While folks my age are sometimes referred to as “elderly” victims in newspaper stories about phone and Internet scams, I resist and object to the implication that I am less than sharp and worrisomely vulnerable to being duped.

I hang up when a stranger calls to warn me that I am about to be audited by the Internal Revenue Service and asks for my Social Security number. I double-delete e-mails purported to come from my Internet provider that ask for my e-mail address and password. I’m no pushover.

However, I fear that over the last 20 years of my practice career, I was duped by several of my adolescent patients on more than one occasion. I hope that I had a reputation in town as one of the physicians least likely to leap to the diagnosis of attention-deficit/hyperactivity disorder (ADHD) and even less likely to pull out my pad and prescribe stimulants.

I was particularly hesitant to make the diagnosis of ADHD in an adolescent whose academic career and behavior in grade school had been unremarkable. But from time to time I was presented with a case that included a combination of apparently reliable teachers’ reports, parental pleas, and patient complaints that was hard to ignore. Having ruled out anxiety, depression, learning disabilities, and severe sleep deprivation (all my teenage patients were sleep deprived to some degree) I would reluctantly agree to a trial of stimulant medication.

As you can imagine, assessing success or failure took time because we were usually looking for improvement in academic performance. For adolescents, this often means waiting to the end of the semester or grading period. If the academic improvement was less than dramatic as it was in the usual scenario, I was left relying on the patient’s report of his subjective observations and waiting another 6 months for more information from the school. Occasionally, the patient would report that the medication made him feel weird and that he wanted to stop it. More often, the patient would report that he was able to pay attention in class more easily, even though he had difficulty pointing to a documented improvement in his performance.

So what does one do? Sometimes I could convince the patient and his family that the trial had failed and that we should stop the medication and work harder to find a better match between his learning style, study habits, and the demands of the school. In other cases, I would adjust dosages and switch medications. The results were seldom dramatic. However, if the patient continued to claim a benefit, I would continue to prescribe the stimulant. I would make phone assessments with every refill, and face-to-face visits at least once a year.

While it may be that a few of those adolescents without clearly demonstrable benefit were indeed being helped by the stimulants, I am now convinced that I was being duped more often than I cared to admit then. I know there were stimulants available on the streets and in the school hallways and parking lots because some of my patients told me that they were easy to find and had tried them. I have to believe that some of those pills on the street were ones I had prescribed. I worry when I consider how many.

The national statistics are staggering and embarrassing. In 2013, the federal Substance Abuse and Mental Health Services Administration reported that ED visits associated with the nonmedical use of prescribed stimulants among adults aged 18-34 years had tripled from 2005 to 2011. (“Workers Seeking Productivity in a Pill Are Abusing ADHD Drugs,” by Alan Schwarz, New York Times, April 18, 2015). How many of the pills associated with those visits were originally prescribed for adolescent who didn’t have ADHD?

How many of my patients were just trying to be good friends by sharing their pills and how many were selling them? How many of the pills I prescribed were fueling all-night parties, and how many were being used as performance-enhancing drugs by students who needed to finish a term paper on time?

I don’t know. But I do know that although I miss practicing pediatrics, I am glad I no longer have to face the dilemma of the adolescent with ADHD-like complaints, because I hate being duped.

While folks my age are sometimes referred to as “elderly” victims in newspaper stories about phone and Internet scams, I resist and object to the implication that I am less than sharp and worrisomely vulnerable to being duped.

I hang up when a stranger calls to warn me that I am about to be audited by the Internal Revenue Service and asks for my Social Security number. I double-delete e-mails purported to come from my Internet provider that ask for my e-mail address and password. I’m no pushover.

However, I fear that over the last 20 years of my practice career, I was duped by several of my adolescent patients on more than one occasion. I hope that I had a reputation in town as one of the physicians least likely to leap to the diagnosis of attention-deficit/hyperactivity disorder (ADHD) and even less likely to pull out my pad and prescribe stimulants.

I was particularly hesitant to make the diagnosis of ADHD in an adolescent whose academic career and behavior in grade school had been unremarkable. But from time to time I was presented with a case that included a combination of apparently reliable teachers’ reports, parental pleas, and patient complaints that was hard to ignore. Having ruled out anxiety, depression, learning disabilities, and severe sleep deprivation (all my teenage patients were sleep deprived to some degree) I would reluctantly agree to a trial of stimulant medication.

As you can imagine, assessing success or failure took time because we were usually looking for improvement in academic performance. For adolescents, this often means waiting to the end of the semester or grading period. If the academic improvement was less than dramatic as it was in the usual scenario, I was left relying on the patient’s report of his subjective observations and waiting another 6 months for more information from the school. Occasionally, the patient would report that the medication made him feel weird and that he wanted to stop it. More often, the patient would report that he was able to pay attention in class more easily, even though he had difficulty pointing to a documented improvement in his performance.

So what does one do? Sometimes I could convince the patient and his family that the trial had failed and that we should stop the medication and work harder to find a better match between his learning style, study habits, and the demands of the school. In other cases, I would adjust dosages and switch medications. The results were seldom dramatic. However, if the patient continued to claim a benefit, I would continue to prescribe the stimulant. I would make phone assessments with every refill, and face-to-face visits at least once a year.

While it may be that a few of those adolescents without clearly demonstrable benefit were indeed being helped by the stimulants, I am now convinced that I was being duped more often than I cared to admit then. I know there were stimulants available on the streets and in the school hallways and parking lots because some of my patients told me that they were easy to find and had tried them. I have to believe that some of those pills on the street were ones I had prescribed. I worry when I consider how many.

The national statistics are staggering and embarrassing. In 2013, the federal Substance Abuse and Mental Health Services Administration reported that ED visits associated with the nonmedical use of prescribed stimulants among adults aged 18-34 years had tripled from 2005 to 2011. (“Workers Seeking Productivity in a Pill Are Abusing ADHD Drugs,” by Alan Schwarz, New York Times, April 18, 2015). How many of the pills associated with those visits were originally prescribed for adolescent who didn’t have ADHD?

How many of my patients were just trying to be good friends by sharing their pills and how many were selling them? How many of the pills I prescribed were fueling all-night parties, and how many were being used as performance-enhancing drugs by students who needed to finish a term paper on time?

I don’t know. But I do know that although I miss practicing pediatrics, I am glad I no longer have to face the dilemma of the adolescent with ADHD-like complaints, because I hate being duped.

While folks my age are sometimes referred to as “elderly” victims in newspaper stories about phone and Internet scams, I resist and object to the implication that I am less than sharp and worrisomely vulnerable to being duped.

I hang up when a stranger calls to warn me that I am about to be audited by the Internal Revenue Service and asks for my Social Security number. I double-delete e-mails purported to come from my Internet provider that ask for my e-mail address and password. I’m no pushover.

However, I fear that over the last 20 years of my practice career, I was duped by several of my adolescent patients on more than one occasion. I hope that I had a reputation in town as one of the physicians least likely to leap to the diagnosis of attention-deficit/hyperactivity disorder (ADHD) and even less likely to pull out my pad and prescribe stimulants.

I was particularly hesitant to make the diagnosis of ADHD in an adolescent whose academic career and behavior in grade school had been unremarkable. But from time to time I was presented with a case that included a combination of apparently reliable teachers’ reports, parental pleas, and patient complaints that was hard to ignore. Having ruled out anxiety, depression, learning disabilities, and severe sleep deprivation (all my teenage patients were sleep deprived to some degree) I would reluctantly agree to a trial of stimulant medication.

As you can imagine, assessing success or failure took time because we were usually looking for improvement in academic performance. For adolescents, this often means waiting to the end of the semester or grading period. If the academic improvement was less than dramatic as it was in the usual scenario, I was left relying on the patient’s report of his subjective observations and waiting another 6 months for more information from the school. Occasionally, the patient would report that the medication made him feel weird and that he wanted to stop it. More often, the patient would report that he was able to pay attention in class more easily, even though he had difficulty pointing to a documented improvement in his performance.

So what does one do? Sometimes I could convince the patient and his family that the trial had failed and that we should stop the medication and work harder to find a better match between his learning style, study habits, and the demands of the school. In other cases, I would adjust dosages and switch medications. The results were seldom dramatic. However, if the patient continued to claim a benefit, I would continue to prescribe the stimulant. I would make phone assessments with every refill, and face-to-face visits at least once a year.

While it may be that a few of those adolescents without clearly demonstrable benefit were indeed being helped by the stimulants, I am now convinced that I was being duped more often than I cared to admit then. I know there were stimulants available on the streets and in the school hallways and parking lots because some of my patients told me that they were easy to find and had tried them. I have to believe that some of those pills on the street were ones I had prescribed. I worry when I consider how many.

