Four pivotal breast cancer trials were presented at the 2016 annual meeting of the American Society of Clinical Oncology in Chicago. The MA.17R trial, which was the plenary talk by Dr Paul Goss, looked at extending adjuvant aromatase inhibitors to 10 years or beyond in postmenopausal women; two presentations reported on mutations after progression in metastatic breast cancer, one on first-line AIs and the other on prior endocrine therapy (PALOMA-3); and results from the Z0011 trial showed that sentinel lymph node dissection without axillary lymph node dissection might show promising 10-year loco-regional control and survival outcomes.

Click on the PDF icon at the top of this introduction to read the full article.

Four pivotal breast cancer trials were presented at the 2016 annual meeting of the American Society of Clinical Oncology in Chicago. The MA.17R trial, which was the plenary talk by Dr Paul Goss, looked at extending adjuvant aromatase inhibitors to 10 years or beyond in postmenopausal women; two presentations reported on mutations after progression in metastatic breast cancer, one on first-line AIs and the other on prior endocrine therapy (PALOMA-3); and results from the Z0011 trial showed that sentinel lymph node dissection without axillary lymph node dissection might show promising 10-year loco-regional control and survival outcomes.

Click on the PDF icon at the top of this introduction to read the full article.

Four pivotal breast cancer trials were presented at the 2016 annual meeting of the American Society of Clinical Oncology in Chicago. The MA.17R trial, which was the plenary talk by Dr Paul Goss, looked at extending adjuvant aromatase inhibitors to 10 years or beyond in postmenopausal women; two presentations reported on mutations after progression in metastatic breast cancer, one on first-line AIs and the other on prior endocrine therapy (PALOMA-3); and results from the Z0011 trial showed that sentinel lymph node dissection without axillary lymph node dissection might show promising 10-year loco-regional control and survival outcomes.

Click on the PDF icon at the top of this introduction to read the full article.

LAS VEGAS – Pay attention to GI symptoms in your scleroderma patients. Gut involvement in scleroderma, a result of vasculopathy and fibrosis affecting the GI tract, is common and can be debilitating, said Daniel Furst, MD.

Speaking at the annual Perspectives in Rheumatologic Diseases presented by the Global Academy for Medical Education, Dr. Furst said that the progression often begins at the mouth and esophagus, and progresses through the digestive system, eventually reaching the rectum and anus.

“You think about motility issues early on, in the esophagus,” and early oral symptoms can include mouth dryness, said Dr. Furst, who is associated with the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence (Italy).

As scleroderma begins to affect the midgut, Dr. Furst said that the secondary results of the decrease in motility are symptoms such as heartburn, nausea, vomiting, and early satiety.

“When you have a decrease in motility, then the normal ... housekeeping waves of the midgut and the colon are decreased,” he said. Bacteria from the colon can then invade the small bowel, causing overgrowth of the midgut by species not normally seen there. Not only gas, but also malnutrition can eventually result, he said.

When scleroderma affects the lower gut, patients can have bloating, diarrhea, and constipation, and finally, incontinence of the bowel, a condition with often devastating psychosocial consequences.

The choice of promotility agents depends on the area affected; erythromycin and metoclopramide help in the upper GI tract, while tegaserod can be helpful in the lower gut.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Pay attention to GI symptoms in your scleroderma patients. Gut involvement in scleroderma, a result of vasculopathy and fibrosis affecting the GI tract, is common and can be debilitating, said Daniel Furst, MD.

Speaking at the annual Perspectives in Rheumatologic Diseases presented by the Global Academy for Medical Education, Dr. Furst said that the progression often begins at the mouth and esophagus, and progresses through the digestive system, eventually reaching the rectum and anus.

“You think about motility issues early on, in the esophagus,” and early oral symptoms can include mouth dryness, said Dr. Furst, who is associated with the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence (Italy).

As scleroderma begins to affect the midgut, Dr. Furst said that the secondary results of the decrease in motility are symptoms such as heartburn, nausea, vomiting, and early satiety.

“When you have a decrease in motility, then the normal ... housekeeping waves of the midgut and the colon are decreased,” he said. Bacteria from the colon can then invade the small bowel, causing overgrowth of the midgut by species not normally seen there. Not only gas, but also malnutrition can eventually result, he said.

When scleroderma affects the lower gut, patients can have bloating, diarrhea, and constipation, and finally, incontinence of the bowel, a condition with often devastating psychosocial consequences.

The choice of promotility agents depends on the area affected; erythromycin and metoclopramide help in the upper GI tract, while tegaserod can be helpful in the lower gut.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – Pay attention to GI symptoms in your scleroderma patients. Gut involvement in scleroderma, a result of vasculopathy and fibrosis affecting the GI tract, is common and can be debilitating, said Daniel Furst, MD.

Speaking at the annual Perspectives in Rheumatologic Diseases presented by the Global Academy for Medical Education, Dr. Furst said that the progression often begins at the mouth and esophagus, and progresses through the digestive system, eventually reaching the rectum and anus.

“You think about motility issues early on, in the esophagus,” and early oral symptoms can include mouth dryness, said Dr. Furst, who is associated with the University of California, Los Angeles, the University of Washington, Seattle, and the University of Florence (Italy).

As scleroderma begins to affect the midgut, Dr. Furst said that the secondary results of the decrease in motility are symptoms such as heartburn, nausea, vomiting, and early satiety.

“When you have a decrease in motility, then the normal ... housekeeping waves of the midgut and the colon are decreased,” he said. Bacteria from the colon can then invade the small bowel, causing overgrowth of the midgut by species not normally seen there. Not only gas, but also malnutrition can eventually result, he said.

When scleroderma affects the lower gut, patients can have bloating, diarrhea, and constipation, and finally, incontinence of the bowel, a condition with often devastating psychosocial consequences.

The choice of promotility agents depends on the area affected; erythromycin and metoclopramide help in the upper GI tract, while tegaserod can be helpful in the lower gut.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

Does habitual cannabis use trigger psychosis, or does a tendency toward psychosis predict increased cannabis use?

“[Our] results suggest that it is more likely than not that continued cannabis use after onset of psychosis is causally associated with increased risk of relapse of psychosis, resulting in psychiatric hospitalization,” reported the authors of a study published online Sept. 28 in JAMA Psychiatry.

It is well established that cannabis use after first-episode psychosis is associated with poor outcomes; what is not so well established is why. The three most prominent theories so far are that cannabis use and psychosis share inherent genetic and/or environmental vulnerabilities, impending psychosis impels increased cannabis use, and conversely, cannabis use has a causal effect on psychosis (Lancet Psychiatry. 2016:3[5]:401) and (Lancet Psychiatry. 2015;3[5]401-2).

©KatarzynaBialasiewicz/thinkstockphotos.com

After conducting a 10-year, prospective cohort investigation of 220 people who presented to psychiatric services at numerous sites in London between April 2002 and July 2013, Tabea Schoeler and her associates in the current study found that the odds of a relapse of psychosis during periods of cannabis use was increased by 1.13, compared with periods of no cannabis use (95% confidence interval, 1.03-1.24) (JAMA Psychiatry. 2016 Sep 28. doi: 10.1001/jamapsychiatry.2016.2427). Further, those who used cannabis continually after first-episode psychosis were found to have a 59.1% higher risk of relapsing psychosis in that 10-year period, compared with a 28.5% increased risk in those who quit using cannabis entirely (P less than .001).

The only true way to measure causality in this area would be to administer cannabis to participants in a randomized, clinically controlled trial, thus challenging the ethics of clinical study. Instead, Ms. Schoeler of the Institute of Psychiatry, Psychology, and Neuroscience at King’s College London and her associates – including Sir Robin M. Murray, MD, a psychiatrist who has been a leading voice in favor of the view that cannabis use and psychotic episodes are often linked – used patient self-reports to assess changes in cannabis use over time. This allowed the investigators to more clearly differentiate between confounders that cannot be readily observed, and that are not likely to change over time, such as any shared genetic or environmental factors, and confounders that can be observed and that do have the potential to change, such as the change in cannabis use status over time, including nonuser vs. user status, and the pattern and frequency of use after onset of illness.

The data were collected in two separate assessments, one was conducted near the time of illness onset, and again at least 2 years after the first episode of psychosis. If interviews were not possible to complete in person, they were conducted over the phone. These data were combined with patient clinical records across the study period. Frequency of cannabis use was measured based on the Cannabis Experience Questionnaire. A patient was considered to have relapsed if he or she was admitted to an inpatient psychiatric facility for exacerbated symptoms of psychosis within 2 years of the first episode of psychosis.

