Hospitalist Ateev Mehrotra, MD, MPH, garnered an audience in Congress last month with his speech on telemedicine that called on lawmakers to take a deliberate approach to the healthcare strategy.

Dr. Mehrotra, a staff physician at Beth Israel Deaconess Medical Center in Boston and a policy analyst for RAND Corporation in Santa Monica, Calif., testified before a health subcommittee of the Energy & Commerce Committee[PDF]. He urged politicians to understand that telemedicine has immense potential but needs to be implemented deliberately to ensure that it provides quality care, improves access to those who need it most, and is used in the most cost-efficient manner.

He spoke with The Hospitalist after testifying:

Question: What do you hope the committee took away from your speech?

Answer: Go in with [your] eyes wide open. Experience tells us this is going to work in some ways and is not going to work in some ways. I think some people are naive and think telemedicine is perfect.

Q: Overutilization is a fear of yours. Tell me why.

A: For every great and remarkable intervention we have introduced in medicine, there has been this potential concern. I gave the example of cardiac catheterization, [which] has saved tens of thousands of lives probably. I can cite many other examples from MRIs to CTs [computed tomography] to robot-assisted surgery, etc., where that overuse issue is very significant. Economists believe [new technologies] are one of the greatest drivers of increased healthcare spending in the United States. With that as background, one shouldn’t be surprised that telemedicine would face the same issues.

Q: With a national push for telemedicine, is that overall a good thing?

A: Maybe I’m just too much of a doctor, but I think about this very much like I think about a drug. You have positive benefits, and you’ve got side effects. You need to be aware of the side effects … it doesn’t mean in many cases you don’t prescribe the drug because the drug is helping overall. If you take that same framework to telemedicine, I would say I’m overall very enthusiastic about the multitude of benefits … but not all telemedicine is the same. TH

Visit our website for more information on telemedicine and hospitalists.

Hospitalist Ateev Mehrotra, MD, MPH, garnered an audience in Congress last month with his speech on telemedicine that called on lawmakers to take a deliberate approach to the healthcare strategy.

Dr. Mehrotra, a staff physician at Beth Israel Deaconess Medical Center in Boston and a policy analyst for RAND Corporation in Santa Monica, Calif., testified before a health subcommittee of the Energy & Commerce Committee[PDF]. He urged politicians to understand that telemedicine has immense potential but needs to be implemented deliberately to ensure that it provides quality care, improves access to those who need it most, and is used in the most cost-efficient manner.

He spoke with The Hospitalist after testifying:

Question: What do you hope the committee took away from your speech?

Answer: Go in with [your] eyes wide open. Experience tells us this is going to work in some ways and is not going to work in some ways. I think some people are naive and think telemedicine is perfect.

Q: Overutilization is a fear of yours. Tell me why.

A: For every great and remarkable intervention we have introduced in medicine, there has been this potential concern. I gave the example of cardiac catheterization, [which] has saved tens of thousands of lives probably. I can cite many other examples from MRIs to CTs [computed tomography] to robot-assisted surgery, etc., where that overuse issue is very significant. Economists believe [new technologies] are one of the greatest drivers of increased healthcare spending in the United States. With that as background, one shouldn’t be surprised that telemedicine would face the same issues.

Q: With a national push for telemedicine, is that overall a good thing?

A: Maybe I’m just too much of a doctor, but I think about this very much like I think about a drug. You have positive benefits, and you’ve got side effects. You need to be aware of the side effects … it doesn’t mean in many cases you don’t prescribe the drug because the drug is helping overall. If you take that same framework to telemedicine, I would say I’m overall very enthusiastic about the multitude of benefits … but not all telemedicine is the same. TH

Visit our website for more information on telemedicine and hospitalists.

Hospitalist Ateev Mehrotra, MD, MPH, garnered an audience in Congress last month with his speech on telemedicine that called on lawmakers to take a deliberate approach to the healthcare strategy.

Dr. Mehrotra, a staff physician at Beth Israel Deaconess Medical Center in Boston and a policy analyst for RAND Corporation in Santa Monica, Calif., testified before a health subcommittee of the Energy & Commerce Committee[PDF]. He urged politicians to understand that telemedicine has immense potential but needs to be implemented deliberately to ensure that it provides quality care, improves access to those who need it most, and is used in the most cost-efficient manner.

He spoke with The Hospitalist after testifying:

Question: What do you hope the committee took away from your speech?

Answer: Go in with [your] eyes wide open. Experience tells us this is going to work in some ways and is not going to work in some ways. I think some people are naive and think telemedicine is perfect.

Q: Overutilization is a fear of yours. Tell me why.

A: For every great and remarkable intervention we have introduced in medicine, there has been this potential concern. I gave the example of cardiac catheterization, [which] has saved tens of thousands of lives probably. I can cite many other examples from MRIs to CTs [computed tomography] to robot-assisted surgery, etc., where that overuse issue is very significant. Economists believe [new technologies] are one of the greatest drivers of increased healthcare spending in the United States. With that as background, one shouldn’t be surprised that telemedicine would face the same issues.

Q: With a national push for telemedicine, is that overall a good thing?

A: Maybe I’m just too much of a doctor, but I think about this very much like I think about a drug. You have positive benefits, and you’ve got side effects. You need to be aware of the side effects … it doesn’t mean in many cases you don’t prescribe the drug because the drug is helping overall. If you take that same framework to telemedicine, I would say I’m overall very enthusiastic about the multitude of benefits … but not all telemedicine is the same. TH

Visit our website for more information on telemedicine and hospitalists.

As hospitalist workloads increase, so do hospital costs and patients' lengths of stay (LOS), according to findings in a recent study.

Those results, says SHM President Burke T. Kealey, MD, SFHM, provide a good starting point to determine an ideal patient census for hospitalists.

"Pushing hospitalist workloads ever higher to meet the demands of patient-care needs or flawed payment models has costs associated with it," says Dr. Kealey, associate medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn. "The costs may be borne by the system or by patients, but there are costs."

For the study published in JAMA Internal Medicine, researchers analyzed data from 20,241 hospitalizations involving 13,916 patients seen by hospitalists at the Christiana Care Health System in Newark, Del., between February 2008 and January 2011.

For hospital occupancies less than 75%, they found that LOS increased from 5.5 to 7.5 days as workload increased. For occupancies of 75% to 85%, LOS increased to about 8 days with higher workloads. For occupancies greater than 85%, the LOS decreased slightly and then increased significantly with higher workloads, with this change occurring at about 15 patients or more per hospitalist.

Costs were also significantly associated with an increase in workload. As the study notes, benchmark recommendations for an individual hospitalist’s workload range from 10 to 15 patient encounters per day.

Dr. Kealey says the findings seem to support the conventional wisdom that hospitalists should ideally see no more than 15 patients a day. He notes, however, that deciding the optimal number of cases for a given practice depends on several factors, including duration of shift, the availability of physician extenders, and the addition of surgical or cardiology cases.

"We won't be able as a specialty to fully realize our potential until we understand and apply the learnings about workload into our practices to ensure hospitalist career sustainability, system health, and best patient care," Dr. Kealey says. "This paper really gets the discussion going."

For more from Dr. Kealey on hospitalist workloads, read his recent blog post on "The Hospital Leader." TH

Visit our website for more information about hospitalist workloads.

As hospitalist workloads increase, so do hospital costs and patients' lengths of stay (LOS), according to findings in a recent study.

Those results, says SHM President Burke T. Kealey, MD, SFHM, provide a good starting point to determine an ideal patient census for hospitalists.

"Pushing hospitalist workloads ever higher to meet the demands of patient-care needs or flawed payment models has costs associated with it," says Dr. Kealey, associate medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn. "The costs may be borne by the system or by patients, but there are costs."

For the study published in JAMA Internal Medicine, researchers analyzed data from 20,241 hospitalizations involving 13,916 patients seen by hospitalists at the Christiana Care Health System in Newark, Del., between February 2008 and January 2011.

For hospital occupancies less than 75%, they found that LOS increased from 5.5 to 7.5 days as workload increased. For occupancies of 75% to 85%, LOS increased to about 8 days with higher workloads. For occupancies greater than 85%, the LOS decreased slightly and then increased significantly with higher workloads, with this change occurring at about 15 patients or more per hospitalist.

Costs were also significantly associated with an increase in workload. As the study notes, benchmark recommendations for an individual hospitalist’s workload range from 10 to 15 patient encounters per day.

Dr. Kealey says the findings seem to support the conventional wisdom that hospitalists should ideally see no more than 15 patients a day. He notes, however, that deciding the optimal number of cases for a given practice depends on several factors, including duration of shift, the availability of physician extenders, and the addition of surgical or cardiology cases.

"We won't be able as a specialty to fully realize our potential until we understand and apply the learnings about workload into our practices to ensure hospitalist career sustainability, system health, and best patient care," Dr. Kealey says. "This paper really gets the discussion going."