The national statistics are staggering and embarrassing. In 2013, the federal Substance Abuse and Mental Health Services Administration reported that ED visits associated with the nonmedical use of prescribed stimulants among adults aged 18-34 years had tripled from 2005 to 2011. (“Workers Seeking Productivity in a Pill Are Abusing ADHD Drugs,” by Alan Schwarz, New York Times, April 18, 2015). How many of the pills associated with those visits were originally prescribed for adolescent who didn’t have ADHD?

How many of my patients were just trying to be good friends by sharing their pills and how many were selling them? How many of the pills I prescribed were fueling all-night parties, and how many were being used as performance-enhancing drugs by students who needed to finish a term paper on time?

I don’t know. But I do know that although I miss practicing pediatrics, I am glad I no longer have to face the dilemma of the adolescent with ADHD-like complaints, because I hate being duped.

Individuals with biopsy-confirmed celiac disease have more than double the risk of receiving a diagnosis of neuropathy when compared with the general population, and the risk persists even when other potentially contributing conditions and lifestyle factors are considered.

The use of Swedish population registries enabled first author Dr. Sujata P. Thawani of Columbia University, New York, and her colleagues to find that the risk of neuropathy was increased both before and after a diagnosis of celiac disease (CD).

“We found an increased risk of neuropathy in patients with CD that persists after CD diagnosis. Although absolute risks for neuropathy are low, CD is a potentially treatable condition with a young age of onset. Our findings suggest that screening could be beneficial in patients with neuropathy,” they wrote (JAMA Neurol. 2015 May 11 [doi:10.1001/jamaneurol.2015.0475]).Neuropathy has a known association with CD, an immune-mediated disorder characterized by sensitivity to gluten with an incidence of about 1% in Western Europe. Previous studies had reported that up to one-third of celiac disease patients also experienced neuropathy, but the literature had not completely characterized the prevalence of neuropathy in the CD population.

©xrender/thinkstockphotos.com

Dr. Thawani and her associates used Swedish pathology registers to identify individuals whose small intestine biopsies showed villous atrophy between 1969 and 2008 (Marsh stage 3, n = 28,232). These individuals were categorized as having CD. Neuropathy diagnoses were drawn from national patient and pharmacy registers. Each CD patient was matched with up to five age- and sex-matched controls (n = 139,473) from the Swedish Total Population Registry, all of whom were diagnosed in the same year and were from the same county as the matched CD patient.

Although 41.7% of CD patients were diagnosed in childhood, the median age at diagnosis was 29 years. About 62% of patients in both groups were female. For CD patients, the absolute risk of neuropathy was 64 per 100,000 patient-years, compared with 15 per 100,000 patients-years in the control group (hazard ratio, 2.5; 95% confidence interval, 2.0-2.9; P < .001).

The risk of neuropathy for patients with CD was not affected by gender, absolute age, or age at diagnosis. The risk of neuropathy for those with CD remained about 2.5 times higher than the matched controls, even after accounting for diabetes status, the presence of other autoimmune disorders, vitamin deficiencies, and alcohol use. Although vitamin B₁₂ deficiency has been associated with CD and may contribute to neuropathy, the investigators noted that, “in our analysis, the influence of vitamin deficiencies did not significantly affect our risk estimate.”

Nonspecified neuropathy was the most commonly reported type of neuropathy. Other subtypes of neuropathy were tracked, but limitations of coding and reporting prevented tracking sensory ganglionopathy, the second most commonly reported neuropathy in CD.

The strengths of the study included the large sample size and the study’s statistical strengths. The retrospective nature of the study was an overall limitation, and the homogeneous study population (over 90% of patients in both arms were of Nordic heritage) limited the study’s generalizability.

Surveillance bias may account for some of the increased risk for neuropathy, noted Dr. Thawani and her colleagues. This was hinted at by the fact that a diagnosis of neuropathy tended to follow closely on the CD diagnosis; physicians may have been more attuned to detecting potential sequelae of the CD diagnosis during this time period. Notably, though, patients with a prior neuropathy diagnosis also were more likely to be diagnosed with CD, showing a bidirectional relationship.

“These data may also suggest that the two diseases may share risk factors or a common underlying etiology for the development of neuropathy, such as a potential role of immunologic mechanisms,” they wrote.

The authors reported no conflicts of interest. The investigators received support from the Swedish Society of Medicine, the Swedish Research Council, and the National Center for Advancing Translational Sciences.

Individuals with biopsy-confirmed celiac disease have more than double the risk of receiving a diagnosis of neuropathy when compared with the general population, and the risk persists even when other potentially contributing conditions and lifestyle factors are considered.

The use of Swedish population registries enabled first author Dr. Sujata P. Thawani of Columbia University, New York, and her colleagues to find that the risk of neuropathy was increased both before and after a diagnosis of celiac disease (CD).

“We found an increased risk of neuropathy in patients with CD that persists after CD diagnosis. Although absolute risks for neuropathy are low, CD is a potentially treatable condition with a young age of onset. Our findings suggest that screening could be beneficial in patients with neuropathy,” they wrote (JAMA Neurol. 2015 May 11 [doi:10.1001/jamaneurol.2015.0475]).Neuropathy has a known association with CD, an immune-mediated disorder characterized by sensitivity to gluten with an incidence of about 1% in Western Europe. Previous studies had reported that up to one-third of celiac disease patients also experienced neuropathy, but the literature had not completely characterized the prevalence of neuropathy in the CD population.

©xrender/thinkstockphotos.com

Dr. Thawani and her associates used Swedish pathology registers to identify individuals whose small intestine biopsies showed villous atrophy between 1969 and 2008 (Marsh stage 3, n = 28,232). These individuals were categorized as having CD. Neuropathy diagnoses were drawn from national patient and pharmacy registers. Each CD patient was matched with up to five age- and sex-matched controls (n = 139,473) from the Swedish Total Population Registry, all of whom were diagnosed in the same year and were from the same county as the matched CD patient.

Although 41.7% of CD patients were diagnosed in childhood, the median age at diagnosis was 29 years. About 62% of patients in both groups were female. For CD patients, the absolute risk of neuropathy was 64 per 100,000 patient-years, compared with 15 per 100,000 patients-years in the control group (hazard ratio, 2.5; 95% confidence interval, 2.0-2.9; P < .001).

The risk of neuropathy for patients with CD was not affected by gender, absolute age, or age at diagnosis. The risk of neuropathy for those with CD remained about 2.5 times higher than the matched controls, even after accounting for diabetes status, the presence of other autoimmune disorders, vitamin deficiencies, and alcohol use. Although vitamin B₁₂ deficiency has been associated with CD and may contribute to neuropathy, the investigators noted that, “in our analysis, the influence of vitamin deficiencies did not significantly affect our risk estimate.”

Nonspecified neuropathy was the most commonly reported type of neuropathy. Other subtypes of neuropathy were tracked, but limitations of coding and reporting prevented tracking sensory ganglionopathy, the second most commonly reported neuropathy in CD.

The strengths of the study included the large sample size and the study’s statistical strengths. The retrospective nature of the study was an overall limitation, and the homogeneous study population (over 90% of patients in both arms were of Nordic heritage) limited the study’s generalizability.

Surveillance bias may account for some of the increased risk for neuropathy, noted Dr. Thawani and her colleagues. This was hinted at by the fact that a diagnosis of neuropathy tended to follow closely on the CD diagnosis; physicians may have been more attuned to detecting potential sequelae of the CD diagnosis during this time period. Notably, though, patients with a prior neuropathy diagnosis also were more likely to be diagnosed with CD, showing a bidirectional relationship.

“These data may also suggest that the two diseases may share risk factors or a common underlying etiology for the development of neuropathy, such as a potential role of immunologic mechanisms,” they wrote.

The authors reported no conflicts of interest. The investigators received support from the Swedish Society of Medicine, the Swedish Research Council, and the National Center for Advancing Translational Sciences.

Individuals with biopsy-confirmed celiac disease have more than double the risk of receiving a diagnosis of neuropathy when compared with the general population, and the risk persists even when other potentially contributing conditions and lifestyle factors are considered.

The use of Swedish population registries enabled first author Dr. Sujata P. Thawani of Columbia University, New York, and her colleagues to find that the risk of neuropathy was increased both before and after a diagnosis of celiac disease (CD).