As for the study population, 59.1% of whom were men with an average age of 29 years, there were no significant differences as to whether they had been diagnosed with either affective or nonaffective psychosis. However, there were significant differences between the risk of relapse and the frequency of cannabis use 2 years after onset of illness. In the nonuser group, 28.5% of patients relapsed. In the intermittent user group, 36% relapsed. In the continuous use group, 59.1% relapsed (P less than .001).

Differences also were found across the three groups in medication adherence rates. Among the nonusers, 47.7% reportedly complied with treatment. The rate was 32% among intermittent users and 20.5% among habitual users (P = .02). Illicit use of other drugs was also higher in the continuous cannabis use group: 27.3% vs. 4% in the cannabis nonuse group and 12% in the intermittent use group (P less than .001).

Also noteworthy was the age of psychosis onset across the groups. While the average age of onset across the study was 28.62 years, for habitual users the average age of illness onset was 25.44 years, compared with 29.52 in nonusers and 28.79 in intermittent users (P = .02).

These results should be viewed in light of their retrospective and self-reported nature – neither of which take into account either premorbid cannabis use or age of illness onset as either predictors or moderators – but the data suggest a dose-response relationship between cannabis use and psychosis, according to the investigators. If so, the implications of the data could reach beyond patient outcomes.

“Because cannabis use is a potentially modifiable risk factor that has an adverse influence on the risk of relapse of psychosis and hospitalization in a given individual, with limited efficacy of existing interventions, these results underscore the importance of developing novel intervention strategies and demand urgent attention from clinicians and health care policy makers,” the authors wrote.

Whether the study conclusively demonstrates that it is cannabis use – and not genetic liability or reverse causation – that drives relapse of psychosis is still not clear. By the investigators’ own admission, the effect of discontinuing cannabis use on patient outcomes has not been tested, leaving the question of a definite causal relationship between continual cannabis use and relapse of psychosis still open for debate.

Ms. Schoeler and the other investigators – with the exception of Dr. Murray – reported no conflicts of interest. Dr. Murray reported that he has received honoraria from Janssen, Sunovion, Otsuka, and Lundbeck. The study was funded in large part by the U.K.’s National Institute for Health Research and by King’s College London.

[email protected]

On Twitter @whitneymcknight

Does habitual cannabis use trigger psychosis, or does a tendency toward psychosis predict increased cannabis use?

“[Our] results suggest that it is more likely than not that continued cannabis use after onset of psychosis is causally associated with increased risk of relapse of psychosis, resulting in psychiatric hospitalization,” reported the authors of a study published online Sept. 28 in JAMA Psychiatry.

It is well established that cannabis use after first-episode psychosis is associated with poor outcomes; what is not so well established is why. The three most prominent theories so far are that cannabis use and psychosis share inherent genetic and/or environmental vulnerabilities, impending psychosis impels increased cannabis use, and conversely, cannabis use has a causal effect on psychosis (Lancet Psychiatry. 2016:3[5]:401) and (Lancet Psychiatry. 2015;3[5]401-2).

©KatarzynaBialasiewicz/thinkstockphotos.com

After conducting a 10-year, prospective cohort investigation of 220 people who presented to psychiatric services at numerous sites in London between April 2002 and July 2013, Tabea Schoeler and her associates in the current study found that the odds of a relapse of psychosis during periods of cannabis use was increased by 1.13, compared with periods of no cannabis use (95% confidence interval, 1.03-1.24) (JAMA Psychiatry. 2016 Sep 28. doi: 10.1001/jamapsychiatry.2016.2427). Further, those who used cannabis continually after first-episode psychosis were found to have a 59.1% higher risk of relapsing psychosis in that 10-year period, compared with a 28.5% increased risk in those who quit using cannabis entirely (P less than .001).

The only true way to measure causality in this area would be to administer cannabis to participants in a randomized, clinically controlled trial, thus challenging the ethics of clinical study. Instead, Ms. Schoeler of the Institute of Psychiatry, Psychology, and Neuroscience at King’s College London and her associates – including Sir Robin M. Murray, MD, a psychiatrist who has been a leading voice in favor of the view that cannabis use and psychotic episodes are often linked – used patient self-reports to assess changes in cannabis use over time. This allowed the investigators to more clearly differentiate between confounders that cannot be readily observed, and that are not likely to change over time, such as any shared genetic or environmental factors, and confounders that can be observed and that do have the potential to change, such as the change in cannabis use status over time, including nonuser vs. user status, and the pattern and frequency of use after onset of illness.

The data were collected in two separate assessments, one was conducted near the time of illness onset, and again at least 2 years after the first episode of psychosis. If interviews were not possible to complete in person, they were conducted over the phone. These data were combined with patient clinical records across the study period. Frequency of cannabis use was measured based on the Cannabis Experience Questionnaire. A patient was considered to have relapsed if he or she was admitted to an inpatient psychiatric facility for exacerbated symptoms of psychosis within 2 years of the first episode of psychosis.

As for the study population, 59.1% of whom were men with an average age of 29 years, there were no significant differences as to whether they had been diagnosed with either affective or nonaffective psychosis. However, there were significant differences between the risk of relapse and the frequency of cannabis use 2 years after onset of illness. In the nonuser group, 28.5% of patients relapsed. In the intermittent user group, 36% relapsed. In the continuous use group, 59.1% relapsed (P less than .001).

Differences also were found across the three groups in medication adherence rates. Among the nonusers, 47.7% reportedly complied with treatment. The rate was 32% among intermittent users and 20.5% among habitual users (P = .02). Illicit use of other drugs was also higher in the continuous cannabis use group: 27.3% vs. 4% in the cannabis nonuse group and 12% in the intermittent use group (P less than .001).

Also noteworthy was the age of psychosis onset across the groups. While the average age of onset across the study was 28.62 years, for habitual users the average age of illness onset was 25.44 years, compared with 29.52 in nonusers and 28.79 in intermittent users (P = .02).

These results should be viewed in light of their retrospective and self-reported nature – neither of which take into account either premorbid cannabis use or age of illness onset as either predictors or moderators – but the data suggest a dose-response relationship between cannabis use and psychosis, according to the investigators. If so, the implications of the data could reach beyond patient outcomes.

“Because cannabis use is a potentially modifiable risk factor that has an adverse influence on the risk of relapse of psychosis and hospitalization in a given individual, with limited efficacy of existing interventions, these results underscore the importance of developing novel intervention strategies and demand urgent attention from clinicians and health care policy makers,” the authors wrote.

Whether the study conclusively demonstrates that it is cannabis use – and not genetic liability or reverse causation – that drives relapse of psychosis is still not clear. By the investigators’ own admission, the effect of discontinuing cannabis use on patient outcomes has not been tested, leaving the question of a definite causal relationship between continual cannabis use and relapse of psychosis still open for debate.

Ms. Schoeler and the other investigators – with the exception of Dr. Murray – reported no conflicts of interest. Dr. Murray reported that he has received honoraria from Janssen, Sunovion, Otsuka, and Lundbeck. The study was funded in large part by the U.K.’s National Institute for Health Research and by King’s College London.

[email protected]

On Twitter @whitneymcknight

Does habitual cannabis use trigger psychosis, or does a tendency toward psychosis predict increased cannabis use?

“[Our] results suggest that it is more likely than not that continued cannabis use after onset of psychosis is causally associated with increased risk of relapse of psychosis, resulting in psychiatric hospitalization,” reported the authors of a study published online Sept. 28 in JAMA Psychiatry.

It is well established that cannabis use after first-episode psychosis is associated with poor outcomes; what is not so well established is why. The three most prominent theories so far are that cannabis use and psychosis share inherent genetic and/or environmental vulnerabilities, impending psychosis impels increased cannabis use, and conversely, cannabis use has a causal effect on psychosis (Lancet Psychiatry. 2016:3[5]:401) and (Lancet Psychiatry. 2015;3[5]401-2).

©KatarzynaBialasiewicz/thinkstockphotos.com

After conducting a 10-year, prospective cohort investigation of 220 people who presented to psychiatric services at numerous sites in London between April 2002 and July 2013, Tabea Schoeler and her associates in the current study found that the odds of a relapse of psychosis during periods of cannabis use was increased by 1.13, compared with periods of no cannabis use (95% confidence interval, 1.03-1.24) (JAMA Psychiatry. 2016 Sep 28. doi: 10.1001/jamapsychiatry.2016.2427). Further, those who used cannabis continually after first-episode psychosis were found to have a 59.1% higher risk of relapsing psychosis in that 10-year period, compared with a 28.5% increased risk in those who quit using cannabis entirely (P less than .001).

