now be identified as being concerned not only about patients who fill their prescriptions there, but also about the health and well-being of the communities in which the pharmacies operate. If another pharmacy chain follows suit, great, but CVS was first.
This attention will also garner attention to the other health care services that the retail chain provides, and it will increase the likelihood that hospitals, clinics, and ACOs will partner with the company.
Retail pharmacies will undoubtedly be a significant player in the delivery of health care, and medical organizations should be partnering with these companies. Unlike large medical institutions, which may be slow to action, a company like CVS could be more nimble and able to implement models of care in many of its more than 7,600 stores.
This could have a true population impact – arguably, more of an impact than training more physicians to provide care using traditional models. CVS’s announcement demonstrates that they are a willing and able partner in improving public health and engaging in health care delivery.
Dr. Ebbert is a professor of medicine at the Mayo Clinic, Rochester, Minn. He disclosed having financial relationships with Pfizer and GlaxoSmithKline, manufacturers of tobacco-dependence treatments.
Zinc for colds
Zinc was recognized as an element in 1509 and as an essential mineral much later. In 1961, zinc deficiency was linked with hypogonadism. Zinc is included in almost all over-the-counter daily vitamins and mineral supplements, typically in the form of zinc oxide, zinc acetate, and zinc gluconate. Zinc is absorbed through the small bowel with an efficiency of 20%-40%. It is the second most important metal in the body after iron and is present in virtually 100% of proteins.
Zinc inhibits viral replication. Because of this, it has been investigated as a way to decrease the duration of symptoms from the common cold. With some evidence suggesting that it works, we know little about the right dose for zinc to exert its magical effects.
In a recently published systematic review, Singh and Das updated a previous Cochrane systematic review and, once again, evaluated the efficacy of zinc in reducing the incidence, severity, and duration of common cold symptoms (Cochrane Database Syst. Rev. 2013;6:CD001364). Studies were included if they were randomized, double-blind, placebo-controlled trials using zinc for at least 5 days for treatment or 5 months for prevention of the common cold.
Sixteen therapeutic trails involving a total of 1,387 people, and two preventive trials with 394 participants were included in the meta-analysis. Zinc came in the form of syrup, lozenges, or tablets. Zinc was associated with statistically significant reductions in the duration but not the severity of symptoms. The mean difference in reduction duration was 1 day (95% confidence interval, –1.72 to –0.34). After 7 days of treatment, significantly fewer subjects had symptoms. Zinc was associated with a reduced incidence of colds, absences from school, and receipt of antibiotics. Bad taste and nausea were significantly higher in patients treated with zinc. The authors suggested that there is a significant reduction in the duration of cold symptoms at a dose of at least 75 mg/day in the lozenge form.
Inhaled zinc can cause permanent anosmia, and so this delivery route was not investigated. Lozenges may be the best bet, since we know the daily dose should be at least 75 mg for treatment. For patients interested in using zinc for prevention, no clear dosage recommendations can be made. Megadose supplementation or high zinc intake has been associated with abdominal pain, diarrhea, nausea, and vomiting. Zinc may interfere with copper absorption, and high zinc intake (greater than 150 mg/day) can lead to copper deficiency and should be avoided.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Zinc was recognized as an element in 1509 and as an essential mineral much later. In 1961, zinc deficiency was linked with hypogonadism. Zinc is included in almost all over-the-counter daily vitamins and mineral supplements, typically in the form of zinc oxide, zinc acetate, and zinc gluconate. Zinc is absorbed through the small bowel with an efficiency of 20%-40%. It is the second most important metal in the body after iron and is present in virtually 100% of proteins.
Zinc inhibits viral replication. Because of this, it has been investigated as a way to decrease the duration of symptoms from the common cold. With some evidence suggesting that it works, we know little about the right dose for zinc to exert its magical effects.
