AGA Clinical Practice Update: Best practices for POEM in achalasia

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Peroral endoscopic myotomy, or POEM, should be considered as primary therapy for type III achalasia and as a treatment option comparable with laparoscopic Heller myotomy for any of the achalasia syndromes – but only when physicians with expertise are available, according to a clinical practice update from the American Gastroenterological Association.

Further, post-POEM patients should be considered at high risk of developing reflux esophagitis and should be advised of the management considerations, including potential indefinite proton pump inhibitor therapy and/or surveillance endoscopy, prior to undergoing the procedure, Peter J. Kahrilas, MD, of Northwestern University, Chicago, and his colleagues wrote in the update, which is published in the November issue of Gastroenterology (2017. doi: 10.1053/j.gastro.2017.10.001).

In an effort to describe the place for POEM among the currently available robust treatments for achalasia, the authors conducted a literature review – their “best practice” recommendations are based on the findings from relevant publications and on expert opinion.

Dr. Peter J. Kahrilas
In determining the need for achalasia therapy, they agreed that patient-specific parameters should be considered along with published efficacy data. Important parameters include Chicago Classification subtype, comorbidities, early vs. late disease, and primary or secondary causes.

Additionally, they said POEM should be performed by experienced physicians in high-volume centers since the procedure is complex and an estimated 20-30 procedures are needed to achieve competence.

The update and these proposed best practices follow the evolution of POEM over the last decade: it began as an exciting concept and is now a mainstream treatment option for achalasia, the authors said.

“Uncontrolled outcome data have been very promising comparing POEM with the standard surgical treatment for achalasia, laparoscopic Heller myotomy (LHM). However, concerns remain regarding post-POEM reflux, the durability of the procedure, and the learning curve for endoscopists adopting the technique,” they wrote, which, when coupled with recent randomized controlled study data showing excellent and equivalent 5-year outcomes with pneumatic dilation and LHM, make the role of POEM somewhat controversial.

As part of the review, they considered the strengths and weaknesses of both POEM and LHM. The data comparing POEM with LHM or pneumatic dilation remain very limited, but based on those that do exist, the authors concluded that “POEM appears to be a safe, effective, and minimally invasive management option in achalasia in the short term.”

Long-term durability data are not yet available, they noted.

Dr. Kahrilas received funding from the U.S. Public Health Service.

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Peroral endoscopic myotomy, or POEM, should be considered as primary therapy for type III achalasia and as a treatment option comparable with laparoscopic Heller myotomy for any of the achalasia syndromes – but only when physicians with expertise are available, according to a clinical practice update from the American Gastroenterological Association.

Further, post-POEM patients should be considered at high risk of developing reflux esophagitis and should be advised of the management considerations, including potential indefinite proton pump inhibitor therapy and/or surveillance endoscopy, prior to undergoing the procedure, Peter J. Kahrilas, MD, of Northwestern University, Chicago, and his colleagues wrote in the update, which is published in the November issue of Gastroenterology (2017. doi: 10.1053/j.gastro.2017.10.001).

In an effort to describe the place for POEM among the currently available robust treatments for achalasia, the authors conducted a literature review – their “best practice” recommendations are based on the findings from relevant publications and on expert opinion.

Dr. Peter J. Kahrilas
In determining the need for achalasia therapy, they agreed that patient-specific parameters should be considered along with published efficacy data. Important parameters include Chicago Classification subtype, comorbidities, early vs. late disease, and primary or secondary causes.

Additionally, they said POEM should be performed by experienced physicians in high-volume centers since the procedure is complex and an estimated 20-30 procedures are needed to achieve competence.

The update and these proposed best practices follow the evolution of POEM over the last decade: it began as an exciting concept and is now a mainstream treatment option for achalasia, the authors said.

“Uncontrolled outcome data have been very promising comparing POEM with the standard surgical treatment for achalasia, laparoscopic Heller myotomy (LHM). However, concerns remain regarding post-POEM reflux, the durability of the procedure, and the learning curve for endoscopists adopting the technique,” they wrote, which, when coupled with recent randomized controlled study data showing excellent and equivalent 5-year outcomes with pneumatic dilation and LHM, make the role of POEM somewhat controversial.

As part of the review, they considered the strengths and weaknesses of both POEM and LHM. The data comparing POEM with LHM or pneumatic dilation remain very limited, but based on those that do exist, the authors concluded that “POEM appears to be a safe, effective, and minimally invasive management option in achalasia in the short term.”

Long-term durability data are not yet available, they noted.

Dr. Kahrilas received funding from the U.S. Public Health Service.

 

Peroral endoscopic myotomy, or POEM, should be considered as primary therapy for type III achalasia and as a treatment option comparable with laparoscopic Heller myotomy for any of the achalasia syndromes – but only when physicians with expertise are available, according to a clinical practice update from the American Gastroenterological Association.

Further, post-POEM patients should be considered at high risk of developing reflux esophagitis and should be advised of the management considerations, including potential indefinite proton pump inhibitor therapy and/or surveillance endoscopy, prior to undergoing the procedure, Peter J. Kahrilas, MD, of Northwestern University, Chicago, and his colleagues wrote in the update, which is published in the November issue of Gastroenterology (2017. doi: 10.1053/j.gastro.2017.10.001).

In an effort to describe the place for POEM among the currently available robust treatments for achalasia, the authors conducted a literature review – their “best practice” recommendations are based on the findings from relevant publications and on expert opinion.

Dr. Peter J. Kahrilas
In determining the need for achalasia therapy, they agreed that patient-specific parameters should be considered along with published efficacy data. Important parameters include Chicago Classification subtype, comorbidities, early vs. late disease, and primary or secondary causes.

Additionally, they said POEM should be performed by experienced physicians in high-volume centers since the procedure is complex and an estimated 20-30 procedures are needed to achieve competence.

The update and these proposed best practices follow the evolution of POEM over the last decade: it began as an exciting concept and is now a mainstream treatment option for achalasia, the authors said.