“We found an increased risk of neuropathy in patients with CD that persists after CD diagnosis. Although absolute risks for neuropathy are low, CD is a potentially treatable condition with a young age of onset. Our findings suggest that screening could be beneficial in patients with neuropathy,” they wrote (JAMA Neurol. 2015 May 11 [doi:10.1001/jamaneurol.2015.0475]).Neuropathy has a known association with CD, an immune-mediated disorder characterized by sensitivity to gluten with an incidence of about 1% in Western Europe. Previous studies had reported that up to one-third of celiac disease patients also experienced neuropathy, but the literature had not completely characterized the prevalence of neuropathy in the CD population.

©xrender/thinkstockphotos.com

Dr. Thawani and her associates used Swedish pathology registers to identify individuals whose small intestine biopsies showed villous atrophy between 1969 and 2008 (Marsh stage 3, n = 28,232). These individuals were categorized as having CD. Neuropathy diagnoses were drawn from national patient and pharmacy registers. Each CD patient was matched with up to five age- and sex-matched controls (n = 139,473) from the Swedish Total Population Registry, all of whom were diagnosed in the same year and were from the same county as the matched CD patient.

Although 41.7% of CD patients were diagnosed in childhood, the median age at diagnosis was 29 years. About 62% of patients in both groups were female. For CD patients, the absolute risk of neuropathy was 64 per 100,000 patient-years, compared with 15 per 100,000 patients-years in the control group (hazard ratio, 2.5; 95% confidence interval, 2.0-2.9; P < .001).

The risk of neuropathy for patients with CD was not affected by gender, absolute age, or age at diagnosis. The risk of neuropathy for those with CD remained about 2.5 times higher than the matched controls, even after accounting for diabetes status, the presence of other autoimmune disorders, vitamin deficiencies, and alcohol use. Although vitamin B₁₂ deficiency has been associated with CD and may contribute to neuropathy, the investigators noted that, “in our analysis, the influence of vitamin deficiencies did not significantly affect our risk estimate.”

Nonspecified neuropathy was the most commonly reported type of neuropathy. Other subtypes of neuropathy were tracked, but limitations of coding and reporting prevented tracking sensory ganglionopathy, the second most commonly reported neuropathy in CD.

The strengths of the study included the large sample size and the study’s statistical strengths. The retrospective nature of the study was an overall limitation, and the homogeneous study population (over 90% of patients in both arms were of Nordic heritage) limited the study’s generalizability.

Surveillance bias may account for some of the increased risk for neuropathy, noted Dr. Thawani and her colleagues. This was hinted at by the fact that a diagnosis of neuropathy tended to follow closely on the CD diagnosis; physicians may have been more attuned to detecting potential sequelae of the CD diagnosis during this time period. Notably, though, patients with a prior neuropathy diagnosis also were more likely to be diagnosed with CD, showing a bidirectional relationship.

“These data may also suggest that the two diseases may share risk factors or a common underlying etiology for the development of neuropathy, such as a potential role of immunologic mechanisms,” they wrote.

The authors reported no conflicts of interest. The investigators received support from the Swedish Society of Medicine, the Swedish Research Council, and the National Center for Advancing Translational Sciences.

I’ve written about the Physician Payment Sunshine Act several times since it became law in 2013. My basic opinion – that it is a tempest in a teapot – has not changed. Nonetheless, now is the time to review the 2014 data reported under your name – and if necessary, initiate a dispute – before the information is posted publicly on June 30.

A quick review: The Sunshine Act, known officially as the “Open Payments Program,” requires all manufacturers of drugs, devices, and medical supplies covered by federal health care programs to report to the Centers for Medicare & Medicaid Services any financial interactions with physicians and teaching hospitals.

Reportable interactions include consulting, food, ownership or investment interest, direct compensation for speakers at education programs, and research. Compensation for clinical trials must be reported but is not made public until the product receives FDA approval, or until 4 years after the payment, whichever is earlier. Payments for trials involving a new indication for an approved drug are posted the following year.

Exemptions include CME activities funded by manufacturers and product samples for patient use. Medical students and residents are exempted entirely.

You are allowed to review your data and request corrections before information is posted publicly. You will have an additional 2 years to pursue corrections after the content goes live at the end of June, but any erroneous information will remain online until the next scheduled update, so you should find and fix errors as promptly as possible.

If you don’t see drug reps, accept sponsored lunches, or give sponsored talks, don’t assume that you won’t be on the website. Check anyway: You might be indirectly involved in a compensation that you were not aware of, or you might have been reported in error.

To review your data, register at the CMS Enterprise Portal (https://portal.cms.gov/wps/portal/unauthportal/home/) and request access to the Open Payments system.

The question remains as to what effect the law might be having on research, continuing education, or physicians’ relationships with the pharmaceutical industry. The short answer is that no one knows. The first data posting this past September came and went with little fanfare, and no repercussions directly attributable to the program have been reported as of this writing.

Sunshine laws have been in effect for several years in six states: California, Colorado, Massachusetts, Minnesota, Vermont, and West Virginia, plus the District of Columbia. (Maine repealed its law in 2011.) Observers disagree on their impact. Studies in Maine and West Virginia showed no significant public reaction or changes in prescribing patterns, according to a 2012 article in the Archives of Internal Medicine (now JAMA Internal Medicine).

Reactions from the public are equally inscrutable. Do citizens think less of doctors who accept the occasional industry-sponsored lunch for their employees? Do they think more of doctors who speak at meetings, or conduct industry-sponsored clinical research? There are no objective data. Anecdotally, I haven’t heard a peep – positive, negative, or indifferent – from any of my patients, nor have any other physicians that I’ve asked.

As of now, I stand by my initial prediction that attorneys, activists, and the occasional reporter will data-mine the information for various purposes, but few patients will bother to visit. Of course, that doesn’t mean you should ignore it as well. As always, I suggest you review the accuracy of anything posted about you, in any form or context, on any venue. This year’s data (reflecting all 2014 reports) have been available for review since April 6. You can initiate a dispute at any time over the next 2 years, before or after public release on June 30, but the sooner the better. Corrections are made each time CMS updates the system.

Maintaining accurate financial records has always been important, but it will be even more important now to support your disputes. CMS won’t simply take your word for it. A free app is available to help you track payments and other reportable industry interactions; search for “Open Payments” at your favorite app store.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News.

I’ve written about the Physician Payment Sunshine Act several times since it became law in 2013. My basic opinion – that it is a tempest in a teapot – has not changed. Nonetheless, now is the time to review the 2014 data reported under your name – and if necessary, initiate a dispute – before the information is posted publicly on June 30.

A quick review: The Sunshine Act, known officially as the “Open Payments Program,” requires all manufacturers of drugs, devices, and medical supplies covered by federal health care programs to report to the Centers for Medicare & Medicaid Services any financial interactions with physicians and teaching hospitals.

Reportable interactions include consulting, food, ownership or investment interest, direct compensation for speakers at education programs, and research. Compensation for clinical trials must be reported but is not made public until the product receives FDA approval, or until 4 years after the payment, whichever is earlier. Payments for trials involving a new indication for an approved drug are posted the following year.

Exemptions include CME activities funded by manufacturers and product samples for patient use. Medical students and residents are exempted entirely.

You are allowed to review your data and request corrections before information is posted publicly. You will have an additional 2 years to pursue corrections after the content goes live at the end of June, but any erroneous information will remain online until the next scheduled update, so you should find and fix errors as promptly as possible.

If you don’t see drug reps, accept sponsored lunches, or give sponsored talks, don’t assume that you won’t be on the website. Check anyway: You might be indirectly involved in a compensation that you were not aware of, or you might have been reported in error.

To review your data, register at the CMS Enterprise Portal (https://portal.cms.gov/wps/portal/unauthportal/home/) and request access to the Open Payments system.

The question remains as to what effect the law might be having on research, continuing education, or physicians’ relationships with the pharmaceutical industry. The short answer is that no one knows. The first data posting this past September came and went with little fanfare, and no repercussions directly attributable to the program have been reported as of this writing.

Sunshine laws have been in effect for several years in six states: California, Colorado, Massachusetts, Minnesota, Vermont, and West Virginia, plus the District of Columbia. (Maine repealed its law in 2011.) Observers disagree on their impact. Studies in Maine and West Virginia showed no significant public reaction or changes in prescribing patterns, according to a 2012 article in the Archives of Internal Medicine (now JAMA Internal Medicine).