The only true way to measure causality in this area would be to administer cannabis to participants in a randomized, clinically controlled trial, thus challenging the ethics of clinical study. Instead, Ms. Schoeler of the Institute of Psychiatry, Psychology, and Neuroscience at King’s College London and her associates – including Sir Robin M. Murray, MD, a psychiatrist who has been a leading voice in favor of the view that cannabis use and psychotic episodes are often linked – used patient self-reports to assess changes in cannabis use over time. This allowed the investigators to more clearly differentiate between confounders that cannot be readily observed, and that are not likely to change over time, such as any shared genetic or environmental factors, and confounders that can be observed and that do have the potential to change, such as the change in cannabis use status over time, including nonuser vs. user status, and the pattern and frequency of use after onset of illness.

The data were collected in two separate assessments, one was conducted near the time of illness onset, and again at least 2 years after the first episode of psychosis. If interviews were not possible to complete in person, they were conducted over the phone. These data were combined with patient clinical records across the study period. Frequency of cannabis use was measured based on the Cannabis Experience Questionnaire. A patient was considered to have relapsed if he or she was admitted to an inpatient psychiatric facility for exacerbated symptoms of psychosis within 2 years of the first episode of psychosis.

As for the study population, 59.1% of whom were men with an average age of 29 years, there were no significant differences as to whether they had been diagnosed with either affective or nonaffective psychosis. However, there were significant differences between the risk of relapse and the frequency of cannabis use 2 years after onset of illness. In the nonuser group, 28.5% of patients relapsed. In the intermittent user group, 36% relapsed. In the continuous use group, 59.1% relapsed (P less than .001).

Differences also were found across the three groups in medication adherence rates. Among the nonusers, 47.7% reportedly complied with treatment. The rate was 32% among intermittent users and 20.5% among habitual users (P = .02). Illicit use of other drugs was also higher in the continuous cannabis use group: 27.3% vs. 4% in the cannabis nonuse group and 12% in the intermittent use group (P less than .001).

Also noteworthy was the age of psychosis onset across the groups. While the average age of onset across the study was 28.62 years, for habitual users the average age of illness onset was 25.44 years, compared with 29.52 in nonusers and 28.79 in intermittent users (P = .02).

These results should be viewed in light of their retrospective and self-reported nature – neither of which take into account either premorbid cannabis use or age of illness onset as either predictors or moderators – but the data suggest a dose-response relationship between cannabis use and psychosis, according to the investigators. If so, the implications of the data could reach beyond patient outcomes.

“Because cannabis use is a potentially modifiable risk factor that has an adverse influence on the risk of relapse of psychosis and hospitalization in a given individual, with limited efficacy of existing interventions, these results underscore the importance of developing novel intervention strategies and demand urgent attention from clinicians and health care policy makers,” the authors wrote.

Whether the study conclusively demonstrates that it is cannabis use – and not genetic liability or reverse causation – that drives relapse of psychosis is still not clear. By the investigators’ own admission, the effect of discontinuing cannabis use on patient outcomes has not been tested, leaving the question of a definite causal relationship between continual cannabis use and relapse of psychosis still open for debate.

Ms. Schoeler and the other investigators – with the exception of Dr. Murray – reported no conflicts of interest. Dr. Murray reported that he has received honoraria from Janssen, Sunovion, Otsuka, and Lundbeck. The study was funded in large part by the U.K.’s National Institute for Health Research and by King’s College London.

[email protected]

On Twitter @whitneymcknight

The National Ambulatory Medical Care Survey^1,2 (NAMCS) indicates that less than 1 out of 4 (23%) psychiatrists provide smoking cessation counseling to their patients, and even fewer prescribe medications.

What gives? How is it that so many psychiatrists endorse having recently helped a patient quit smoking when the data from large-scale surveys^1,2 indicate they do not?

From the “glass is half-full” perspective, the discrepancy might indicate that psychiatrists finally have bought into the message put forth 20 years ago when the American Psychiatric Association first published its clinical practice guidelines for treating nicotine dependence.³ Because the figures I cited from NAMCS reflect data from 2006 to 2010, it is possible that in the last 5 years more psychiatrists have started to help their patients quit smoking. Such an hypothesis is further supported by the increasing number of research papers on smoking cessation in individuals with mental illness published over the past 8 years—a period that coincides with the release of the second edition of the Treating tobacco use and dependence clinical practice guideline from the U.S. Agency for Healthcare Research and Quality, which highlighted the need for more research in this population of smokers.⁴

Regardless of the reason, the fact that my informal surveys indicate a likely uptick in activity among psychiatrists to help their patients quit smoking is welcome news. With nearly 1 out of 2 cigarettes sold in the United States being smoked by individuals with psychiatric and substance use disorders,⁵ psychiatrists and other mental health professionals play a vital role in addressing this epidemic. That our patients smoke at rates 2- to 4-times that of the general population and die decades earlier than their non-smoking, non-mentally ill counterparts⁶ are compelling reasons urging us to end our complacency and help our patients quit smoking.

EAGLES trial results help debunk the latest myth about smoking cessation

In an article that I wrote for Current Psychiatry 11 years ago,⁷ I attempted to debunk 3 myths that might have influenced some psychiatrists’ approach and motivation to intervene in tobacco dependence. Since that article appeared, a fourth myth has been promulgated—that the non-nicotine smoking cessation medications, bupropion and varenicline, are unsafe to use in patients with stable psychiatric disorders and cause serious neuropsychiatric adverse events (AEs) including suicide. Indeed, that is one implication of the “black-box” warning both of these medications received in July 2009, which caution that, “the risks of Zyban^®/Chantix^® should be weighed against the benefits of [their] use.”^8,9 For an illness that causes 480,000 deaths each year in the United States,¹⁰ and nearly 6 million across the globe,¹¹ tobacco treatment specialists find themselves in a quandary when 2 of the only 3 approved medications available—nicotine replacement therapy being the third—carry such a stern warning.

In addition to applying the “black-box” warning, the FDA issued a post-marketing requirement to the manufacturers of bupropion and varenicline to conduct a large randomized controlled trial—Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES)—the top-line results of which were published in The Lancet this spring.¹²

The researchers found no significant increase in serious neuropsychiatric AEs—a composite measure assessing depression, anxiety, suicidality, and 13 other symptom clusters—attributable to varenicline or bupropion compared with placebo or the nicotine patch in smokers with or without psychiatric disorders. The study did detect a significant difference—approximately 4% (2% in non-psychiatric cohort vs 6% in psychiatric cohort)—in the rate of serious neuropsychiatric AEs regardless of treatment condition. In both cohorts, varenicline was more effective than bupropion, which had similar efficacy to the nicotine patch; all interventions were superior to placebo. Importantly, all 3 medications significantly improved quit rates in smokers with and without psychiatric disorders. Although the efficacy of medications in smokers with or without psychiatric disorders was similar in terms of odds ratios, overall, those with psychiatric disorders had 20% to 30% lower quit rates compared with non-psychiatrically ill smokers.

The EAGLES study results, when viewed in the context of findings from other clinical trials and large-scale observational studies, provide further evidence that smokers with stable mental illness can use bupropion and varenicline safely. It also demonstrates that moderate to severe neuropsychiatric AEs occur during a smoking cessation attempt regardless of the medication used, therefore, monitoring smokers—especially those with psychiatric disorders—is important, a role that psychiatrists are uniquely poised to play.

That all 3 smoking cessation medications are effective in patients with mood, anxiety, and psychotic disorders is good news for our patients. Combined with the EAGLES safety findings, there is no better time to intervene in tobacco dependence

The National Ambulatory Medical Care Survey^1,2 (NAMCS) indicates that less than 1 out of 4 (23%) psychiatrists provide smoking cessation counseling to their patients, and even fewer prescribe medications.

What gives? How is it that so many psychiatrists endorse having recently helped a patient quit smoking when the data from large-scale surveys^1,2 indicate they do not?

