Blood-brain barrier imaging can serve as a biomarker for progression of disease in adults with bipolar disorder, results from a small study suggest.

“While the pathophysiology of bipolar disorder remains poorly understood, converging evidence points to the presence of neuroinflammation in bipolar patients,” wrote Lyna Kamintsky, a PhD candidate at Dalhousie University, Halifax, N.S., and colleagues.

The researchers examined MRI data from 36 patients with bipolar disorder and compared them with 14 matched controls. The average age of the patients was 49 years and the average duration of illness was 28 years. The study was published in NeuroImage: Clinical (2019 Oct 22. doi: 10.1016/j.nicl.2019.102049).

“Leakage rates were considered pathological when exceeding 0.02, the 95th percentile of all values in a cohort of control subjects,” the researchers said. Overall, 10 subjects (all patients with bipolar disorder) met criteria for “extensive blood-brain barrier leakage.” The researchers found that those patients also had higher rates of chronic illness, more frequent and/or severe manic episodes, and more severe anxiety, depression, and social/occupational dysfunction, compared with those without blood-brain barrier leakage.

The patients with extensive blood-brain barrier leakage also had higher body mass indexes, greater risk of cardiovascular disease, and advanced heart age. In addition, all patients in this group had comorbid insulin resistance.

The study findings were limited by the small sample size, but the results suggest that blood-brain barrier imaging could be a biomarker for bipolar disease progression with implications for treatment, the researchers said.

The study was supported by the European Union’s Seventh Framework Program, the Nova Scotia Health Research Foundation, Brain Canada, and the Brain & Behavior Research Foundation. The researchers disclosed having no financial conflicts.

SOURCE: Kamintsky L et al. NeuroImage: Clinical. 2019 Oct 22. doi: 10.1016/j.nicl.2019.102049.

Blood-brain barrier imaging can serve as a biomarker for progression of disease in adults with bipolar disorder, results from a small study suggest.

“While the pathophysiology of bipolar disorder remains poorly understood, converging evidence points to the presence of neuroinflammation in bipolar patients,” wrote Lyna Kamintsky, a PhD candidate at Dalhousie University, Halifax, N.S., and colleagues.

The researchers examined MRI data from 36 patients with bipolar disorder and compared them with 14 matched controls. The average age of the patients was 49 years and the average duration of illness was 28 years. The study was published in NeuroImage: Clinical (2019 Oct 22. doi: 10.1016/j.nicl.2019.102049).

“Leakage rates were considered pathological when exceeding 0.02, the 95th percentile of all values in a cohort of control subjects,” the researchers said. Overall, 10 subjects (all patients with bipolar disorder) met criteria for “extensive blood-brain barrier leakage.” The researchers found that those patients also had higher rates of chronic illness, more frequent and/or severe manic episodes, and more severe anxiety, depression, and social/occupational dysfunction, compared with those without blood-brain barrier leakage.

The patients with extensive blood-brain barrier leakage also had higher body mass indexes, greater risk of cardiovascular disease, and advanced heart age. In addition, all patients in this group had comorbid insulin resistance.

The study findings were limited by the small sample size, but the results suggest that blood-brain barrier imaging could be a biomarker for bipolar disease progression with implications for treatment, the researchers said.

The study was supported by the European Union’s Seventh Framework Program, the Nova Scotia Health Research Foundation, Brain Canada, and the Brain & Behavior Research Foundation. The researchers disclosed having no financial conflicts.

SOURCE: Kamintsky L et al. NeuroImage: Clinical. 2019 Oct 22. doi: 10.1016/j.nicl.2019.102049.

Blood-brain barrier imaging can serve as a biomarker for progression of disease in adults with bipolar disorder, results from a small study suggest.

“While the pathophysiology of bipolar disorder remains poorly understood, converging evidence points to the presence of neuroinflammation in bipolar patients,” wrote Lyna Kamintsky, a PhD candidate at Dalhousie University, Halifax, N.S., and colleagues.

The researchers examined MRI data from 36 patients with bipolar disorder and compared them with 14 matched controls. The average age of the patients was 49 years and the average duration of illness was 28 years. The study was published in NeuroImage: Clinical (2019 Oct 22. doi: 10.1016/j.nicl.2019.102049).

“Leakage rates were considered pathological when exceeding 0.02, the 95th percentile of all values in a cohort of control subjects,” the researchers said. Overall, 10 subjects (all patients with bipolar disorder) met criteria for “extensive blood-brain barrier leakage.” The researchers found that those patients also had higher rates of chronic illness, more frequent and/or severe manic episodes, and more severe anxiety, depression, and social/occupational dysfunction, compared with those without blood-brain barrier leakage.

The patients with extensive blood-brain barrier leakage also had higher body mass indexes, greater risk of cardiovascular disease, and advanced heart age. In addition, all patients in this group had comorbid insulin resistance.

The study findings were limited by the small sample size, but the results suggest that blood-brain barrier imaging could be a biomarker for bipolar disease progression with implications for treatment, the researchers said.

The study was supported by the European Union’s Seventh Framework Program, the Nova Scotia Health Research Foundation, Brain Canada, and the Brain & Behavior Research Foundation. The researchers disclosed having no financial conflicts.

SOURCE: Kamintsky L et al. NeuroImage: Clinical. 2019 Oct 22. doi: 10.1016/j.nicl.2019.102049.

Aklief Cream Topical Retinoid Approved for Acne Vulgaris

Galderma Laboratories, LP, announces US Food and Drug Administration approval of Aklief (trifarotene) Cream 0.005% for the treatment of acne vulgaris in patients 9 years and older. Trifarotene is a retinoid that selectively targets retinoic acid receptor γ. Aklief Cream treats both facial and truncal acne. Aklief Cream is expected to be available in the United States in November 2019 in a 45-g pump. For more information, visit www.galderma.com.

Altreno Lotion Now Available in a 20-g Tube for Dermatologist Dispensing

Ortho Dermatologics launches a 20-g tube of Altreno (tretinoin) Lotion 0.05% for dermatologists to dispense in their offices. Offering the product in the physician’s office helps ensure that patients will be ready to begin their acne regimen, increasing patient compliance. Altreno Lotion is approved for the treatment of acne vulgaris in patients 9 years and older. It provides efficacy and tolerability in a once-daily dosing regimen. For more information, visit www.altrenohcp.com.

Amzeeq Topical Minocycline Approved for Acne

Foamix Pharmaceuticals Ltd receives US Food and Drug Administration approval of Amzeeq (minocycline) Foam 4% for the treatment of moderate to severe acne vulgaris in patients 9 years and older. Foamix’s proprietary Molecule Stabilizing Technology is used to effectively deliver minocycline—a broad-spectrum antibiotic—in a foam-based vehicle for once-daily application. Amzeeq is expected to be available for prescribing in January 2020. For more information, visit www.foamix.com.

FDA Clears Protego Antimicrobial Wound Dressing

Turn Therapeutics, Inc, receives US Food and Drug Administration clearance of Protego antimicrobial wound dressing for acute and chronic wound management. Protego wound dressings are single-use, sterile, antimicrobial gauze dressings impregnated with Hexagen, a proprietary petrolatum-based wound care emulsion. Protego offers patients the utility of traditional petrolatum-saturated gauze dressings with the added benefit of broad-spectrum antimicrobial protection against bacteria, fungi, and yeasts. For more information, visit www.turntherapeutics.com.

Skin Cancer Foundation Champions for Change Gala Raises More Than $700,000

The Skin Cancer Foundation held its 23rd annual Champions for Change Gala on October 17, 2019. The foundation’s signature fundraising event raised more than $700,000 to support educational campaigns, community programs, and research initiatives. More than 400 guests attended the event at The Plaza Hotel in New York, New York. The event was emceed by comedian Tom Kelly, and President Dr. Deborah S. Sarnoff reflected on the 40th birthday of the foundation, reinforcing the goal “to change behaviors and save lives.” For more information, visit www.skincancer.org.



If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

Aklief Cream Topical Retinoid Approved for Acne Vulgaris

Galderma Laboratories, LP, announces US Food and Drug Administration approval of Aklief (trifarotene) Cream 0.005% for the treatment of acne vulgaris in patients 9 years and older. Trifarotene is a retinoid that selectively targets retinoic acid receptor γ. Aklief Cream treats both facial and truncal acne. Aklief Cream is expected to be available in the United States in November 2019 in a 45-g pump. For more information, visit www.galderma.com.

Altreno Lotion Now Available in a 20-g Tube for Dermatologist Dispensing

Ortho Dermatologics launches a 20-g tube of Altreno (tretinoin) Lotion 0.05% for dermatologists to dispense in their offices. Offering the product in the physician’s office helps ensure that patients will be ready to begin their acne regimen, increasing patient compliance. Altreno Lotion is approved for the treatment of acne vulgaris in patients 9 years and older. It provides efficacy and tolerability in a once-daily dosing regimen. For more information, visit www.altrenohcp.com.

Amzeeq Topical Minocycline Approved for Acne

Foamix Pharmaceuticals Ltd receives US Food and Drug Administration approval of Amzeeq (minocycline) Foam 4% for the treatment of moderate to severe acne vulgaris in patients 9 years and older. Foamix’s proprietary Molecule Stabilizing Technology is used to effectively deliver minocycline—a broad-spectrum antibiotic—in a foam-based vehicle for once-daily application. Amzeeq is expected to be available for prescribing in January 2020. For more information, visit www.foamix.com.

FDA Clears Protego Antimicrobial Wound Dressing

Turn Therapeutics, Inc, receives US Food and Drug Administration clearance of Protego antimicrobial wound dressing for acute and chronic wound management. Protego wound dressings are single-use, sterile, antimicrobial gauze dressings impregnated with Hexagen, a proprietary petrolatum-based wound care emulsion. Protego offers patients the utility of traditional petrolatum-saturated gauze dressings with the added benefit of broad-spectrum antimicrobial protection against bacteria, fungi, and yeasts. For more information, visit www.turntherapeutics.com.

Skin Cancer Foundation Champions for Change Gala Raises More Than $700,000

The Skin Cancer Foundation held its 23rd annual Champions for Change Gala on October 17, 2019. The foundation’s signature fundraising event raised more than $700,000 to support educational campaigns, community programs, and research initiatives. More than 400 guests attended the event at The Plaza Hotel in New York, New York. The event was emceed by comedian Tom Kelly, and President Dr. Deborah S. Sarnoff reflected on the 40th birthday of the foundation, reinforcing the goal “to change behaviors and save lives.” For more information, visit www.skincancer.org.



If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

Aklief Cream Topical Retinoid Approved for Acne Vulgaris

Galderma Laboratories, LP, announces US Food and Drug Administration approval of Aklief (trifarotene) Cream 0.005% for the treatment of acne vulgaris in patients 9 years and older. Trifarotene is a retinoid that selectively targets retinoic acid receptor γ. Aklief Cream treats both facial and truncal acne. Aklief Cream is expected to be available in the United States in November 2019 in a 45-g pump. For more information, visit www.galderma.com.