Reactions from the public are equally inscrutable. Do citizens think less of doctors who accept the occasional industry-sponsored lunch for their employees? Do they think more of doctors who speak at meetings, or conduct industry-sponsored clinical research? There are no objective data. Anecdotally, I haven’t heard a peep – positive, negative, or indifferent – from any of my patients, nor have any other physicians that I’ve asked.

As of now, I stand by my initial prediction that attorneys, activists, and the occasional reporter will data-mine the information for various purposes, but few patients will bother to visit. Of course, that doesn’t mean you should ignore it as well. As always, I suggest you review the accuracy of anything posted about you, in any form or context, on any venue. This year’s data (reflecting all 2014 reports) have been available for review since April 6. You can initiate a dispute at any time over the next 2 years, before or after public release on June 30, but the sooner the better. Corrections are made each time CMS updates the system.

Maintaining accurate financial records has always been important, but it will be even more important now to support your disputes. CMS won’t simply take your word for it. A free app is available to help you track payments and other reportable industry interactions; search for “Open Payments” at your favorite app store.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News.

I’ve written about the Physician Payment Sunshine Act several times since it became law in 2013. My basic opinion – that it is a tempest in a teapot – has not changed. Nonetheless, now is the time to review the 2014 data reported under your name – and if necessary, initiate a dispute – before the information is posted publicly on June 30.

A quick review: The Sunshine Act, known officially as the “Open Payments Program,” requires all manufacturers of drugs, devices, and medical supplies covered by federal health care programs to report to the Centers for Medicare & Medicaid Services any financial interactions with physicians and teaching hospitals.

Reportable interactions include consulting, food, ownership or investment interest, direct compensation for speakers at education programs, and research. Compensation for clinical trials must be reported but is not made public until the product receives FDA approval, or until 4 years after the payment, whichever is earlier. Payments for trials involving a new indication for an approved drug are posted the following year.

Exemptions include CME activities funded by manufacturers and product samples for patient use. Medical students and residents are exempted entirely.

You are allowed to review your data and request corrections before information is posted publicly. You will have an additional 2 years to pursue corrections after the content goes live at the end of June, but any erroneous information will remain online until the next scheduled update, so you should find and fix errors as promptly as possible.

If you don’t see drug reps, accept sponsored lunches, or give sponsored talks, don’t assume that you won’t be on the website. Check anyway: You might be indirectly involved in a compensation that you were not aware of, or you might have been reported in error.

To review your data, register at the CMS Enterprise Portal (https://portal.cms.gov/wps/portal/unauthportal/home/) and request access to the Open Payments system.

The question remains as to what effect the law might be having on research, continuing education, or physicians’ relationships with the pharmaceutical industry. The short answer is that no one knows. The first data posting this past September came and went with little fanfare, and no repercussions directly attributable to the program have been reported as of this writing.

Sunshine laws have been in effect for several years in six states: California, Colorado, Massachusetts, Minnesota, Vermont, and West Virginia, plus the District of Columbia. (Maine repealed its law in 2011.) Observers disagree on their impact. Studies in Maine and West Virginia showed no significant public reaction or changes in prescribing patterns, according to a 2012 article in the Archives of Internal Medicine (now JAMA Internal Medicine).

Reactions from the public are equally inscrutable. Do citizens think less of doctors who accept the occasional industry-sponsored lunch for their employees? Do they think more of doctors who speak at meetings, or conduct industry-sponsored clinical research? There are no objective data. Anecdotally, I haven’t heard a peep – positive, negative, or indifferent – from any of my patients, nor have any other physicians that I’ve asked.

As of now, I stand by my initial prediction that attorneys, activists, and the occasional reporter will data-mine the information for various purposes, but few patients will bother to visit. Of course, that doesn’t mean you should ignore it as well. As always, I suggest you review the accuracy of anything posted about you, in any form or context, on any venue. This year’s data (reflecting all 2014 reports) have been available for review since April 6. You can initiate a dispute at any time over the next 2 years, before or after public release on June 30, but the sooner the better. Corrections are made each time CMS updates the system.

Maintaining accurate financial records has always been important, but it will be even more important now to support your disputes. CMS won’t simply take your word for it. A free app is available to help you track payments and other reportable industry interactions; search for “Open Payments” at your favorite app store.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News.

Woman on a scale

Researchers have identified several factors that may influence the risk of obesity in childhood cancer survivors.

Previous research showed that obesity rates are elevated in childhood cancer survivors who were exposed to cranial radiation.

But the new study has shown that other types of treatment, a patient’s age, and certain genetic variants are associated with obesity in this population.

Carmen Wilson, PhD, of St. Jude Children’s Research Hospital in Memphis, Tennessee, and her colleagues reported these findings in Cancer.

The researchers evaluated 1,996 childhood cancer survivors treated at St. Jude. The patients’ median age at diagnosis was 7.2 years (range, 0.1-24.8), and their median age at follow-up was 32.4 years (range, 18.9-63.8).

At the time of evaluation, 645 patients (32.3%) were of normal weight, 71 (3.6%) were underweight, 556 (27.9%) were overweight, and 723 (36.2%) were obese.

The prevalence of obesity was highest in male leukemia survivors (42.5%) and females who survived neuroblastoma (43.6%), followed closely by those who survived leukemia (43.1%).

Multivariable analyses showed that 3 factors were independently associated with an increased risk of obesity: older age at the time of evaluation (≥30 years vs <30 years; P<0.001), undergoing cranial radiation (P<0.001), and receiving glucocorticoids (P=0.004).

On the other hand, receiving chest, abdominal, or pelvic radiation was associated with a decreased risk of obesity (P<0.001).

The researchers also identified 166 single nucleotide polymorphisms that were associated with obesity among cancer survivors who had received cranial radiation. The strongest association was in variants of genes involved in neuron growth, repair, and connectivity.

Among survivors who did not receive cranial radiation, only 1 single nucleotide polymorphism—rs12073359, located on chromosome 1—was associated with an increased risk of obesity.

Dr Wilson said these findings might help us identify the childhood cancer survivors who are most likely to become obese. The results may also provide a foundation for future research efforts aimed at characterizing molecular pathways involved in the link between childhood cancer treatment and obesity.

Woman on a scale

Researchers have identified several factors that may influence the risk of obesity in childhood cancer survivors.

Previous research showed that obesity rates are elevated in childhood cancer survivors who were exposed to cranial radiation.

But the new study has shown that other types of treatment, a patient’s age, and certain genetic variants are associated with obesity in this population.

Carmen Wilson, PhD, of St. Jude Children’s Research Hospital in Memphis, Tennessee, and her colleagues reported these findings in Cancer.

The researchers evaluated 1,996 childhood cancer survivors treated at St. Jude. The patients’ median age at diagnosis was 7.2 years (range, 0.1-24.8), and their median age at follow-up was 32.4 years (range, 18.9-63.8).

At the time of evaluation, 645 patients (32.3%) were of normal weight, 71 (3.6%) were underweight, 556 (27.9%) were overweight, and 723 (36.2%) were obese.

The prevalence of obesity was highest in male leukemia survivors (42.5%) and females who survived neuroblastoma (43.6%), followed closely by those who survived leukemia (43.1%).

Multivariable analyses showed that 3 factors were independently associated with an increased risk of obesity: older age at the time of evaluation (≥30 years vs <30 years; P<0.001), undergoing cranial radiation (P<0.001), and receiving glucocorticoids (P=0.004).

On the other hand, receiving chest, abdominal, or pelvic radiation was associated with a decreased risk of obesity (P<0.001).

The researchers also identified 166 single nucleotide polymorphisms that were associated with obesity among cancer survivors who had received cranial radiation. The strongest association was in variants of genes involved in neuron growth, repair, and connectivity.

Among survivors who did not receive cranial radiation, only 1 single nucleotide polymorphism—rs12073359, located on chromosome 1—was associated with an increased risk of obesity.

Dr Wilson said these findings might help us identify the childhood cancer survivors who are most likely to become obese. The results may also provide a foundation for future research efforts aimed at characterizing molecular pathways involved in the link between childhood cancer treatment and obesity.

Woman on a scale

Researchers have identified several factors that may influence the risk of obesity in childhood cancer survivors.

Previous research showed that obesity rates are elevated in childhood cancer survivors who were exposed to cranial radiation.

But the new study has shown that other types of treatment, a patient’s age, and certain genetic variants are associated with obesity in this population.

Carmen Wilson, PhD, of St. Jude Children’s Research Hospital in Memphis, Tennessee, and her colleagues reported these findings in Cancer.

The researchers evaluated 1,996 childhood cancer survivors treated at St. Jude. The patients’ median age at diagnosis was 7.2 years (range, 0.1-24.8), and their median age at follow-up was 32.4 years (range, 18.9-63.8).