From the “glass is half-full” perspective, the discrepancy might indicate that psychiatrists finally have bought into the message put forth 20 years ago when the American Psychiatric Association first published its clinical practice guidelines for treating nicotine dependence.³ Because the figures I cited from NAMCS reflect data from 2006 to 2010, it is possible that in the last 5 years more psychiatrists have started to help their patients quit smoking. Such an hypothesis is further supported by the increasing number of research papers on smoking cessation in individuals with mental illness published over the past 8 years—a period that coincides with the release of the second edition of the Treating tobacco use and dependence clinical practice guideline from the U.S. Agency for Healthcare Research and Quality, which highlighted the need for more research in this population of smokers.⁴

Regardless of the reason, the fact that my informal surveys indicate a likely uptick in activity among psychiatrists to help their patients quit smoking is welcome news. With nearly 1 out of 2 cigarettes sold in the United States being smoked by individuals with psychiatric and substance use disorders,⁵ psychiatrists and other mental health professionals play a vital role in addressing this epidemic. That our patients smoke at rates 2- to 4-times that of the general population and die decades earlier than their non-smoking, non-mentally ill counterparts⁶ are compelling reasons urging us to end our complacency and help our patients quit smoking.

EAGLES trial results help debunk the latest myth about smoking cessation

In an article that I wrote for Current Psychiatry 11 years ago,⁷ I attempted to debunk 3 myths that might have influenced some psychiatrists’ approach and motivation to intervene in tobacco dependence. Since that article appeared, a fourth myth has been promulgated—that the non-nicotine smoking cessation medications, bupropion and varenicline, are unsafe to use in patients with stable psychiatric disorders and cause serious neuropsychiatric adverse events (AEs) including suicide. Indeed, that is one implication of the “black-box” warning both of these medications received in July 2009, which caution that, “the risks of Zyban^®/Chantix^® should be weighed against the benefits of [their] use.”^8,9 For an illness that causes 480,000 deaths each year in the United States,¹⁰ and nearly 6 million across the globe,¹¹ tobacco treatment specialists find themselves in a quandary when 2 of the only 3 approved medications available—nicotine replacement therapy being the third—carry such a stern warning.

In addition to applying the “black-box” warning, the FDA issued a post-marketing requirement to the manufacturers of bupropion and varenicline to conduct a large randomized controlled trial—Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES)—the top-line results of which were published in The Lancet this spring.¹²

The researchers found no significant increase in serious neuropsychiatric AEs—a composite measure assessing depression, anxiety, suicidality, and 13 other symptom clusters—attributable to varenicline or bupropion compared with placebo or the nicotine patch in smokers with or without psychiatric disorders. The study did detect a significant difference—approximately 4% (2% in non-psychiatric cohort vs 6% in psychiatric cohort)—in the rate of serious neuropsychiatric AEs regardless of treatment condition. In both cohorts, varenicline was more effective than bupropion, which had similar efficacy to the nicotine patch; all interventions were superior to placebo. Importantly, all 3 medications significantly improved quit rates in smokers with and without psychiatric disorders. Although the efficacy of medications in smokers with or without psychiatric disorders was similar in terms of odds ratios, overall, those with psychiatric disorders had 20% to 30% lower quit rates compared with non-psychiatrically ill smokers.

The EAGLES study results, when viewed in the context of findings from other clinical trials and large-scale observational studies, provide further evidence that smokers with stable mental illness can use bupropion and varenicline safely. It also demonstrates that moderate to severe neuropsychiatric AEs occur during a smoking cessation attempt regardless of the medication used, therefore, monitoring smokers—especially those with psychiatric disorders—is important, a role that psychiatrists are uniquely poised to play.

That all 3 smoking cessation medications are effective in patients with mood, anxiety, and psychotic disorders is good news for our patients. Combined with the EAGLES safety findings, there is no better time to intervene in tobacco dependence

The National Ambulatory Medical Care Survey^1,2 (NAMCS) indicates that less than 1 out of 4 (23%) psychiatrists provide smoking cessation counseling to their patients, and even fewer prescribe medications.

What gives? How is it that so many psychiatrists endorse having recently helped a patient quit smoking when the data from large-scale surveys^1,2 indicate they do not?

From the “glass is half-full” perspective, the discrepancy might indicate that psychiatrists finally have bought into the message put forth 20 years ago when the American Psychiatric Association first published its clinical practice guidelines for treating nicotine dependence.³ Because the figures I cited from NAMCS reflect data from 2006 to 2010, it is possible that in the last 5 years more psychiatrists have started to help their patients quit smoking. Such an hypothesis is further supported by the increasing number of research papers on smoking cessation in individuals with mental illness published over the past 8 years—a period that coincides with the release of the second edition of the Treating tobacco use and dependence clinical practice guideline from the U.S. Agency for Healthcare Research and Quality, which highlighted the need for more research in this population of smokers.⁴

Regardless of the reason, the fact that my informal surveys indicate a likely uptick in activity among psychiatrists to help their patients quit smoking is welcome news. With nearly 1 out of 2 cigarettes sold in the United States being smoked by individuals with psychiatric and substance use disorders,⁵ psychiatrists and other mental health professionals play a vital role in addressing this epidemic. That our patients smoke at rates 2- to 4-times that of the general population and die decades earlier than their non-smoking, non-mentally ill counterparts⁶ are compelling reasons urging us to end our complacency and help our patients quit smoking.

EAGLES trial results help debunk the latest myth about smoking cessation

In an article that I wrote for Current Psychiatry 11 years ago,⁷ I attempted to debunk 3 myths that might have influenced some psychiatrists’ approach and motivation to intervene in tobacco dependence. Since that article appeared, a fourth myth has been promulgated—that the non-nicotine smoking cessation medications, bupropion and varenicline, are unsafe to use in patients with stable psychiatric disorders and cause serious neuropsychiatric adverse events (AEs) including suicide. Indeed, that is one implication of the “black-box” warning both of these medications received in July 2009, which caution that, “the risks of Zyban^®/Chantix^® should be weighed against the benefits of [their] use.”^8,9 For an illness that causes 480,000 deaths each year in the United States,¹⁰ and nearly 6 million across the globe,¹¹ tobacco treatment specialists find themselves in a quandary when 2 of the only 3 approved medications available—nicotine replacement therapy being the third—carry such a stern warning.

In addition to applying the “black-box” warning, the FDA issued a post-marketing requirement to the manufacturers of bupropion and varenicline to conduct a large randomized controlled trial—Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES)—the top-line results of which were published in The Lancet this spring.¹²

The researchers found no significant increase in serious neuropsychiatric AEs—a composite measure assessing depression, anxiety, suicidality, and 13 other symptom clusters—attributable to varenicline or bupropion compared with placebo or the nicotine patch in smokers with or without psychiatric disorders. The study did detect a significant difference—approximately 4% (2% in non-psychiatric cohort vs 6% in psychiatric cohort)—in the rate of serious neuropsychiatric AEs regardless of treatment condition. In both cohorts, varenicline was more effective than bupropion, which had similar efficacy to the nicotine patch; all interventions were superior to placebo. Importantly, all 3 medications significantly improved quit rates in smokers with and without psychiatric disorders. Although the efficacy of medications in smokers with or without psychiatric disorders was similar in terms of odds ratios, overall, those with psychiatric disorders had 20% to 30% lower quit rates compared with non-psychiatrically ill smokers.

The EAGLES study results, when viewed in the context of findings from other clinical trials and large-scale observational studies, provide further evidence that smokers with stable mental illness can use bupropion and varenicline safely. It also demonstrates that moderate to severe neuropsychiatric AEs occur during a smoking cessation attempt regardless of the medication used, therefore, monitoring smokers—especially those with psychiatric disorders—is important, a role that psychiatrists are uniquely poised to play.

That all 3 smoking cessation medications are effective in patients with mood, anxiety, and psychotic disorders is good news for our patients. Combined with the EAGLES safety findings, there is no better time to intervene in tobacco dependence

It has been almost 10 years since the Advisory Committee on Immunization Practices (ACIP) recommended administration of human papillomavirus (HPV) vaccine for 11- to 12-year-old girls and young women up to 26 years of age. Routine administration in preteen boys and young adult males up to 21 years of age was recommended in 2011. An HPV series should be completed by 13 years. So how well are we protecting our patients?

Vaccine coverage

The National Immunization Survey–Teen (NIS-Teen) monitors vaccine coverage annually among adolescents 13-17 years. Data are obtained from individuals from the 50 states, the District of Columbia, the U.S. Virgin Islands, and six major urban areas (MMWR. 2016 Aug 26;65[33]:850-8).