“Uncontrolled outcome data have been very promising comparing POEM with the standard surgical treatment for achalasia, laparoscopic Heller myotomy (LHM). However, concerns remain regarding post-POEM reflux, the durability of the procedure, and the learning curve for endoscopists adopting the technique,” they wrote, which, when coupled with recent randomized controlled study data showing excellent and equivalent 5-year outcomes with pneumatic dilation and LHM, make the role of POEM somewhat controversial.

As part of the review, they considered the strengths and weaknesses of both POEM and LHM. The data comparing POEM with LHM or pneumatic dilation remain very limited, but based on those that do exist, the authors concluded that “POEM appears to be a safe, effective, and minimally invasive management option in achalasia in the short term.”

Long-term durability data are not yet available, they noted.

Dr. Kahrilas received funding from the U.S. Public Health Service.

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New RA JAK inhibitor, monoclonal antibody trial results scheduled for ACR 2017

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New results from several investigational oral Janus kinase inhibitor trials and an antifractalkine monoclonal antibody trial for patients with rheumatoid arthritis will be made available for the first time to attendees of the annual meeting of the American College of Rheumatology on Nov. 6 and 7 in San Diego.

Selective JAK-1 inhibitor upadacitinib

Two double-blind, randomized, controlled phase 3 studies of the oral, selective JAK-1 inhibitor upadacitinib (ABT-494) will be presented at the meeting, both involving once-daily extended-release formulations of the drug at 15 mg or 30 mg. The first trial, to be presented during an ACR abstract session on Monday, Nov. 6, showed that the drug met ACR 20 response criteria at significantly higher rates than did placebo at week 12 (63.8% for 15 mg, 66.2% for 30 mg, and 35.7% for placebo) in 661 patients with active RA and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Patients on the study drug also achieved low disease activity (28-joint Disease Activity Score using C-reactive protein [DAS28-CRP] of 3.2 or less) in higher proportions than did those who received placebo (48.4% for 15 mg, 47.9% for 30 mg, and 17.2% for placebo). More infections occurred in patients on 15 mg and 30 mg upadacitinib (29.0% and 31.5%, respectively), compared with placebo (21.3%), but there were no differences in serious infections. Three of the total four cases of herpes zoster infection were in patients taking upadacitinib.

A second upadacitinib trial, which involved patients on stable csDMARD therapy who could not tolerate or had disease refractory to a biologic DMARD, will be presented during a late-breaking poster session on Tuesday, Nov. 7. The study randomized 499 patients who had severe, refractory disease for a mean duration of 13 years. At 12 weeks, treatment with upadacitinib resulted in ACR 20 responses in 64.6% at 15 mg and 56.4% at 30 mg, compared with 28.4% for placebo. Responses at 12 weeks of 3.2 or less for DAS28-CRP also occurred at significantly higher rates of 43.3% for 15 mg and 42.4% for 30 mg, compared with 14.2% for placebo. Patients who were switched from placebo to active treatment at week 12 also achieved these responses at week 24, and the people who stayed on treatment with upadacitinib maintained or improved their response at week 24. More adverse events and infections tended to occur with upadacitinib at 30 mg than with 15 mg, and there were more herpes zoster infections with 30 mg (n = 4) vs. 15 mg (n = 1) and placebo (n = 1).
 

Antifractalkine monoclonal antibody

The Monday afternoon RA therapy abstract session will also feature the first-in-patient results at 52 weeks for the antifractalkine monoclonal antibody E6011 in an open-label phase 1/2 study of Japanese RA patients with active disease who had an inadequate response or intolerance to methotrexate or a TNF inhibitor. The results from the small trial of the biologic, which targets the chemokine that regulates chemotaxis and the adhesion of inflammatory cells that express CX3C chemokine receptor 1 (CX3CR1), indicate that the treatment has durable efficacy and is safe and well tolerated. Adverse events (AEs) developed in 84% of 28 patients who participated in the 52-week extension study, including a rate of 48% for treatment-emergent adverse events (TEAEs) and 14% for serious AEs. ACR 20 rates at week 52 ranged from 58% for 100 mg of E6011 to 73% for 200 mg and 60% for 400 mg.

Filgotinib safety in an extension trial

The long-term, open-label results from two phase 2b studies of the JAK-1 inhibitor filgotinib that’s in development for RA also will be presented during the same Monday abstract session. These safety data out to 84 weeks from the long-term extension study of the DARWIN 1 and 2 studies, called DARWIN 3, show that, among patients who received at least one dose of filgotinib 100 mg twice daily or 200 mg once daily in addition to methotrexate, the rate of TEAEs ranged from about 146 to 153 per 100 patient-years of exposure (PYE), including about 41-45 infections per 100 PYE. For filgotinib monotherapy, the rate of TEAEs was 150 per 100 PYE for 200 mg once daily, including 38 infections per 100 PYE.

Total cholesterol of 200-239 mg/dL occurred at a rate of about 79 per 100 PYE and a level of 240 mg/dL or greater was seen in 61-64 per 100 PYE for patients who took filgotinib plus methotrexate. Filgotinib monotherapy at 200 mg once daily gave rates of about 94 and 71 per 100 PYE for those respective total cholesterol levels.

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New results from several investigational oral Janus kinase inhibitor trials and an antifractalkine monoclonal antibody trial for patients with rheumatoid arthritis will be made available for the first time to attendees of the annual meeting of the American College of Rheumatology on Nov. 6 and 7 in San Diego.