At the time of evaluation, 645 patients (32.3%) were of normal weight, 71 (3.6%) were underweight, 556 (27.9%) were overweight, and 723 (36.2%) were obese.

The prevalence of obesity was highest in male leukemia survivors (42.5%) and females who survived neuroblastoma (43.6%), followed closely by those who survived leukemia (43.1%).

Multivariable analyses showed that 3 factors were independently associated with an increased risk of obesity: older age at the time of evaluation (≥30 years vs <30 years; P<0.001), undergoing cranial radiation (P<0.001), and receiving glucocorticoids (P=0.004).

On the other hand, receiving chest, abdominal, or pelvic radiation was associated with a decreased risk of obesity (P<0.001).

The researchers also identified 166 single nucleotide polymorphisms that were associated with obesity among cancer survivors who had received cranial radiation. The strongest association was in variants of genes involved in neuron growth, repair, and connectivity.

Among survivors who did not receive cranial radiation, only 1 single nucleotide polymorphism—rs12073359, located on chromosome 1—was associated with an increased risk of obesity.

Dr Wilson said these findings might help us identify the childhood cancer survivors who are most likely to become obese. The results may also provide a foundation for future research efforts aimed at characterizing molecular pathways involved in the link between childhood cancer treatment and obesity.

Pill production

Photo courtesy of the FDA

The antimalarial drug chloroquine is not currently available from US suppliers, according to the Centers for Disease Control and Prevention (CDC).

The agency said it will provide updates as more information becomes available from the Food and Drug Administration.

Chloroquine is used as malaria treatment and prophylaxis, but hydroxychloroquine sulfate can be prescribed in place of chloroquine when indicated.

Healthcare providers who need assistance diagnosing or managing suspected or confirmed cases of malaria can call the CDC Malaria Hotline at 1-855-856-4713 (Monday through Friday, 9 am to 5pm, Eastern time).

For emergency consultation after hours, providers can call 1-770-488-7100 and ask to speak with a CDC Malaria Branch clinician.

Pill production

Photo courtesy of the FDA

The antimalarial drug chloroquine is not currently available from US suppliers, according to the Centers for Disease Control and Prevention (CDC).

The agency said it will provide updates as more information becomes available from the Food and Drug Administration.

Chloroquine is used as malaria treatment and prophylaxis, but hydroxychloroquine sulfate can be prescribed in place of chloroquine when indicated.

Healthcare providers who need assistance diagnosing or managing suspected or confirmed cases of malaria can call the CDC Malaria Hotline at 1-855-856-4713 (Monday through Friday, 9 am to 5pm, Eastern time).

For emergency consultation after hours, providers can call 1-770-488-7100 and ask to speak with a CDC Malaria Branch clinician.

Pill production

Photo courtesy of the FDA

The antimalarial drug chloroquine is not currently available from US suppliers, according to the Centers for Disease Control and Prevention (CDC).

The agency said it will provide updates as more information becomes available from the Food and Drug Administration.

Chloroquine is used as malaria treatment and prophylaxis, but hydroxychloroquine sulfate can be prescribed in place of chloroquine when indicated.

Healthcare providers who need assistance diagnosing or managing suspected or confirmed cases of malaria can call the CDC Malaria Hotline at 1-855-856-4713 (Monday through Friday, 9 am to 5pm, Eastern time).

For emergency consultation after hours, providers can call 1-770-488-7100 and ask to speak with a CDC Malaria Branch clinician.

CHICAGO – Adult survivors of childhood burns have significantly higher rates of Axis I mental and physical disorders years after their injury, a population-based study shows.

“We think it is really important to screen for, identify, and treat these illnesses not only in that acute period and shortly after the burn injury, but well into adulthood,” study author James Stone said at the annual meeting of the American Burn Association.

Patrice Wendling/Frontline Medical News

He reported on 745 adult burn survivors identified using administrative data from a regional pediatric burn center registry in Manitoba, Canada, who were matched 1:5 with 3,725 controls from the general Manitoba population based on age, sex, and geographic location. The burn survivors had an average age of 5.9 years at the time of burn injury, burns involved an average 12% of total body surface area, and 65% of burn survivors were male. The average follow-up was nearly 15 years (range 2.8-24.7 years).

In unadjusted univariate analysis, adult survivors had significantly higher rates than matched controls for any lifetime physical disorder (rate ratio, 1.17), arthritis (RR, 1.23), cancer (RR, 1.94), diabetes (RR, 1.69), fractures (RR, 1.45), and total respiratory morbidity (RR, 1.15).

After adjustment for gender, geography, and income, any physical disorder (RR, 1.15; P value < .01), arthritis (RR, 1.24; P < .01), fractures (RR, 1.37; P .001), and total respiratory morbidity (RR, 1.13; P < .05) remained significant, Mr. Stone, from the University of Manitoba, Winnipeg, Canada, reported.

Further, 81% of burn survivors had a lifetime physical illness compared with 69% of controls.

“The fact that 81% of our burn cohort was diagnosed with a physical illness is definitely concerning,” he said. “We hypothesize that the prolonged hyperinflammatory and hypermetabolic state that has been previously reported makes these individuals more susceptible to these illnesses down the road.”

The burn cohort also had significantly higher unadjusted rate ratios for any Axis 1 mental disorder (RR, 1.62), major depressive disorder (RR, 1.64), anxiety (RR, 1.57), substance abuse (RR, 2.86), and suicide attempts (RR, 5.00).

All disorders remained statistically significant after adjustment with rate ratios of 1.54 (P < .001), 1.54 (P < .001), 1.50 (P < .001), 2.35 (P < .001), and 4.33 (P < .01), respectively.

The high rates of substance abuse and suicide attempts are consistent with previous clinical interview studies, but are still cause for great concern, Mr. Stone said.

The risk for any mental or physical disorder was not significantly impacted by burn location or by burns that affected more than 30% of total body surface area. Age older than 5 years at the time of the burn significantly increased the risk of any mental disorder (relative risk, 1.92; P < .001).

Limitations of the study include the potential for bias because the data relied on individuals presenting to physicians, discrepancies between ICD codes for physician billings and hospital claims, and some survivors may have moved out of the province, Mr. Stone said. The study, however, had a sample size three times greater than the next largest study of its kind, and importantly, matched burn patients to the general population.

[email protected]

CHICAGO – Adult survivors of childhood burns have significantly higher rates of Axis I mental and physical disorders years after their injury, a population-based study shows.

“We think it is really important to screen for, identify, and treat these illnesses not only in that acute period and shortly after the burn injury, but well into adulthood,” study author James Stone said at the annual meeting of the American Burn Association.

Patrice Wendling/Frontline Medical News

He reported on 745 adult burn survivors identified using administrative data from a regional pediatric burn center registry in Manitoba, Canada, who were matched 1:5 with 3,725 controls from the general Manitoba population based on age, sex, and geographic location. The burn survivors had an average age of 5.9 years at the time of burn injury, burns involved an average 12% of total body surface area, and 65% of burn survivors were male. The average follow-up was nearly 15 years (range 2.8-24.7 years).

In unadjusted univariate analysis, adult survivors had significantly higher rates than matched controls for any lifetime physical disorder (rate ratio, 1.17), arthritis (RR, 1.23), cancer (RR, 1.94), diabetes (RR, 1.69), fractures (RR, 1.45), and total respiratory morbidity (RR, 1.15).

After adjustment for gender, geography, and income, any physical disorder (RR, 1.15; P value < .01), arthritis (RR, 1.24; P < .01), fractures (RR, 1.37; P .001), and total respiratory morbidity (RR, 1.13; P < .05) remained significant, Mr. Stone, from the University of Manitoba, Winnipeg, Canada, reported.

Further, 81% of burn survivors had a lifetime physical illness compared with 69% of controls.

“The fact that 81% of our burn cohort was diagnosed with a physical illness is definitely concerning,” he said. “We hypothesize that the prolonged hyperinflammatory and hypermetabolic state that has been previously reported makes these individuals more susceptible to these illnesses down the road.”

The burn cohort also had significantly higher unadjusted rate ratios for any Axis 1 mental disorder (RR, 1.62), major depressive disorder (RR, 1.64), anxiety (RR, 1.57), substance abuse (RR, 2.86), and suicide attempts (RR, 5.00).

All disorders remained statistically significant after adjustment with rate ratios of 1.54 (P < .001), 1.54 (P < .001), 1.50 (P < .001), 2.35 (P < .001), and 4.33 (P < .01), respectively.