Altreno Lotion Now Available in a 20-g Tube for Dermatologist Dispensing

Ortho Dermatologics launches a 20-g tube of Altreno (tretinoin) Lotion 0.05% for dermatologists to dispense in their offices. Offering the product in the physician’s office helps ensure that patients will be ready to begin their acne regimen, increasing patient compliance. Altreno Lotion is approved for the treatment of acne vulgaris in patients 9 years and older. It provides efficacy and tolerability in a once-daily dosing regimen. For more information, visit www.altrenohcp.com.

Amzeeq Topical Minocycline Approved for Acne

Foamix Pharmaceuticals Ltd receives US Food and Drug Administration approval of Amzeeq (minocycline) Foam 4% for the treatment of moderate to severe acne vulgaris in patients 9 years and older. Foamix’s proprietary Molecule Stabilizing Technology is used to effectively deliver minocycline—a broad-spectrum antibiotic—in a foam-based vehicle for once-daily application. Amzeeq is expected to be available for prescribing in January 2020. For more information, visit www.foamix.com.

FDA Clears Protego Antimicrobial Wound Dressing

Turn Therapeutics, Inc, receives US Food and Drug Administration clearance of Protego antimicrobial wound dressing for acute and chronic wound management. Protego wound dressings are single-use, sterile, antimicrobial gauze dressings impregnated with Hexagen, a proprietary petrolatum-based wound care emulsion. Protego offers patients the utility of traditional petrolatum-saturated gauze dressings with the added benefit of broad-spectrum antimicrobial protection against bacteria, fungi, and yeasts. For more information, visit www.turntherapeutics.com.

Skin Cancer Foundation Champions for Change Gala Raises More Than $700,000

The Skin Cancer Foundation held its 23rd annual Champions for Change Gala on October 17, 2019. The foundation’s signature fundraising event raised more than $700,000 to support educational campaigns, community programs, and research initiatives. More than 400 guests attended the event at The Plaza Hotel in New York, New York. The event was emceed by comedian Tom Kelly, and President Dr. Deborah S. Sarnoff reflected on the 40th birthday of the foundation, reinforcing the goal “to change behaviors and save lives.” For more information, visit www.skincancer.org.



If you would like your product included in Product News, please email a press release to the Editorial Office at [email protected].

I became a better doctor on the day I became a cardiac patient. On that day, I experienced the helpless, vulnerable, and needy feelings of a patient’s dependency and blind trust of a physician whom I did not know. I suddenly realized how it feels to be a patient.

Courtesy Richard W. Cohen

My entire life, I had always been an athlete in excellent shape. My 7-day-a-week daily schedule included seeing patients, being an expert psychiatric witness for disability cases, playing 2 hours of tennis, walking/running for 1 hour, and ending the night with 1 hour on a stationary bike.

I get to see my children all the time. I am so fortunate to get to travel with them and play national father-son and father-daughter tennis tournaments. We have been ranked No. 1 in the country many times. I have won 16 gold balls in these tournaments, each symbolic of a U.S. championship.

As a busy board-certified psychiatrist, I had been featured in an article, “Well being: Tennis is doctor’s favorite medicine,” by Art Carey, in the Philadelphia Inquirer, posted May 2, 2011. The author discussed my diet and exercise regime, and how I used exercise to stay healthy and to deal with the stress of being a physician.
 

‘Take me to the hospital’

At the end of 2018, I had a complete blood count performed, and the results indicated that I had a lipid panel of a healthy 30-year-old; however, my delusional bubble burst in March 2019. I was the No. 1 seed in a National Father-Daughter Tennis Tournament in Chicago. We were in the semifinal match, we had won the first set, and we were up 3-0. I fell, hit my head on the net post, and was feeling nauseated. I checked for bleeding and continued playing, though I was not feeling well. Five minutes later, I experienced symptoms of very extreme gastrointestinal pain and nausea. I ran off the tennis court wanting to vomit and get rid of the symptom so I could go back and finish the match. I wanted to play in the finals the following day and try to win the tournament.

The kind, competent, compassionate, and warm tournament director said I looked gray – and he promptly called 911. The paramedics came and said they thought I may be having a heart attack. I was in denial since I had no chest pain and I thought I was super healthy; therefore, I could not be experiencing an acute myocardial infarction. I finally agreed to let technicians perform an EKG, and they told me that I had ST elevation. Reality finally set in and I realized I was having a heart attack. “Take me to the hospital,” I said.

At the Chicago hospital where I was taken, I told doctors and staff I was a physician. To my surprise, they did not care. I was not going to get any prioritized treatment. Despite all of my devotion to medicine, I was not even getting their top physician to treat me. I was being evaluated by a resident. I felt even more deflated.

They performed a cardiac catheterization and put in one stent in one vessel in the right cardiac vessel. I had many questions to ask, but everyone seemed very impatient and abrupt with me, acting like this was just a very routine procedure. No one ever adequately answered my questions. I was very disillusioned, and I felt very insignificant, scared, and invisible.

I was discharged a few days later and was told my heart problem was fixed. I was instructed to follow up with a cardiologist in Philadelphia when I got home.

The first night home, I experienced chest pain. I was alarmed and thought my stent may have collapsed, so I went to the emergency room of the Philadelphia area hospital I knew had the best cardiac staff. After another blood test, indicating raised troponin levels, I was informed they needed to perform another cardiac catheterization. I learned I had two more coronary artery blockages, each 95%-99%, in the left ventricle.

I was shocked. How could the doctor in Chicago have made such a significant mistake? What happened? I would never know.

The interventional cardiologist in Philadelphia was able to repair one coronary artery, but the other blockage in the LED vessel (yes, the widow maker) had calcified too much for a stent. I would need cardiac bypass surgery. This was very unbelievable to me, and furthermore, I would have to wait 2 long weeks for the anticoagulant effect of the Brilinta to wear off before I could undergo bypass surgery.

While I anxiously waited for the big day, I was calling either my cardiologist, surgeon, or his nurse practitioner almost daily with questions and concerns; after all, this was a life-threatening and momentous event. Thankfully, I was met with great patience, understanding, and promptness of detailed answers and explanations by all involved with my cardiac care. The reactions of the staff made me mindful of the importance of really hearing my patients’ concerns and addressing their issues in a prompt, nonjudgmental, patient, and genuine manner. I am grateful that my robotic cardiac bypass surgery on March 26, 2019, went very well, and I am now back to work, playing tennis, jogging slowly, and riding my stationery bike.
 

Changed perspective on practice

I had always thought of myself as a warm, caring, and empathic psychiatrist, but my experience as a cardiac patient made me realize that there is always room for improvement in treating my patients.

Remember, every doctor will become a patient one day, and the reality of illness, injury, and mortality may really hit you hard, as it did me. You may not receive any prioritized treatment and you will know what it feels like to be helpless, vulnerable, and at the mercy of a physician while you regress in the service of the ego and become a patient.

You can be a better doctor now if you are mindful that whatever the physical, emotional, or mental issue facing your patients, the problem may be catastrophic to them. They need your undivided attention. Any problem is a significant event to your presenting patient. Really listen to his or her concerns or questions, and address every one with patience, understanding, and accurate information. Be genuine, empathetic, and nonjudgmental toward your patient so he or she will be open and honest with you. If you follow these lessons, which I learned the hard way, you can become a better doctor.

I followed my doctor’s instructions and I started hitting tennis balls gradually. I worked myself back into shape and with my daughter Julia Cohen, and we won the USTA National Father Daughter Clay Court Championship in Florida 6 months after I had the heart attack during a national tennis tournament. This is the comeback of the year in tennis!
 

Dr. Cohen has had a private practice in psychiatry for more than 35 years. He is a former professor of psychiatry, family medicine, and otolaryngology at Thomas Jefferson University in Philadelphia. Dr. Cohen has been a nationally ranked tennis player from age 12 to the present, served as captain of the University of Pennsylvania tennis team, and ranked No. 1 in tennis in the middle states section and in the country in various categories and times. He was inducted into the Philadelphia Jewish Sports Hall of Fame in 2012.

I became a better doctor on the day I became a cardiac patient. On that day, I experienced the helpless, vulnerable, and needy feelings of a patient’s dependency and blind trust of a physician whom I did not know. I suddenly realized how it feels to be a patient.

Courtesy Richard W. Cohen

My entire life, I had always been an athlete in excellent shape. My 7-day-a-week daily schedule included seeing patients, being an expert psychiatric witness for disability cases, playing 2 hours of tennis, walking/running for 1 hour, and ending the night with 1 hour on a stationary bike.

I get to see my children all the time. I am so fortunate to get to travel with them and play national father-son and father-daughter tennis tournaments. We have been ranked No. 1 in the country many times. I have won 16 gold balls in these tournaments, each symbolic of a U.S. championship.

As a busy board-certified psychiatrist, I had been featured in an article, “Well being: Tennis is doctor’s favorite medicine,” by Art Carey, in the Philadelphia Inquirer, posted May 2, 2011. The author discussed my diet and exercise regime, and how I used exercise to stay healthy and to deal with the stress of being a physician.
 

‘Take me to the hospital’

At the end of 2018, I had a complete blood count performed, and the results indicated that I had a lipid panel of a healthy 30-year-old; however, my delusional bubble burst in March 2019. I was the No. 1 seed in a National Father-Daughter Tennis Tournament in Chicago. We were in the semifinal match, we had won the first set, and we were up 3-0. I fell, hit my head on the net post, and was feeling nauseated. I checked for bleeding and continued playing, though I was not feeling well. Five minutes later, I experienced symptoms of very extreme gastrointestinal pain and nausea. I ran off the tennis court wanting to vomit and get rid of the symptom so I could go back and finish the match. I wanted to play in the finals the following day and try to win the tournament.

The kind, competent, compassionate, and warm tournament director said I looked gray – and he promptly called 911. The paramedics came and said they thought I may be having a heart attack. I was in denial since I had no chest pain and I thought I was super healthy; therefore, I could not be experiencing an acute myocardial infarction. I finally agreed to let technicians perform an EKG, and they told me that I had ST elevation. Reality finally set in and I realized I was having a heart attack. “Take me to the hospital,” I said.

At the Chicago hospital where I was taken, I told doctors and staff I was a physician. To my surprise, they did not care. I was not going to get any prioritized treatment. Despite all of my devotion to medicine, I was not even getting their top physician to treat me. I was being evaluated by a resident. I felt even more deflated.

They performed a cardiac catheterization and put in one stent in one vessel in the right cardiac vessel. I had many questions to ask, but everyone seemed very impatient and abrupt with me, acting like this was just a very routine procedure. No one ever adequately answered my questions. I was very disillusioned, and I felt very insignificant, scared, and invisible.

I was discharged a few days later and was told my heart problem was fixed. I was instructed to follow up with a cardiologist in Philadelphia when I got home.

The first night home, I experienced chest pain. I was alarmed and thought my stent may have collapsed, so I went to the emergency room of the Philadelphia area hospital I knew had the best cardiac staff. After another blood test, indicating raised troponin levels, I was informed they needed to perform another cardiac catheterization. I learned I had two more coronary artery blockages, each 95%-99%, in the left ventricle.

I was shocked. How could the doctor in Chicago have made such a significant mistake? What happened? I would never know.

The interventional cardiologist in Philadelphia was able to repair one coronary artery, but the other blockage in the LED vessel (yes, the widow maker) had calcified too much for a stent. I would need cardiac bypass surgery. This was very unbelievable to me, and furthermore, I would have to wait 2 long weeks for the anticoagulant effect of the Brilinta to wear off before I could undergo bypass surgery.