In a recently published systematic review, Singh and Das updated a previous Cochrane systematic review and, once again, evaluated the efficacy of zinc in reducing the incidence, severity, and duration of common cold symptoms (Cochrane Database Syst. Rev. 2013;6:CD001364). Studies were included if they were randomized, double-blind, placebo-controlled trials using zinc for at least 5 days for treatment or 5 months for prevention of the common cold.
Sixteen therapeutic trails involving a total of 1,387 people, and two preventive trials with 394 participants were included in the meta-analysis. Zinc came in the form of syrup, lozenges, or tablets. Zinc was associated with statistically significant reductions in the duration but not the severity of symptoms. The mean difference in reduction duration was 1 day (95% confidence interval, –1.72 to –0.34). After 7 days of treatment, significantly fewer subjects had symptoms. Zinc was associated with a reduced incidence of colds, absences from school, and receipt of antibiotics. Bad taste and nausea were significantly higher in patients treated with zinc. The authors suggested that there is a significant reduction in the duration of cold symptoms at a dose of at least 75 mg/day in the lozenge form.
Inhaled zinc can cause permanent anosmia, and so this delivery route was not investigated. Lozenges may be the best bet, since we know the daily dose should be at least 75 mg for treatment. For patients interested in using zinc for prevention, no clear dosage recommendations can be made. Megadose supplementation or high zinc intake has been associated with abdominal pain, diarrhea, nausea, and vomiting. Zinc may interfere with copper absorption, and high zinc intake (greater than 150 mg/day) can lead to copper deficiency and should be avoided.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
Zinc was recognized as an element in 1509 and as an essential mineral much later. In 1961, zinc deficiency was linked with hypogonadism. Zinc is included in almost all over-the-counter daily vitamins and mineral supplements, typically in the form of zinc oxide, zinc acetate, and zinc gluconate. Zinc is absorbed through the small bowel with an efficiency of 20%-40%. It is the second most important metal in the body after iron and is present in virtually 100% of proteins.
Zinc inhibits viral replication. Because of this, it has been investigated as a way to decrease the duration of symptoms from the common cold. With some evidence suggesting that it works, we know little about the right dose for zinc to exert its magical effects.
In a recently published systematic review, Singh and Das updated a previous Cochrane systematic review and, once again, evaluated the efficacy of zinc in reducing the incidence, severity, and duration of common cold symptoms (Cochrane Database Syst. Rev. 2013;6:CD001364). Studies were included if they were randomized, double-blind, placebo-controlled trials using zinc for at least 5 days for treatment or 5 months for prevention of the common cold.
Sixteen therapeutic trails involving a total of 1,387 people, and two preventive trials with 394 participants were included in the meta-analysis. Zinc came in the form of syrup, lozenges, or tablets. Zinc was associated with statistically significant reductions in the duration but not the severity of symptoms. The mean difference in reduction duration was 1 day (95% confidence interval, –1.72 to –0.34). After 7 days of treatment, significantly fewer subjects had symptoms. Zinc was associated with a reduced incidence of colds, absences from school, and receipt of antibiotics. Bad taste and nausea were significantly higher in patients treated with zinc. The authors suggested that there is a significant reduction in the duration of cold symptoms at a dose of at least 75 mg/day in the lozenge form.
Inhaled zinc can cause permanent anosmia, and so this delivery route was not investigated. Lozenges may be the best bet, since we know the daily dose should be at least 75 mg for treatment. For patients interested in using zinc for prevention, no clear dosage recommendations can be made. Megadose supplementation or high zinc intake has been associated with abdominal pain, diarrhea, nausea, and vomiting. Zinc may interfere with copper absorption, and high zinc intake (greater than 150 mg/day) can lead to copper deficiency and should be avoided.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reports no conflicts of interest.
What Matters: Bacterial vaginosis
The most common cause of vaginal discharge in women of childbearing age is bacterial vaginosis, which is characterized by a complex change in the vaginal flora with a reduction of lactobacilli and an increase in anaerobic bacteria such as Gardnerella vaginalis.