Selective JAK-1 inhibitor upadacitinib

Two double-blind, randomized, controlled phase 3 studies of the oral, selective JAK-1 inhibitor upadacitinib (ABT-494) will be presented at the meeting, both involving once-daily extended-release formulations of the drug at 15 mg or 30 mg. The first trial, to be presented during an ACR abstract session on Monday, Nov. 6, showed that the drug met ACR 20 response criteria at significantly higher rates than did placebo at week 12 (63.8% for 15 mg, 66.2% for 30 mg, and 35.7% for placebo) in 661 patients with active RA and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Patients on the study drug also achieved low disease activity (28-joint Disease Activity Score using C-reactive protein [DAS28-CRP] of 3.2 or less) in higher proportions than did those who received placebo (48.4% for 15 mg, 47.9% for 30 mg, and 17.2% for placebo). More infections occurred in patients on 15 mg and 30 mg upadacitinib (29.0% and 31.5%, respectively), compared with placebo (21.3%), but there were no differences in serious infections. Three of the total four cases of herpes zoster infection were in patients taking upadacitinib.

A second upadacitinib trial, which involved patients on stable csDMARD therapy who could not tolerate or had disease refractory to a biologic DMARD, will be presented during a late-breaking poster session on Tuesday, Nov. 7. The study randomized 499 patients who had severe, refractory disease for a mean duration of 13 years. At 12 weeks, treatment with upadacitinib resulted in ACR 20 responses in 64.6% at 15 mg and 56.4% at 30 mg, compared with 28.4% for placebo. Responses at 12 weeks of 3.2 or less for DAS28-CRP also occurred at significantly higher rates of 43.3% for 15 mg and 42.4% for 30 mg, compared with 14.2% for placebo. Patients who were switched from placebo to active treatment at week 12 also achieved these responses at week 24, and the people who stayed on treatment with upadacitinib maintained or improved their response at week 24. More adverse events and infections tended to occur with upadacitinib at 30 mg than with 15 mg, and there were more herpes zoster infections with 30 mg (n = 4) vs. 15 mg (n = 1) and placebo (n = 1).
 

Antifractalkine monoclonal antibody

The Monday afternoon RA therapy abstract session will also feature the first-in-patient results at 52 weeks for the antifractalkine monoclonal antibody E6011 in an open-label phase 1/2 study of Japanese RA patients with active disease who had an inadequate response or intolerance to methotrexate or a TNF inhibitor. The results from the small trial of the biologic, which targets the chemokine that regulates chemotaxis and the adhesion of inflammatory cells that express CX3C chemokine receptor 1 (CX3CR1), indicate that the treatment has durable efficacy and is safe and well tolerated. Adverse events (AEs) developed in 84% of 28 patients who participated in the 52-week extension study, including a rate of 48% for treatment-emergent adverse events (TEAEs) and 14% for serious AEs. ACR 20 rates at week 52 ranged from 58% for 100 mg of E6011 to 73% for 200 mg and 60% for 400 mg.

Filgotinib safety in an extension trial

The long-term, open-label results from two phase 2b studies of the JAK-1 inhibitor filgotinib that’s in development for RA also will be presented during the same Monday abstract session. These safety data out to 84 weeks from the long-term extension study of the DARWIN 1 and 2 studies, called DARWIN 3, show that, among patients who received at least one dose of filgotinib 100 mg twice daily or 200 mg once daily in addition to methotrexate, the rate of TEAEs ranged from about 146 to 153 per 100 patient-years of exposure (PYE), including about 41-45 infections per 100 PYE. For filgotinib monotherapy, the rate of TEAEs was 150 per 100 PYE for 200 mg once daily, including 38 infections per 100 PYE.

Total cholesterol of 200-239 mg/dL occurred at a rate of about 79 per 100 PYE and a level of 240 mg/dL or greater was seen in 61-64 per 100 PYE for patients who took filgotinib plus methotrexate. Filgotinib monotherapy at 200 mg once daily gave rates of about 94 and 71 per 100 PYE for those respective total cholesterol levels.

 

New results from several investigational oral Janus kinase inhibitor trials and an antifractalkine monoclonal antibody trial for patients with rheumatoid arthritis will be made available for the first time to attendees of the annual meeting of the American College of Rheumatology on Nov. 6 and 7 in San Diego.

Selective JAK-1 inhibitor upadacitinib

Two double-blind, randomized, controlled phase 3 studies of the oral, selective JAK-1 inhibitor upadacitinib (ABT-494) will be presented at the meeting, both involving once-daily extended-release formulations of the drug at 15 mg or 30 mg. The first trial, to be presented during an ACR abstract session on Monday, Nov. 6, showed that the drug met ACR 20 response criteria at significantly higher rates than did placebo at week 12 (63.8% for 15 mg, 66.2% for 30 mg, and 35.7% for placebo) in 661 patients with active RA and an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). Patients on the study drug also achieved low disease activity (28-joint Disease Activity Score using C-reactive protein [DAS28-CRP] of 3.2 or less) in higher proportions than did those who received placebo (48.4% for 15 mg, 47.9% for 30 mg, and 17.2% for placebo). More infections occurred in patients on 15 mg and 30 mg upadacitinib (29.0% and 31.5%, respectively), compared with placebo (21.3%), but there were no differences in serious infections. Three of the total four cases of herpes zoster infection were in patients taking upadacitinib.

A second upadacitinib trial, which involved patients on stable csDMARD therapy who could not tolerate or had disease refractory to a biologic DMARD, will be presented during a late-breaking poster session on Tuesday, Nov. 7. The study randomized 499 patients who had severe, refractory disease for a mean duration of 13 years. At 12 weeks, treatment with upadacitinib resulted in ACR 20 responses in 64.6% at 15 mg and 56.4% at 30 mg, compared with 28.4% for placebo. Responses at 12 weeks of 3.2 or less for DAS28-CRP also occurred at significantly higher rates of 43.3% for 15 mg and 42.4% for 30 mg, compared with 14.2% for placebo. Patients who were switched from placebo to active treatment at week 12 also achieved these responses at week 24, and the people who stayed on treatment with upadacitinib maintained or improved their response at week 24. More adverse events and infections tended to occur with upadacitinib at 30 mg than with 15 mg, and there were more herpes zoster infections with 30 mg (n = 4) vs. 15 mg (n = 1) and placebo (n = 1).
 