While I anxiously waited for the big day, I was calling either my cardiologist, surgeon, or his nurse practitioner almost daily with questions and concerns; after all, this was a life-threatening and momentous event. Thankfully, I was met with great patience, understanding, and promptness of detailed answers and explanations by all involved with my cardiac care. The reactions of the staff made me mindful of the importance of really hearing my patients’ concerns and addressing their issues in a prompt, nonjudgmental, patient, and genuine manner. I am grateful that my robotic cardiac bypass surgery on March 26, 2019, went very well, and I am now back to work, playing tennis, jogging slowly, and riding my stationery bike.
 

Changed perspective on practice

I had always thought of myself as a warm, caring, and empathic psychiatrist, but my experience as a cardiac patient made me realize that there is always room for improvement in treating my patients.

Remember, every doctor will become a patient one day, and the reality of illness, injury, and mortality may really hit you hard, as it did me. You may not receive any prioritized treatment and you will know what it feels like to be helpless, vulnerable, and at the mercy of a physician while you regress in the service of the ego and become a patient.

You can be a better doctor now if you are mindful that whatever the physical, emotional, or mental issue facing your patients, the problem may be catastrophic to them. They need your undivided attention. Any problem is a significant event to your presenting patient. Really listen to his or her concerns or questions, and address every one with patience, understanding, and accurate information. Be genuine, empathetic, and nonjudgmental toward your patient so he or she will be open and honest with you. If you follow these lessons, which I learned the hard way, you can become a better doctor.

I followed my doctor’s instructions and I started hitting tennis balls gradually. I worked myself back into shape and with my daughter Julia Cohen, and we won the USTA National Father Daughter Clay Court Championship in Florida 6 months after I had the heart attack during a national tennis tournament. This is the comeback of the year in tennis!
 

Dr. Cohen has had a private practice in psychiatry for more than 35 years. He is a former professor of psychiatry, family medicine, and otolaryngology at Thomas Jefferson University in Philadelphia. Dr. Cohen has been a nationally ranked tennis player from age 12 to the present, served as captain of the University of Pennsylvania tennis team, and ranked No. 1 in tennis in the middle states section and in the country in various categories and times. He was inducted into the Philadelphia Jewish Sports Hall of Fame in 2012.

I became a better doctor on the day I became a cardiac patient. On that day, I experienced the helpless, vulnerable, and needy feelings of a patient’s dependency and blind trust of a physician whom I did not know. I suddenly realized how it feels to be a patient.

Courtesy Richard W. Cohen

My entire life, I had always been an athlete in excellent shape. My 7-day-a-week daily schedule included seeing patients, being an expert psychiatric witness for disability cases, playing 2 hours of tennis, walking/running for 1 hour, and ending the night with 1 hour on a stationary bike.

I get to see my children all the time. I am so fortunate to get to travel with them and play national father-son and father-daughter tennis tournaments. We have been ranked No. 1 in the country many times. I have won 16 gold balls in these tournaments, each symbolic of a U.S. championship.

As a busy board-certified psychiatrist, I had been featured in an article, “Well being: Tennis is doctor’s favorite medicine,” by Art Carey, in the Philadelphia Inquirer, posted May 2, 2011. The author discussed my diet and exercise regime, and how I used exercise to stay healthy and to deal with the stress of being a physician.
 

‘Take me to the hospital’

At the end of 2018, I had a complete blood count performed, and the results indicated that I had a lipid panel of a healthy 30-year-old; however, my delusional bubble burst in March 2019. I was the No. 1 seed in a National Father-Daughter Tennis Tournament in Chicago. We were in the semifinal match, we had won the first set, and we were up 3-0. I fell, hit my head on the net post, and was feeling nauseated. I checked for bleeding and continued playing, though I was not feeling well. Five minutes later, I experienced symptoms of very extreme gastrointestinal pain and nausea. I ran off the tennis court wanting to vomit and get rid of the symptom so I could go back and finish the match. I wanted to play in the finals the following day and try to win the tournament.

The kind, competent, compassionate, and warm tournament director said I looked gray – and he promptly called 911. The paramedics came and said they thought I may be having a heart attack. I was in denial since I had no chest pain and I thought I was super healthy; therefore, I could not be experiencing an acute myocardial infarction. I finally agreed to let technicians perform an EKG, and they told me that I had ST elevation. Reality finally set in and I realized I was having a heart attack. “Take me to the hospital,” I said.

At the Chicago hospital where I was taken, I told doctors and staff I was a physician. To my surprise, they did not care. I was not going to get any prioritized treatment. Despite all of my devotion to medicine, I was not even getting their top physician to treat me. I was being evaluated by a resident. I felt even more deflated.

They performed a cardiac catheterization and put in one stent in one vessel in the right cardiac vessel. I had many questions to ask, but everyone seemed very impatient and abrupt with me, acting like this was just a very routine procedure. No one ever adequately answered my questions. I was very disillusioned, and I felt very insignificant, scared, and invisible.

I was discharged a few days later and was told my heart problem was fixed. I was instructed to follow up with a cardiologist in Philadelphia when I got home.

The first night home, I experienced chest pain. I was alarmed and thought my stent may have collapsed, so I went to the emergency room of the Philadelphia area hospital I knew had the best cardiac staff. After another blood test, indicating raised troponin levels, I was informed they needed to perform another cardiac catheterization. I learned I had two more coronary artery blockages, each 95%-99%, in the left ventricle.

I was shocked. How could the doctor in Chicago have made such a significant mistake? What happened? I would never know.

The interventional cardiologist in Philadelphia was able to repair one coronary artery, but the other blockage in the LED vessel (yes, the widow maker) had calcified too much for a stent. I would need cardiac bypass surgery. This was very unbelievable to me, and furthermore, I would have to wait 2 long weeks for the anticoagulant effect of the Brilinta to wear off before I could undergo bypass surgery.

While I anxiously waited for the big day, I was calling either my cardiologist, surgeon, or his nurse practitioner almost daily with questions and concerns; after all, this was a life-threatening and momentous event. Thankfully, I was met with great patience, understanding, and promptness of detailed answers and explanations by all involved with my cardiac care. The reactions of the staff made me mindful of the importance of really hearing my patients’ concerns and addressing their issues in a prompt, nonjudgmental, patient, and genuine manner. I am grateful that my robotic cardiac bypass surgery on March 26, 2019, went very well, and I am now back to work, playing tennis, jogging slowly, and riding my stationery bike.
 

Changed perspective on practice

I had always thought of myself as a warm, caring, and empathic psychiatrist, but my experience as a cardiac patient made me realize that there is always room for improvement in treating my patients.

Remember, every doctor will become a patient one day, and the reality of illness, injury, and mortality may really hit you hard, as it did me. You may not receive any prioritized treatment and you will know what it feels like to be helpless, vulnerable, and at the mercy of a physician while you regress in the service of the ego and become a patient.

You can be a better doctor now if you are mindful that whatever the physical, emotional, or mental issue facing your patients, the problem may be catastrophic to them. They need your undivided attention. Any problem is a significant event to your presenting patient. Really listen to his or her concerns or questions, and address every one with patience, understanding, and accurate information. Be genuine, empathetic, and nonjudgmental toward your patient so he or she will be open and honest with you. If you follow these lessons, which I learned the hard way, you can become a better doctor.

I followed my doctor’s instructions and I started hitting tennis balls gradually. I worked myself back into shape and with my daughter Julia Cohen, and we won the USTA National Father Daughter Clay Court Championship in Florida 6 months after I had the heart attack during a national tennis tournament. This is the comeback of the year in tennis!
 

Dr. Cohen has had a private practice in psychiatry for more than 35 years. He is a former professor of psychiatry, family medicine, and otolaryngology at Thomas Jefferson University in Philadelphia. Dr. Cohen has been a nationally ranked tennis player from age 12 to the present, served as captain of the University of Pennsylvania tennis team, and ranked No. 1 in tennis in the middle states section and in the country in various categories and times. He was inducted into the Philadelphia Jewish Sports Hall of Fame in 2012.

ATLANTA – Guselkumab improved outcomes in psoriatic arthritis patients regardless of past treatment with tumor necrosis factor inhibitors in the phase 3 DISCOVER-1 trial.

The anti-interleukin-23p19 monoclonal antibody is approved in the United States for the treatment of moderate to severe plaque psoriasis (PsO).

The response rates with guselkumab versus placebo were seen regardless of prior TNFi use, he said.

The study included 381 patients with active PsA, defined as three or more swollen joints, three or more tender joints, and C-reactive protein of 0.3 mg/dL or greater despite standard therapies. About 30% were exposed to up to two TNFi therapies and 10% were nonresponders or inadequate responders to those therapies.

Concomitant use of select nonbiologic disease-modifying antirheumatic drugs, oral corticosteroids, and NSAIDs was allowed, and patients with less than 5% improvement in tender plus swollen joints at week 16 could initiate or increase the dose of the permitted medications while continuing study treatment, Dr. Deodhar said.

The mean body surface area with PsO involvement was 13.4%; 42.5% of patients had an IGA of 3-4 for skin involvement. Mean swollen and tender joint counts were 9.8 and 19.3, respectively, indicating a population with moderate to severe disease, he added.

Serious adverse events, serious infections, and death occurred in 2.4%, 0.5%, and 0.3% of patients, respectively.

“Both guselkumab regimens were safe and well tolerated through week 24,” Dr. Deodhar said, noting that the safety profile was consistent with that established in the treatment of PsO and described in the label.

DISCOVER-1 was funded by Janssen Research & Development. Dr. Deodhar reported relationships (advisory board activity, consulting, and/or research grant funding) with several pharmaceutical companies including Janssen. Several coauthors are employees of Janssen.

[email protected]

SOURCE: Deodhar A et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 807.

ATLANTA – Guselkumab improved outcomes in psoriatic arthritis patients regardless of past treatment with tumor necrosis factor inhibitors in the phase 3 DISCOVER-1 trial.

The anti-interleukin-23p19 monoclonal antibody is approved in the United States for the treatment of moderate to severe plaque psoriasis (PsO).

The response rates with guselkumab versus placebo were seen regardless of prior TNFi use, he said.

The study included 381 patients with active PsA, defined as three or more swollen joints, three or more tender joints, and C-reactive protein of 0.3 mg/dL or greater despite standard therapies. About 30% were exposed to up to two TNFi therapies and 10% were nonresponders or inadequate responders to those therapies.

Concomitant use of select nonbiologic disease-modifying antirheumatic drugs, oral corticosteroids, and NSAIDs was allowed, and patients with less than 5% improvement in tender plus swollen joints at week 16 could initiate or increase the dose of the permitted medications while continuing study treatment, Dr. Deodhar said.

The mean body surface area with PsO involvement was 13.4%; 42.5% of patients had an IGA of 3-4 for skin involvement. Mean swollen and tender joint counts were 9.8 and 19.3, respectively, indicating a population with moderate to severe disease, he added.

Serious adverse events, serious infections, and death occurred in 2.4%, 0.5%, and 0.3% of patients, respectively.