Among women with bacterial vaginosis (BV), 50%-75% are asymptomatic. Symptomatic women usually present with vaginal odor and/or discharge that is off-white, thin, and homogeneous in most cases. BV can create complications in pregnancy, but up to half of cases resolve spontaneously. Treatment is usually with antibiotics, but BV will recur in 69% of women within 1 year. Other than treatment with antibiotics, are there alternative ways to manage this disease?
Both oral and vaginal delivery of lactobacilli are known to renew vaginal microbiota. But is oral lactobacillus alone effective for treating BV?
Vujic et al. conducted a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a probiotic containing lactobacilli for the treatment of women with BV (Eur. J. Obstet. Gynecol. Reprod. Biol. 2013;168:75-9). Women were eligible for inclusion if they were older than 18 years of age and diagnosed with vaginal infection including BV, candidiasis, trichomoniasis, or a combination of these conditions. Women were excluded if they were pregnant, lactating, or menstruating. Subjects received either two capsules containing greater than 1 x 109 CFU lactobacillus daily or matching placebo for 6 weeks. At 6 and 12 weeks after randomization, subjects underwent gynecologic examinations for a wet mount evaluation and recovery of vaginal flora on agar plates. The primary outcome of the study was the rate of restitution of normal vaginal microbiota at 6 weeks.
In all, 544 subjects were randomized (395 to probiotic and 149 to placebo). Adherence to medication was greater than 90% in both groups. Restitution of balanced vaginal microbiota was evident in 243 subjects (61.5%) in the probiotic group and 40 subjects (26.9%) in the placebo group (P less than .001). At 12 weeks, normal vaginal microbiota was present in 51% of subjects in the probiotic group but only 21% of subjects taking placebo (P less than .001). The number-needed-to-treat was 2.9 with a relative risk reduction of 47.4% at 6 weeks.
For nonpregnant women with mild symptoms, the use of oral probiotics may be a reasonable option. For women who have recurrent episodes of BV, data suggest that probiotics could prevent future episodes, but more data is needed to evaluate this hypothesis.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.
The most common cause of vaginal discharge in women of childbearing age is bacterial vaginosis, which is characterized by a complex change in the vaginal flora with a reduction of lactobacilli and an increase in anaerobic bacteria such as Gardnerella vaginalis.
Among women with bacterial vaginosis (BV), 50%-75% are asymptomatic. Symptomatic women usually present with vaginal odor and/or discharge that is off-white, thin, and homogeneous in most cases. BV can create complications in pregnancy, but up to half of cases resolve spontaneously. Treatment is usually with antibiotics, but BV will recur in 69% of women within 1 year. Other than treatment with antibiotics, are there alternative ways to manage this disease?
Both oral and vaginal delivery of lactobacilli are known to renew vaginal microbiota. But is oral lactobacillus alone effective for treating BV?
Vujic et al. conducted a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a probiotic containing lactobacilli for the treatment of women with BV (Eur. J. Obstet. Gynecol. Reprod. Biol. 2013;168:75-9). Women were eligible for inclusion if they were older than 18 years of age and diagnosed with vaginal infection including BV, candidiasis, trichomoniasis, or a combination of these conditions. Women were excluded if they were pregnant, lactating, or menstruating. Subjects received either two capsules containing greater than 1 x 109 CFU lactobacillus daily or matching placebo for 6 weeks. At 6 and 12 weeks after randomization, subjects underwent gynecologic examinations for a wet mount evaluation and recovery of vaginal flora on agar plates. The primary outcome of the study was the rate of restitution of normal vaginal microbiota at 6 weeks.
In all, 544 subjects were randomized (395 to probiotic and 149 to placebo). Adherence to medication was greater than 90% in both groups. Restitution of balanced vaginal microbiota was evident in 243 subjects (61.5%) in the probiotic group and 40 subjects (26.9%) in the placebo group (P less than .001). At 12 weeks, normal vaginal microbiota was present in 51% of subjects in the probiotic group but only 21% of subjects taking placebo (P less than .001). The number-needed-to-treat was 2.9 with a relative risk reduction of 47.4% at 6 weeks.