HPV vaccination continues to lag behind Tdap and the meningococcal conjugate vaccine (MCV), although each one is recommended to be administered at the 11- to 12-year visit. In 2015, coverage for receiving at least one dose of HPV vaccine among females was almost 62.8 % and for at least three doses was 41.9%; among males, coverage with at least one dose was 49.8% and for at least three doses was 28.1%. Compared with 2014, coverage for at least one dose of HPV vaccine increased 2.8% in females and 8.1% in males. Males also had a 7.6% for receipt of at least two doses of HPV vaccine, compared with 2014. HPV vaccine coverage in females aged 13 and younger also was lower than for those aged 15 and older. Coverage did not differ for males based on age.

HPV vaccination coverage also differed by state. In 2015, 28 states reported increased coverage in males, but only 7 states had increased coverage in females. Among all adolescents, coverage with at least one dose of HPV vaccine was 56.1%, at least two doses was 45.4%, and at least three doses was 34.9%. In contrast, 86.4% of all adolescents received at least one dose of Tdap, and 81.3% received at least one dose of MCV.

HPV-associated cancers

HPV is the most common sexually transmitted infection in both men and women. It is estimated that 79 million Americans are infected and 14 million new infections occur annually, usually in teens and young adults. Although most infections are asymptomatic and clear spontaneously, persistent infection with oncogenic types can progress to cancer. Cervical and oropharyngeal cancer were the most common HPV-associated cancers in women and men, respectively, in 2008-2012 (MMWR 2016;65:661-6).

All three HPV vaccines protect against HPV types 16 and 18. These types are estimated to account for the majority of cervical and oropharyngeal cancers, 66% and 62%, respectively. The additional types in the 9-valent HPV will protect against HPV types that cause approximately 15% of cervical cancers.

The association between HPV and cancer is clear. So why isn’t this vaccine being embraced? HPV vaccine is all about cancer prevention. Isn’t it? What are the barriers to HPV vaccination? Are parental concerns the only barrier? Are we recommending this vaccine as strongly as others?

Vaccine safety and efficacy

Safety has been a concern voiced by some parents. Collectively, HPV vaccines were studied in more than 95,000 individuals prior to licensure. Almost 90 million doses of vaccine have been distributed in the United States and more than 183 million, worldwide. The federal government utilizes three systems to monitor vaccine safety once a vaccine is licensed: The Vaccine Adverse Event Reporting System (VAERS), the Vaccine Safety Datalink (VSD), and the Clinical Immunization Safety Assessment (CISA) Network. Ongoing safety studies also are conducted by vaccine manufacturers. Since licensure, no serious safety concerns have been identified. Postvaccination syncope, first identified in the VAERS database in 2006, has declined since observation post injection was recommended by ACIP. Multiple studies in the United States and abroad have not demonstrated a causal association with HPV vaccine and any autoimmune and/or neurologic condition or increased risk for thromboembolism.

Mélanie Drolet, PhD, and her colleagues reviewed 20 studies in nine countries with at least 50% coverage in female adolescents aged 13-19 years. There was a 68% reduction in the prevalence of HPV types 16 and 18 and a 61% reduction in anal warts in the postvaccine era (Lancet Infect Dis. 2015 May;15[5]:565-80). Studies also indicate there is no indication of waning immunity.

Parental perceptions

Some parents feel the vaccine is not necessary because their child is not sexually active and/or is not at risk for acquiring a sexually transmitted infection. Others opt to delay initiation. NHANES (National Health and Nutrition Examination Survey) data from 2011 to 2014 revealed that among females aged 14-26 years whose age was known at the time of their first dose of HPV vaccine, 43% had reported having sex before or in the same year that they received their first dose.

One consistent reason parents indicate for not vaccinating is the lack of recommendation from their child’s health provider. Differences in age and sex recommendations also are reported. NIS-Teen 2013 demonstrated that parents of girls were more likely than parents of boys to receive a provider recommendation (65% vs.42%.) Only 29% of female parents indicated they’d received a provider recommendation to have their child vaccinated with HPV by ages 11-12 years.

Mandy A. Allison, MD, and her colleagues reviewed primary care physician perspectives about HPV vaccine in a national survey among 364 pediatricians and 218 family physicians (FPs). Although 84% of pediatricians and 75% of FPs indicated they always discuss HPV vaccination, only 60% of pediatricians and 59% of FPs strongly recommend HPV vaccine for 11- to 12-year-old girls; for boys it was 52% and 41%. More than half reported parental deferral. For pediatricians who almost never discussed the topic, the reasons included that the patient was not sexually active (54%), the child was young (38%), and the patient was already receiving other vaccines (35%) (Pediatrics. 2016 Feb;137[2]:e20152488).

Providers can be influenced by their perceptions of what value parents place on vaccines. In one study, parents were asked to put a value on specific vaccines. Providers were then asked to estimate how parents ranked the vaccines on a scale of 0-10. Providers underestimated the value placed on HPV vaccine (9.3 vs 5.2) (Vaccine 2014;32:579-84).

Improving HPV coverage: Preventing future HPV-related cancers

HPV vaccine should be recommended with as much conviction as Tdap and MCV at the 11- to 12-year visit for both girls and boys. Administration of all three should occur on the same day. Clinician recommendation is the No. 1 reason parents decide to vaccinate. The mantra “same way, same day” should become synonymous with the 11- to 12-year visit. All who have contact with the patient, beginning with the front desk staff, should know the importance of HPV vaccine, and when and why it is recommended. Often, families spend more time with support staff and have discussions prior to interacting with you.

Anticipate questions about HPV. Why give the vaccine when the child is so young and not sexually active? Is my child really at risk? Is it safe? I read on the Internet. … Questions should be interpreted as a need for additional information and reassurance from you.

Remember to emphasize that HPV vaccine is important because it prevents cancer and it is most effective prior to exposure to HPV.

Additional resources to facilitate your discussions about HPV can be found at www.cdc.gov/hpv.

Dr. Word is a pediatric infectious disease specialist and director of the Houston Travel Medicine Clinic. She said she had no relevant financial disclosures.

It has been almost 10 years since the Advisory Committee on Immunization Practices (ACIP) recommended administration of human papillomavirus (HPV) vaccine for 11- to 12-year-old girls and young women up to 26 years of age. Routine administration in preteen boys and young adult males up to 21 years of age was recommended in 2011. An HPV series should be completed by 13 years. So how well are we protecting our patients?

Vaccine coverage

The National Immunization Survey–Teen (NIS-Teen) monitors vaccine coverage annually among adolescents 13-17 years. Data are obtained from individuals from the 50 states, the District of Columbia, the U.S. Virgin Islands, and six major urban areas (MMWR. 2016 Aug 26;65[33]:850-8).

HPV vaccination continues to lag behind Tdap and the meningococcal conjugate vaccine (MCV), although each one is recommended to be administered at the 11- to 12-year visit. In 2015, coverage for receiving at least one dose of HPV vaccine among females was almost 62.8 % and for at least three doses was 41.9%; among males, coverage with at least one dose was 49.8% and for at least three doses was 28.1%. Compared with 2014, coverage for at least one dose of HPV vaccine increased 2.8% in females and 8.1% in males. Males also had a 7.6% for receipt of at least two doses of HPV vaccine, compared with 2014. HPV vaccine coverage in females aged 13 and younger also was lower than for those aged 15 and older. Coverage did not differ for males based on age.

HPV vaccination coverage also differed by state. In 2015, 28 states reported increased coverage in males, but only 7 states had increased coverage in females. Among all adolescents, coverage with at least one dose of HPV vaccine was 56.1%, at least two doses was 45.4%, and at least three doses was 34.9%. In contrast, 86.4% of all adolescents received at least one dose of Tdap, and 81.3% received at least one dose of MCV.

HPV-associated cancers

HPV is the most common sexually transmitted infection in both men and women. It is estimated that 79 million Americans are infected and 14 million new infections occur annually, usually in teens and young adults. Although most infections are asymptomatic and clear spontaneously, persistent infection with oncogenic types can progress to cancer. Cervical and oropharyngeal cancer were the most common HPV-associated cancers in women and men, respectively, in 2008-2012 (MMWR 2016;65:661-6).

All three HPV vaccines protect against HPV types 16 and 18. These types are estimated to account for the majority of cervical and oropharyngeal cancers, 66% and 62%, respectively. The additional types in the 9-valent HPV will protect against HPV types that cause approximately 15% of cervical cancers.