Antifractalkine monoclonal antibody

The Monday afternoon RA therapy abstract session will also feature the first-in-patient results at 52 weeks for the antifractalkine monoclonal antibody E6011 in an open-label phase 1/2 study of Japanese RA patients with active disease who had an inadequate response or intolerance to methotrexate or a TNF inhibitor. The results from the small trial of the biologic, which targets the chemokine that regulates chemotaxis and the adhesion of inflammatory cells that express CX3C chemokine receptor 1 (CX3CR1), indicate that the treatment has durable efficacy and is safe and well tolerated. Adverse events (AEs) developed in 84% of 28 patients who participated in the 52-week extension study, including a rate of 48% for treatment-emergent adverse events (TEAEs) and 14% for serious AEs. ACR 20 rates at week 52 ranged from 58% for 100 mg of E6011 to 73% for 200 mg and 60% for 400 mg.

Filgotinib safety in an extension trial

The long-term, open-label results from two phase 2b studies of the JAK-1 inhibitor filgotinib that’s in development for RA also will be presented during the same Monday abstract session. These safety data out to 84 weeks from the long-term extension study of the DARWIN 1 and 2 studies, called DARWIN 3, show that, among patients who received at least one dose of filgotinib 100 mg twice daily or 200 mg once daily in addition to methotrexate, the rate of TEAEs ranged from about 146 to 153 per 100 patient-years of exposure (PYE), including about 41-45 infections per 100 PYE. For filgotinib monotherapy, the rate of TEAEs was 150 per 100 PYE for 200 mg once daily, including 38 infections per 100 PYE.

Total cholesterol of 200-239 mg/dL occurred at a rate of about 79 per 100 PYE and a level of 240 mg/dL or greater was seen in 61-64 per 100 PYE for patients who took filgotinib plus methotrexate. Filgotinib monotherapy at 200 mg once daily gave rates of about 94 and 71 per 100 PYE for those respective total cholesterol levels.

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Infections, psoriasis, facial fillers heat up Las Vegas Dermatology Seminar

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Mon, 01/14/2019 - 10:11

 

Updates on vaccines and infections, as well as the latest acne treatments and the Psoriasis Forum are among the hot topics at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Dr. Joseph F. Fowler Jr.
“For the psoriasis forum, we have updated information on new biological agents and biosimilars,” Dr. Stein Gold said in an interview.

Dr. Stein Gold, along with Julie Harper, MD, will direct a rosacea forum on Thursday to review the latest information on pathology and treatment. The day’s acne forum will include details on sebum-reduction products in the pipeline, as well as data on benzoyl peroxide.

The psoriasis forum on Friday will feature “long-term information on the safety of current drugs,” and also look ahead to more data on IL-23 inhibitors, Dr. Fowler said in an interview.

Aesthetic dermatology highlights from Saturday’s scheduled presentations include Dr. Zachary’s review of options for facial rejuvenation and what clinicians need to know about body contouring. Kristin M. Kelly, MD, of the University of California, Irvine, will discuss devices and how they can be best used to modulate scarring, and Howard Steinman, MD, who is in private practice in Irving, Tex., will share tips on “avoiding the danger zones” when using toxins and fillers.

SDEF and this news organization are owned by the same parent company.

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Updates on vaccines and infections, as well as the latest acne treatments and the Psoriasis Forum are among the hot topics at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Dr. Joseph F. Fowler Jr.
“For the psoriasis forum, we have updated information on new biological agents and biosimilars,” Dr. Stein Gold said in an interview.

Dr. Stein Gold, along with Julie Harper, MD, will direct a rosacea forum on Thursday to review the latest information on pathology and treatment. The day’s acne forum will include details on sebum-reduction products in the pipeline, as well as data on benzoyl peroxide.

The psoriasis forum on Friday will feature “long-term information on the safety of current drugs,” and also look ahead to more data on IL-23 inhibitors, Dr. Fowler said in an interview.

Aesthetic dermatology highlights from Saturday’s scheduled presentations include Dr. Zachary’s review of options for facial rejuvenation and what clinicians need to know about body contouring. Kristin M. Kelly, MD, of the University of California, Irvine, will discuss devices and how they can be best used to modulate scarring, and Howard Steinman, MD, who is in private practice in Irving, Tex., will share tips on “avoiding the danger zones” when using toxins and fillers.

SDEF and this news organization are owned by the same parent company.

 

Updates on vaccines and infections, as well as the latest acne treatments and the Psoriasis Forum are among the hot topics at Skin Disease Education Foundation’s annual Las Vegas Dermatology Seminar.

Dr. Joseph F. Fowler Jr.
“For the psoriasis forum, we have updated information on new biological agents and biosimilars,” Dr. Stein Gold said in an interview.

Dr. Stein Gold, along with Julie Harper, MD, will direct a rosacea forum on Thursday to review the latest information on pathology and treatment. The day’s acne forum will include details on sebum-reduction products in the pipeline, as well as data on benzoyl peroxide.

The psoriasis forum on Friday will feature “long-term information on the safety of current drugs,” and also look ahead to more data on IL-23 inhibitors, Dr. Fowler said in an interview.

Aesthetic dermatology highlights from Saturday’s scheduled presentations include Dr. Zachary’s review of options for facial rejuvenation and what clinicians need to know about body contouring. Kristin M. Kelly, MD, of the University of California, Irvine, will discuss devices and how they can be best used to modulate scarring, and Howard Steinman, MD, who is in private practice in Irving, Tex., will share tips on “avoiding the danger zones” when using toxins and fillers.

SDEF and this news organization are owned by the same parent company.

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Cardiogenic shock boosts PAH readmissions 10-fold

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– Cardiogenic shock, acute kidney injury, and chronic obstructive pulmonary disease were the top drivers of 30-day rehospitalizations in U.S. patients after an index hospitalization for pulmonary artery hypertension, based on an analysis of U.S. national data from 2013.