For nonpregnant women with mild symptoms, the use of oral probiotics may be a reasonable option. For women who have recurrent episodes of BV, data suggest that probiotics could prevent future episodes, but more data is needed to evaluate this hypothesis.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.
The most common cause of vaginal discharge in women of childbearing age is bacterial vaginosis, which is characterized by a complex change in the vaginal flora with a reduction of lactobacilli and an increase in anaerobic bacteria such as Gardnerella vaginalis.
Among women with bacterial vaginosis (BV), 50%-75% are asymptomatic. Symptomatic women usually present with vaginal odor and/or discharge that is off-white, thin, and homogeneous in most cases. BV can create complications in pregnancy, but up to half of cases resolve spontaneously. Treatment is usually with antibiotics, but BV will recur in 69% of women within 1 year. Other than treatment with antibiotics, are there alternative ways to manage this disease?
Both oral and vaginal delivery of lactobacilli are known to renew vaginal microbiota. But is oral lactobacillus alone effective for treating BV?
Vujic et al. conducted a double-blind, randomized, placebo-controlled clinical trial evaluating the efficacy of a probiotic containing lactobacilli for the treatment of women with BV (Eur. J. Obstet. Gynecol. Reprod. Biol. 2013;168:75-9). Women were eligible for inclusion if they were older than 18 years of age and diagnosed with vaginal infection including BV, candidiasis, trichomoniasis, or a combination of these conditions. Women were excluded if they were pregnant, lactating, or menstruating. Subjects received either two capsules containing greater than 1 x 109 CFU lactobacillus daily or matching placebo for 6 weeks. At 6 and 12 weeks after randomization, subjects underwent gynecologic examinations for a wet mount evaluation and recovery of vaginal flora on agar plates. The primary outcome of the study was the rate of restitution of normal vaginal microbiota at 6 weeks.
In all, 544 subjects were randomized (395 to probiotic and 149 to placebo). Adherence to medication was greater than 90% in both groups. Restitution of balanced vaginal microbiota was evident in 243 subjects (61.5%) in the probiotic group and 40 subjects (26.9%) in the placebo group (P less than .001). At 12 weeks, normal vaginal microbiota was present in 51% of subjects in the probiotic group but only 21% of subjects taking placebo (P less than .001). The number-needed-to-treat was 2.9 with a relative risk reduction of 47.4% at 6 weeks.
For nonpregnant women with mild symptoms, the use of oral probiotics may be a reasonable option. For women who have recurrent episodes of BV, data suggest that probiotics could prevent future episodes, but more data is needed to evaluate this hypothesis.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn. The opinions expressed are those of the author.
Combo therapy for tobacco dependence
The Jan. 8 issue of JAMA marked the 50th anniversary of the first surgeon general’s report on smoking and health. We are all witness to the human catastrophe we call tobacco use. What will future generations think when they look back on us and see that we accepted something that killed so many? Or why we don’t have more medications to treat it – only two new drugs in the last two decades.
I have spent the last 15 years researching how to help people quit tobacco use. One may think that I would have a panel free of patients who continue to smoke – or who may know better than to show up for visits with me.
Far from true. I can think of one patient in particular whom I am watching slowly die from this addiction. Three years ago, his forced expiratory volume in 1 second was 1.04 L, and he continues to smoke a pack of cigarettes per day and is now on supplemental oxygen (although, he tells me, not at the same time).
Tobacco addiction engages a dizzying network of neurotransmitters. Given this complexity, one may wonder if we would gain traction by administering therapies attacking the problem from different angles. Previous research, for example, has shown that combining the nicotine patch with bupropion is better than the nicotine patch alone.
Varenicline is one of the most effective therapies for smoking cessation and acts on the acetylcholine nicotinic receptor. Bupropion, the other first-line nonnicotine drug for smoking cessation, inhibits the reuptake of norepinephrine and dopamine. Some researchers have hypothesized that these medications may act together synergistically.