“Both guselkumab regimens were safe and well tolerated through week 24,” Dr. Deodhar said, noting that the safety profile was consistent with that established in the treatment of PsO and described in the label.

DISCOVER-1 was funded by Janssen Research & Development. Dr. Deodhar reported relationships (advisory board activity, consulting, and/or research grant funding) with several pharmaceutical companies including Janssen. Several coauthors are employees of Janssen.

[email protected]

SOURCE: Deodhar A et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 807.

ATLANTA – Guselkumab improved outcomes in psoriatic arthritis patients regardless of past treatment with tumor necrosis factor inhibitors in the phase 3 DISCOVER-1 trial.

The anti-interleukin-23p19 monoclonal antibody is approved in the United States for the treatment of moderate to severe plaque psoriasis (PsO).

The response rates with guselkumab versus placebo were seen regardless of prior TNFi use, he said.

The study included 381 patients with active PsA, defined as three or more swollen joints, three or more tender joints, and C-reactive protein of 0.3 mg/dL or greater despite standard therapies. About 30% were exposed to up to two TNFi therapies and 10% were nonresponders or inadequate responders to those therapies.

Concomitant use of select nonbiologic disease-modifying antirheumatic drugs, oral corticosteroids, and NSAIDs was allowed, and patients with less than 5% improvement in tender plus swollen joints at week 16 could initiate or increase the dose of the permitted medications while continuing study treatment, Dr. Deodhar said.

The mean body surface area with PsO involvement was 13.4%; 42.5% of patients had an IGA of 3-4 for skin involvement. Mean swollen and tender joint counts were 9.8 and 19.3, respectively, indicating a population with moderate to severe disease, he added.

Serious adverse events, serious infections, and death occurred in 2.4%, 0.5%, and 0.3% of patients, respectively.

“Both guselkumab regimens were safe and well tolerated through week 24,” Dr. Deodhar said, noting that the safety profile was consistent with that established in the treatment of PsO and described in the label.

DISCOVER-1 was funded by Janssen Research & Development. Dr. Deodhar reported relationships (advisory board activity, consulting, and/or research grant funding) with several pharmaceutical companies including Janssen. Several coauthors are employees of Janssen.

[email protected]

SOURCE: Deodhar A et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 807.

ANSWER

This ECG shows sinus rhythm with complete heart block and a junctional rhythm with a right-axis deviation. Additionally, ventricular depolarization in the precordial leads is suggestive of an anterior myocardial infarction.

Sinus rhythm is evidenced by the regular, steady progression of P waves with a P-P interval of about 90 beats/min. Complete atrioventricular dissociation indicates complete heart block.

A normal QRS duration of 106 ms at a rate of 56 beats/min supports the diagnosis of a junctional escape rhythm. Right-axis deviation is evidenced by an R axis of 120°.

Finally, poor R-wave progression with deep S waves in leads V₁ through V₅ is suggestive of an anterior myocardial infarction. However, in this case, there is no evidence of ischemia or history of infarction—so these are thought to be early postoperative findings.

ANSWER

This ECG shows sinus rhythm with complete heart block and a junctional rhythm with a right-axis deviation. Additionally, ventricular depolarization in the precordial leads is suggestive of an anterior myocardial infarction.

Sinus rhythm is evidenced by the regular, steady progression of P waves with a P-P interval of about 90 beats/min. Complete atrioventricular dissociation indicates complete heart block.

A normal QRS duration of 106 ms at a rate of 56 beats/min supports the diagnosis of a junctional escape rhythm. Right-axis deviation is evidenced by an R axis of 120°.

Finally, poor R-wave progression with deep S waves in leads V₁ through V₅ is suggestive of an anterior myocardial infarction. However, in this case, there is no evidence of ischemia or history of infarction—so these are thought to be early postoperative findings.

ANSWER

This ECG shows sinus rhythm with complete heart block and a junctional rhythm with a right-axis deviation. Additionally, ventricular depolarization in the precordial leads is suggestive of an anterior myocardial infarction.

Sinus rhythm is evidenced by the regular, steady progression of P waves with a P-P interval of about 90 beats/min. Complete atrioventricular dissociation indicates complete heart block.

A normal QRS duration of 106 ms at a rate of 56 beats/min supports the diagnosis of a junctional escape rhythm. Right-axis deviation is evidenced by an R axis of 120°.

Finally, poor R-wave progression with deep S waves in leads V₁ through V₅ is suggestive of an anterior myocardial infarction. However, in this case, there is no evidence of ischemia or history of infarction—so these are thought to be early postoperative findings.

The Diagnosis: Congenital Self-healing Reticulohistiocytosis 

Biopsy of a representative lesion from this patient was consistent with congenital self-healing reticulohistiocytosis, as shown in the Figure. Characteristic Langerhans cells were present in the dermis that stained CD1a positive, S-100 positive, and CD68 negative to confirm the diagnosis.

Congenital self-healing reticulohistiocytosis, or Hashimoto-Pritzker syndrome, is a rare benign form of Langerhans cell histiocytosis. It is twice as common in males than females and typically noted at birth or early during the neonatal period. Lesions may present as pink, firm, asymptomatic papulonodular lesions that often ulcerate with possible residual hypopigmentation or hyperpigmentation.¹ The differential diagnosis includes congenital infectious and hematologic diseases typically associated with blueberry muffin baby. Thus, varicella, cytomegalovirus, syphilis, toxoplasmosis, rubella, neuroblastoma, leukemia cutis, and extramedullary hematopoiesis, among others, may be considered. Juvenile xanthogranuloma or urticaria pigmentosa also enter the differential diagnosis given the yellow-brown appearance. As a clonal proliferation of Langerhans cells, pathology reveals lesions that stain positive for CD1a and S-100.²  

Although typically absent, evaluation for systemic involvement is warranted, which may be an early presentation of multisystem Langerhans cell histiocytosis. Continued monitoring is recommended given the risk of relapse and associated mortality. Our patient continues to do well. He will continue to be followed by our team and hematology/oncology during early childhood.  

The treatment of congenital self-healing reticulohistiocytosis may include conservative monitoring, topical steroids, topical nitrogen mustard, tacrolimus, or psoralen plus UVA.³ Surgical excision may be considered for large lesions.  

The Diagnosis: Congenital Self-healing Reticulohistiocytosis 

Biopsy of a representative lesion from this patient was consistent with congenital self-healing reticulohistiocytosis, as shown in the Figure. Characteristic Langerhans cells were present in the dermis that stained CD1a positive, S-100 positive, and CD68 negative to confirm the diagnosis.

Congenital self-healing reticulohistiocytosis, or Hashimoto-Pritzker syndrome, is a rare benign form of Langerhans cell histiocytosis. It is twice as common in males than females and typically noted at birth or early during the neonatal period. Lesions may present as pink, firm, asymptomatic papulonodular lesions that often ulcerate with possible residual hypopigmentation or hyperpigmentation.¹ The differential diagnosis includes congenital infectious and hematologic diseases typically associated with blueberry muffin baby. Thus, varicella, cytomegalovirus, syphilis, toxoplasmosis, rubella, neuroblastoma, leukemia cutis, and extramedullary hematopoiesis, among others, may be considered. Juvenile xanthogranuloma or urticaria pigmentosa also enter the differential diagnosis given the yellow-brown appearance. As a clonal proliferation of Langerhans cells, pathology reveals lesions that stain positive for CD1a and S-100.²  

Although typically absent, evaluation for systemic involvement is warranted, which may be an early presentation of multisystem Langerhans cell histiocytosis. Continued monitoring is recommended given the risk of relapse and associated mortality. Our patient continues to do well. He will continue to be followed by our team and hematology/oncology during early childhood.  

The treatment of congenital self-healing reticulohistiocytosis may include conservative monitoring, topical steroids, topical nitrogen mustard, tacrolimus, or psoralen plus UVA.³ Surgical excision may be considered for large lesions.  

The Diagnosis: Congenital Self-healing Reticulohistiocytosis 

Biopsy of a representative lesion from this patient was consistent with congenital self-healing reticulohistiocytosis, as shown in the Figure. Characteristic Langerhans cells were present in the dermis that stained CD1a positive, S-100 positive, and CD68 negative to confirm the diagnosis.

Congenital self-healing reticulohistiocytosis, or Hashimoto-Pritzker syndrome, is a rare benign form of Langerhans cell histiocytosis. It is twice as common in males than females and typically noted at birth or early during the neonatal period. Lesions may present as pink, firm, asymptomatic papulonodular lesions that often ulcerate with possible residual hypopigmentation or hyperpigmentation.¹ The differential diagnosis includes congenital infectious and hematologic diseases typically associated with blueberry muffin baby. Thus, varicella, cytomegalovirus, syphilis, toxoplasmosis, rubella, neuroblastoma, leukemia cutis, and extramedullary hematopoiesis, among others, may be considered. Juvenile xanthogranuloma or urticaria pigmentosa also enter the differential diagnosis given the yellow-brown appearance. As a clonal proliferation of Langerhans cells, pathology reveals lesions that stain positive for CD1a and S-100.²  

Although typically absent, evaluation for systemic involvement is warranted, which may be an early presentation of multisystem Langerhans cell histiocytosis. Continued monitoring is recommended given the risk of relapse and associated mortality. Our patient continues to do well. He will continue to be followed by our team and hematology/oncology during early childhood.  

The treatment of congenital self-healing reticulohistiocytosis may include conservative monitoring, topical steroids, topical nitrogen mustard, tacrolimus, or psoralen plus UVA.³ Surgical excision may be considered for large lesions.  

ATLANTA – A group of patients using a tumor necrosis factor inhibitor safely received the live-attenuated varicella vaccine Zostavax without any cases of herpes zoster in the first 6 weeks after vaccination in the blinded, randomized, placebo-controlled Varicella Zoster Vaccine (VERVE) trial .

According to guidelines from the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, there is a theoretical concern that patients using a tumor necrosis factor inhibitor (TNFi) and other biologic therapies who receive a live-attenuated version of the varicella vaccine (Zostavax) could become infected with varicella from the vaccine. Patients with RA and psoriatic arthritis as well as other autoimmune and inflammatory conditions who are likely to receive TNFi therapy are also at risk for herpes zoster reactivation, Jeffrey Curtis, MD, professor of medicine in the division of clinical immunology and rheumatology of the University of Alabama at Birmingham, said in his presentation at the annual meeting of the American College of Rheumatology. There also exists a risk for patients receiving low-dose glucocorticoids.

“The challenge, of course, is there’s not a great definition and there certainly is not a well-standardized assay for how immunocompromised someone is, and so that led to the uncertainty in this patient population for this and other live-virus vaccines,” Dr. Curtis said.

Dr. Curtis and colleagues enrolled 627 participants from 33 centers into the VERVE trial. Participants were aged at least 50 years, were taking a TNFi, and had not previously received Zostavax.

Patients in both groups had a mean age of about 63 years and about two-thirds were women. The most common indications for TNFi use in the Zostavax group and the placebo group were RA (59.2% vs. 56.0%, respectively), psoriatic arthritis (24.3% vs. 23.9%), and ankylosing spondylitis (7.2% vs. 8.5%), while the anti-TNF agents used were adalimumab (38.1% vs. 27.4%), infliximab (28.4% vs. 34.2%), etanercept (19.0% vs. 23.5%), golimumab (10.0% vs. 8.1%), and certolizumab pegol (4.5% vs. 6.8%). In addition, some patients in the Zostavax and placebo groups were also taking concomitant therapies with TNFi, such as oral glucocorticoids (9.7% vs. 11.4%).