For more from Dr. Kealey on hospitalist workloads, read his recent blog post on "The Hospital Leader." TH

Visit our website for more information about hospitalist workloads.

As hospitalist workloads increase, so do hospital costs and patients' lengths of stay (LOS), according to findings in a recent study.

Those results, says SHM President Burke T. Kealey, MD, SFHM, provide a good starting point to determine an ideal patient census for hospitalists.

"Pushing hospitalist workloads ever higher to meet the demands of patient-care needs or flawed payment models has costs associated with it," says Dr. Kealey, associate medical director of hospital specialties at HealthPartners Medical Group in St. Paul, Minn. "The costs may be borne by the system or by patients, but there are costs."

For the study published in JAMA Internal Medicine, researchers analyzed data from 20,241 hospitalizations involving 13,916 patients seen by hospitalists at the Christiana Care Health System in Newark, Del., between February 2008 and January 2011.

For hospital occupancies less than 75%, they found that LOS increased from 5.5 to 7.5 days as workload increased. For occupancies of 75% to 85%, LOS increased to about 8 days with higher workloads. For occupancies greater than 85%, the LOS decreased slightly and then increased significantly with higher workloads, with this change occurring at about 15 patients or more per hospitalist.

Costs were also significantly associated with an increase in workload. As the study notes, benchmark recommendations for an individual hospitalist’s workload range from 10 to 15 patient encounters per day.

Dr. Kealey says the findings seem to support the conventional wisdom that hospitalists should ideally see no more than 15 patients a day. He notes, however, that deciding the optimal number of cases for a given practice depends on several factors, including duration of shift, the availability of physician extenders, and the addition of surgical or cardiology cases.

"We won't be able as a specialty to fully realize our potential until we understand and apply the learnings about workload into our practices to ensure hospitalist career sustainability, system health, and best patient care," Dr. Kealey says. "This paper really gets the discussion going."

For more from Dr. Kealey on hospitalist workloads, read his recent blog post on "The Hospital Leader." TH

Visit our website for more information about hospitalist workloads.

Nephrolithiasis affects 1 in 11 people in the United States resulting in several million emergency department visits annually. The prevalence of nephrolithiasis is higher among men, obese individuals, and white non-Hispanics. The prevalence of kidney stones also appears to be increasing.

Our patients tell us that few things hurt worse than kidney stones. We may feel especially compelled to make a diagnosis given pain severity in otherwise healthy adults who have "never experienced this kind of pain before." Perhaps because of this, lots of patients are undergoing CT imaging for kidney stones ... in the United States. Interestingly, the European Urology Association recommends ultrasonography as the first-line test for urolithiasis.

Can we predict who has a kidney stone?

Moore and colleagues derived and validated a clinical prediction rule for uncomplicated ureteral stone. The derivation cohort was 1,040 patients undergoing noncontrast CT for suspected uncomplicated kidney stone. The validation cohort was 491 consecutively enrolled patients.

Data analysis revealed five factors that were significantly associated with the presence of a ureteral stone: male sex (2 points), duration of pain to presentation (greater than 24 hours: 0 points; 6-24 hours: 1 point; less than 6 hours: 3 points), nonblack race (3 points), presence of nausea or vomiting (nausea alone: 1 point; vomiting alone: 2 points), and microscopic hematuria (3 points). The points add up to low probability (0-5 points = 10% chance of stone), moderate probability (6-9 points = about 50% chance of stone), and high probability (10-13 points = about 90% chance of stone). Acutely important alternative causes were found in 1.6% of the high-probability group in the validation set. These causes were diverticulitis, appendicitis, mass, pyelonephritis, cholecystitis, pneumonia, bowel obstruction, colitis, aortic aneurysm, and pancreatitis.

This algorithm was derived and validated in the emergency setting so it will have different performance characteristics in the outpatient, ambulatory, phone-triage world. However, as the authors discuss, this algorithm could be used to help institutions make decisions about lowering radiation doses for "stone protocol" scans. Scales such as these should be incorporated into electronic medical record systems to improve care delivery.

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

Nephrolithiasis affects 1 in 11 people in the United States resulting in several million emergency department visits annually. The prevalence of nephrolithiasis is higher among men, obese individuals, and white non-Hispanics. The prevalence of kidney stones also appears to be increasing.

Our patients tell us that few things hurt worse than kidney stones. We may feel especially compelled to make a diagnosis given pain severity in otherwise healthy adults who have "never experienced this kind of pain before." Perhaps because of this, lots of patients are undergoing CT imaging for kidney stones ... in the United States. Interestingly, the European Urology Association recommends ultrasonography as the first-line test for urolithiasis.

Can we predict who has a kidney stone?

Moore and colleagues derived and validated a clinical prediction rule for uncomplicated ureteral stone. The derivation cohort was 1,040 patients undergoing noncontrast CT for suspected uncomplicated kidney stone. The validation cohort was 491 consecutively enrolled patients.

Data analysis revealed five factors that were significantly associated with the presence of a ureteral stone: male sex (2 points), duration of pain to presentation (greater than 24 hours: 0 points; 6-24 hours: 1 point; less than 6 hours: 3 points), nonblack race (3 points), presence of nausea or vomiting (nausea alone: 1 point; vomiting alone: 2 points), and microscopic hematuria (3 points). The points add up to low probability (0-5 points = 10% chance of stone), moderate probability (6-9 points = about 50% chance of stone), and high probability (10-13 points = about 90% chance of stone). Acutely important alternative causes were found in 1.6% of the high-probability group in the validation set. These causes were diverticulitis, appendicitis, mass, pyelonephritis, cholecystitis, pneumonia, bowel obstruction, colitis, aortic aneurysm, and pancreatitis.

This algorithm was derived and validated in the emergency setting so it will have different performance characteristics in the outpatient, ambulatory, phone-triage world. However, as the authors discuss, this algorithm could be used to help institutions make decisions about lowering radiation doses for "stone protocol" scans. Scales such as these should be incorporated into electronic medical record systems to improve care delivery.

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

Nephrolithiasis affects 1 in 11 people in the United States resulting in several million emergency department visits annually. The prevalence of nephrolithiasis is higher among men, obese individuals, and white non-Hispanics. The prevalence of kidney stones also appears to be increasing.

Our patients tell us that few things hurt worse than kidney stones. We may feel especially compelled to make a diagnosis given pain severity in otherwise healthy adults who have "never experienced this kind of pain before." Perhaps because of this, lots of patients are undergoing CT imaging for kidney stones ... in the United States. Interestingly, the European Urology Association recommends ultrasonography as the first-line test for urolithiasis.

Can we predict who has a kidney stone?

Moore and colleagues derived and validated a clinical prediction rule for uncomplicated ureteral stone. The derivation cohort was 1,040 patients undergoing noncontrast CT for suspected uncomplicated kidney stone. The validation cohort was 491 consecutively enrolled patients.

Data analysis revealed five factors that were significantly associated with the presence of a ureteral stone: male sex (2 points), duration of pain to presentation (greater than 24 hours: 0 points; 6-24 hours: 1 point; less than 6 hours: 3 points), nonblack race (3 points), presence of nausea or vomiting (nausea alone: 1 point; vomiting alone: 2 points), and microscopic hematuria (3 points). The points add up to low probability (0-5 points = 10% chance of stone), moderate probability (6-9 points = about 50% chance of stone), and high probability (10-13 points = about 90% chance of stone). Acutely important alternative causes were found in 1.6% of the high-probability group in the validation set. These causes were diverticulitis, appendicitis, mass, pyelonephritis, cholecystitis, pneumonia, bowel obstruction, colitis, aortic aneurysm, and pancreatitis.

This algorithm was derived and validated in the emergency setting so it will have different performance characteristics in the outpatient, ambulatory, phone-triage world. However, as the authors discuss, this algorithm could be used to help institutions make decisions about lowering radiation doses for "stone protocol" scans. Scales such as these should be incorporated into electronic medical record systems to improve care delivery.

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

For a problem that has been on the back burner for decades, the treatment of atrial fibrillation has suddenly become a "marquis" diagnosis.

Age and technology have led to an explosion of interest in this arcane cardiac problem. Advertisements for new anticoagulants and thrombin inhibitors for "A Fib" have become almost as common as those for male impotency. The aging of the world population certainly has been a major factor in its increased incidence. New technology and pharmacology has driven the increase in clinical interest and has advanced our knowledge about the disease. Epidemiology data have provided important information about the natural history of paroxysmal atrial fibrillation (AF), and its relationship to chronic AF and its adverse effects on long-term mortality.

The importance of anticoagulant therapy for the prevention of systemic emboli and stroke has been the mainstay of therapy for almost 50 years. Although we have struggled with a variety of antiarrhythmic drugs, their shortcomings have been more than apparent. Most of us now use a rate-control strategy to control the tachycardia inherent in AF. The development of new factor Xa and direct thrombin inhibitor drugs have made the logistics of providing adequate thrombus prevention much simpler, if somewhat more expensive.