An episode of cardiogenic shock boosted 30-day rehospitalizations nearly 10-fold in recently discharged pulmonary artery hypertension (PAH) patients. A history of chronic obstructive pulmonary disease (COPD) linked with a threefold higher rehospitalization rate, and acute kidney injury linked with a doubled number of 30-day rehospitalizations, Kshitij Chatterjee, MD, said at the CHEST annual meeting.

Mitchel L. Zoler/Frontline Medical News
Dr. Kshitij Chatterjee
“We were surprised” that acute disorders – cardiogenic shock and acute kidney injury – played such a key role in triggering readmissions, said Dr. Chatterjee, a hospitalist at the University of Arkansas for Medical Science in Little Rock. He contrasted the impact of these acute disorders on PAH with the main drivers of rehospitalization for other diseases, such as COPD and pneumonia, that more often link with chronic comorbidities.

The powerful impact of cardiogenic shock in particular suggests that interventions that improve patient compliance with stabilizing treatments following an index PAH hospitalization might be effective at preventing a patient’s quick return to the hospital. Contacting PAH patients a week after their index hospitalization discharge to make sure they are compliant with their diuretic regimen, for example, might help prevent a decompensation that then leads to cardiogenic shock and a return trip to the hospital, Dr. Chatterjee suggested.

Follow-up of PAH patients after an index hospitalization “is probably the single most important thing, because it can help with compliance,” he said in an interview.

The rehospitalizations he studied could be for any cause. His analysis showed that the most common cause of rehospitalization was heart failure, which caused 23% of the rehospitalizations, followed by pulmonary hypertension that caused 20%, and acute kidney injury, responsible for 11% of the 30-day rehospitalizations.

Dr. Chatterjee’s study used data collected during 2013 in the National Readmissions Database, run by the federal Agency for Healthcare Quality and Research. During that period, 776 patients entered a U.S. hospital with a primary diagnosis of PAH. During the 30 days following discharge, 114 (15%) returned to the hospital. During the second hospitalization 8% died, and the median length of stay for those who remained alive was 7 days.

Dr. Chatterjee highlighted that the modest number of index hospitalizations for PAH, as well as 30-day rehospitalizations he found in 2013, make it highly unlikely that PAH rehospitalizations will become a target for Medicare penalties as has been done for heart failure, pneumonia, COPD, and a few other disorders. But he stressed that patients with PAH who need rehospitalization generally have a highly compromised quality of life that potentially could be avoided by better management, which could prevent the need for rehospitalization.

Dr. Chatterjee had no disclosures.

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– Cardiogenic shock, acute kidney injury, and chronic obstructive pulmonary disease were the top drivers of 30-day rehospitalizations in U.S. patients after an index hospitalization for pulmonary artery hypertension, based on an analysis of U.S. national data from 2013.

An episode of cardiogenic shock boosted 30-day rehospitalizations nearly 10-fold in recently discharged pulmonary artery hypertension (PAH) patients. A history of chronic obstructive pulmonary disease (COPD) linked with a threefold higher rehospitalization rate, and acute kidney injury linked with a doubled number of 30-day rehospitalizations, Kshitij Chatterjee, MD, said at the CHEST annual meeting.

Mitchel L. Zoler/Frontline Medical News
Dr. Kshitij Chatterjee
“We were surprised” that acute disorders – cardiogenic shock and acute kidney injury – played such a key role in triggering readmissions, said Dr. Chatterjee, a hospitalist at the University of Arkansas for Medical Science in Little Rock. He contrasted the impact of these acute disorders on PAH with the main drivers of rehospitalization for other diseases, such as COPD and pneumonia, that more often link with chronic comorbidities.

The powerful impact of cardiogenic shock in particular suggests that interventions that improve patient compliance with stabilizing treatments following an index PAH hospitalization might be effective at preventing a patient’s quick return to the hospital. Contacting PAH patients a week after their index hospitalization discharge to make sure they are compliant with their diuretic regimen, for example, might help prevent a decompensation that then leads to cardiogenic shock and a return trip to the hospital, Dr. Chatterjee suggested.

Follow-up of PAH patients after an index hospitalization “is probably the single most important thing, because it can help with compliance,” he said in an interview.

The rehospitalizations he studied could be for any cause. His analysis showed that the most common cause of rehospitalization was heart failure, which caused 23% of the rehospitalizations, followed by pulmonary hypertension that caused 20%, and acute kidney injury, responsible for 11% of the 30-day rehospitalizations.

Dr. Chatterjee’s study used data collected during 2013 in the National Readmissions Database, run by the federal Agency for Healthcare Quality and Research. During that period, 776 patients entered a U.S. hospital with a primary diagnosis of PAH. During the 30 days following discharge, 114 (15%) returned to the hospital. During the second hospitalization 8% died, and the median length of stay for those who remained alive was 7 days.

Dr. Chatterjee highlighted that the modest number of index hospitalizations for PAH, as well as 30-day rehospitalizations he found in 2013, make it highly unlikely that PAH rehospitalizations will become a target for Medicare penalties as has been done for heart failure, pneumonia, COPD, and a few other disorders. But he stressed that patients with PAH who need rehospitalization generally have a highly compromised quality of life that potentially could be avoided by better management, which could prevent the need for rehospitalization.

Dr. Chatterjee had no disclosures.

 

– Cardiogenic shock, acute kidney injury, and chronic obstructive pulmonary disease were the top drivers of 30-day rehospitalizations in U.S. patients after an index hospitalization for pulmonary artery hypertension, based on an analysis of U.S. national data from 2013.

An episode of cardiogenic shock boosted 30-day rehospitalizations nearly 10-fold in recently discharged pulmonary artery hypertension (PAH) patients. A history of chronic obstructive pulmonary disease (COPD) linked with a threefold higher rehospitalization rate, and acute kidney injury linked with a doubled number of 30-day rehospitalizations, Kshitij Chatterjee, MD, said at the CHEST annual meeting.