The researchers randomized participants to receive Zostavax or placebo (saline) and then followed them for 6 weeks, and looked for signs of wild-type or vaccine-strain varicella infection. If participants were suspected to have varicella, they were assessed clinically, underwent polymerase chain reaction testing, and rashes were photographed. At baseline and at 6 weeks, the researchers collected serum and peripheral blood mononuclear cells to determine patient immunity to varicella. After 6 months, participants were unmasked to the treatment arm of the study.

Dr. Curtis and colleagues found no confirmed varicella infection cases at 6 weeks. “To the extent that 0 cases out of 317 vaccinated people is reassuring, there were no cases, so that was exceedingly heartening as a result,” he said.

Out of 20 serious adverse events total in the groups, 15 events occurred before 6 months, including 8 suspected varicella cases in the Zostavax group and 7 in the placebo group. However, there were no positive cases of varicella – either wild type or vaccine type – after polymerase chain reaction tests. Overall, there were 268 adverse events in 195 participants, with 73 events (27.2%) consisting of injection-site reactions. The researchers also found no difference in the rate of disease flares, and found no differences in adverse reactions between groups, apart from a higher rate of injection-site reactions in the varicella group (19.4% vs. 4.2%).

With regard to immunogenicity, the humoral immune response was measured through IgG, which showed an immune response in the varicella group at 6 weeks (geometric mean fold ratio, 1.33; 95% confidence interval, 1.18-1.51), compared with the placebo group (GMFR, 1.02; 95% CI, 0.91-1.14); cell-mediated immune response was measured by interferon-gamma, which also showed an immune response in the live-vaccine group (GMFR, 1.49; 95% CI, 1.14-1.94), compared with participants who received placebo (GMFR, 1.14; 95% CI, 0.87-1.48). In preliminary 1-year data, IgG immune response was elevated in the varicella group (GMFR, 1.46; 95% CI, 1.08-1.99), but there was no elevated immune response for interferon-gamma (GMFR, 0.78; 95% CI, 0.49-1.25).

“I think the trial is encouraging not only for its result with the live zoster vaccine and TNF-treated patients, but also challenge the notion that, if you need to, a live-virus vaccine may in fact be able to be safely given to people with autoimmune and inflammatory diseases, even those treated with biologics like tumor necrosis factor inhibitors,” Dr. Curtis said.

As patients in VERVE consented to long-term follow-up in health plan claims and EHR data, it will be possible to follow these patients in the future to assess herpes zoster reactivation. Dr. Curtis also noted that a new trial involving the recombinant, adjuvanted zoster vaccine (Shingrix) is currently in development and should begin next year.

The VERVE trial was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Curtis reported serving as a current member of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices Herpes Zoster Work Group. He and some of the other authors reported financial relationships with many pharmaceutical companies.

SOURCE: Curtis J et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 824.

ATLANTA – A group of patients using a tumor necrosis factor inhibitor safely received the live-attenuated varicella vaccine Zostavax without any cases of herpes zoster in the first 6 weeks after vaccination in the blinded, randomized, placebo-controlled Varicella Zoster Vaccine (VERVE) trial .

According to guidelines from the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, there is a theoretical concern that patients using a tumor necrosis factor inhibitor (TNFi) and other biologic therapies who receive a live-attenuated version of the varicella vaccine (Zostavax) could become infected with varicella from the vaccine. Patients with RA and psoriatic arthritis as well as other autoimmune and inflammatory conditions who are likely to receive TNFi therapy are also at risk for herpes zoster reactivation, Jeffrey Curtis, MD, professor of medicine in the division of clinical immunology and rheumatology of the University of Alabama at Birmingham, said in his presentation at the annual meeting of the American College of Rheumatology. There also exists a risk for patients receiving low-dose glucocorticoids.

“The challenge, of course, is there’s not a great definition and there certainly is not a well-standardized assay for how immunocompromised someone is, and so that led to the uncertainty in this patient population for this and other live-virus vaccines,” Dr. Curtis said.

Dr. Curtis and colleagues enrolled 627 participants from 33 centers into the VERVE trial. Participants were aged at least 50 years, were taking a TNFi, and had not previously received Zostavax.

Patients in both groups had a mean age of about 63 years and about two-thirds were women. The most common indications for TNFi use in the Zostavax group and the placebo group were RA (59.2% vs. 56.0%, respectively), psoriatic arthritis (24.3% vs. 23.9%), and ankylosing spondylitis (7.2% vs. 8.5%), while the anti-TNF agents used were adalimumab (38.1% vs. 27.4%), infliximab (28.4% vs. 34.2%), etanercept (19.0% vs. 23.5%), golimumab (10.0% vs. 8.1%), and certolizumab pegol (4.5% vs. 6.8%). In addition, some patients in the Zostavax and placebo groups were also taking concomitant therapies with TNFi, such as oral glucocorticoids (9.7% vs. 11.4%).

The researchers randomized participants to receive Zostavax or placebo (saline) and then followed them for 6 weeks, and looked for signs of wild-type or vaccine-strain varicella infection. If participants were suspected to have varicella, they were assessed clinically, underwent polymerase chain reaction testing, and rashes were photographed. At baseline and at 6 weeks, the researchers collected serum and peripheral blood mononuclear cells to determine patient immunity to varicella. After 6 months, participants were unmasked to the treatment arm of the study.

Dr. Curtis and colleagues found no confirmed varicella infection cases at 6 weeks. “To the extent that 0 cases out of 317 vaccinated people is reassuring, there were no cases, so that was exceedingly heartening as a result,” he said.

Out of 20 serious adverse events total in the groups, 15 events occurred before 6 months, including 8 suspected varicella cases in the Zostavax group and 7 in the placebo group. However, there were no positive cases of varicella – either wild type or vaccine type – after polymerase chain reaction tests. Overall, there were 268 adverse events in 195 participants, with 73 events (27.2%) consisting of injection-site reactions. The researchers also found no difference in the rate of disease flares, and found no differences in adverse reactions between groups, apart from a higher rate of injection-site reactions in the varicella group (19.4% vs. 4.2%).

With regard to immunogenicity, the humoral immune response was measured through IgG, which showed an immune response in the varicella group at 6 weeks (geometric mean fold ratio, 1.33; 95% confidence interval, 1.18-1.51), compared with the placebo group (GMFR, 1.02; 95% CI, 0.91-1.14); cell-mediated immune response was measured by interferon-gamma, which also showed an immune response in the live-vaccine group (GMFR, 1.49; 95% CI, 1.14-1.94), compared with participants who received placebo (GMFR, 1.14; 95% CI, 0.87-1.48). In preliminary 1-year data, IgG immune response was elevated in the varicella group (GMFR, 1.46; 95% CI, 1.08-1.99), but there was no elevated immune response for interferon-gamma (GMFR, 0.78; 95% CI, 0.49-1.25).

“I think the trial is encouraging not only for its result with the live zoster vaccine and TNF-treated patients, but also challenge the notion that, if you need to, a live-virus vaccine may in fact be able to be safely given to people with autoimmune and inflammatory diseases, even those treated with biologics like tumor necrosis factor inhibitors,” Dr. Curtis said.

As patients in VERVE consented to long-term follow-up in health plan claims and EHR data, it will be possible to follow these patients in the future to assess herpes zoster reactivation. Dr. Curtis also noted that a new trial involving the recombinant, adjuvanted zoster vaccine (Shingrix) is currently in development and should begin next year.

The VERVE trial was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Curtis reported serving as a current member of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices Herpes Zoster Work Group. He and some of the other authors reported financial relationships with many pharmaceutical companies.

SOURCE: Curtis J et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 824.

ATLANTA – A group of patients using a tumor necrosis factor inhibitor safely received the live-attenuated varicella vaccine Zostavax without any cases of herpes zoster in the first 6 weeks after vaccination in the blinded, randomized, placebo-controlled Varicella Zoster Vaccine (VERVE) trial .

According to guidelines from the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, there is a theoretical concern that patients using a tumor necrosis factor inhibitor (TNFi) and other biologic therapies who receive a live-attenuated version of the varicella vaccine (Zostavax) could become infected with varicella from the vaccine. Patients with RA and psoriatic arthritis as well as other autoimmune and inflammatory conditions who are likely to receive TNFi therapy are also at risk for herpes zoster reactivation, Jeffrey Curtis, MD, professor of medicine in the division of clinical immunology and rheumatology of the University of Alabama at Birmingham, said in his presentation at the annual meeting of the American College of Rheumatology. There also exists a risk for patients receiving low-dose glucocorticoids.

“The challenge, of course, is there’s not a great definition and there certainly is not a well-standardized assay for how immunocompromised someone is, and so that led to the uncertainty in this patient population for this and other live-virus vaccines,” Dr. Curtis said.

Dr. Curtis and colleagues enrolled 627 participants from 33 centers into the VERVE trial. Participants were aged at least 50 years, were taking a TNFi, and had not previously received Zostavax.

Patients in both groups had a mean age of about 63 years and about two-thirds were women. The most common indications for TNFi use in the Zostavax group and the placebo group were RA (59.2% vs. 56.0%, respectively), psoriatic arthritis (24.3% vs. 23.9%), and ankylosing spondylitis (7.2% vs. 8.5%), while the anti-TNF agents used were adalimumab (38.1% vs. 27.4%), infliximab (28.4% vs. 34.2%), etanercept (19.0% vs. 23.5%), golimumab (10.0% vs. 8.1%), and certolizumab pegol (4.5% vs. 6.8%). In addition, some patients in the Zostavax and placebo groups were also taking concomitant therapies with TNFi, such as oral glucocorticoids (9.7% vs. 11.4%).

The researchers randomized participants to receive Zostavax or placebo (saline) and then followed them for 6 weeks, and looked for signs of wild-type or vaccine-strain varicella infection. If participants were suspected to have varicella, they were assessed clinically, underwent polymerase chain reaction testing, and rashes were photographed. At baseline and at 6 weeks, the researchers collected serum and peripheral blood mononuclear cells to determine patient immunity to varicella. After 6 months, participants were unmasked to the treatment arm of the study.

Dr. Curtis and colleagues found no confirmed varicella infection cases at 6 weeks. “To the extent that 0 cases out of 317 vaccinated people is reassuring, there were no cases, so that was exceedingly heartening as a result,” he said.

Out of 20 serious adverse events total in the groups, 15 events occurred before 6 months, including 8 suspected varicella cases in the Zostavax group and 7 in the placebo group. However, there were no positive cases of varicella – either wild type or vaccine type – after polymerase chain reaction tests. Overall, there were 268 adverse events in 195 participants, with 73 events (27.2%) consisting of injection-site reactions. The researchers also found no difference in the rate of disease flares, and found no differences in adverse reactions between groups, apart from a higher rate of injection-site reactions in the varicella group (19.4% vs. 4.2%).