The elephant in the room is the increasing use of radiofrequency catheter ablation technology that has had some success in the prevention of AF arising from the tissue in the pulmonary vein–atrial interface. Numerous small studies have reported that this technology surpasses rhythm control with antiarrhythmic agents, a hurdle not too difficult to beat. The best results have been observed in patients with recurrent paroxysmal AF where maintenance of regular sinus rhythm has been the primary outcome measurement (JAMA 2014;311:692-700). Even here, recurrence after ablation has been common. The benefit of ablation therapy in patients with initial paroxysmal AF (N. Engl. J. Med. 2012;367:1587-95) or chronic persistent AF has been uncertain at best. As a result, the AHA/ACC/HRS (American Heart Association/American College of Cardiology/Heart Rhythm Society) guidelines have given a class I (evidence level A) recommendation for ablation therapy for symptomatic paroxysmal AF and class IIa (evidence level A) and IIb (evidence level B) for symptomatic recurrent paroxysmal and longstanding persistent AF when balanced against drug tolerability, respectively (J. Am. Coll. Cardiol. 2014 [doi:10.1016/j.jacc.2014.03.021]).

All of these clinical data are exciting and have led to enthusiasm for ablation technology despite the potential for nonfatal and rare fatal complication, based almost entirely on its ability to improve upon the dismal benefits of antiarrhythmic rhythm control. Even as we consider the benefit of ablation therapy, new techniques are being developed. The lack of mortality and morbidity data is a result of the short follow-up, usually limited to a year or two, and small sample size. This lack of long-term outcome data for ablation therapy should be of some concern to clinicians who have lived through the last few years. Many of my readers had not been born when we embarked on the ineffective and dangerous pharmacologic prevention of sudden death by pharmacologic suppression of ambient ventricular premature beats. Numerous surrogate measures of clinical benefit of a variety of therapeutic interventions have been disproven and disposed of in the subsequent years. The use of surrogate measures like the partial suppression of AF rather than morbidity and mortality outcomes to establish clinical benefit, have been largely discarded as a dead end.

The Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation Trial (CABANA), which is beginning to recruit more than 2,000 patients with new-onset or undertreated paroxysmal, persistent, or longstanding AF to be followed for over 4 years may answer the question of whether radiofrequency ablation therapy, rate control, or rhythm control provides the best clinical treatment of atrial fibrillation. The primary outcome will be the composite endpoint of total mortality, disabling stroke or serious bleeding, or cardiac arrest. An important secondary endpoint will be total mortality. Until its conclusion, we should proceed cautiously with expanding radiofrequency ablation therapy for the treatment of AF.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

For a problem that has been on the back burner for decades, the treatment of atrial fibrillation has suddenly become a "marquis" diagnosis.

Age and technology have led to an explosion of interest in this arcane cardiac problem. Advertisements for new anticoagulants and thrombin inhibitors for "A Fib" have become almost as common as those for male impotency. The aging of the world population certainly has been a major factor in its increased incidence. New technology and pharmacology has driven the increase in clinical interest and has advanced our knowledge about the disease. Epidemiology data have provided important information about the natural history of paroxysmal atrial fibrillation (AF), and its relationship to chronic AF and its adverse effects on long-term mortality.

The importance of anticoagulant therapy for the prevention of systemic emboli and stroke has been the mainstay of therapy for almost 50 years. Although we have struggled with a variety of antiarrhythmic drugs, their shortcomings have been more than apparent. Most of us now use a rate-control strategy to control the tachycardia inherent in AF. The development of new factor Xa and direct thrombin inhibitor drugs have made the logistics of providing adequate thrombus prevention much simpler, if somewhat more expensive.

The elephant in the room is the increasing use of radiofrequency catheter ablation technology that has had some success in the prevention of AF arising from the tissue in the pulmonary vein–atrial interface. Numerous small studies have reported that this technology surpasses rhythm control with antiarrhythmic agents, a hurdle not too difficult to beat. The best results have been observed in patients with recurrent paroxysmal AF where maintenance of regular sinus rhythm has been the primary outcome measurement (JAMA 2014;311:692-700). Even here, recurrence after ablation has been common. The benefit of ablation therapy in patients with initial paroxysmal AF (N. Engl. J. Med. 2012;367:1587-95) or chronic persistent AF has been uncertain at best. As a result, the AHA/ACC/HRS (American Heart Association/American College of Cardiology/Heart Rhythm Society) guidelines have given a class I (evidence level A) recommendation for ablation therapy for symptomatic paroxysmal AF and class IIa (evidence level A) and IIb (evidence level B) for symptomatic recurrent paroxysmal and longstanding persistent AF when balanced against drug tolerability, respectively (J. Am. Coll. Cardiol. 2014 [doi:10.1016/j.jacc.2014.03.021]).

All of these clinical data are exciting and have led to enthusiasm for ablation technology despite the potential for nonfatal and rare fatal complication, based almost entirely on its ability to improve upon the dismal benefits of antiarrhythmic rhythm control. Even as we consider the benefit of ablation therapy, new techniques are being developed. The lack of mortality and morbidity data is a result of the short follow-up, usually limited to a year or two, and small sample size. This lack of long-term outcome data for ablation therapy should be of some concern to clinicians who have lived through the last few years. Many of my readers had not been born when we embarked on the ineffective and dangerous pharmacologic prevention of sudden death by pharmacologic suppression of ambient ventricular premature beats. Numerous surrogate measures of clinical benefit of a variety of therapeutic interventions have been disproven and disposed of in the subsequent years. The use of surrogate measures like the partial suppression of AF rather than morbidity and mortality outcomes to establish clinical benefit, have been largely discarded as a dead end.

The Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation Trial (CABANA), which is beginning to recruit more than 2,000 patients with new-onset or undertreated paroxysmal, persistent, or longstanding AF to be followed for over 4 years may answer the question of whether radiofrequency ablation therapy, rate control, or rhythm control provides the best clinical treatment of atrial fibrillation. The primary outcome will be the composite endpoint of total mortality, disabling stroke or serious bleeding, or cardiac arrest. An important secondary endpoint will be total mortality. Until its conclusion, we should proceed cautiously with expanding radiofrequency ablation therapy for the treatment of AF.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

For a problem that has been on the back burner for decades, the treatment of atrial fibrillation has suddenly become a "marquis" diagnosis.

Age and technology have led to an explosion of interest in this arcane cardiac problem. Advertisements for new anticoagulants and thrombin inhibitors for "A Fib" have become almost as common as those for male impotency. The aging of the world population certainly has been a major factor in its increased incidence. New technology and pharmacology has driven the increase in clinical interest and has advanced our knowledge about the disease. Epidemiology data have provided important information about the natural history of paroxysmal atrial fibrillation (AF), and its relationship to chronic AF and its adverse effects on long-term mortality.

The importance of anticoagulant therapy for the prevention of systemic emboli and stroke has been the mainstay of therapy for almost 50 years. Although we have struggled with a variety of antiarrhythmic drugs, their shortcomings have been more than apparent. Most of us now use a rate-control strategy to control the tachycardia inherent in AF. The development of new factor Xa and direct thrombin inhibitor drugs have made the logistics of providing adequate thrombus prevention much simpler, if somewhat more expensive.

The elephant in the room is the increasing use of radiofrequency catheter ablation technology that has had some success in the prevention of AF arising from the tissue in the pulmonary vein–atrial interface. Numerous small studies have reported that this technology surpasses rhythm control with antiarrhythmic agents, a hurdle not too difficult to beat. The best results have been observed in patients with recurrent paroxysmal AF where maintenance of regular sinus rhythm has been the primary outcome measurement (JAMA 2014;311:692-700). Even here, recurrence after ablation has been common. The benefit of ablation therapy in patients with initial paroxysmal AF (N. Engl. J. Med. 2012;367:1587-95) or chronic persistent AF has been uncertain at best. As a result, the AHA/ACC/HRS (American Heart Association/American College of Cardiology/Heart Rhythm Society) guidelines have given a class I (evidence level A) recommendation for ablation therapy for symptomatic paroxysmal AF and class IIa (evidence level A) and IIb (evidence level B) for symptomatic recurrent paroxysmal and longstanding persistent AF when balanced against drug tolerability, respectively (J. Am. Coll. Cardiol. 2014 [doi:10.1016/j.jacc.2014.03.021]).

All of these clinical data are exciting and have led to enthusiasm for ablation technology despite the potential for nonfatal and rare fatal complication, based almost entirely on its ability to improve upon the dismal benefits of antiarrhythmic rhythm control. Even as we consider the benefit of ablation therapy, new techniques are being developed. The lack of mortality and morbidity data is a result of the short follow-up, usually limited to a year or two, and small sample size. This lack of long-term outcome data for ablation therapy should be of some concern to clinicians who have lived through the last few years. Many of my readers had not been born when we embarked on the ineffective and dangerous pharmacologic prevention of sudden death by pharmacologic suppression of ambient ventricular premature beats. Numerous surrogate measures of clinical benefit of a variety of therapeutic interventions have been disproven and disposed of in the subsequent years. The use of surrogate measures like the partial suppression of AF rather than morbidity and mortality outcomes to establish clinical benefit, have been largely discarded as a dead end.

The Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation Trial (CABANA), which is beginning to recruit more than 2,000 patients with new-onset or undertreated paroxysmal, persistent, or longstanding AF to be followed for over 4 years may answer the question of whether radiofrequency ablation therapy, rate control, or rhythm control provides the best clinical treatment of atrial fibrillation. The primary outcome will be the composite endpoint of total mortality, disabling stroke or serious bleeding, or cardiac arrest. An important secondary endpoint will be total mortality. Until its conclusion, we should proceed cautiously with expanding radiofrequency ablation therapy for the treatment of AF.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The Diagnosis: Blaschkoid Punctate Vitiligo

Based on the patient’s clinical appearance as well as the histologic findings, the diagnosis of vitiligo was made. Although vitiligo is certainly not uncommon and punctate vitiligo is a known clinical presentation,¹ punctate vitiliginous depigmentation conforming to lines of Blaschko is unique. Follicular repigmentation in a patch of vitiligo potentially could lead to this “spotty” appearance, but our patient maintained that the band was never confluently depigmented and that small macules arose within normally pigmented skin. The patient’s adult age at onset makes this case even more unusual.

Follicular repigmentation in vitiligo is fairly well understood, as the perifollicular pigment is formed by upward migration of activated melanoblasts in the outer root sheath.² Follicular depigmentation as well as selective or initial loss of melanocytes around hair follicles in early vitiligo has not been described. It is unclear if the seemingly folliculocentric nature of the patient’s vitiliginous macules was a false observation, coincidental, or actually related to selective melanocyte loss around follicles.

Blaschkoid distribution has been described in numerous skin disorders and is known to be based on genetic mosaicism.³ Most of these disorders are X-linked and/or congenital. However, many acquired skin conditions have been described exhibiting blaschkoid distribution, such as vitiligo, psoriasis, lichen planus, atopic dermatitis, and mycosis fungoides.^4,5

Confettilike depigmentation has been described as an unusual clinical variant of vitiligo.¹ It also has been reported after psoralen plus UVA therapy in patients with more classic vitiligo,⁶ numerous domestic chemicals,⁷ and in association with mycosis fungoides.⁸ In these cases, punctate lesions were disseminated, symmetric on extremities, or limited to areas exposed to chemicals.

The Diagnosis: Blaschkoid Punctate Vitiligo

Based on the patient’s clinical appearance as well as the histologic findings, the diagnosis of vitiligo was made. Although vitiligo is certainly not uncommon and punctate vitiligo is a known clinical presentation,¹ punctate vitiliginous depigmentation conforming to lines of Blaschko is unique. Follicular repigmentation in a patch of vitiligo potentially could lead to this “spotty” appearance, but our patient maintained that the band was never confluently depigmented and that small macules arose within normally pigmented skin. The patient’s adult age at onset makes this case even more unusual.

Follicular repigmentation in vitiligo is fairly well understood, as the perifollicular pigment is formed by upward migration of activated melanoblasts in the outer root sheath.² Follicular depigmentation as well as selective or initial loss of melanocytes around hair follicles in early vitiligo has not been described. It is unclear if the seemingly folliculocentric nature of the patient’s vitiliginous macules was a false observation, coincidental, or actually related to selective melanocyte loss around follicles.

Blaschkoid distribution has been described in numerous skin disorders and is known to be based on genetic mosaicism.³ Most of these disorders are X-linked and/or congenital. However, many acquired skin conditions have been described exhibiting blaschkoid distribution, such as vitiligo, psoriasis, lichen planus, atopic dermatitis, and mycosis fungoides.^4,5

Confettilike depigmentation has been described as an unusual clinical variant of vitiligo.¹ It also has been reported after psoralen plus UVA therapy in patients with more classic vitiligo,⁶ numerous domestic chemicals,⁷ and in association with mycosis fungoides.⁸ In these cases, punctate lesions were disseminated, symmetric on extremities, or limited to areas exposed to chemicals.

The Diagnosis: Blaschkoid Punctate Vitiligo

Based on the patient’s clinical appearance as well as the histologic findings, the diagnosis of vitiligo was made. Although vitiligo is certainly not uncommon and punctate vitiligo is a known clinical presentation,¹ punctate vitiliginous depigmentation conforming to lines of Blaschko is unique. Follicular repigmentation in a patch of vitiligo potentially could lead to this “spotty” appearance, but our patient maintained that the band was never confluently depigmented and that small macules arose within normally pigmented skin. The patient’s adult age at onset makes this case even more unusual.

Follicular repigmentation in vitiligo is fairly well understood, as the perifollicular pigment is formed by upward migration of activated melanoblasts in the outer root sheath.² Follicular depigmentation as well as selective or initial loss of melanocytes around hair follicles in early vitiligo has not been described. It is unclear if the seemingly folliculocentric nature of the patient’s vitiliginous macules was a false observation, coincidental, or actually related to selective melanocyte loss around follicles.

Blaschkoid distribution has been described in numerous skin disorders and is known to be based on genetic mosaicism.³ Most of these disorders are X-linked and/or congenital. However, many acquired skin conditions have been described exhibiting blaschkoid distribution, such as vitiligo, psoriasis, lichen planus, atopic dermatitis, and mycosis fungoides.^4,5

Confettilike depigmentation has been described as an unusual clinical variant of vitiligo.¹ It also has been reported after psoralen plus UVA therapy in patients with more classic vitiligo,⁶ numerous domestic chemicals,⁷ and in association with mycosis fungoides.⁸ In these cases, punctate lesions were disseminated, symmetric on extremities, or limited to areas exposed to chemicals.

Micrograph showing AML cells

Credit: Lance Liotta

New research has revealed a mechanism of drug resistance in acute myeloid leukemia (AML) that may also occur in other cancers.

Investigators found evidence suggesting that glioma-associated protein 1 (GLI1) and the UDP glucuronosyltransferase (UGT1A) family of enzymes drive resistance to 2 drugs—ribavirin and cytarabine—in AML.

But the researchers were able to overcome this resistance by genetic or pharmacologic inhibition of GLI1.

They described this research in a letter to Nature.

“By studying drug-resistant cancer cells from AML patients and head and neck tumors, we found that a gene called GLI1 is dramatically overactive in these cells,” said study author Hiba Zahreddine, a doctoral student at the University of Montreal in Canada.

“[W[e were then able to show that this results in a specific chemical change to the drugs that prevents their toxicity toward the cancer cells,” said author Kathy Borden, PhD, of the University of Montreal’s Institute for Research in Immunology and Cancer.

Specifically, the investigators found that UGT1A enzymes add glucuronic acid to the drugs, thereby modifying their activity. And GLI1 alone is sufficient to drive UGT1A-dependent glucuronidation of ribavirin and cytarabine, which fuels drug resistance.

Fortunately, the researchers found that inhibiting GLI1, either genetically or with pharmacologic inhibitors, could force cancer cells to revert to a treatment-sensitive state.

The team therefore hopes that using GLI1 inhibitors in combination with ribavirin, cytarabine, or other therapies can overcome treatment resistance in patients with AML. The investigators have received approval from Health Canada to conduct a new clinical trial to test this theory.

“If this new approach is successful, it could have very broad applications, since the mode of action of ribavirin suggests that it could be effective against up to 30% of all cancers, including some types of breast, prostate, colon, stomach, and head and neck cancers, in addition to AML,” said Morris Goodman, co-founder and Chairman of the Board of Pharmascience Inc., the company that manufactured the ribavirin for this research.

Micrograph showing AML cells

Credit: Lance Liotta

New research has revealed a mechanism of drug resistance in acute myeloid leukemia (AML) that may also occur in other cancers.

Investigators found evidence suggesting that glioma-associated protein 1 (GLI1) and the UDP glucuronosyltransferase (UGT1A) family of enzymes drive resistance to 2 drugs—ribavirin and cytarabine—in AML.

But the researchers were able to overcome this resistance by genetic or pharmacologic inhibition of GLI1.

They described this research in a letter to Nature.

“By studying drug-resistant cancer cells from AML patients and head and neck tumors, we found that a gene called GLI1 is dramatically overactive in these cells,” said study author Hiba Zahreddine, a doctoral student at the University of Montreal in Canada.

“[W[e were then able to show that this results in a specific chemical change to the drugs that prevents their toxicity toward the cancer cells,” said author Kathy Borden, PhD, of the University of Montreal’s Institute for Research in Immunology and Cancer.

Specifically, the investigators found that UGT1A enzymes add glucuronic acid to the drugs, thereby modifying their activity. And GLI1 alone is sufficient to drive UGT1A-dependent glucuronidation of ribavirin and cytarabine, which fuels drug resistance.

Fortunately, the researchers found that inhibiting GLI1, either genetically or with pharmacologic inhibitors, could force cancer cells to revert to a treatment-sensitive state.