In that 50th anniversary issue, we published data from our multicenter, randomized clinical trial with our colleagues at the University of Minnesota (JAMA 2014;311:155-63). In this study, we randomized 506 smokers to either combination therapy with bupropion sustained release (SR) and varenicline or varenicline alone given for 3 months.
We were particularly intrigued by the subgroup analysis, which showed that among heavier (20 or more cigarettes per day) and more dependent smokers, combination therapy was superior to monotherapy out to 12 months. Importantly, 12 months is 9 months after stopping the medications.
As a treating clinician who sees smokers in both my primary care and addiction practices, I find these data helpful and motivating.
Helpful because they lead me to conclude that varenicline will work for my lighter smokers, and varenicline combined with bupropion SR may increase the chances of success in heavier ones. As in all good clinical practice, patients should be alerted to the possibility of mood changes and symptoms.
Motivating because I now have data supporting me to step up my game in helping my patients quit before they become another statistic.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reported ties to Pfizer, GlaxoSmithKline, Orexigen, and JHP Pharmaceuticals.
The Jan. 8 issue of JAMA marked the 50th anniversary of the first surgeon general’s report on smoking and health. We are all witness to the human catastrophe we call tobacco use. What will future generations think when they look back on us and see that we accepted something that killed so many? Or why we don’t have more medications to treat it – only two new drugs in the last two decades.
I have spent the last 15 years researching how to help people quit tobacco use. One may think that I would have a panel free of patients who continue to smoke – or who may know better than to show up for visits with me.
Far from true. I can think of one patient in particular whom I am watching slowly die from this addiction. Three years ago, his forced expiratory volume in 1 second was 1.04 L, and he continues to smoke a pack of cigarettes per day and is now on supplemental oxygen (although, he tells me, not at the same time).
Tobacco addiction engages a dizzying network of neurotransmitters. Given this complexity, one may wonder if we would gain traction by administering therapies attacking the problem from different angles. Previous research, for example, has shown that combining the nicotine patch with bupropion is better than the nicotine patch alone.
Varenicline is one of the most effective therapies for smoking cessation and acts on the acetylcholine nicotinic receptor. Bupropion, the other first-line nonnicotine drug for smoking cessation, inhibits the reuptake of norepinephrine and dopamine. Some researchers have hypothesized that these medications may act together synergistically.
In that 50th anniversary issue, we published data from our multicenter, randomized clinical trial with our colleagues at the University of Minnesota (JAMA 2014;311:155-63). In this study, we randomized 506 smokers to either combination therapy with bupropion sustained release (SR) and varenicline or varenicline alone given for 3 months.
We were particularly intrigued by the subgroup analysis, which showed that among heavier (20 or more cigarettes per day) and more dependent smokers, combination therapy was superior to monotherapy out to 12 months. Importantly, 12 months is 9 months after stopping the medications.
As a treating clinician who sees smokers in both my primary care and addiction practices, I find these data helpful and motivating.
Helpful because they lead me to conclude that varenicline will work for my lighter smokers, and varenicline combined with bupropion SR may increase the chances of success in heavier ones. As in all good clinical practice, patients should be alerted to the possibility of mood changes and symptoms.
Motivating because I now have data supporting me to step up my game in helping my patients quit before they become another statistic.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reported ties to Pfizer, GlaxoSmithKline, Orexigen, and JHP Pharmaceuticals.
The Jan. 8 issue of JAMA marked the 50th anniversary of the first surgeon general’s report on smoking and health. We are all witness to the human catastrophe we call tobacco use. What will future generations think when they look back on us and see that we accepted something that killed so many? Or why we don’t have more medications to treat it – only two new drugs in the last two decades.
I have spent the last 15 years researching how to help people quit tobacco use. One may think that I would have a panel free of patients who continue to smoke – or who may know better than to show up for visits with me.
Far from true. I can think of one patient in particular whom I am watching slowly die from this addiction. Three years ago, his forced expiratory volume in 1 second was 1.04 L, and he continues to smoke a pack of cigarettes per day and is now on supplemental oxygen (although, he tells me, not at the same time).