With regard to immunogenicity, the humoral immune response was measured through IgG, which showed an immune response in the varicella group at 6 weeks (geometric mean fold ratio, 1.33; 95% confidence interval, 1.18-1.51), compared with the placebo group (GMFR, 1.02; 95% CI, 0.91-1.14); cell-mediated immune response was measured by interferon-gamma, which also showed an immune response in the live-vaccine group (GMFR, 1.49; 95% CI, 1.14-1.94), compared with participants who received placebo (GMFR, 1.14; 95% CI, 0.87-1.48). In preliminary 1-year data, IgG immune response was elevated in the varicella group (GMFR, 1.46; 95% CI, 1.08-1.99), but there was no elevated immune response for interferon-gamma (GMFR, 0.78; 95% CI, 0.49-1.25).

“I think the trial is encouraging not only for its result with the live zoster vaccine and TNF-treated patients, but also challenge the notion that, if you need to, a live-virus vaccine may in fact be able to be safely given to people with autoimmune and inflammatory diseases, even those treated with biologics like tumor necrosis factor inhibitors,” Dr. Curtis said.

As patients in VERVE consented to long-term follow-up in health plan claims and EHR data, it will be possible to follow these patients in the future to assess herpes zoster reactivation. Dr. Curtis also noted that a new trial involving the recombinant, adjuvanted zoster vaccine (Shingrix) is currently in development and should begin next year.

The VERVE trial was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Curtis reported serving as a current member of the Center for Disease Control and Prevention’s Advisory Committee on Immunization Practices Herpes Zoster Work Group. He and some of the other authors reported financial relationships with many pharmaceutical companies.

SOURCE: Curtis J et al. Arthritis Rheumatol. 2019;71(suppl 10), Abstract 824.

A study of more than 5 million Kaiser Permanente/Northern California patients suggests that the prevalence of adults diagnosed with ADHD has dramatically increased over the last 10 years (JAMA Netw Open. 2019 Nov 1. doi: 10.1001/jamanetworkopen.2019.14344).

SIphotography/Getty Images

Over the interval between 2007 and 2016, the prevalence of ADHD went from 0.43% to 0.96%, an increase of more than 120%. For adults, being white, male, younger, employed, and better educated increased one’s chances of receiving an ADHD diagnosis. Having a comorbid mental health diagnosis such as an eating disorder, anxiety, depression, or being labeled as bipolar also increased the odds of acquiring the ADHD label.

Should this observed increase in adults with ADHD be a warning to pediatricians that we have been underdiagnosing the condition in our patients? Are our screening tools too coarse, allowing a significant number of children to slip through the cracks only to land in the laps of our colleagues in internal medicine and family practice? If this were the case, does this mean that adult and youth ADHD are basically the same condition, but in some individuals the signs and symptoms become more obvious with aging? Does it also suggest that there is a genetic basis to ADHD with variable expression? Could it be that individuals with adult ADHD exhibited a few of the hallmarks of the diagnosis when they were young, but aggravating factors in the environment such as job stress or marital discord unmasked the signs and symptoms that had been percolating just under our radar for decades?

As usual, there is no simple answer that explains the findings unearthed by these researchers. One gets a sense from reading their paper that the authors feel that ADHD is being diagnosed more often as more individuals have access to physicians and other professionals who are attuned to the diagnosis. The fact that white, better-educated, and employed men are more likely to acquire the diagnosis might support the argument that as segments of the population who have been underserved by the health care system come on board we will continue to see a rise in the number of adults with the diagnosis. The more patients who see health care providers who are primed to make the diagnosis, the more often the diagnosis will be made.

I am sure there is a segment of the population who enter the world with some genetically mediated chemical or structural vulnerability that results in the signs and symptoms of ADHD. Most, but not all, of these individuals have symptoms that are so obvious that they present in childhood. However, a larger number of children and most adults who are labeled with ADHD are exhibiting the symptoms of inattention, distractibility, and impulsiveness as the result of environmental factors such as sleep deprivation, family or job stress, and other comorbid mental health conditions, or simply because they were young for their school cohort.

Pediatricians need not feel that we have missed another opportunity for prevention because the prevalence of the diagnosis of adult ADHD is increasing dramatically. However, that increase should serve as another reminder to us that there can be multiple factors that can result in signs and symptoms that attract the label of ADHD. We must be careful and look long and hard before we diagnose and reach for our prescription pad.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

A study of more than 5 million Kaiser Permanente/Northern California patients suggests that the prevalence of adults diagnosed with ADHD has dramatically increased over the last 10 years (JAMA Netw Open. 2019 Nov 1. doi: 10.1001/jamanetworkopen.2019.14344).

SIphotography/Getty Images

Over the interval between 2007 and 2016, the prevalence of ADHD went from 0.43% to 0.96%, an increase of more than 120%. For adults, being white, male, younger, employed, and better educated increased one’s chances of receiving an ADHD diagnosis. Having a comorbid mental health diagnosis such as an eating disorder, anxiety, depression, or being labeled as bipolar also increased the odds of acquiring the ADHD label.

Should this observed increase in adults with ADHD be a warning to pediatricians that we have been underdiagnosing the condition in our patients? Are our screening tools too coarse, allowing a significant number of children to slip through the cracks only to land in the laps of our colleagues in internal medicine and family practice? If this were the case, does this mean that adult and youth ADHD are basically the same condition, but in some individuals the signs and symptoms become more obvious with aging? Does it also suggest that there is a genetic basis to ADHD with variable expression? Could it be that individuals with adult ADHD exhibited a few of the hallmarks of the diagnosis when they were young, but aggravating factors in the environment such as job stress or marital discord unmasked the signs and symptoms that had been percolating just under our radar for decades?

As usual, there is no simple answer that explains the findings unearthed by these researchers. One gets a sense from reading their paper that the authors feel that ADHD is being diagnosed more often as more individuals have access to physicians and other professionals who are attuned to the diagnosis. The fact that white, better-educated, and employed men are more likely to acquire the diagnosis might support the argument that as segments of the population who have been underserved by the health care system come on board we will continue to see a rise in the number of adults with the diagnosis. The more patients who see health care providers who are primed to make the diagnosis, the more often the diagnosis will be made.

I am sure there is a segment of the population who enter the world with some genetically mediated chemical or structural vulnerability that results in the signs and symptoms of ADHD. Most, but not all, of these individuals have symptoms that are so obvious that they present in childhood. However, a larger number of children and most adults who are labeled with ADHD are exhibiting the symptoms of inattention, distractibility, and impulsiveness as the result of environmental factors such as sleep deprivation, family or job stress, and other comorbid mental health conditions, or simply because they were young for their school cohort.

Pediatricians need not feel that we have missed another opportunity for prevention because the prevalence of the diagnosis of adult ADHD is increasing dramatically. However, that increase should serve as another reminder to us that there can be multiple factors that can result in signs and symptoms that attract the label of ADHD. We must be careful and look long and hard before we diagnose and reach for our prescription pad.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

A study of more than 5 million Kaiser Permanente/Northern California patients suggests that the prevalence of adults diagnosed with ADHD has dramatically increased over the last 10 years (JAMA Netw Open. 2019 Nov 1. doi: 10.1001/jamanetworkopen.2019.14344).

SIphotography/Getty Images

Over the interval between 2007 and 2016, the prevalence of ADHD went from 0.43% to 0.96%, an increase of more than 120%. For adults, being white, male, younger, employed, and better educated increased one’s chances of receiving an ADHD diagnosis. Having a comorbid mental health diagnosis such as an eating disorder, anxiety, depression, or being labeled as bipolar also increased the odds of acquiring the ADHD label.

Should this observed increase in adults with ADHD be a warning to pediatricians that we have been underdiagnosing the condition in our patients? Are our screening tools too coarse, allowing a significant number of children to slip through the cracks only to land in the laps of our colleagues in internal medicine and family practice? If this were the case, does this mean that adult and youth ADHD are basically the same condition, but in some individuals the signs and symptoms become more obvious with aging? Does it also suggest that there is a genetic basis to ADHD with variable expression? Could it be that individuals with adult ADHD exhibited a few of the hallmarks of the diagnosis when they were young, but aggravating factors in the environment such as job stress or marital discord unmasked the signs and symptoms that had been percolating just under our radar for decades?

As usual, there is no simple answer that explains the findings unearthed by these researchers. One gets a sense from reading their paper that the authors feel that ADHD is being diagnosed more often as more individuals have access to physicians and other professionals who are attuned to the diagnosis. The fact that white, better-educated, and employed men are more likely to acquire the diagnosis might support the argument that as segments of the population who have been underserved by the health care system come on board we will continue to see a rise in the number of adults with the diagnosis. The more patients who see health care providers who are primed to make the diagnosis, the more often the diagnosis will be made.

I am sure there is a segment of the population who enter the world with some genetically mediated chemical or structural vulnerability that results in the signs and symptoms of ADHD. Most, but not all, of these individuals have symptoms that are so obvious that they present in childhood. However, a larger number of children and most adults who are labeled with ADHD are exhibiting the symptoms of inattention, distractibility, and impulsiveness as the result of environmental factors such as sleep deprivation, family or job stress, and other comorbid mental health conditions, or simply because they were young for their school cohort.

Pediatricians need not feel that we have missed another opportunity for prevention because the prevalence of the diagnosis of adult ADHD is increasing dramatically. However, that increase should serve as another reminder to us that there can be multiple factors that can result in signs and symptoms that attract the label of ADHD. We must be careful and look long and hard before we diagnose and reach for our prescription pad.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

Postcolonoscopy colorectal cancers were more likely to arise in the proximal colon and to show microsatellite instability, according to the results of a retrospective population-based study of 168 adults with incident colorectal cancers.

In all, 64% of postcolonoscopy colorectal cancers were located in the proximal colon, compared with 44% of detected colorectal cancers (P = .016), reported Niloy Jewel Samadder, MD, of the University of Utah in Salt Lake City, together with his associates. Furthermore, microsatellite instability (MSI) was detected in 32% of postcolonoscopy colorectal cancers, versus 13% of detected colorectal cancers (P = .005). These findings may point to differences in the underlying biology of postcolonoscopy colorectal cancers and detected colorectal cancers, they said. Studies are needed “to determine if postcolonoscopy cancers arise through a specific genetic pathway that may accelerate neoplastic progression,” they wrote in Clinical Gastroenterology and Hepatology.

Postcolonoscopy colorectal cancers are a “small but clinically important subset of colorectal cancers” that are diagnosed after the patient has a colonoscopy in which no cancer is detected, the researchers noted. These cancers have an estimated global prevalence ranging from 3% to 9% and an estimated pooled prevalence of 3.7% (Am J Gastroenterol. 2014;109:1375-89). Risk factors for postcolonoscopy colorectal cancers include low adenoma detection rates, rural facilities, and care by physicians who are not gastroenterologists. However, tumor-specific and patient-specific factors, including location within the colon and superior survival, compared with detected cancers, raises the possibility of underlying molecular differences related to tumorigenesis, the researchers said.

To investigate this idea, they retrospectively analyzed data from residents of Utah between 50 and 80 years old who had a colonoscopy between, Feb. 15, 1995, and Jan. 31, 2009, at one of two large clinical facilities in Utah (Intermountain Healthcare or the University of Utah Health Sciences). Using a state population-based database, they merged medical information from these patients with cancer histories from the Utah Cancer Registry. This enabled them to compare all 84 postcolonoscopy colorectal cancers (defined as those detected within 6-60 months of colonoscopy) with tissue available for analysis with 84 detected colorectal cancers (detected within 6 months of a colonoscopy).