The team therefore hopes that using GLI1 inhibitors in combination with ribavirin, cytarabine, or other therapies can overcome treatment resistance in patients with AML. The investigators have received approval from Health Canada to conduct a new clinical trial to test this theory.

“If this new approach is successful, it could have very broad applications, since the mode of action of ribavirin suggests that it could be effective against up to 30% of all cancers, including some types of breast, prostate, colon, stomach, and head and neck cancers, in addition to AML,” said Morris Goodman, co-founder and Chairman of the Board of Pharmascience Inc., the company that manufactured the ribavirin for this research.

Micrograph showing AML cells

Credit: Lance Liotta

New research has revealed a mechanism of drug resistance in acute myeloid leukemia (AML) that may also occur in other cancers.

Investigators found evidence suggesting that glioma-associated protein 1 (GLI1) and the UDP glucuronosyltransferase (UGT1A) family of enzymes drive resistance to 2 drugs—ribavirin and cytarabine—in AML.

But the researchers were able to overcome this resistance by genetic or pharmacologic inhibition of GLI1.

They described this research in a letter to Nature.

“By studying drug-resistant cancer cells from AML patients and head and neck tumors, we found that a gene called GLI1 is dramatically overactive in these cells,” said study author Hiba Zahreddine, a doctoral student at the University of Montreal in Canada.

“[W[e were then able to show that this results in a specific chemical change to the drugs that prevents their toxicity toward the cancer cells,” said author Kathy Borden, PhD, of the University of Montreal’s Institute for Research in Immunology and Cancer.

Specifically, the investigators found that UGT1A enzymes add glucuronic acid to the drugs, thereby modifying their activity. And GLI1 alone is sufficient to drive UGT1A-dependent glucuronidation of ribavirin and cytarabine, which fuels drug resistance.

Fortunately, the researchers found that inhibiting GLI1, either genetically or with pharmacologic inhibitors, could force cancer cells to revert to a treatment-sensitive state.

The team therefore hopes that using GLI1 inhibitors in combination with ribavirin, cytarabine, or other therapies can overcome treatment resistance in patients with AML. The investigators have received approval from Health Canada to conduct a new clinical trial to test this theory.

“If this new approach is successful, it could have very broad applications, since the mode of action of ribavirin suggests that it could be effective against up to 30% of all cancers, including some types of breast, prostate, colon, stomach, and head and neck cancers, in addition to AML,” said Morris Goodman, co-founder and Chairman of the Board of Pharmascience Inc., the company that manufactured the ribavirin for this research.

CHICAGO – Two laboratory measurements that are commonly used to assess the cause of symptomatic ascites before liver transplant may be deceptive when used to assess posttransplant ascites, a retrospective study of 15 patients suggested.

Before liver transplant, a serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL differentiates ascites due to portal hypertension rather than other causes 97% of the time. An ascites total protein (aTP) measurement has a lower accuracy for portal hypertension of 57%, but when used in conjunction with SAAG, an aTP of 2.5 g/dL or greater suggests that the cause is cardiac ascites, tuberculous ascites, or peritoneal carcinomatosis, Dr. Jeffrey LaFond explained at the annual Digestive Disease Week.

He and his associates studied the records of 15 patients who developed symptomatic post-transplant ascites that had enough volume to require therapeutic paracentesis. The ascites occurred a mean of 515 days after transplantation (ranging from 14 to 2,744 days). In the work-up for ascites, the sensitivity of SAAG for portal hypertension was 82% and the sensitivity of aTP for portal hypertension was 50%.

Three of 12 patients who had a posttransplant SAAG had a gradient below 1.1 g/dL even though other tests found no evidence of another cause for ascites besides portal hypertension, and two of those three patients had confirmed portal hypertension, he reported. Five of 10 patients with an aTP had a value greater than 2.5 g/dL, even though they had confirmed portal hypertension and normal cardiac function, he reported.

"Assessment of ascites due to portal hypertension and/or vascular stricture in the posttransplant period using SAAG and aTP can be deceiving and cannot be relied upon to make diagnostic interventional decisions," said Dr. LaFond of the University of Virginia, Charlottesville. "A hepatic venogram should be performed early on in patients with posttransplant ascites to evaluate for strictures and portal hypertension.

Records showed that all patients in the study had ascites confirmed by imaging and/or paracenteses and had diagnostic studies to rule out heart failure, opportunistic infection, or malignancy as the source of ascites. Suspected portal hypertension was confirmed by pressure measurements or the presence of vascular strictures on venogram, with portal hypertension defined as a sinusoidal or portosystemic gradient greater than 5 or the presence of a stricture with a gradient of at least 3.

An estimated 3%-7% of patients develop ascites after liver transplant, which has been associated with an increased risk of renal impairment, prolonged hospitalization, and abdominal infections, he said.

Dr. LaFond reported having no financial disclosures.

[email protected]

On Twitter @sherryboschert

*This story was updated 6/3/2014.

CHICAGO – Two laboratory measurements that are commonly used to assess the cause of symptomatic ascites before liver transplant may be deceptive when used to assess posttransplant ascites, a retrospective study of 15 patients suggested.

Before liver transplant, a serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL differentiates ascites due to portal hypertension rather than other causes 97% of the time. An ascites total protein (aTP) measurement has a lower accuracy for portal hypertension of 57%, but when used in conjunction with SAAG, an aTP of 2.5 g/dL or greater suggests that the cause is cardiac ascites, tuberculous ascites, or peritoneal carcinomatosis, Dr. Jeffrey LaFond explained at the annual Digestive Disease Week.

He and his associates studied the records of 15 patients who developed symptomatic post-transplant ascites that had enough volume to require therapeutic paracentesis. The ascites occurred a mean of 515 days after transplantation (ranging from 14 to 2,744 days). In the work-up for ascites, the sensitivity of SAAG for portal hypertension was 82% and the sensitivity of aTP for portal hypertension was 50%.

Three of 12 patients who had a posttransplant SAAG had a gradient below 1.1 g/dL even though other tests found no evidence of another cause for ascites besides portal hypertension, and two of those three patients had confirmed portal hypertension, he reported. Five of 10 patients with an aTP had a value greater than 2.5 g/dL, even though they had confirmed portal hypertension and normal cardiac function, he reported.

"Assessment of ascites due to portal hypertension and/or vascular stricture in the posttransplant period using SAAG and aTP can be deceiving and cannot be relied upon to make diagnostic interventional decisions," said Dr. LaFond of the University of Virginia, Charlottesville. "A hepatic venogram should be performed early on in patients with posttransplant ascites to evaluate for strictures and portal hypertension.

Records showed that all patients in the study had ascites confirmed by imaging and/or paracenteses and had diagnostic studies to rule out heart failure, opportunistic infection, or malignancy as the source of ascites. Suspected portal hypertension was confirmed by pressure measurements or the presence of vascular strictures on venogram, with portal hypertension defined as a sinusoidal or portosystemic gradient greater than 5 or the presence of a stricture with a gradient of at least 3.

An estimated 3%-7% of patients develop ascites after liver transplant, which has been associated with an increased risk of renal impairment, prolonged hospitalization, and abdominal infections, he said.

Dr. LaFond reported having no financial disclosures.

[email protected]

On Twitter @sherryboschert

*This story was updated 6/3/2014.

CHICAGO – Two laboratory measurements that are commonly used to assess the cause of symptomatic ascites before liver transplant may be deceptive when used to assess posttransplant ascites, a retrospective study of 15 patients suggested.

Before liver transplant, a serum-ascites albumin gradient (SAAG) greater than 1.1 g/dL differentiates ascites due to portal hypertension rather than other causes 97% of the time. An ascites total protein (aTP) measurement has a lower accuracy for portal hypertension of 57%, but when used in conjunction with SAAG, an aTP of 2.5 g/dL or greater suggests that the cause is cardiac ascites, tuberculous ascites, or peritoneal carcinomatosis, Dr. Jeffrey LaFond explained at the annual Digestive Disease Week.

He and his associates studied the records of 15 patients who developed symptomatic post-transplant ascites that had enough volume to require therapeutic paracentesis. The ascites occurred a mean of 515 days after transplantation (ranging from 14 to 2,744 days). In the work-up for ascites, the sensitivity of SAAG for portal hypertension was 82% and the sensitivity of aTP for portal hypertension was 50%.

Three of 12 patients who had a posttransplant SAAG had a gradient below 1.1 g/dL even though other tests found no evidence of another cause for ascites besides portal hypertension, and two of those three patients had confirmed portal hypertension, he reported. Five of 10 patients with an aTP had a value greater than 2.5 g/dL, even though they had confirmed portal hypertension and normal cardiac function, he reported.

"Assessment of ascites due to portal hypertension and/or vascular stricture in the posttransplant period using SAAG and aTP can be deceiving and cannot be relied upon to make diagnostic interventional decisions," said Dr. LaFond of the University of Virginia, Charlottesville. "A hepatic venogram should be performed early on in patients with posttransplant ascites to evaluate for strictures and portal hypertension.