The high rates of substance abuse and suicide attempts are consistent with previous clinical interview studies, but are still cause for great concern, Mr. Stone said.

The risk for any mental or physical disorder was not significantly impacted by burn location or by burns that affected more than 30% of total body surface area. Age older than 5 years at the time of the burn significantly increased the risk of any mental disorder (relative risk, 1.92; P < .001).

Limitations of the study include the potential for bias because the data relied on individuals presenting to physicians, discrepancies between ICD codes for physician billings and hospital claims, and some survivors may have moved out of the province, Mr. Stone said. The study, however, had a sample size three times greater than the next largest study of its kind, and importantly, matched burn patients to the general population.

[email protected]

CHICAGO – Adult survivors of childhood burns have significantly higher rates of Axis I mental and physical disorders years after their injury, a population-based study shows.

“We think it is really important to screen for, identify, and treat these illnesses not only in that acute period and shortly after the burn injury, but well into adulthood,” study author James Stone said at the annual meeting of the American Burn Association.

Patrice Wendling/Frontline Medical News

He reported on 745 adult burn survivors identified using administrative data from a regional pediatric burn center registry in Manitoba, Canada, who were matched 1:5 with 3,725 controls from the general Manitoba population based on age, sex, and geographic location. The burn survivors had an average age of 5.9 years at the time of burn injury, burns involved an average 12% of total body surface area, and 65% of burn survivors were male. The average follow-up was nearly 15 years (range 2.8-24.7 years).

In unadjusted univariate analysis, adult survivors had significantly higher rates than matched controls for any lifetime physical disorder (rate ratio, 1.17), arthritis (RR, 1.23), cancer (RR, 1.94), diabetes (RR, 1.69), fractures (RR, 1.45), and total respiratory morbidity (RR, 1.15).

After adjustment for gender, geography, and income, any physical disorder (RR, 1.15; P value < .01), arthritis (RR, 1.24; P < .01), fractures (RR, 1.37; P .001), and total respiratory morbidity (RR, 1.13; P < .05) remained significant, Mr. Stone, from the University of Manitoba, Winnipeg, Canada, reported.

Further, 81% of burn survivors had a lifetime physical illness compared with 69% of controls.

“The fact that 81% of our burn cohort was diagnosed with a physical illness is definitely concerning,” he said. “We hypothesize that the prolonged hyperinflammatory and hypermetabolic state that has been previously reported makes these individuals more susceptible to these illnesses down the road.”

The burn cohort also had significantly higher unadjusted rate ratios for any Axis 1 mental disorder (RR, 1.62), major depressive disorder (RR, 1.64), anxiety (RR, 1.57), substance abuse (RR, 2.86), and suicide attempts (RR, 5.00).

All disorders remained statistically significant after adjustment with rate ratios of 1.54 (P < .001), 1.54 (P < .001), 1.50 (P < .001), 2.35 (P < .001), and 4.33 (P < .01), respectively.

The high rates of substance abuse and suicide attempts are consistent with previous clinical interview studies, but are still cause for great concern, Mr. Stone said.

The risk for any mental or physical disorder was not significantly impacted by burn location or by burns that affected more than 30% of total body surface area. Age older than 5 years at the time of the burn significantly increased the risk of any mental disorder (relative risk, 1.92; P < .001).

Limitations of the study include the potential for bias because the data relied on individuals presenting to physicians, discrepancies between ICD codes for physician billings and hospital claims, and some survivors may have moved out of the province, Mr. Stone said. The study, however, had a sample size three times greater than the next largest study of its kind, and importantly, matched burn patients to the general population.

[email protected]

Acute hepatitis C virus infections more than tripled among young people in Kentucky, Tennessee, Virginia, and West Virginia between 2006 and 2012, investigators reported online May 8 in Morbidity and Mortality Weekly Report.

“The increase in acute HCV infections in central Appalachia is highly correlated with the region’s epidemic of prescription opioid abuse and facilitated by an upsurge in the number of persons who inject drugs,” said Dr. Jon Zibbell at the Centers for Disease Control and Prevention and his associates.

Nationally, acute HCV infections have risen most steeply in states east of the Mississippi. To further explore the trend, the researchers examined HCV case data from the National Notifiable Disease Surveillance System, and data on 217,789 admissions to substance abuse treatment centers related to opioid or injection drug abuse (MMWR 2015;64:453-8).

Confirmed HCV cases among individuals aged 30 years and younger rose by 364% in the four Appalachian states during 2006-2012, the investigators found. “The increasing incidence among nonurban residents was at least double that of urban residents each year,” they said. Among patients with known risk factors for HCV infection, 73% reported injection drug use.

During the same time, treatment admissions for opioid dependency among individuals aged 12-29 years rose by 21% in the four states, and self-reported injection drug use rose by more than 12%, the researchers said. “Evidence-based strategies as well as integrated-service provision are urgently needed in drug treatment programs to ensure patients are tested for HCV, and persons found to be HCV infected are linked to care and receive appropriate treatment,” they concluded. “These efforts will require further collaboration among federal partners and state and local health departments to better address the syndemic of opioid abuse and HCV infection.”

The investigators declared no funding sources or financial conflicts of interest.

Acute hepatitis C virus infections more than tripled among young people in Kentucky, Tennessee, Virginia, and West Virginia between 2006 and 2012, investigators reported online May 8 in Morbidity and Mortality Weekly Report.

“The increase in acute HCV infections in central Appalachia is highly correlated with the region’s epidemic of prescription opioid abuse and facilitated by an upsurge in the number of persons who inject drugs,” said Dr. Jon Zibbell at the Centers for Disease Control and Prevention and his associates.

Nationally, acute HCV infections have risen most steeply in states east of the Mississippi. To further explore the trend, the researchers examined HCV case data from the National Notifiable Disease Surveillance System, and data on 217,789 admissions to substance abuse treatment centers related to opioid or injection drug abuse (MMWR 2015;64:453-8).

Confirmed HCV cases among individuals aged 30 years and younger rose by 364% in the four Appalachian states during 2006-2012, the investigators found. “The increasing incidence among nonurban residents was at least double that of urban residents each year,” they said. Among patients with known risk factors for HCV infection, 73% reported injection drug use.

During the same time, treatment admissions for opioid dependency among individuals aged 12-29 years rose by 21% in the four states, and self-reported injection drug use rose by more than 12%, the researchers said. “Evidence-based strategies as well as integrated-service provision are urgently needed in drug treatment programs to ensure patients are tested for HCV, and persons found to be HCV infected are linked to care and receive appropriate treatment,” they concluded. “These efforts will require further collaboration among federal partners and state and local health departments to better address the syndemic of opioid abuse and HCV infection.”

The investigators declared no funding sources or financial conflicts of interest.

Acute hepatitis C virus infections more than tripled among young people in Kentucky, Tennessee, Virginia, and West Virginia between 2006 and 2012, investigators reported online May 8 in Morbidity and Mortality Weekly Report.

“The increase in acute HCV infections in central Appalachia is highly correlated with the region’s epidemic of prescription opioid abuse and facilitated by an upsurge in the number of persons who inject drugs,” said Dr. Jon Zibbell at the Centers for Disease Control and Prevention and his associates.

Nationally, acute HCV infections have risen most steeply in states east of the Mississippi. To further explore the trend, the researchers examined HCV case data from the National Notifiable Disease Surveillance System, and data on 217,789 admissions to substance abuse treatment centers related to opioid or injection drug abuse (MMWR 2015;64:453-8).

Confirmed HCV cases among individuals aged 30 years and younger rose by 364% in the four Appalachian states during 2006-2012, the investigators found. “The increasing incidence among nonurban residents was at least double that of urban residents each year,” they said. Among patients with known risk factors for HCV infection, 73% reported injection drug use.

During the same time, treatment admissions for opioid dependency among individuals aged 12-29 years rose by 21% in the four states, and self-reported injection drug use rose by more than 12%, the researchers said. “Evidence-based strategies as well as integrated-service provision are urgently needed in drug treatment programs to ensure patients are tested for HCV, and persons found to be HCV infected are linked to care and receive appropriate treatment,” they concluded. “These efforts will require further collaboration among federal partners and state and local health departments to better address the syndemic of opioid abuse and HCV infection.”

The investigators declared no funding sources or financial conflicts of interest.

How often have nonphysicians told you that they could never work the hours you do?