The association between HPV and cancer is clear. So why isn’t this vaccine being embraced? HPV vaccine is all about cancer prevention. Isn’t it? What are the barriers to HPV vaccination? Are parental concerns the only barrier? Are we recommending this vaccine as strongly as others?

Vaccine safety and efficacy

Safety has been a concern voiced by some parents. Collectively, HPV vaccines were studied in more than 95,000 individuals prior to licensure. Almost 90 million doses of vaccine have been distributed in the United States and more than 183 million, worldwide. The federal government utilizes three systems to monitor vaccine safety once a vaccine is licensed: The Vaccine Adverse Event Reporting System (VAERS), the Vaccine Safety Datalink (VSD), and the Clinical Immunization Safety Assessment (CISA) Network. Ongoing safety studies also are conducted by vaccine manufacturers. Since licensure, no serious safety concerns have been identified. Postvaccination syncope, first identified in the VAERS database in 2006, has declined since observation post injection was recommended by ACIP. Multiple studies in the United States and abroad have not demonstrated a causal association with HPV vaccine and any autoimmune and/or neurologic condition or increased risk for thromboembolism.

Mélanie Drolet, PhD, and her colleagues reviewed 20 studies in nine countries with at least 50% coverage in female adolescents aged 13-19 years. There was a 68% reduction in the prevalence of HPV types 16 and 18 and a 61% reduction in anal warts in the postvaccine era (Lancet Infect Dis. 2015 May;15[5]:565-80). Studies also indicate there is no indication of waning immunity.

Parental perceptions

Some parents feel the vaccine is not necessary because their child is not sexually active and/or is not at risk for acquiring a sexually transmitted infection. Others opt to delay initiation. NHANES (National Health and Nutrition Examination Survey) data from 2011 to 2014 revealed that among females aged 14-26 years whose age was known at the time of their first dose of HPV vaccine, 43% had reported having sex before or in the same year that they received their first dose.

One consistent reason parents indicate for not vaccinating is the lack of recommendation from their child’s health provider. Differences in age and sex recommendations also are reported. NIS-Teen 2013 demonstrated that parents of girls were more likely than parents of boys to receive a provider recommendation (65% vs.42%.) Only 29% of female parents indicated they’d received a provider recommendation to have their child vaccinated with HPV by ages 11-12 years.

Mandy A. Allison, MD, and her colleagues reviewed primary care physician perspectives about HPV vaccine in a national survey among 364 pediatricians and 218 family physicians (FPs). Although 84% of pediatricians and 75% of FPs indicated they always discuss HPV vaccination, only 60% of pediatricians and 59% of FPs strongly recommend HPV vaccine for 11- to 12-year-old girls; for boys it was 52% and 41%. More than half reported parental deferral. For pediatricians who almost never discussed the topic, the reasons included that the patient was not sexually active (54%), the child was young (38%), and the patient was already receiving other vaccines (35%) (Pediatrics. 2016 Feb;137[2]:e20152488).

Providers can be influenced by their perceptions of what value parents place on vaccines. In one study, parents were asked to put a value on specific vaccines. Providers were then asked to estimate how parents ranked the vaccines on a scale of 0-10. Providers underestimated the value placed on HPV vaccine (9.3 vs 5.2) (Vaccine 2014;32:579-84).

Improving HPV coverage: Preventing future HPV-related cancers

HPV vaccine should be recommended with as much conviction as Tdap and MCV at the 11- to 12-year visit for both girls and boys. Administration of all three should occur on the same day. Clinician recommendation is the No. 1 reason parents decide to vaccinate. The mantra “same way, same day” should become synonymous with the 11- to 12-year visit. All who have contact with the patient, beginning with the front desk staff, should know the importance of HPV vaccine, and when and why it is recommended. Often, families spend more time with support staff and have discussions prior to interacting with you.

Anticipate questions about HPV. Why give the vaccine when the child is so young and not sexually active? Is my child really at risk? Is it safe? I read on the Internet. … Questions should be interpreted as a need for additional information and reassurance from you.

Remember to emphasize that HPV vaccine is important because it prevents cancer and it is most effective prior to exposure to HPV.

Additional resources to facilitate your discussions about HPV can be found at www.cdc.gov/hpv.

Dr. Word is a pediatric infectious disease specialist and director of the Houston Travel Medicine Clinic. She said she had no relevant financial disclosures.

It has been almost 10 years since the Advisory Committee on Immunization Practices (ACIP) recommended administration of human papillomavirus (HPV) vaccine for 11- to 12-year-old girls and young women up to 26 years of age. Routine administration in preteen boys and young adult males up to 21 years of age was recommended in 2011. An HPV series should be completed by 13 years. So how well are we protecting our patients?

Vaccine coverage

The National Immunization Survey–Teen (NIS-Teen) monitors vaccine coverage annually among adolescents 13-17 years. Data are obtained from individuals from the 50 states, the District of Columbia, the U.S. Virgin Islands, and six major urban areas (MMWR. 2016 Aug 26;65[33]:850-8).

HPV vaccination continues to lag behind Tdap and the meningococcal conjugate vaccine (MCV), although each one is recommended to be administered at the 11- to 12-year visit. In 2015, coverage for receiving at least one dose of HPV vaccine among females was almost 62.8 % and for at least three doses was 41.9%; among males, coverage with at least one dose was 49.8% and for at least three doses was 28.1%. Compared with 2014, coverage for at least one dose of HPV vaccine increased 2.8% in females and 8.1% in males. Males also had a 7.6% for receipt of at least two doses of HPV vaccine, compared with 2014. HPV vaccine coverage in females aged 13 and younger also was lower than for those aged 15 and older. Coverage did not differ for males based on age.

HPV vaccination coverage also differed by state. In 2015, 28 states reported increased coverage in males, but only 7 states had increased coverage in females. Among all adolescents, coverage with at least one dose of HPV vaccine was 56.1%, at least two doses was 45.4%, and at least three doses was 34.9%. In contrast, 86.4% of all adolescents received at least one dose of Tdap, and 81.3% received at least one dose of MCV.

HPV-associated cancers

HPV is the most common sexually transmitted infection in both men and women. It is estimated that 79 million Americans are infected and 14 million new infections occur annually, usually in teens and young adults. Although most infections are asymptomatic and clear spontaneously, persistent infection with oncogenic types can progress to cancer. Cervical and oropharyngeal cancer were the most common HPV-associated cancers in women and men, respectively, in 2008-2012 (MMWR 2016;65:661-6).

All three HPV vaccines protect against HPV types 16 and 18. These types are estimated to account for the majority of cervical and oropharyngeal cancers, 66% and 62%, respectively. The additional types in the 9-valent HPV will protect against HPV types that cause approximately 15% of cervical cancers.

The association between HPV and cancer is clear. So why isn’t this vaccine being embraced? HPV vaccine is all about cancer prevention. Isn’t it? What are the barriers to HPV vaccination? Are parental concerns the only barrier? Are we recommending this vaccine as strongly as others?

Vaccine safety and efficacy

Safety has been a concern voiced by some parents. Collectively, HPV vaccines were studied in more than 95,000 individuals prior to licensure. Almost 90 million doses of vaccine have been distributed in the United States and more than 183 million, worldwide. The federal government utilizes three systems to monitor vaccine safety once a vaccine is licensed: The Vaccine Adverse Event Reporting System (VAERS), the Vaccine Safety Datalink (VSD), and the Clinical Immunization Safety Assessment (CISA) Network. Ongoing safety studies also are conducted by vaccine manufacturers. Since licensure, no serious safety concerns have been identified. Postvaccination syncope, first identified in the VAERS database in 2006, has declined since observation post injection was recommended by ACIP. Multiple studies in the United States and abroad have not demonstrated a causal association with HPV vaccine and any autoimmune and/or neurologic condition or increased risk for thromboembolism.

Mélanie Drolet, PhD, and her colleagues reviewed 20 studies in nine countries with at least 50% coverage in female adolescents aged 13-19 years. There was a 68% reduction in the prevalence of HPV types 16 and 18 and a 61% reduction in anal warts in the postvaccine era (Lancet Infect Dis. 2015 May;15[5]:565-80). Studies also indicate there is no indication of waning immunity.

Parental perceptions

Some parents feel the vaccine is not necessary because their child is not sexually active and/or is not at risk for acquiring a sexually transmitted infection. Others opt to delay initiation. NHANES (National Health and Nutrition Examination Survey) data from 2011 to 2014 revealed that among females aged 14-26 years whose age was known at the time of their first dose of HPV vaccine, 43% had reported having sex before or in the same year that they received their first dose.