In the multivariable analysis, MSI was the only molecular feature that was significantly more frequent in postcolonoscopy versus detected colorectal cancers (odds ratio, 4.20; 95% confidence interval, 1.58-11.14). However, postcolonoscopy colorectal cancers were significantly more likely to be early stage (86% versus 69% for detected colorectal cancers; P = .040). Five-year survival did not significantly differ between the groups.

“The molecular signatures of postcolonoscopy colorectal cancers in our study overlap with those of sporadic MSI and serrated pathways, suggesting these mechanisms play a disproportionate role in postcolonoscopy colorectal cancers.” the researchers said. “Additional studies are needed to determine whether these postcolonoscopy colorectal cancers arise through a familial cancer pathway and/or serrated neoplastic pathway of sporadic lesions.

Funders included the American College of Gastroenterology, the National Cancer Institute, the Huntsman Cancer Foundation, the University of Utah, and the Utah Department of Health. Dr. Samadder reported consulting relationships with Cancer Prevention Pharmaceuticals and Janssen Research and Development. The other researchers reported having no conflicts of interest.
 

SOURCE: Samadder NJ et al. Clin Gastroenterol Hepatol. 2019 Mar 28. doi: 10.1016/j.cgh.2019.02.040.

Postcolonoscopy colorectal cancers were more likely to arise in the proximal colon and to show microsatellite instability, according to the results of a retrospective population-based study of 168 adults with incident colorectal cancers.

In all, 64% of postcolonoscopy colorectal cancers were located in the proximal colon, compared with 44% of detected colorectal cancers (P = .016), reported Niloy Jewel Samadder, MD, of the University of Utah in Salt Lake City, together with his associates. Furthermore, microsatellite instability (MSI) was detected in 32% of postcolonoscopy colorectal cancers, versus 13% of detected colorectal cancers (P = .005). These findings may point to differences in the underlying biology of postcolonoscopy colorectal cancers and detected colorectal cancers, they said. Studies are needed “to determine if postcolonoscopy cancers arise through a specific genetic pathway that may accelerate neoplastic progression,” they wrote in Clinical Gastroenterology and Hepatology.

Postcolonoscopy colorectal cancers are a “small but clinically important subset of colorectal cancers” that are diagnosed after the patient has a colonoscopy in which no cancer is detected, the researchers noted. These cancers have an estimated global prevalence ranging from 3% to 9% and an estimated pooled prevalence of 3.7% (Am J Gastroenterol. 2014;109:1375-89). Risk factors for postcolonoscopy colorectal cancers include low adenoma detection rates, rural facilities, and care by physicians who are not gastroenterologists. However, tumor-specific and patient-specific factors, including location within the colon and superior survival, compared with detected cancers, raises the possibility of underlying molecular differences related to tumorigenesis, the researchers said.

To investigate this idea, they retrospectively analyzed data from residents of Utah between 50 and 80 years old who had a colonoscopy between, Feb. 15, 1995, and Jan. 31, 2009, at one of two large clinical facilities in Utah (Intermountain Healthcare or the University of Utah Health Sciences). Using a state population-based database, they merged medical information from these patients with cancer histories from the Utah Cancer Registry. This enabled them to compare all 84 postcolonoscopy colorectal cancers (defined as those detected within 6-60 months of colonoscopy) with tissue available for analysis with 84 detected colorectal cancers (detected within 6 months of a colonoscopy).

In the multivariable analysis, MSI was the only molecular feature that was significantly more frequent in postcolonoscopy versus detected colorectal cancers (odds ratio, 4.20; 95% confidence interval, 1.58-11.14). However, postcolonoscopy colorectal cancers were significantly more likely to be early stage (86% versus 69% for detected colorectal cancers; P = .040). Five-year survival did not significantly differ between the groups.

“The molecular signatures of postcolonoscopy colorectal cancers in our study overlap with those of sporadic MSI and serrated pathways, suggesting these mechanisms play a disproportionate role in postcolonoscopy colorectal cancers.” the researchers said. “Additional studies are needed to determine whether these postcolonoscopy colorectal cancers arise through a familial cancer pathway and/or serrated neoplastic pathway of sporadic lesions.

Funders included the American College of Gastroenterology, the National Cancer Institute, the Huntsman Cancer Foundation, the University of Utah, and the Utah Department of Health. Dr. Samadder reported consulting relationships with Cancer Prevention Pharmaceuticals and Janssen Research and Development. The other researchers reported having no conflicts of interest.
 

SOURCE: Samadder NJ et al. Clin Gastroenterol Hepatol. 2019 Mar 28. doi: 10.1016/j.cgh.2019.02.040.

Postcolonoscopy colorectal cancers were more likely to arise in the proximal colon and to show microsatellite instability, according to the results of a retrospective population-based study of 168 adults with incident colorectal cancers.

In all, 64% of postcolonoscopy colorectal cancers were located in the proximal colon, compared with 44% of detected colorectal cancers (P = .016), reported Niloy Jewel Samadder, MD, of the University of Utah in Salt Lake City, together with his associates. Furthermore, microsatellite instability (MSI) was detected in 32% of postcolonoscopy colorectal cancers, versus 13% of detected colorectal cancers (P = .005). These findings may point to differences in the underlying biology of postcolonoscopy colorectal cancers and detected colorectal cancers, they said. Studies are needed “to determine if postcolonoscopy cancers arise through a specific genetic pathway that may accelerate neoplastic progression,” they wrote in Clinical Gastroenterology and Hepatology.

Postcolonoscopy colorectal cancers are a “small but clinically important subset of colorectal cancers” that are diagnosed after the patient has a colonoscopy in which no cancer is detected, the researchers noted. These cancers have an estimated global prevalence ranging from 3% to 9% and an estimated pooled prevalence of 3.7% (Am J Gastroenterol. 2014;109:1375-89). Risk factors for postcolonoscopy colorectal cancers include low adenoma detection rates, rural facilities, and care by physicians who are not gastroenterologists. However, tumor-specific and patient-specific factors, including location within the colon and superior survival, compared with detected cancers, raises the possibility of underlying molecular differences related to tumorigenesis, the researchers said.

To investigate this idea, they retrospectively analyzed data from residents of Utah between 50 and 80 years old who had a colonoscopy between, Feb. 15, 1995, and Jan. 31, 2009, at one of two large clinical facilities in Utah (Intermountain Healthcare or the University of Utah Health Sciences). Using a state population-based database, they merged medical information from these patients with cancer histories from the Utah Cancer Registry. This enabled them to compare all 84 postcolonoscopy colorectal cancers (defined as those detected within 6-60 months of colonoscopy) with tissue available for analysis with 84 detected colorectal cancers (detected within 6 months of a colonoscopy).

In the multivariable analysis, MSI was the only molecular feature that was significantly more frequent in postcolonoscopy versus detected colorectal cancers (odds ratio, 4.20; 95% confidence interval, 1.58-11.14). However, postcolonoscopy colorectal cancers were significantly more likely to be early stage (86% versus 69% for detected colorectal cancers; P = .040). Five-year survival did not significantly differ between the groups.

“The molecular signatures of postcolonoscopy colorectal cancers in our study overlap with those of sporadic MSI and serrated pathways, suggesting these mechanisms play a disproportionate role in postcolonoscopy colorectal cancers.” the researchers said. “Additional studies are needed to determine whether these postcolonoscopy colorectal cancers arise through a familial cancer pathway and/or serrated neoplastic pathway of sporadic lesions.

Funders included the American College of Gastroenterology, the National Cancer Institute, the Huntsman Cancer Foundation, the University of Utah, and the Utah Department of Health. Dr. Samadder reported consulting relationships with Cancer Prevention Pharmaceuticals and Janssen Research and Development. The other researchers reported having no conflicts of interest.
 

SOURCE: Samadder NJ et al. Clin Gastroenterol Hepatol. 2019 Mar 28. doi: 10.1016/j.cgh.2019.02.040.

Stoners, beware: Young, frequent marijuana users who also smoke cigarettes are at a nearly three-fold increased risk for stroke, and people with cannabis use disorder are at a 50% greater risk of being hospitalized for arrhythmias, according to new research presented at the American Heart Association Scientific Sessions 2019.

An analysis of pooled data on nearly 44,000 participants in a cross-sectional survey showed that, among the 13.6% who reported using marijuana within the last 30 days, the adjusted odds ratio for young-onset stroke (aged 18-44 years), compared with non-users, was 2.75, reported Tarang Parekh, MBBS, a health policy researcher of George Mason University in Fairfax, Va., and colleagues.

In a separate study, a retrospective analysis of national inpatient data showed that people diagnosed with cannabis use disorder – a pathological pattern of impaired control, social impairment, risky behavior or physiological adaptation similar in nature to alcoholism – had a 47%-52% increased likelihood of hospitalization for an arrhythmia, reported Rikinkumar S. Patel, MD, a psychiatry resident at Griffin Memorial Hospital in Norman, Okla.

“As these [cannabis] products become increasingly used across the country, getting clearer, scientifically rigorous data is going to be important as we try to understand the overall health effects of cannabis,” said AHA President Robert Harrington, MD, of Stanford (Calif.) University in a statement.

Currently, use of both medical and recreational marijuana is fully legal in 11 U.S. states and the District of Columbia. Medical marijuana is legal with recreational use decriminalized (or penalties reduced) in 28 other states, and totally illegal in 11 other states, according to employee screening firm DISA Global Solutions.
 

Stroke study

In an oral presentation with simultaneous publication in the AHA journal Stroke, Dr. Parekh and colleagues presented an analysis of pooled data from the Behavioral Risk Factor Surveillance System (BRFSS), a nationally representative cross-sectional survey collected by the Centers for Disease Control and Prevention in 2016 and 2017.

They looked at baseline sociodemographic data and created multivariable logistic regression models with state fixed effects to determine whether marijuana use within the last 30 days was associated with young-onset stroke.

They identified 43,860 participants representing a weighted sample of 35.5 million Americans. Of the sample, 63.3% were male, and 13.6 % of all participants reported using marijuana in the last 30 days.

They found in an unadjusted model that marijuana users had an odds ratio for stroke, compared with nonusers, of 1.59 (P less than.1), and in a model adjusted for demographic factors (gender, race, ethnicity, and education) the OR increased to 1.76 (P less than .05).

When they threw risk behavior into the model (physical activity, body mass index, heavy drinking, and cigarette smoking), they saw that the OR for stroke shot up to 2.75 (P less than .01).

“Physicians should ask patients if they use cannabis and counsel them about its potential stroke risk as part of regular doctor visits,” Dr. Parekh said in a statement.
 

Arrhythmias study

Based on recent studies suggesting that cannabis use may trigger cardiovascular events, Dr. Patel and colleagues studied whether cannabis use disorder may be related to arrhythmias, approaching the question through hospital records.

“The effects of using cannabis are seen within 15 minutes and last for around 3 hours. At lower doses, it is linked to a rapid heartbeat. At higher doses, it is linked to a too-slow heartbeat,” he said in a statement.