Most people think physicians are a unique breed, and in some respects, we are. But in important ways we are just like everyone else. When we work long hours under stressful conditions and go without adequate sleep or nourishment, we cannot function at peak performance. Just like everyone else, we can become irritable, grumpy, and cynical when our basic needs are not met. We are human too, and we are at higher risk than most people for burnout, depression, and even suicide.

An article in the Journal of Hospital Medicine in 2014 noted that slightly over 50% of hospitalists were affected by burnout. We scored high on the emotional exhaustion subscale, and 40.3% of us had symptoms of depression, with a surprising 9.2% rate of recent suicidality. Hospital medicine definitely has its advantages over many other fields of medicine, but as this study demonstrates, there is still much to be desired in our “work-life balance.”

Each practice has its own perks and negatives, and what will enhance the lives of hospitalists in one group may make intolerable the lives of members of another group. For instance, it is no surprise that 12-hour shifts with 7-on, 7-off block scheduling can be exhausting. If you have a family, this schedule leaves plenty of fun time on the weeks you are off, but you may still be missing 50% of your family’s life if you leave for work before your kids wake up and return after they go to bed.

Whatever your concerns and stressors may be, rest assured, you are not alone, and if enough of the members of your group have similar issues, you may be successful addressing them with your director or hospital administrator. Retaining good hospitalists is vital to the financial success of many hospitals, and being flexible enough to truly meet their reasonable needs can literally make or break a hospitalist team.

How often have nonphysicians told you that they could never work the hours you do?

Most people think physicians are a unique breed, and in some respects, we are. But in important ways we are just like everyone else. When we work long hours under stressful conditions and go without adequate sleep or nourishment, we cannot function at peak performance. Just like everyone else, we can become irritable, grumpy, and cynical when our basic needs are not met. We are human too, and we are at higher risk than most people for burnout, depression, and even suicide.

An article in the Journal of Hospital Medicine in 2014 noted that slightly over 50% of hospitalists were affected by burnout. We scored high on the emotional exhaustion subscale, and 40.3% of us had symptoms of depression, with a surprising 9.2% rate of recent suicidality. Hospital medicine definitely has its advantages over many other fields of medicine, but as this study demonstrates, there is still much to be desired in our “work-life balance.”

Each practice has its own perks and negatives, and what will enhance the lives of hospitalists in one group may make intolerable the lives of members of another group. For instance, it is no surprise that 12-hour shifts with 7-on, 7-off block scheduling can be exhausting. If you have a family, this schedule leaves plenty of fun time on the weeks you are off, but you may still be missing 50% of your family’s life if you leave for work before your kids wake up and return after they go to bed.

Whatever your concerns and stressors may be, rest assured, you are not alone, and if enough of the members of your group have similar issues, you may be successful addressing them with your director or hospital administrator. Retaining good hospitalists is vital to the financial success of many hospitals, and being flexible enough to truly meet their reasonable needs can literally make or break a hospitalist team.

How often have nonphysicians told you that they could never work the hours you do?

Most people think physicians are a unique breed, and in some respects, we are. But in important ways we are just like everyone else. When we work long hours under stressful conditions and go without adequate sleep or nourishment, we cannot function at peak performance. Just like everyone else, we can become irritable, grumpy, and cynical when our basic needs are not met. We are human too, and we are at higher risk than most people for burnout, depression, and even suicide.

An article in the Journal of Hospital Medicine in 2014 noted that slightly over 50% of hospitalists were affected by burnout. We scored high on the emotional exhaustion subscale, and 40.3% of us had symptoms of depression, with a surprising 9.2% rate of recent suicidality. Hospital medicine definitely has its advantages over many other fields of medicine, but as this study demonstrates, there is still much to be desired in our “work-life balance.”

Each practice has its own perks and negatives, and what will enhance the lives of hospitalists in one group may make intolerable the lives of members of another group. For instance, it is no surprise that 12-hour shifts with 7-on, 7-off block scheduling can be exhausting. If you have a family, this schedule leaves plenty of fun time on the weeks you are off, but you may still be missing 50% of your family’s life if you leave for work before your kids wake up and return after they go to bed.

Whatever your concerns and stressors may be, rest assured, you are not alone, and if enough of the members of your group have similar issues, you may be successful addressing them with your director or hospital administrator. Retaining good hospitalists is vital to the financial success of many hospitals, and being flexible enough to truly meet their reasonable needs can literally make or break a hospitalist team.

A gametocyte-infected red

blood cell that has stiffened

after treatment

© 2015 Ramdani et al.

The erectile dysfunction drug sildenafil (Viagra) could prevent transmission of the malaria parasite, according to research published in PLOS Pathogens.

Investigators found that sildenafil increases the stiffness of erythrocytes infected by the parasite Plasmodium falciparum.

This allows the cells to be eliminated from the bloodstream and may therefore reduce transmission of the malaria parasite from humans to mosquitoes.

The investigators noted that P falciparum has a complex developmental cycle that is completed partly in humans and partly in mosquitoes. Treatments for malaria target the asexual forms of this parasite that cause symptoms, but not the sexual forms transmitted from a human to a mosquito.

Malaria eradication therefore necessitates new types of treatments against sexual forms of the parasite in order to block transmission and prevent dissemination of the disease.

The sexual forms of P falciparum develop in human erythrocytes sequestered in the bone marrow before they are released into the blood. They are then accessible to mosquitoes, which can ingest them when they bite.

Circulating erythrocytes are deformable, thus preventing their clearance via the spleen. And gametocyte-infected erythrocytes can easily pass through the spleen and persist for several days in the blood circulation.

With this in mind, Ghania Ramdani, of Université Paris Descartes in France, and colleagues sought to stiffen the infected erythrocytes so they would be removed from circulation.

The team found that the deformability of gametocyte-infected erythrocytes is regulated by a signaling pathway that involves cAMP. When cAMP molecules accumulate, an erythrocyte becomes stiffer. And cAMP is degraded by the enzyme phosphodiesterase, which promotes erythrocyte deformability.

Using an in vitro model reproducing filtration by the spleen, the investigators were able to identify several pharmacological agents that inhibit phosophodiesterases and can therefore increase the stiffness of infected erythrocytes.

One of these agents is sildenafil. The team showed that a standard dose of the drug had the potential to increase the stiffness of sexual forms of the parasite and therefore favor the elimination of infected erythrocytes from the circulation.

This discovery could lead to new ways to stop the spread of malaria, the investigators said. They believe that modifying the active substance in sildenafil to block its erectile effect, or testing similar agents devoid of this effect, could indeed result in a treatment to prevent transmission of the parasite from humans to mosquitoes.

A gametocyte-infected red

blood cell that has stiffened

after treatment

© 2015 Ramdani et al.

The erectile dysfunction drug sildenafil (Viagra) could prevent transmission of the malaria parasite, according to research published in PLOS Pathogens.

Investigators found that sildenafil increases the stiffness of erythrocytes infected by the parasite Plasmodium falciparum.

This allows the cells to be eliminated from the bloodstream and may therefore reduce transmission of the malaria parasite from humans to mosquitoes.

The investigators noted that P falciparum has a complex developmental cycle that is completed partly in humans and partly in mosquitoes. Treatments for malaria target the asexual forms of this parasite that cause symptoms, but not the sexual forms transmitted from a human to a mosquito.

Malaria eradication therefore necessitates new types of treatments against sexual forms of the parasite in order to block transmission and prevent dissemination of the disease.

The sexual forms of P falciparum develop in human erythrocytes sequestered in the bone marrow before they are released into the blood. They are then accessible to mosquitoes, which can ingest them when they bite.

Circulating erythrocytes are deformable, thus preventing their clearance via the spleen. And gametocyte-infected erythrocytes can easily pass through the spleen and persist for several days in the blood circulation.

With this in mind, Ghania Ramdani, of Université Paris Descartes in France, and colleagues sought to stiffen the infected erythrocytes so they would be removed from circulation.

The team found that the deformability of gametocyte-infected erythrocytes is regulated by a signaling pathway that involves cAMP. When cAMP molecules accumulate, an erythrocyte becomes stiffer. And cAMP is degraded by the enzyme phosphodiesterase, which promotes erythrocyte deformability.

Using an in vitro model reproducing filtration by the spleen, the investigators were able to identify several pharmacological agents that inhibit phosophodiesterases and can therefore increase the stiffness of infected erythrocytes.

One of these agents is sildenafil. The team showed that a standard dose of the drug had the potential to increase the stiffness of sexual forms of the parasite and therefore favor the elimination of infected erythrocytes from the circulation.