Tobacco addiction engages a dizzying network of neurotransmitters. Given this complexity, one may wonder if we would gain traction by administering therapies attacking the problem from different angles. Previous research, for example, has shown that combining the nicotine patch with bupropion is better than the nicotine patch alone.
Varenicline is one of the most effective therapies for smoking cessation and acts on the acetylcholine nicotinic receptor. Bupropion, the other first-line nonnicotine drug for smoking cessation, inhibits the reuptake of norepinephrine and dopamine. Some researchers have hypothesized that these medications may act together synergistically.
In that 50th anniversary issue, we published data from our multicenter, randomized clinical trial with our colleagues at the University of Minnesota (JAMA 2014;311:155-63). In this study, we randomized 506 smokers to either combination therapy with bupropion sustained release (SR) and varenicline or varenicline alone given for 3 months.
We were particularly intrigued by the subgroup analysis, which showed that among heavier (20 or more cigarettes per day) and more dependent smokers, combination therapy was superior to monotherapy out to 12 months. Importantly, 12 months is 9 months after stopping the medications.
As a treating clinician who sees smokers in both my primary care and addiction practices, I find these data helpful and motivating.
Helpful because they lead me to conclude that varenicline will work for my lighter smokers, and varenicline combined with bupropion SR may increase the chances of success in heavier ones. As in all good clinical practice, patients should be alerted to the possibility of mood changes and symptoms.
Motivating because I now have data supporting me to step up my game in helping my patients quit before they become another statistic.
Dr. Ebbert is professor of medicine and a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. He reported ties to Pfizer, GlaxoSmithKline, Orexigen, and JHP Pharmaceuticals.
Fiber in the new year
The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.
Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.
Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).
But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?
In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).
The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.
The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.
Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.
The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.
Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.
Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).
But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?
In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).
The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.
The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.
Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.
The start of a new year provides us the opportunity to reflect on the past year, relish in our successes, ruminate about things we did less well, and make resolutions. For 2014, I resolve to take better stock of, and encourage in my patients an increased use of, fiber.
Fiber is a simple and cheap intervention. So simple and cheap that I have increasingly neglected to assess and instruct my patients on its use and benefits. The recommended amount of dietary fiber is 20-35 g/day, and some of us may feel quite sure that many of our patients are not coming close to this amount of intake.
Recall that total dietary fiber is a combination of both insoluble (e.g., wheat bran, whole grains, vegetables) and soluble (e.g., psyllium, nuts, and some fruits and vegetables) components. Soluble fiber can reduce the risk for type 2 diabetes, control blood glucose in individuals who already have diabetes, and reduce the risk for coronary heart disease (CHD) and cardiovascular disease (CVD, i.e., fatal or incident stroke plus CHD).
But how much does fiber reduce the risk for cardiovascular disease? Is there a dose effect?
In a recent systematic review of the literature, investigators endeavored to determine the dose-response relationship between dietary fiber and reductions in CHD and CVD risks. Prospective studies reporting associations between fiber intake and CHD and CVD endpoints were included if they had a minimum of 3 years of follow-up and were published between 1990 and 2013 (BMJ 2013;347:f6879).
The literature review included 22 studies. Total dietary fiber intake was associated with a reduced risk for CVD (risk ratio, 0.91 per 7 g/day; 95% CI: 0.88-0.94) and CHD (RR, 0.91; 95% CI: 0.87-0.94). Insoluble fiber seemed to have the greatest reduction, although the authors encouraged caution in the interpretation of the data on the specific subtypes of fiber, which need further study. We should focus on the total daily intake.
The take-home message is that patients should be encouraged to increase their intake of whole foods (unprocessed and unrefined). For every additional 7 g of total fiber per day, a 9% lower risk for CVD and CHD clinical endpoints can be achieved. For patients who are unable to achieve higher fiber intake through diet, supplementation with psyllium or methylcelluose, soluble fibers common in popular OTC brands, may be beneficial.
Dr. Ebbert is a professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author. He reported having no conflicts of interest.