One consistent reason parents indicate for not vaccinating is the lack of recommendation from their child’s health provider. Differences in age and sex recommendations also are reported. NIS-Teen 2013 demonstrated that parents of girls were more likely than parents of boys to receive a provider recommendation (65% vs.42%.) Only 29% of female parents indicated they’d received a provider recommendation to have their child vaccinated with HPV by ages 11-12 years.

Mandy A. Allison, MD, and her colleagues reviewed primary care physician perspectives about HPV vaccine in a national survey among 364 pediatricians and 218 family physicians (FPs). Although 84% of pediatricians and 75% of FPs indicated they always discuss HPV vaccination, only 60% of pediatricians and 59% of FPs strongly recommend HPV vaccine for 11- to 12-year-old girls; for boys it was 52% and 41%. More than half reported parental deferral. For pediatricians who almost never discussed the topic, the reasons included that the patient was not sexually active (54%), the child was young (38%), and the patient was already receiving other vaccines (35%) (Pediatrics. 2016 Feb;137[2]:e20152488).

Providers can be influenced by their perceptions of what value parents place on vaccines. In one study, parents were asked to put a value on specific vaccines. Providers were then asked to estimate how parents ranked the vaccines on a scale of 0-10. Providers underestimated the value placed on HPV vaccine (9.3 vs 5.2) (Vaccine 2014;32:579-84).

Improving HPV coverage: Preventing future HPV-related cancers

HPV vaccine should be recommended with as much conviction as Tdap and MCV at the 11- to 12-year visit for both girls and boys. Administration of all three should occur on the same day. Clinician recommendation is the No. 1 reason parents decide to vaccinate. The mantra “same way, same day” should become synonymous with the 11- to 12-year visit. All who have contact with the patient, beginning with the front desk staff, should know the importance of HPV vaccine, and when and why it is recommended. Often, families spend more time with support staff and have discussions prior to interacting with you.

Anticipate questions about HPV. Why give the vaccine when the child is so young and not sexually active? Is my child really at risk? Is it safe? I read on the Internet. … Questions should be interpreted as a need for additional information and reassurance from you.

Remember to emphasize that HPV vaccine is important because it prevents cancer and it is most effective prior to exposure to HPV.

Additional resources to facilitate your discussions about HPV can be found at www.cdc.gov/hpv.

Dr. Word is a pediatric infectious disease specialist and director of the Houston Travel Medicine Clinic. She said she had no relevant financial disclosures.

A frameshift mutation in the CSF2RB gene that is common in Ashkenazi Jews has been linked to Crohn’s disease, according to a report in Gastroenterology.

The Ashkenazi Jewish population has a four- to sevenfold higher prevalence of Crohn’s disease than does the general population. To identify possible genetic mutations associated with the disease, researchers performed exome sequencing of samples from 1,477 Ashkenazi Jewish patients with Crohn’s disease and 2,614 Ashkenazi Jewish control subjects who didn’t have the disorder. All the study participants were enrolled at medical centers throughout North America, Europe, and Israel, noted Ling-Shiang Chuang, PhD, a postdoctoral fellow in genetics and genomic sciences, Mount Sinai Medical Center, New York, and his associates.

They genotyped 224 frameshift mutations and identified one in the colony-stimulating factor 2–receptor beta common subunit (CSF2RB) gene that was significantly associated with Crohn’s disease. They validated this association in a replication cohort of 1,515 Ashkenazi Jewish patients with Crohn’s disease and 7,052 health Ashkenazi control subjects, observing nearly identical allele frequencies and odds ratios as in the discovery cohort.

©SilverV/Thinkstock.com

Since the CSF2RB gene encodes for the receptor for GM-CSF (granulocyte-macrophage colony-stimulating factor) cytokines, the mutation would be expected to reduce GM-CSF signaling in monocytes obtained from carriers. The investigators found this was true when they examined monocytes taken from intestinal-tissue samples and peripheral-blood samples from affected patients.

“The present findings of a loss-of-function frameshift variant in the CSF2RB gene argue for a primary pathogenic role of decreased GM-CSF signaling in driving a subset of Crohn’s disease cases. As many as 30% of cases have increased levels of anti-GM-CSF antibodies, which can neutralize GM-CSF activity, indicating that impaired GM-CSF signaling plays a major role in Crohn’s disease,” Dr. Chuang and his associates wrote (Gastroenterol. 2016;151:710-23.e2. doi: 10.1053/j.gastro.2016.06.045).

Future research may identify subgroups of Crohn’s patients in which treatments that target GM-CSF signaling may be effective, and it may also point the way to novel therapies for the broader population of patients with Crohn’s disease, they added.

This study was supported by the National Institutes of Health, the Inflammatory Bowel Disease Genetics Consortium, the Genetic Research Center at Mount Sinai Medical Center, New York’s Crohn’s Foundation, and several others. Dr. Chuang and his associates reported having no relevant financial disclosures.

A frameshift mutation in the CSF2RB gene that is common in Ashkenazi Jews has been linked to Crohn’s disease, according to a report in Gastroenterology.

The Ashkenazi Jewish population has a four- to sevenfold higher prevalence of Crohn’s disease than does the general population. To identify possible genetic mutations associated with the disease, researchers performed exome sequencing of samples from 1,477 Ashkenazi Jewish patients with Crohn’s disease and 2,614 Ashkenazi Jewish control subjects who didn’t have the disorder. All the study participants were enrolled at medical centers throughout North America, Europe, and Israel, noted Ling-Shiang Chuang, PhD, a postdoctoral fellow in genetics and genomic sciences, Mount Sinai Medical Center, New York, and his associates.

They genotyped 224 frameshift mutations and identified one in the colony-stimulating factor 2–receptor beta common subunit (CSF2RB) gene that was significantly associated with Crohn’s disease. They validated this association in a replication cohort of 1,515 Ashkenazi Jewish patients with Crohn’s disease and 7,052 health Ashkenazi control subjects, observing nearly identical allele frequencies and odds ratios as in the discovery cohort.

©SilverV/Thinkstock.com

Since the CSF2RB gene encodes for the receptor for GM-CSF (granulocyte-macrophage colony-stimulating factor) cytokines, the mutation would be expected to reduce GM-CSF signaling in monocytes obtained from carriers. The investigators found this was true when they examined monocytes taken from intestinal-tissue samples and peripheral-blood samples from affected patients.

“The present findings of a loss-of-function frameshift variant in the CSF2RB gene argue for a primary pathogenic role of decreased GM-CSF signaling in driving a subset of Crohn’s disease cases. As many as 30% of cases have increased levels of anti-GM-CSF antibodies, which can neutralize GM-CSF activity, indicating that impaired GM-CSF signaling plays a major role in Crohn’s disease,” Dr. Chuang and his associates wrote (Gastroenterol. 2016;151:710-23.e2. doi: 10.1053/j.gastro.2016.06.045).

Future research may identify subgroups of Crohn’s patients in which treatments that target GM-CSF signaling may be effective, and it may also point the way to novel therapies for the broader population of patients with Crohn’s disease, they added.

This study was supported by the National Institutes of Health, the Inflammatory Bowel Disease Genetics Consortium, the Genetic Research Center at Mount Sinai Medical Center, New York’s Crohn’s Foundation, and several others. Dr. Chuang and his associates reported having no relevant financial disclosures.

A frameshift mutation in the CSF2RB gene that is common in Ashkenazi Jews has been linked to Crohn’s disease, according to a report in Gastroenterology.

The Ashkenazi Jewish population has a four- to sevenfold higher prevalence of Crohn’s disease than does the general population. To identify possible genetic mutations associated with the disease, researchers performed exome sequencing of samples from 1,477 Ashkenazi Jewish patients with Crohn’s disease and 2,614 Ashkenazi Jewish control subjects who didn’t have the disorder. All the study participants were enrolled at medical centers throughout North America, Europe, and Israel, noted Ling-Shiang Chuang, PhD, a postdoctoral fellow in genetics and genomic sciences, Mount Sinai Medical Center, New York, and his associates.

They genotyped 224 frameshift mutations and identified one in the colony-stimulating factor 2–receptor beta common subunit (CSF2RB) gene that was significantly associated with Crohn’s disease. They validated this association in a replication cohort of 1,515 Ashkenazi Jewish patients with Crohn’s disease and 7,052 health Ashkenazi control subjects, observing nearly identical allele frequencies and odds ratios as in the discovery cohort.