Mitchel L. Zoler/Frontline Medical News
Dr. Kshitij Chatterjee
“We were surprised” that acute disorders – cardiogenic shock and acute kidney injury – played such a key role in triggering readmissions, said Dr. Chatterjee, a hospitalist at the University of Arkansas for Medical Science in Little Rock. He contrasted the impact of these acute disorders on PAH with the main drivers of rehospitalization for other diseases, such as COPD and pneumonia, that more often link with chronic comorbidities.

The powerful impact of cardiogenic shock in particular suggests that interventions that improve patient compliance with stabilizing treatments following an index PAH hospitalization might be effective at preventing a patient’s quick return to the hospital. Contacting PAH patients a week after their index hospitalization discharge to make sure they are compliant with their diuretic regimen, for example, might help prevent a decompensation that then leads to cardiogenic shock and a return trip to the hospital, Dr. Chatterjee suggested.

Follow-up of PAH patients after an index hospitalization “is probably the single most important thing, because it can help with compliance,” he said in an interview.

The rehospitalizations he studied could be for any cause. His analysis showed that the most common cause of rehospitalization was heart failure, which caused 23% of the rehospitalizations, followed by pulmonary hypertension that caused 20%, and acute kidney injury, responsible for 11% of the 30-day rehospitalizations.

Dr. Chatterjee’s study used data collected during 2013 in the National Readmissions Database, run by the federal Agency for Healthcare Quality and Research. During that period, 776 patients entered a U.S. hospital with a primary diagnosis of PAH. During the 30 days following discharge, 114 (15%) returned to the hospital. During the second hospitalization 8% died, and the median length of stay for those who remained alive was 7 days.

Dr. Chatterjee highlighted that the modest number of index hospitalizations for PAH, as well as 30-day rehospitalizations he found in 2013, make it highly unlikely that PAH rehospitalizations will become a target for Medicare penalties as has been done for heart failure, pneumonia, COPD, and a few other disorders. But he stressed that patients with PAH who need rehospitalization generally have a highly compromised quality of life that potentially could be avoided by better management, which could prevent the need for rehospitalization.

Dr. Chatterjee had no disclosures.

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Key clinical point: Cardiogenic shock, COPD, and acute kidney injury were independently associated with increased 30-day rehospitalization after index hospitalization for PAH.

Major finding: Patients with cardiogenic shock following PAH hospitalization had a 9.7-fold increased rate of 30-day rehospitalization, compared with patients without shock.

Data source: The National Readmissions Database, which included 776 index U.S. hospitalizations for pulmonary arterial hospitalization during 2013.

Disclosures: Dr. Chatterjee had no disclosures.

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DDSEP® 8 Quick quiz - November 2017 Question 2

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Answer: C


Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.


Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

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Answer: C


Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.


Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Answer: C


Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.


Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

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DDSEP® 8 Quick quiz - November 2017 Question 2
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A 26-year-old woman is evaluated for assistance with weight management. She denies any significant medical or surgical history, but her BMI is 42 kg/m2. She does not understand why she maintains this weight. She insists that she follows a careful diet of healthy foods, noting that she has several servings each day of fruits and vegetables. She does not go to a gym, but walks when she can and takes the stairs more frequently than the elevator. Upon further review, she does admit to “stress eating” episodes just once or twice each week, but dismisses this as noncontributory, since this has been normal behavior for her since high school, when she was not considered to be overweight. She describes these episodes as more typically occurring after a stressful work day, during which she may treat herself to a bag of cookies or a carton of ice cream, usually alone in her apartment in the evening after dinner. She denies nausea, vomiting, or using laxatives. She denies sleep disturbance, is usually well rested in the morning, and eats “a healthy breakfast.” A routine electrolyte profile and complete blood count are unremarkable. She seeks your advice on endoscopic devices for weight loss management.

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Government uncertainty drives jump in ACA silver plan insurance premiums

Comment by Dr. Mike Nelson, MD, FCCP
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Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News
Other drivers of this increase include lower than anticipated enrollment in the marketplace, limited insurer participation, insufficient action by the government to reimburse plans that cover higher-cost enrollees, and general volatility around the policies governing exchanges, according to the Avalere research.

The expected premium changes are highly variable by state. Iowa has the highest change in its silver plans, with an average premium increase of 69% for its silver plans, while at the other end of the spectrum, Alaska is actually seeing a 22% decrease.

“These rates may change prior to open enrollment depending on how states respond to the elimination of CSR [cost-sharing reduction] funding for the 2018 plan year,” Avalere notes in its new analysis, adding that states may allow plans to refile for rate hikes now that CSR funding is likely dead. “In states where this occurs, it is expected that the newly updated rates will be substantially higher for the 2018 plan year.”

There was a glimmer of hope that the CSR payments would resume after a compromise was reached in the Senate Health, Education, Labor & Pensions Committee by Chairman Lamar Alexander (R-Tenn.) and Ranking Member Patty Murray (D-Wash.) that would offer 2 years of funding along with flexibility in the waiver program to allow states to tweak Affordable Care Act requirements. However, Speaker Paul Ryan (R-Wisc.) said the House would not be taking on any more health care action for the remainder of the year.

A spokeswoman from America’s Health Insurance Plans said in an interview that, although the CSR payments are no more, premium tax credits still exist to help lower-income individuals obtain insurance coverage.

Body

Mike Nelson, MD, FCCP, comments: One need not “google” too long to find that the United States performs quite poorly in overall health care when compared with other nations, despite spending more than any of the comparators…we’re 37th this year. This information from Avalere Health portends a further drop in our ranking next year. The privilege of good health is a responsibility of the individual, but the right to affordable health care is a responsibility of the government. It is time for our legislators to stop playing partisan politics and start communicating to propose a workable and affordable solution.

Dr. Mike Nelson

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Mike Nelson, MD, FCCP, comments: One need not “google” too long to find that the United States performs quite poorly in overall health care when compared with other nations, despite spending more than any of the comparators…we’re 37th this year. This information from Avalere Health portends a further drop in our ranking next year. The privilege of good health is a responsibility of the individual, but the right to affordable health care is a responsibility of the government. It is time for our legislators to stop playing partisan politics and start communicating to propose a workable and affordable solution.