Records showed that all patients in the study had ascites confirmed by imaging and/or paracenteses and had diagnostic studies to rule out heart failure, opportunistic infection, or malignancy as the source of ascites. Suspected portal hypertension was confirmed by pressure measurements or the presence of vascular strictures on venogram, with portal hypertension defined as a sinusoidal or portosystemic gradient greater than 5 or the presence of a stricture with a gradient of at least 3.

An estimated 3%-7% of patients develop ascites after liver transplant, which has been associated with an increased risk of renal impairment, prolonged hospitalization, and abdominal infections, he said.

Dr. LaFond reported having no financial disclosures.

[email protected]

On Twitter @sherryboschert

*This story was updated 6/3/2014.

Naomi is a 61-year-old woman who has lived with bipolar disorder and its stigma for 30 years. After a major manic episode and hospitalization, she entered into family treatment at the urging of her three daughters. Previously, her husband had been the primary force in guiding her psychiatric care, and she had been in treatment with a psychiatrist who is his professional colleague.

The patient’s first depressive episode began in the postpartum period, but she did not seek help at that time because she thought that her feelings were normal for a new mother. She did not receive any psychiatric attention until she cycled into mania and called the police for fear her child was being poisoned by neighbors. Her most recent manic episode occurred after she stopped her medications because of concerns about side effects. She was too embarrassed to tell her husband or doctor. She routinely fails to tell her other medical doctors that she is on mood stabilizers, because she does not want them to know she has bipolar disorder.

How stigma gets in the way

As discussed previously by Dr. Alison M. Heru ("Mental illness stigma is a family affair," Clinical Psychiatry News, April 2014, p. 8), stigma, when internalized or self-directed, can lead to psychological distress, decreased self-esteem and life satisfaction, and increased depression and suicidality (Compr. Psychiatry 2010;51:603-6). Close family members of those with mental disorders are affected by stigma, commonly referred to as "stigma by association" or "courtesy stigma."

Up to 92% of caregivers of people with psychiatric disorders have reported internalized stigma (J. Psychiatr. Ment. Health Nurs. 2012;19:665-71). These family members become distant and avoidant, resulting in a reduced quality of life and an impaired ability to provide critical support for their loved ones. Caregiver anxiety is inversely related to patient anxiety, stigma, and poor alliance (J. Nerv. Ment. Disease 2011;199:18-24).

As a result of these factors, while people with psychiatric disorders have to cope with their own mental illness as well as the public and self-stigma that alienate them from society, they also are at risk of losing their family connections.

In order to confront stigma, the Family Center for Bipolar Disorder in New York City, for example, uses a Family Inclusive Treatment (FIT) model. The FIT model includes an engagement period at the initiation of treatment that is focused on psychoeducation and relapse prevention planning. FIT is unique in that every patient is required to sign a release of information giving permission for full, open communication at all times between the patient’s clinician and a treatment partner of their choice. After the initial engagement period, there are quarterly family visits to supplement regular individual treatment sessions. FIT treatment promotes open communication about symptoms and medications. FIT strives to minimize patient isolation from families; they can talk openly with one another and their clinician.

After seeing many families enter treatment, FIT staff noticed the prominence of stigma.

We have begun to ask about stigma directly. Do people with more stigma do worse in treatment? Do they adhere more poorly to treatment? Do their families tend to become less involved over time? To begin, Dr. Mednick and staff examined demographic data looking for factors that might predispose a person to experience increased stigma.

In terms of diagnosis, people with more internalizing disorders such as depression and anxiety disorders tend to experience more stigma. Distress is experienced internally. As Dr. Bassirnia and her colleagues wrote in a poster presented at the recent American Psychiatric Association meeting, people with externalizing disorders, such as substance abuse and antisocial disorders, are more likely to express their distress outwardly and are less likely to suffer from stigma ("The relationship between personality traits and perceived internalized stigma in bipolar patients and their caregivers," 2014).

Meanwhile, two systematic review studies have reported moderate to high levels of internalized stigma in people with bipolar disorder. In these studies, a higher level of internalized stigma had a negative correlation with self-esteem, social adjustment, and perceived social support, and positive correlation with severity of symptoms, functional impairment, and rehospitalization. In spite of having more severe symptoms; people with higher levels of self-stigma are less likely to seek professional help and adhere to their treatment. Stigma by association and its negative consequences in caregivers of people with mental disorders also have been reported (J. Affect. Disord. 2013;150:181-91).

A useful and easy to administer scale that helps to identify stigma is the "Perceived Criticism Scale" (J. Abnorm. Psychol. 1989;98:225-35). By asking four questions, the clinician can get a good sense of family dynamics and can monitor the progress and change over time. The questions rate perception on a scale of 1-10, where "X" is the other person involved in treatment, either patient or caregiver. Here are the questions:

1. How critical do you think you are of X?

2. How critical do you think X is of you?

3. When X criticizes you, how upset do you get?

4. When you criticize X, how upset does he/she get?

For families with high scores, follow-up is needed. The Internalized Stigma of Mental Illness (ISMI) scale (Psychiatry Res. 2003;121:31-49) can be used. The ISMI scale makes statements about stigma for which participants rate their agreement on a Likert scale, such as:

• I don’t talk about myself much because I don’t want to burden others with my mental illness.

• Being around people who don’t have a mental illness makes me feel out of place or inadequate.

• People can tell that I have a mental illness by the way I look.

• Mentally ill people tend to be violent.

• I feel out of place in the world because I have a mental illness.

The ISMI scale contains 29 short, simple statements like the ones above and can be completed in less than 10 minutes. The statements are designed to avoid hypothetical situations, stay focused in the present, and address the participant’s own identity and experience.

Using the tools in practice

Naomi entered family treatment with her husband and daughters. Using the ISMI to measure the stigma of mental illness that each family member was experiencing, Naomi was shocked to see that her daughters felt far less stigma about having a mother with mental illness than she had assumed. In turn, her daughters were shocked at how much stigma Naomi was experiencing. Naomi’s husband scored between them. This data paved the way for an open family conversation about how Naomi’s illness had affected their lives, and especially how Naomi’s husband and his perceptions of her illness had affected her treatment course.

Caregivers play a very important role in bipolar disorder. After all, the illness can lead to difficulty functioning and can threaten the family’s stability. Sometimes caregivers can serve as a source of strength and a beacon of stability in the occasional storm. It is hard for the family between the storms, when the same flashing beacon can be a constant reminder to the patient of their illness. Often, well intentioned concerns become constant checking up, making the patient feel stigmatized and expected to fail.

"Good" caregivers will be aware of the stigma and the impact it has on their loved one and on themselves, without becoming a source of stigma.

Dr. Mednick is an attending psychiatrist at the Family Center for Bipolar at Mount Sinai Beth Israel in New York City. Dr. Bassirnia is a second-year psychiatry resident at Mount Sinai Beth Israel. Scan the QR code to read more Families in Psychiatry columns at clinicalpsychiatrynews.com.

Naomi is a 61-year-old woman who has lived with bipolar disorder and its stigma for 30 years. After a major manic episode and hospitalization, she entered into family treatment at the urging of her three daughters. Previously, her husband had been the primary force in guiding her psychiatric care, and she had been in treatment with a psychiatrist who is his professional colleague.

The patient’s first depressive episode began in the postpartum period, but she did not seek help at that time because she thought that her feelings were normal for a new mother. She did not receive any psychiatric attention until she cycled into mania and called the police for fear her child was being poisoned by neighbors. Her most recent manic episode occurred after she stopped her medications because of concerns about side effects. She was too embarrassed to tell her husband or doctor. She routinely fails to tell her other medical doctors that she is on mood stabilizers, because she does not want them to know she has bipolar disorder.

How stigma gets in the way

As discussed previously by Dr. Alison M. Heru ("Mental illness stigma is a family affair," Clinical Psychiatry News, April 2014, p. 8), stigma, when internalized or self-directed, can lead to psychological distress, decreased self-esteem and life satisfaction, and increased depression and suicidality (Compr. Psychiatry 2010;51:603-6). Close family members of those with mental disorders are affected by stigma, commonly referred to as "stigma by association" or "courtesy stigma."

Up to 92% of caregivers of people with psychiatric disorders have reported internalized stigma (J. Psychiatr. Ment. Health Nurs. 2012;19:665-71). These family members become distant and avoidant, resulting in a reduced quality of life and an impaired ability to provide critical support for their loved ones. Caregiver anxiety is inversely related to patient anxiety, stigma, and poor alliance (J. Nerv. Ment. Disease 2011;199:18-24).

As a result of these factors, while people with psychiatric disorders have to cope with their own mental illness as well as the public and self-stigma that alienate them from society, they also are at risk of losing their family connections.