©SilverV/Thinkstock.com

Since the CSF2RB gene encodes for the receptor for GM-CSF (granulocyte-macrophage colony-stimulating factor) cytokines, the mutation would be expected to reduce GM-CSF signaling in monocytes obtained from carriers. The investigators found this was true when they examined monocytes taken from intestinal-tissue samples and peripheral-blood samples from affected patients.

“The present findings of a loss-of-function frameshift variant in the CSF2RB gene argue for a primary pathogenic role of decreased GM-CSF signaling in driving a subset of Crohn’s disease cases. As many as 30% of cases have increased levels of anti-GM-CSF antibodies, which can neutralize GM-CSF activity, indicating that impaired GM-CSF signaling plays a major role in Crohn’s disease,” Dr. Chuang and his associates wrote (Gastroenterol. 2016;151:710-23.e2. doi: 10.1053/j.gastro.2016.06.045).

Future research may identify subgroups of Crohn’s patients in which treatments that target GM-CSF signaling may be effective, and it may also point the way to novel therapies for the broader population of patients with Crohn’s disease, they added.

This study was supported by the National Institutes of Health, the Inflammatory Bowel Disease Genetics Consortium, the Genetic Research Center at Mount Sinai Medical Center, New York’s Crohn’s Foundation, and several others. Dr. Chuang and his associates reported having no relevant financial disclosures.

Several simple, inexpensive operational interventions substantially improve care for viral hepatitis, according to a report published in the Lancet.

Recent advances in treatment for chronic hepatitis B and chronic hepatitis C have the potential to halt or even reverse the progression of associated liver disease and to reduce related mortality, reported Kali Zhou, MD, of the division of gastroenterology, University of California, San Francisco, and her associates. But they can do so only if affected individuals are engaged and retained in the relatively long continuum of care, from diagnosis through viral suppression or cure.

To assess the usefulness of interventions that promote such patient engagement and retention, Dr. Zhou and her colleagues reviewed the scientific literature and performed a meta-analysis of 56 studies. They examined 15 studies on HBV care, 38 on HCV care, and 3 on both types of hepatitis (Lancet Infect Dis. 2016 Sep 5. doi: 10.1016/S1473-3099[16]30208-0).

Among their findings:

• Educating a single lay health worker to improve knowledge about the disease in his or her community and to promote diagnostic testing nearly tripled the testing rate (relative risk, 2.68), compared with no such intervention.

• Clinician reminders during regular office visits to consider hepatitis testing – such as prompts in the patients’ electronic medical records or stickers on their charts – nearly quadrupled the testing rate (RR, 3.70), compared with no clinician reminders.

• Providing guided referral to a hepatitis specialist for people at risk for the disorder markedly improved the rate of visits to such specialists (RR, 1.57), compared with no such referrals.

• Providing psychological counseling and motivational therapy for mental health and/or substance misuse problems along with medical care for hepatitis dramatically increased the number of patients treated (OR, 3.42) and raised the rate of treatment completion (RR, 1.14).

• Combining mental health, substance misuse, and hepatitis treatment services at one location increased the rate of treatment initiation (RR, 1.36), treatment adherence (RR, 1.22), and cure as measured by sustained virologic response rate (RR, 1.21), compared with usual care.

These interventions might be useful in augmenting hepatitis treatment programs worldwide, Dr. Zhou and her associates said.

The World Health Organization and the U.S. Fulbright Program supported the study. Dr. Zhou and her associates reported having no relevant financial disclosures.

Several simple, inexpensive operational interventions substantially improve care for viral hepatitis, according to a report published in the Lancet.

Recent advances in treatment for chronic hepatitis B and chronic hepatitis C have the potential to halt or even reverse the progression of associated liver disease and to reduce related mortality, reported Kali Zhou, MD, of the division of gastroenterology, University of California, San Francisco, and her associates. But they can do so only if affected individuals are engaged and retained in the relatively long continuum of care, from diagnosis through viral suppression or cure.

To assess the usefulness of interventions that promote such patient engagement and retention, Dr. Zhou and her colleagues reviewed the scientific literature and performed a meta-analysis of 56 studies. They examined 15 studies on HBV care, 38 on HCV care, and 3 on both types of hepatitis (Lancet Infect Dis. 2016 Sep 5. doi: 10.1016/S1473-3099[16]30208-0).

Among their findings:

• Educating a single lay health worker to improve knowledge about the disease in his or her community and to promote diagnostic testing nearly tripled the testing rate (relative risk, 2.68), compared with no such intervention.

• Clinician reminders during regular office visits to consider hepatitis testing – such as prompts in the patients’ electronic medical records or stickers on their charts – nearly quadrupled the testing rate (RR, 3.70), compared with no clinician reminders.

• Providing guided referral to a hepatitis specialist for people at risk for the disorder markedly improved the rate of visits to such specialists (RR, 1.57), compared with no such referrals.

• Providing psychological counseling and motivational therapy for mental health and/or substance misuse problems along with medical care for hepatitis dramatically increased the number of patients treated (OR, 3.42) and raised the rate of treatment completion (RR, 1.14).

• Combining mental health, substance misuse, and hepatitis treatment services at one location increased the rate of treatment initiation (RR, 1.36), treatment adherence (RR, 1.22), and cure as measured by sustained virologic response rate (RR, 1.21), compared with usual care.

These interventions might be useful in augmenting hepatitis treatment programs worldwide, Dr. Zhou and her associates said.

The World Health Organization and the U.S. Fulbright Program supported the study. Dr. Zhou and her associates reported having no relevant financial disclosures.

Several simple, inexpensive operational interventions substantially improve care for viral hepatitis, according to a report published in the Lancet.

Recent advances in treatment for chronic hepatitis B and chronic hepatitis C have the potential to halt or even reverse the progression of associated liver disease and to reduce related mortality, reported Kali Zhou, MD, of the division of gastroenterology, University of California, San Francisco, and her associates. But they can do so only if affected individuals are engaged and retained in the relatively long continuum of care, from diagnosis through viral suppression or cure.

To assess the usefulness of interventions that promote such patient engagement and retention, Dr. Zhou and her colleagues reviewed the scientific literature and performed a meta-analysis of 56 studies. They examined 15 studies on HBV care, 38 on HCV care, and 3 on both types of hepatitis (Lancet Infect Dis. 2016 Sep 5. doi: 10.1016/S1473-3099[16]30208-0).

Among their findings:

• Educating a single lay health worker to improve knowledge about the disease in his or her community and to promote diagnostic testing nearly tripled the testing rate (relative risk, 2.68), compared with no such intervention.

• Clinician reminders during regular office visits to consider hepatitis testing – such as prompts in the patients’ electronic medical records or stickers on their charts – nearly quadrupled the testing rate (RR, 3.70), compared with no clinician reminders.

• Providing guided referral to a hepatitis specialist for people at risk for the disorder markedly improved the rate of visits to such specialists (RR, 1.57), compared with no such referrals.

• Providing psychological counseling and motivational therapy for mental health and/or substance misuse problems along with medical care for hepatitis dramatically increased the number of patients treated (OR, 3.42) and raised the rate of treatment completion (RR, 1.14).

• Combining mental health, substance misuse, and hepatitis treatment services at one location increased the rate of treatment initiation (RR, 1.36), treatment adherence (RR, 1.22), and cure as measured by sustained virologic response rate (RR, 1.21), compared with usual care.

These interventions might be useful in augmenting hepatitis treatment programs worldwide, Dr. Zhou and her associates said.

The World Health Organization and the U.S. Fulbright Program supported the study. Dr. Zhou and her associates reported having no relevant financial disclosures.

Background Prostate cancer affects not only men with the disease, but their partners and families as well. These affects can include changes to everyday lifestyle activities, incontinence, and sexual dysfunction, and sometimes, relationships.

Click on the PDF icon at the top of this introduction to read the full article.

Background Prostate cancer affects not only men with the disease, but their partners and families as well. These affects can include changes to everyday lifestyle activities, incontinence, and sexual dysfunction, and sometimes, relationships.

Click on the PDF icon at the top of this introduction to read the full article.

Background Prostate cancer affects not only men with the disease, but their partners and families as well. These affects can include changes to everyday lifestyle activities, incontinence, and sexual dysfunction, and sometimes, relationships.

Click on the PDF icon at the top of this introduction to read the full article.