Dr. Patel and colleagues conducted a retrospective analysis of the Nationwide Inpatient Sample from 2010-2014, a period during which medical marijuana became legal in several states and recreational marijuana became legal in Colorado and Washington. The sample is a database maintained by the Healthcare Cost and Utilization Project of the U.S. Office of Disease Prevention and Health Promotion.

They identified 570,557 patients aged 15-54 years with a primary diagnosis of arrhythmia, and compared them with a sample of 67,662,082 patients hospitalized with no arrhythmia diagnosed during the same period.

They found a 2.6% incidence of cannabis use disorder among patients hospitalized for arrhythmias. Patients with cannabis use disorder tended to be younger (15- to 24-years-old; OR, 4.23), male (OR, 1.70) and African American (OR, 2.70).

In regression analysis adjusted for demographics and comorbidities, cannabis use disorder was associated with higher odds of arrhythmia hospitalization in young patients, at 1.28 times among 15- to 24-year-olds (95% confidence interval, 1.229-1.346) and 1.52 times for 25- to 34-year-olds (95% CI, 1.469-1.578).

“As medical and recreational cannabis is legalized in many states, it is important to know the difference between therapeutic cannabis dosing for medical purposes and the consequences of cannabis abuse. We urgently need additional research to understand these issues,” Dr. Patel said.

“It’s not proving that there’s a direct link, but it’s raising a suggestion in an observational analysis that [this] indeed might be the case. What that means for clinicians is that, if you’re seeing a patient who is presenting with a symptomatic arrhythmia, adding cannabis usage to your list of questions as you begin to try to understand possible precipitating factors for this arrhythmia seems to be a reasonable thing to do,” Dr. Harrington commented.

Stoners, beware: Young, frequent marijuana users who also smoke cigarettes are at a nearly three-fold increased risk for stroke, and people with cannabis use disorder are at a 50% greater risk of being hospitalized for arrhythmias, according to new research presented at the American Heart Association Scientific Sessions 2019.

An analysis of pooled data on nearly 44,000 participants in a cross-sectional survey showed that, among the 13.6% who reported using marijuana within the last 30 days, the adjusted odds ratio for young-onset stroke (aged 18-44 years), compared with non-users, was 2.75, reported Tarang Parekh, MBBS, a health policy researcher of George Mason University in Fairfax, Va., and colleagues.

In a separate study, a retrospective analysis of national inpatient data showed that people diagnosed with cannabis use disorder – a pathological pattern of impaired control, social impairment, risky behavior or physiological adaptation similar in nature to alcoholism – had a 47%-52% increased likelihood of hospitalization for an arrhythmia, reported Rikinkumar S. Patel, MD, a psychiatry resident at Griffin Memorial Hospital in Norman, Okla.

“As these [cannabis] products become increasingly used across the country, getting clearer, scientifically rigorous data is going to be important as we try to understand the overall health effects of cannabis,” said AHA President Robert Harrington, MD, of Stanford (Calif.) University in a statement.

Currently, use of both medical and recreational marijuana is fully legal in 11 U.S. states and the District of Columbia. Medical marijuana is legal with recreational use decriminalized (or penalties reduced) in 28 other states, and totally illegal in 11 other states, according to employee screening firm DISA Global Solutions.
 

Stroke study

In an oral presentation with simultaneous publication in the AHA journal Stroke, Dr. Parekh and colleagues presented an analysis of pooled data from the Behavioral Risk Factor Surveillance System (BRFSS), a nationally representative cross-sectional survey collected by the Centers for Disease Control and Prevention in 2016 and 2017.

They looked at baseline sociodemographic data and created multivariable logistic regression models with state fixed effects to determine whether marijuana use within the last 30 days was associated with young-onset stroke.

They identified 43,860 participants representing a weighted sample of 35.5 million Americans. Of the sample, 63.3% were male, and 13.6 % of all participants reported using marijuana in the last 30 days.

They found in an unadjusted model that marijuana users had an odds ratio for stroke, compared with nonusers, of 1.59 (P less than.1), and in a model adjusted for demographic factors (gender, race, ethnicity, and education) the OR increased to 1.76 (P less than .05).

When they threw risk behavior into the model (physical activity, body mass index, heavy drinking, and cigarette smoking), they saw that the OR for stroke shot up to 2.75 (P less than .01).

“Physicians should ask patients if they use cannabis and counsel them about its potential stroke risk as part of regular doctor visits,” Dr. Parekh said in a statement.
 

Arrhythmias study

Based on recent studies suggesting that cannabis use may trigger cardiovascular events, Dr. Patel and colleagues studied whether cannabis use disorder may be related to arrhythmias, approaching the question through hospital records.

“The effects of using cannabis are seen within 15 minutes and last for around 3 hours. At lower doses, it is linked to a rapid heartbeat. At higher doses, it is linked to a too-slow heartbeat,” he said in a statement.

Dr. Patel and colleagues conducted a retrospective analysis of the Nationwide Inpatient Sample from 2010-2014, a period during which medical marijuana became legal in several states and recreational marijuana became legal in Colorado and Washington. The sample is a database maintained by the Healthcare Cost and Utilization Project of the U.S. Office of Disease Prevention and Health Promotion.

They identified 570,557 patients aged 15-54 years with a primary diagnosis of arrhythmia, and compared them with a sample of 67,662,082 patients hospitalized with no arrhythmia diagnosed during the same period.

They found a 2.6% incidence of cannabis use disorder among patients hospitalized for arrhythmias. Patients with cannabis use disorder tended to be younger (15- to 24-years-old; OR, 4.23), male (OR, 1.70) and African American (OR, 2.70).

In regression analysis adjusted for demographics and comorbidities, cannabis use disorder was associated with higher odds of arrhythmia hospitalization in young patients, at 1.28 times among 15- to 24-year-olds (95% confidence interval, 1.229-1.346) and 1.52 times for 25- to 34-year-olds (95% CI, 1.469-1.578).

“As medical and recreational cannabis is legalized in many states, it is important to know the difference between therapeutic cannabis dosing for medical purposes and the consequences of cannabis abuse. We urgently need additional research to understand these issues,” Dr. Patel said.

“It’s not proving that there’s a direct link, but it’s raising a suggestion in an observational analysis that [this] indeed might be the case. What that means for clinicians is that, if you’re seeing a patient who is presenting with a symptomatic arrhythmia, adding cannabis usage to your list of questions as you begin to try to understand possible precipitating factors for this arrhythmia seems to be a reasonable thing to do,” Dr. Harrington commented.

Stoners, beware: Young, frequent marijuana users who also smoke cigarettes are at a nearly three-fold increased risk for stroke, and people with cannabis use disorder are at a 50% greater risk of being hospitalized for arrhythmias, according to new research presented at the American Heart Association Scientific Sessions 2019.

An analysis of pooled data on nearly 44,000 participants in a cross-sectional survey showed that, among the 13.6% who reported using marijuana within the last 30 days, the adjusted odds ratio for young-onset stroke (aged 18-44 years), compared with non-users, was 2.75, reported Tarang Parekh, MBBS, a health policy researcher of George Mason University in Fairfax, Va., and colleagues.

In a separate study, a retrospective analysis of national inpatient data showed that people diagnosed with cannabis use disorder – a pathological pattern of impaired control, social impairment, risky behavior or physiological adaptation similar in nature to alcoholism – had a 47%-52% increased likelihood of hospitalization for an arrhythmia, reported Rikinkumar S. Patel, MD, a psychiatry resident at Griffin Memorial Hospital in Norman, Okla.

“As these [cannabis] products become increasingly used across the country, getting clearer, scientifically rigorous data is going to be important as we try to understand the overall health effects of cannabis,” said AHA President Robert Harrington, MD, of Stanford (Calif.) University in a statement.

Currently, use of both medical and recreational marijuana is fully legal in 11 U.S. states and the District of Columbia. Medical marijuana is legal with recreational use decriminalized (or penalties reduced) in 28 other states, and totally illegal in 11 other states, according to employee screening firm DISA Global Solutions.
 

Stroke study

In an oral presentation with simultaneous publication in the AHA journal Stroke, Dr. Parekh and colleagues presented an analysis of pooled data from the Behavioral Risk Factor Surveillance System (BRFSS), a nationally representative cross-sectional survey collected by the Centers for Disease Control and Prevention in 2016 and 2017.

They looked at baseline sociodemographic data and created multivariable logistic regression models with state fixed effects to determine whether marijuana use within the last 30 days was associated with young-onset stroke.

They identified 43,860 participants representing a weighted sample of 35.5 million Americans. Of the sample, 63.3% were male, and 13.6 % of all participants reported using marijuana in the last 30 days.

They found in an unadjusted model that marijuana users had an odds ratio for stroke, compared with nonusers, of 1.59 (P less than.1), and in a model adjusted for demographic factors (gender, race, ethnicity, and education) the OR increased to 1.76 (P less than .05).

When they threw risk behavior into the model (physical activity, body mass index, heavy drinking, and cigarette smoking), they saw that the OR for stroke shot up to 2.75 (P less than .01).

“Physicians should ask patients if they use cannabis and counsel them about its potential stroke risk as part of regular doctor visits,” Dr. Parekh said in a statement.
 

Arrhythmias study

Based on recent studies suggesting that cannabis use may trigger cardiovascular events, Dr. Patel and colleagues studied whether cannabis use disorder may be related to arrhythmias, approaching the question through hospital records.

“The effects of using cannabis are seen within 15 minutes and last for around 3 hours. At lower doses, it is linked to a rapid heartbeat. At higher doses, it is linked to a too-slow heartbeat,” he said in a statement.

Dr. Patel and colleagues conducted a retrospective analysis of the Nationwide Inpatient Sample from 2010-2014, a period during which medical marijuana became legal in several states and recreational marijuana became legal in Colorado and Washington. The sample is a database maintained by the Healthcare Cost and Utilization Project of the U.S. Office of Disease Prevention and Health Promotion.

They identified 570,557 patients aged 15-54 years with a primary diagnosis of arrhythmia, and compared them with a sample of 67,662,082 patients hospitalized with no arrhythmia diagnosed during the same period.

They found a 2.6% incidence of cannabis use disorder among patients hospitalized for arrhythmias. Patients with cannabis use disorder tended to be younger (15- to 24-years-old; OR, 4.23), male (OR, 1.70) and African American (OR, 2.70).

In regression analysis adjusted for demographics and comorbidities, cannabis use disorder was associated with higher odds of arrhythmia hospitalization in young patients, at 1.28 times among 15- to 24-year-olds (95% confidence interval, 1.229-1.346) and 1.52 times for 25- to 34-year-olds (95% CI, 1.469-1.578).

“As medical and recreational cannabis is legalized in many states, it is important to know the difference between therapeutic cannabis dosing for medical purposes and the consequences of cannabis abuse. We urgently need additional research to understand these issues,” Dr. Patel said.

“It’s not proving that there’s a direct link, but it’s raising a suggestion in an observational analysis that [this] indeed might be the case. What that means for clinicians is that, if you’re seeing a patient who is presenting with a symptomatic arrhythmia, adding cannabis usage to your list of questions as you begin to try to understand possible precipitating factors for this arrhythmia seems to be a reasonable thing to do,” Dr. Harrington commented.