In order to confront stigma, the Family Center for Bipolar Disorder in New York City, for example, uses a Family Inclusive Treatment (FIT) model. The FIT model includes an engagement period at the initiation of treatment that is focused on psychoeducation and relapse prevention planning. FIT is unique in that every patient is required to sign a release of information giving permission for full, open communication at all times between the patient’s clinician and a treatment partner of their choice. After the initial engagement period, there are quarterly family visits to supplement regular individual treatment sessions. FIT treatment promotes open communication about symptoms and medications. FIT strives to minimize patient isolation from families; they can talk openly with one another and their clinician.

After seeing many families enter treatment, FIT staff noticed the prominence of stigma.

We have begun to ask about stigma directly. Do people with more stigma do worse in treatment? Do they adhere more poorly to treatment? Do their families tend to become less involved over time? To begin, Dr. Mednick and staff examined demographic data looking for factors that might predispose a person to experience increased stigma.

In terms of diagnosis, people with more internalizing disorders such as depression and anxiety disorders tend to experience more stigma. Distress is experienced internally. As Dr. Bassirnia and her colleagues wrote in a poster presented at the recent American Psychiatric Association meeting, people with externalizing disorders, such as substance abuse and antisocial disorders, are more likely to express their distress outwardly and are less likely to suffer from stigma ("The relationship between personality traits and perceived internalized stigma in bipolar patients and their caregivers," 2014).

Meanwhile, two systematic review studies have reported moderate to high levels of internalized stigma in people with bipolar disorder. In these studies, a higher level of internalized stigma had a negative correlation with self-esteem, social adjustment, and perceived social support, and positive correlation with severity of symptoms, functional impairment, and rehospitalization. In spite of having more severe symptoms; people with higher levels of self-stigma are less likely to seek professional help and adhere to their treatment. Stigma by association and its negative consequences in caregivers of people with mental disorders also have been reported (J. Affect. Disord. 2013;150:181-91).

A useful and easy to administer scale that helps to identify stigma is the "Perceived Criticism Scale" (J. Abnorm. Psychol. 1989;98:225-35). By asking four questions, the clinician can get a good sense of family dynamics and can monitor the progress and change over time. The questions rate perception on a scale of 1-10, where "X" is the other person involved in treatment, either patient or caregiver. Here are the questions:

1. How critical do you think you are of X?

2. How critical do you think X is of you?

3. When X criticizes you, how upset do you get?

4. When you criticize X, how upset does he/she get?

For families with high scores, follow-up is needed. The Internalized Stigma of Mental Illness (ISMI) scale (Psychiatry Res. 2003;121:31-49) can be used. The ISMI scale makes statements about stigma for which participants rate their agreement on a Likert scale, such as:

• I don’t talk about myself much because I don’t want to burden others with my mental illness.

• Being around people who don’t have a mental illness makes me feel out of place or inadequate.

• People can tell that I have a mental illness by the way I look.

• Mentally ill people tend to be violent.

• I feel out of place in the world because I have a mental illness.

The ISMI scale contains 29 short, simple statements like the ones above and can be completed in less than 10 minutes. The statements are designed to avoid hypothetical situations, stay focused in the present, and address the participant’s own identity and experience.

Using the tools in practice

Naomi entered family treatment with her husband and daughters. Using the ISMI to measure the stigma of mental illness that each family member was experiencing, Naomi was shocked to see that her daughters felt far less stigma about having a mother with mental illness than she had assumed. In turn, her daughters were shocked at how much stigma Naomi was experiencing. Naomi’s husband scored between them. This data paved the way for an open family conversation about how Naomi’s illness had affected their lives, and especially how Naomi’s husband and his perceptions of her illness had affected her treatment course.

Caregivers play a very important role in bipolar disorder. After all, the illness can lead to difficulty functioning and can threaten the family’s stability. Sometimes caregivers can serve as a source of strength and a beacon of stability in the occasional storm. It is hard for the family between the storms, when the same flashing beacon can be a constant reminder to the patient of their illness. Often, well intentioned concerns become constant checking up, making the patient feel stigmatized and expected to fail.

"Good" caregivers will be aware of the stigma and the impact it has on their loved one and on themselves, without becoming a source of stigma.

Dr. Mednick is an attending psychiatrist at the Family Center for Bipolar at Mount Sinai Beth Israel in New York City. Dr. Bassirnia is a second-year psychiatry resident at Mount Sinai Beth Israel. Scan the QR code to read more Families in Psychiatry columns at clinicalpsychiatrynews.com.

Naomi is a 61-year-old woman who has lived with bipolar disorder and its stigma for 30 years. After a major manic episode and hospitalization, she entered into family treatment at the urging of her three daughters. Previously, her husband had been the primary force in guiding her psychiatric care, and she had been in treatment with a psychiatrist who is his professional colleague.

The patient’s first depressive episode began in the postpartum period, but she did not seek help at that time because she thought that her feelings were normal for a new mother. She did not receive any psychiatric attention until she cycled into mania and called the police for fear her child was being poisoned by neighbors. Her most recent manic episode occurred after she stopped her medications because of concerns about side effects. She was too embarrassed to tell her husband or doctor. She routinely fails to tell her other medical doctors that she is on mood stabilizers, because she does not want them to know she has bipolar disorder.

How stigma gets in the way

As discussed previously by Dr. Alison M. Heru ("Mental illness stigma is a family affair," Clinical Psychiatry News, April 2014, p. 8), stigma, when internalized or self-directed, can lead to psychological distress, decreased self-esteem and life satisfaction, and increased depression and suicidality (Compr. Psychiatry 2010;51:603-6). Close family members of those with mental disorders are affected by stigma, commonly referred to as "stigma by association" or "courtesy stigma."

Up to 92% of caregivers of people with psychiatric disorders have reported internalized stigma (J. Psychiatr. Ment. Health Nurs. 2012;19:665-71). These family members become distant and avoidant, resulting in a reduced quality of life and an impaired ability to provide critical support for their loved ones. Caregiver anxiety is inversely related to patient anxiety, stigma, and poor alliance (J. Nerv. Ment. Disease 2011;199:18-24).

As a result of these factors, while people with psychiatric disorders have to cope with their own mental illness as well as the public and self-stigma that alienate them from society, they also are at risk of losing their family connections.

In order to confront stigma, the Family Center for Bipolar Disorder in New York City, for example, uses a Family Inclusive Treatment (FIT) model. The FIT model includes an engagement period at the initiation of treatment that is focused on psychoeducation and relapse prevention planning. FIT is unique in that every patient is required to sign a release of information giving permission for full, open communication at all times between the patient’s clinician and a treatment partner of their choice. After the initial engagement period, there are quarterly family visits to supplement regular individual treatment sessions. FIT treatment promotes open communication about symptoms and medications. FIT strives to minimize patient isolation from families; they can talk openly with one another and their clinician.

After seeing many families enter treatment, FIT staff noticed the prominence of stigma.

We have begun to ask about stigma directly. Do people with more stigma do worse in treatment? Do they adhere more poorly to treatment? Do their families tend to become less involved over time? To begin, Dr. Mednick and staff examined demographic data looking for factors that might predispose a person to experience increased stigma.

In terms of diagnosis, people with more internalizing disorders such as depression and anxiety disorders tend to experience more stigma. Distress is experienced internally. As Dr. Bassirnia and her colleagues wrote in a poster presented at the recent American Psychiatric Association meeting, people with externalizing disorders, such as substance abuse and antisocial disorders, are more likely to express their distress outwardly and are less likely to suffer from stigma ("The relationship between personality traits and perceived internalized stigma in bipolar patients and their caregivers," 2014).

Meanwhile, two systematic review studies have reported moderate to high levels of internalized stigma in people with bipolar disorder. In these studies, a higher level of internalized stigma had a negative correlation with self-esteem, social adjustment, and perceived social support, and positive correlation with severity of symptoms, functional impairment, and rehospitalization. In spite of having more severe symptoms; people with higher levels of self-stigma are less likely to seek professional help and adhere to their treatment. Stigma by association and its negative consequences in caregivers of people with mental disorders also have been reported (J. Affect. Disord. 2013;150:181-91).

A useful and easy to administer scale that helps to identify stigma is the "Perceived Criticism Scale" (J. Abnorm. Psychol. 1989;98:225-35). By asking four questions, the clinician can get a good sense of family dynamics and can monitor the progress and change over time. The questions rate perception on a scale of 1-10, where "X" is the other person involved in treatment, either patient or caregiver. Here are the questions:

1. How critical do you think you are of X?

2. How critical do you think X is of you?

3. When X criticizes you, how upset do you get?

4. When you criticize X, how upset does he/she get?

For families with high scores, follow-up is needed. The Internalized Stigma of Mental Illness (ISMI) scale (Psychiatry Res. 2003;121:31-49) can be used. The ISMI scale makes statements about stigma for which participants rate their agreement on a Likert scale, such as:

• I don’t talk about myself much because I don’t want to burden others with my mental illness.

• Being around people who don’t have a mental illness makes me feel out of place or inadequate.

• People can tell that I have a mental illness by the way I look.