This discovery could lead to new ways to stop the spread of malaria, the investigators said. They believe that modifying the active substance in sildenafil to block its erectile effect, or testing similar agents devoid of this effect, could indeed result in a treatment to prevent transmission of the parasite from humans to mosquitoes.

A gametocyte-infected red

blood cell that has stiffened

after treatment

© 2015 Ramdani et al.

The erectile dysfunction drug sildenafil (Viagra) could prevent transmission of the malaria parasite, according to research published in PLOS Pathogens.

Investigators found that sildenafil increases the stiffness of erythrocytes infected by the parasite Plasmodium falciparum.

This allows the cells to be eliminated from the bloodstream and may therefore reduce transmission of the malaria parasite from humans to mosquitoes.

The investigators noted that P falciparum has a complex developmental cycle that is completed partly in humans and partly in mosquitoes. Treatments for malaria target the asexual forms of this parasite that cause symptoms, but not the sexual forms transmitted from a human to a mosquito.

Malaria eradication therefore necessitates new types of treatments against sexual forms of the parasite in order to block transmission and prevent dissemination of the disease.

The sexual forms of P falciparum develop in human erythrocytes sequestered in the bone marrow before they are released into the blood. They are then accessible to mosquitoes, which can ingest them when they bite.

Circulating erythrocytes are deformable, thus preventing their clearance via the spleen. And gametocyte-infected erythrocytes can easily pass through the spleen and persist for several days in the blood circulation.

With this in mind, Ghania Ramdani, of Université Paris Descartes in France, and colleagues sought to stiffen the infected erythrocytes so they would be removed from circulation.

The team found that the deformability of gametocyte-infected erythrocytes is regulated by a signaling pathway that involves cAMP. When cAMP molecules accumulate, an erythrocyte becomes stiffer. And cAMP is degraded by the enzyme phosphodiesterase, which promotes erythrocyte deformability.

Using an in vitro model reproducing filtration by the spleen, the investigators were able to identify several pharmacological agents that inhibit phosophodiesterases and can therefore increase the stiffness of infected erythrocytes.

One of these agents is sildenafil. The team showed that a standard dose of the drug had the potential to increase the stiffness of sexual forms of the parasite and therefore favor the elimination of infected erythrocytes from the circulation.

This discovery could lead to new ways to stop the spread of malaria, the investigators said. They believe that modifying the active substance in sildenafil to block its erectile effect, or testing similar agents devoid of this effect, could indeed result in a treatment to prevent transmission of the parasite from humans to mosquitoes.

I freely admit I am obsessed with research articles about eating habits. I hold out hope that this will eventually unlock the magic bullet to cure us of the modern plague of obesity. At a certain level, our patients need us to be captivated by such literature. We should feel fairly comfortable with the common knowledge that diets are effective if you stay on them and reducing the caloric density of foods can result in meaningful weight loss.

But what about how quickly we eat? In our fast-paced, heavily caffeinated society, we seem to shovel rather than chew. Ever since I was a medical resident, I have practically inhaled my food. Perchance I am operating under the erroneous and illogical assumption that if I don’t taste the food it won’t register as calories. True science has now enlightened me to the error in my thinking.

Dr. Eric Robinson and his colleagues conducted a brilliant systematic review of the impact of eating rate on energy intake and hunger (Am. J. Clin. Nutr. 2014;100:123-51). They included studies for which there was at least one study arm in which participants ate a meal at a statistically significant slower rate than that of a different arm. Twenty-two studies met the criteria for inclusion.

Available evidence suggests that a slower eating rate is associated with lower intake, compared with faster eating. The effect on caloric intake was observed regardless of the intervention used to modify the eating rate, such as modifying food from soft (fast rate) to hard (slow rate) or verbal instruction. No relationship was observed between eating rate and hunger at the end of the meal or several hours later.

Intriguing to me is the hypothesis that eating rate likely affects intake through the duration and intensity of oral exposure to taste. Previous studies have shown that, when eating rate is held constant, increasing sensory exposure leads to a lower energy intake. This seems to relate to our innate wiring that gives us a “sensory specific satiety.” In my understanding, sensory specific satiety turns off appetitive drive when you have had too much chocolate or too many potato chips and you feel slightly ill. Unfortunately, the food industry is on to this game and they have designed foods to be perfectly balanced to not render satiety. These foods can tragically be eaten ceaselessly.

Take-home message: If your patients cannot control the bad foods they eat, they should try to eat them more slowly.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

I freely admit I am obsessed with research articles about eating habits. I hold out hope that this will eventually unlock the magic bullet to cure us of the modern plague of obesity. At a certain level, our patients need us to be captivated by such literature. We should feel fairly comfortable with the common knowledge that diets are effective if you stay on them and reducing the caloric density of foods can result in meaningful weight loss.

But what about how quickly we eat? In our fast-paced, heavily caffeinated society, we seem to shovel rather than chew. Ever since I was a medical resident, I have practically inhaled my food. Perchance I am operating under the erroneous and illogical assumption that if I don’t taste the food it won’t register as calories. True science has now enlightened me to the error in my thinking.

Dr. Eric Robinson and his colleagues conducted a brilliant systematic review of the impact of eating rate on energy intake and hunger (Am. J. Clin. Nutr. 2014;100:123-51). They included studies for which there was at least one study arm in which participants ate a meal at a statistically significant slower rate than that of a different arm. Twenty-two studies met the criteria for inclusion.

Available evidence suggests that a slower eating rate is associated with lower intake, compared with faster eating. The effect on caloric intake was observed regardless of the intervention used to modify the eating rate, such as modifying food from soft (fast rate) to hard (slow rate) or verbal instruction. No relationship was observed between eating rate and hunger at the end of the meal or several hours later.

Intriguing to me is the hypothesis that eating rate likely affects intake through the duration and intensity of oral exposure to taste. Previous studies have shown that, when eating rate is held constant, increasing sensory exposure leads to a lower energy intake. This seems to relate to our innate wiring that gives us a “sensory specific satiety.” In my understanding, sensory specific satiety turns off appetitive drive when you have had too much chocolate or too many potato chips and you feel slightly ill. Unfortunately, the food industry is on to this game and they have designed foods to be perfectly balanced to not render satiety. These foods can tragically be eaten ceaselessly.

Take-home message: If your patients cannot control the bad foods they eat, they should try to eat them more slowly.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.

I freely admit I am obsessed with research articles about eating habits. I hold out hope that this will eventually unlock the magic bullet to cure us of the modern plague of obesity. At a certain level, our patients need us to be captivated by such literature. We should feel fairly comfortable with the common knowledge that diets are effective if you stay on them and reducing the caloric density of foods can result in meaningful weight loss.

But what about how quickly we eat? In our fast-paced, heavily caffeinated society, we seem to shovel rather than chew. Ever since I was a medical resident, I have practically inhaled my food. Perchance I am operating under the erroneous and illogical assumption that if I don’t taste the food it won’t register as calories. True science has now enlightened me to the error in my thinking.

Dr. Eric Robinson and his colleagues conducted a brilliant systematic review of the impact of eating rate on energy intake and hunger (Am. J. Clin. Nutr. 2014;100:123-51). They included studies for which there was at least one study arm in which participants ate a meal at a statistically significant slower rate than that of a different arm. Twenty-two studies met the criteria for inclusion.

Available evidence suggests that a slower eating rate is associated with lower intake, compared with faster eating. The effect on caloric intake was observed regardless of the intervention used to modify the eating rate, such as modifying food from soft (fast rate) to hard (slow rate) or verbal instruction. No relationship was observed between eating rate and hunger at the end of the meal or several hours later.

Intriguing to me is the hypothesis that eating rate likely affects intake through the duration and intensity of oral exposure to taste. Previous studies have shown that, when eating rate is held constant, increasing sensory exposure leads to a lower energy intake. This seems to relate to our innate wiring that gives us a “sensory specific satiety.” In my understanding, sensory specific satiety turns off appetitive drive when you have had too much chocolate or too many potato chips and you feel slightly ill. Unfortunately, the food industry is on to this game and they have designed foods to be perfectly balanced to not render satiety. These foods can tragically be eaten ceaselessly.

Take-home message: If your patients cannot control the bad foods they eat, they should try to eat them more slowly.

Dr. Ebbert is professor of medicine, a general internist at the Mayo Clinic in Rochester, Minn., and a diplomate of the American Board of Addiction Medicine. The opinions expressed are those of the author and do not necessarily represent the views and opinions of the Mayo Clinic. The opinions expressed in this article should not be used to diagnose or treat any medical condition nor should they be used as a substitute for medical advice from a qualified, board-certified practicing clinician.