Dr. Mike Nelson

Body

Mike Nelson, MD, FCCP, comments: One need not “google” too long to find that the United States performs quite poorly in overall health care when compared with other nations, despite spending more than any of the comparators…we’re 37th this year. This information from Avalere Health portends a further drop in our ranking next year. The privilege of good health is a responsibility of the individual, but the right to affordable health care is a responsibility of the government. It is time for our legislators to stop playing partisan politics and start communicating to propose a workable and affordable solution.

Dr. Mike Nelson

Title
Comment by Dr. Mike Nelson, MD, FCCP
Comment by Dr. Mike Nelson, MD, FCCP

 

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News
Other drivers of this increase include lower than anticipated enrollment in the marketplace, limited insurer participation, insufficient action by the government to reimburse plans that cover higher-cost enrollees, and general volatility around the policies governing exchanges, according to the Avalere research.

The expected premium changes are highly variable by state. Iowa has the highest change in its silver plans, with an average premium increase of 69% for its silver plans, while at the other end of the spectrum, Alaska is actually seeing a 22% decrease.

“These rates may change prior to open enrollment depending on how states respond to the elimination of CSR [cost-sharing reduction] funding for the 2018 plan year,” Avalere notes in its new analysis, adding that states may allow plans to refile for rate hikes now that CSR funding is likely dead. “In states where this occurs, it is expected that the newly updated rates will be substantially higher for the 2018 plan year.”

There was a glimmer of hope that the CSR payments would resume after a compromise was reached in the Senate Health, Education, Labor & Pensions Committee by Chairman Lamar Alexander (R-Tenn.) and Ranking Member Patty Murray (D-Wash.) that would offer 2 years of funding along with flexibility in the waiver program to allow states to tweak Affordable Care Act requirements. However, Speaker Paul Ryan (R-Wisc.) said the House would not be taking on any more health care action for the remainder of the year.

A spokeswoman from America’s Health Insurance Plans said in an interview that, although the CSR payments are no more, premium tax credits still exist to help lower-income individuals obtain insurance coverage.

 

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News
Other drivers of this increase include lower than anticipated enrollment in the marketplace, limited insurer participation, insufficient action by the government to reimburse plans that cover higher-cost enrollees, and general volatility around the policies governing exchanges, according to the Avalere research.

The expected premium changes are highly variable by state. Iowa has the highest change in its silver plans, with an average premium increase of 69% for its silver plans, while at the other end of the spectrum, Alaska is actually seeing a 22% decrease.

“These rates may change prior to open enrollment depending on how states respond to the elimination of CSR [cost-sharing reduction] funding for the 2018 plan year,” Avalere notes in its new analysis, adding that states may allow plans to refile for rate hikes now that CSR funding is likely dead. “In states where this occurs, it is expected that the newly updated rates will be substantially higher for the 2018 plan year.”

There was a glimmer of hope that the CSR payments would resume after a compromise was reached in the Senate Health, Education, Labor & Pensions Committee by Chairman Lamar Alexander (R-Tenn.) and Ranking Member Patty Murray (D-Wash.) that would offer 2 years of funding along with flexibility in the waiver program to allow states to tweak Affordable Care Act requirements. However, Speaker Paul Ryan (R-Wisc.) said the House would not be taking on any more health care action for the remainder of the year.

A spokeswoman from America’s Health Insurance Plans said in an interview that, although the CSR payments are no more, premium tax credits still exist to help lower-income individuals obtain insurance coverage.

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Government uncertainty drives jump in ACA silver plan insurance premiums

Article Type
Changed
Thu, 03/28/2019 - 14:45

 

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News
Other drivers of this increase include lower than anticipated enrollment in the marketplace, limited insurer participation, insufficient action by the government to reimburse plans that cover higher-cost enrollees, and general volatility around the policies governing exchanges, according to the Avalere research.

The expected premium changes are highly variable by state. Iowa has the highest change in its silver plans, with an average premium increase of 69% for its silver plans, while at the other end of the spectrum, Alaska is actually seeing a 22% decrease.

“These rates may change prior to open enrollment depending on how states respond to the elimination of CSR [cost-sharing reduction] funding for the 2018 plan year,” Avalere notes in its new analysis, adding that states may allow plans to refile for rate hikes now that CSR funding is likely dead. “In states where this occurs, it is expected that the newly updated rates will be substantially higher for the 2018 plan year.”

There was a glimmer of hope that the CSR payments would resume after a compromise was reached in the Senate Health, Education, Labor & Pensions Committee by Chairman Lamar Alexander (R-Tenn.) and Ranking Member Patty Murray (D-Wash.) that would offer 2 years of funding along with flexibility in the waiver program to allow states to tweak Affordable Care Act requirements, which is supported by AGA (http://www.gastro.org/news_items/aga-supports-alexander-murray-agreement-to-stabilize-individual-market). However, Speaker Paul Ryan (R-Wisc.) said the House would not be taking on any more health care action for the remainder of the year.

A spokeswoman from America’s Health Insurance Plans said in an interview that, although the CSR payments are no more, premium tax credits still exist to help lower-income individuals obtain insurance coverage.

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Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News
Other drivers of this increase include lower than anticipated enrollment in the marketplace, limited insurer participation, insufficient action by the government to reimburse plans that cover higher-cost enrollees, and general volatility around the policies governing exchanges, according to the Avalere research.

The expected premium changes are highly variable by state. Iowa has the highest change in its silver plans, with an average premium increase of 69% for its silver plans, while at the other end of the spectrum, Alaska is actually seeing a 22% decrease.

“These rates may change prior to open enrollment depending on how states respond to the elimination of CSR [cost-sharing reduction] funding for the 2018 plan year,” Avalere notes in its new analysis, adding that states may allow plans to refile for rate hikes now that CSR funding is likely dead. “In states where this occurs, it is expected that the newly updated rates will be substantially higher for the 2018 plan year.”