• Mentally ill people tend to be violent.

• I feel out of place in the world because I have a mental illness.

The ISMI scale contains 29 short, simple statements like the ones above and can be completed in less than 10 minutes. The statements are designed to avoid hypothetical situations, stay focused in the present, and address the participant’s own identity and experience.

Using the tools in practice

Naomi entered family treatment with her husband and daughters. Using the ISMI to measure the stigma of mental illness that each family member was experiencing, Naomi was shocked to see that her daughters felt far less stigma about having a mother with mental illness than she had assumed. In turn, her daughters were shocked at how much stigma Naomi was experiencing. Naomi’s husband scored between them. This data paved the way for an open family conversation about how Naomi’s illness had affected their lives, and especially how Naomi’s husband and his perceptions of her illness had affected her treatment course.

Caregivers play a very important role in bipolar disorder. After all, the illness can lead to difficulty functioning and can threaten the family’s stability. Sometimes caregivers can serve as a source of strength and a beacon of stability in the occasional storm. It is hard for the family between the storms, when the same flashing beacon can be a constant reminder to the patient of their illness. Often, well intentioned concerns become constant checking up, making the patient feel stigmatized and expected to fail.

"Good" caregivers will be aware of the stigma and the impact it has on their loved one and on themselves, without becoming a source of stigma.

Dr. Mednick is an attending psychiatrist at the Family Center for Bipolar at Mount Sinai Beth Israel in New York City. Dr. Bassirnia is a second-year psychiatry resident at Mount Sinai Beth Israel. Scan the QR code to read more Families in Psychiatry columns at clinicalpsychiatrynews.com.

Researchers in the lab

Credit: Rhoda Baer

A scientist’s chances of landing a faculty position at an academic institution are predictable based solely on his or her publication record, according to a study published in Current Biology.

Chances depend mostly on the number of publications the scientist has, the impact factor of the journals in which those papers are published, and the number of papers that receive more citations than expected based on the journal in which they were published, the researchers said.

“We’d like to start a discussion on what factors are taken into account when people are selected to become a principal investigator,” said study author David van Dijk, PhD, of the Weizmann Institute of Science in Rehovot, Israel.

“On the one hand, these results are encouraging, because they suggest that people are promoted based on merit. On the other hand, many of the most groundbreaking papers were not published in high-impact-factor journals and did not initially receive a high number of citations. This filtering method will certainly miss some phenomenal and ahead-of-their time scientists.”

Dr Van Dijk said he and his colleagues were motivated by endless conversations with fellow graduate students and post docs, who were dreaming of their first paper in a prestigious journal. There was the sense that those publications were the tickets to success.

So Dr van Dijk and his colleagues wanted to see if they could find evidence to that effect. And, indeed, they could.

The researchers generated publication record data for more than 25,000 scientists and used a machine-learning approach to generate a model of each individual’s chances of moving from the first-author position, typically reserved for trainees, to the last-author position, a place most often held by principal investigators (PIs).

“We find that whether or not a scientist becomes a PI is largely predictable by their publication record, even taking into account only the first few years of publication,” the researchers reported. “Our model is able to predict with relatively high accuracy who becomes a PI and is also able to predict how long this will take.”

To calculate your own likelihood of success using this model, visit: http://www.pipredictor.com.

Dr Van Dijk said the study results suggest the current system is working. Understanding how it works might be useful for those thinking through their careers or for those on hiring committees who might like to allow factors outside of the publication record to factor more significantly in hiring decisions.

The authors don’t recommend that scientists make decisions about their futures based solely on their PI prediction scores, of course. There are surely plenty of other harder-to-quantify factors that can also play a role. And there is some hopeful news for those who are persistent, even if they haven’t landed that stellar paper just yet.

“There is an element of luck in getting a paper in Nature, Cell, or Science, so it can be frustrating if you think you are a good scientist and want to succeed, but that high-impact-factor paper just doesn’t happen,” Dr van Dijk said.

“It’s encouraging that we find that doing good-quality science on a consistent basis—as evidenced by multiple first-author papers of reasonable impact factor—does seem to be rewarded in the end.”

Researchers in the lab

Credit: Rhoda Baer

A scientist’s chances of landing a faculty position at an academic institution are predictable based solely on his or her publication record, according to a study published in Current Biology.

Chances depend mostly on the number of publications the scientist has, the impact factor of the journals in which those papers are published, and the number of papers that receive more citations than expected based on the journal in which they were published, the researchers said.

“We’d like to start a discussion on what factors are taken into account when people are selected to become a principal investigator,” said study author David van Dijk, PhD, of the Weizmann Institute of Science in Rehovot, Israel.

“On the one hand, these results are encouraging, because they suggest that people are promoted based on merit. On the other hand, many of the most groundbreaking papers were not published in high-impact-factor journals and did not initially receive a high number of citations. This filtering method will certainly miss some phenomenal and ahead-of-their time scientists.”

Dr Van Dijk said he and his colleagues were motivated by endless conversations with fellow graduate students and post docs, who were dreaming of their first paper in a prestigious journal. There was the sense that those publications were the tickets to success.

So Dr van Dijk and his colleagues wanted to see if they could find evidence to that effect. And, indeed, they could.

The researchers generated publication record data for more than 25,000 scientists and used a machine-learning approach to generate a model of each individual’s chances of moving from the first-author position, typically reserved for trainees, to the last-author position, a place most often held by principal investigators (PIs).

“We find that whether or not a scientist becomes a PI is largely predictable by their publication record, even taking into account only the first few years of publication,” the researchers reported. “Our model is able to predict with relatively high accuracy who becomes a PI and is also able to predict how long this will take.”

To calculate your own likelihood of success using this model, visit: http://www.pipredictor.com.

Dr Van Dijk said the study results suggest the current system is working. Understanding how it works might be useful for those thinking through their careers or for those on hiring committees who might like to allow factors outside of the publication record to factor more significantly in hiring decisions.

The authors don’t recommend that scientists make decisions about their futures based solely on their PI prediction scores, of course. There are surely plenty of other harder-to-quantify factors that can also play a role. And there is some hopeful news for those who are persistent, even if they haven’t landed that stellar paper just yet.

“There is an element of luck in getting a paper in Nature, Cell, or Science, so it can be frustrating if you think you are a good scientist and want to succeed, but that high-impact-factor paper just doesn’t happen,” Dr van Dijk said.

“It’s encouraging that we find that doing good-quality science on a consistent basis—as evidenced by multiple first-author papers of reasonable impact factor—does seem to be rewarded in the end.”

Researchers in the lab

Credit: Rhoda Baer

A scientist’s chances of landing a faculty position at an academic institution are predictable based solely on his or her publication record, according to a study published in Current Biology.

Chances depend mostly on the number of publications the scientist has, the impact factor of the journals in which those papers are published, and the number of papers that receive more citations than expected based on the journal in which they were published, the researchers said.

“We’d like to start a discussion on what factors are taken into account when people are selected to become a principal investigator,” said study author David van Dijk, PhD, of the Weizmann Institute of Science in Rehovot, Israel.

“On the one hand, these results are encouraging, because they suggest that people are promoted based on merit. On the other hand, many of the most groundbreaking papers were not published in high-impact-factor journals and did not initially receive a high number of citations. This filtering method will certainly miss some phenomenal and ahead-of-their time scientists.”

Dr Van Dijk said he and his colleagues were motivated by endless conversations with fellow graduate students and post docs, who were dreaming of their first paper in a prestigious journal. There was the sense that those publications were the tickets to success.

So Dr van Dijk and his colleagues wanted to see if they could find evidence to that effect. And, indeed, they could.

The researchers generated publication record data for more than 25,000 scientists and used a machine-learning approach to generate a model of each individual’s chances of moving from the first-author position, typically reserved for trainees, to the last-author position, a place most often held by principal investigators (PIs).

“We find that whether or not a scientist becomes a PI is largely predictable by their publication record, even taking into account only the first few years of publication,” the researchers reported. “Our model is able to predict with relatively high accuracy who becomes a PI and is also able to predict how long this will take.”

To calculate your own likelihood of success using this model, visit: http://www.pipredictor.com.

Dr Van Dijk said the study results suggest the current system is working. Understanding how it works might be useful for those thinking through their careers or for those on hiring committees who might like to allow factors outside of the publication record to factor more significantly in hiring decisions.

The authors don’t recommend that scientists make decisions about their futures based solely on their PI prediction scores, of course. There are surely plenty of other harder-to-quantify factors that can also play a role. And there is some hopeful news for those who are persistent, even if they haven’t landed that stellar paper just yet.

“There is an element of luck in getting a paper in Nature, Cell, or Science, so it can be frustrating if you think you are a good scientist and want to succeed, but that high-impact-factor paper just doesn’t happen,” Dr van Dijk said.

“It’s encouraging that we find that doing good-quality science on a consistent basis—as evidenced by multiple first-author papers of reasonable impact factor—does seem to be rewarded in the end.”