There was a glimmer of hope that the CSR payments would resume after a compromise was reached in the Senate Health, Education, Labor & Pensions Committee by Chairman Lamar Alexander (R-Tenn.) and Ranking Member Patty Murray (D-Wash.) that would offer 2 years of funding along with flexibility in the waiver program to allow states to tweak Affordable Care Act requirements, which is supported by AGA (http://www.gastro.org/news_items/aga-supports-alexander-murray-agreement-to-stabilize-individual-market). However, Speaker Paul Ryan (R-Wisc.) said the House would not be taking on any more health care action for the remainder of the year.

A spokeswoman from America’s Health Insurance Plans said in an interview that, although the CSR payments are no more, premium tax credits still exist to help lower-income individuals obtain insurance coverage.

 

Silver plans on the Affordable Care Act insurance exchanges in 2018 will see an average premium increase of 34% nationwide, according to new research from Avalere Health.

“Plans are raising premiums in 2018 to account for market uncertainty and the federal government’s failure to pay for cost-sharing reductions,” Caroline Pearson, senior vice president at Avalere, said in a statement. “These premium increases may allow insurers to remain in the market and enrollees in all regions to have access to coverage.”

Mary Ellen Schneider/Frontline Medical News
Other drivers of this increase include lower than anticipated enrollment in the marketplace, limited insurer participation, insufficient action by the government to reimburse plans that cover higher-cost enrollees, and general volatility around the policies governing exchanges, according to the Avalere research.

The expected premium changes are highly variable by state. Iowa has the highest change in its silver plans, with an average premium increase of 69% for its silver plans, while at the other end of the spectrum, Alaska is actually seeing a 22% decrease.

“These rates may change prior to open enrollment depending on how states respond to the elimination of CSR [cost-sharing reduction] funding for the 2018 plan year,” Avalere notes in its new analysis, adding that states may allow plans to refile for rate hikes now that CSR funding is likely dead. “In states where this occurs, it is expected that the newly updated rates will be substantially higher for the 2018 plan year.”

There was a glimmer of hope that the CSR payments would resume after a compromise was reached in the Senate Health, Education, Labor & Pensions Committee by Chairman Lamar Alexander (R-Tenn.) and Ranking Member Patty Murray (D-Wash.) that would offer 2 years of funding along with flexibility in the waiver program to allow states to tweak Affordable Care Act requirements, which is supported by AGA (http://www.gastro.org/news_items/aga-supports-alexander-murray-agreement-to-stabilize-individual-market). However, Speaker Paul Ryan (R-Wisc.) said the House would not be taking on any more health care action for the remainder of the year.

A spokeswoman from America’s Health Insurance Plans said in an interview that, although the CSR payments are no more, premium tax credits still exist to help lower-income individuals obtain insurance coverage.

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DDSEP® 8 Quick quiz - November 2017 Question 1

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DDSEP® 8 Quick quiz - November 2017 Question 1

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

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Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

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A 50-year-old woman with no past medical history presents to the emergency department with the acute onset of severe epigastric pain and vomiting. She is afebrile with a blood pressure of 100/50 mm Hg, and pulse of 110 bpm. Physical exam shows right upper-quadrant and epigastric tenderness to palpation without rebound. Labs demonstrate a WBC count of 17,000/mm3, hemoglobin of 16 g/dL, creatinine of 1.4 mg/dL, ALT of 215 U/L, AST of 190 U/L, a total bilirubin of 2.1 mg/dL, and triglycerides of 492 mg/dL. Right upper-quadrant ultrasound reveals gallstones and a 1.2-cm common bile duct. The following day, despite being hydrated aggressively, the patient develops a fever and becomes jaundiced with worsening abdominal pain.

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What’s Eating You? Scabies in the Developing World

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What’s Eating You? Scabies in the Developing World

Scabies is caused by the mite Sarcoptes scabiei var hominis.1 It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.2 Historically, scabies was first described in the Old Testament and by Aristotle,2 but the causative organism was not identified until 1687 using a light microscope.3 Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.1 It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.8 Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.10 As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.12 They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.2 The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,2 in skin burrows within the stratum granulosum.12 Maturation from larva to adult takes 10 to 14 days.12 A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Figure 1. Sarcoptes scabiei mite (A), ova (B) and scybala (fecal material)(C).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.13

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.14 However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.13 Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.12 In adults, sexual contact is an important method of transmission,12 and patients with scabies should be screened for other sexually transmitted diseases.8

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).12 The scalp, face, and neck frequently are involved in infants and children,2 and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.12 Itching is characteristically worse at night.8 In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.15,16 Mika et al10 suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).18 In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).19 Scabies skin infestations and infections are endemic in many remote aboriginal communities20 where 70% of children younger than 2 years have chronic scabies and skin sores.21 In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.22 In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.23 Edison et al24 reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al25 found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al26 concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.27

Figure 2. Scabies rash in an infant with burrows and erythematous papules.

 

 

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al28 found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,13 whereas permethrin cream 5% is the standard treatment in the developed world.29 Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.30 Drug shortages also can contribute to a high prevalence of scabies infestation in the community.31 Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.8 However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.34 Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.35

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.20 Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.34,36

References
  1. Romani L, Whitfeld MJ, Koroivueta J, et al. Mass drug administration for scabies control in a population with endemic disease. N Engl J Med. 2015;373:2305-2313.
  2. Hicks MI, Elston DM. Scabies. Dermatol Ther. 2009;22:279-292.
  3. Ramos-e-Silva M. Giovan Cosimo Bonomo (1663-1696): discoverer of the etiology of scabies. Int J Dermatol. 1998;37:625-630.
  4. Chung SD, Wang KH, Huang CC, et al. Scabies increased the risk of chronic kidney disease: a 5-year follow-up study. J Eur Acad Dermatol Venereol. 2014;28:286-292.
  5. Wong SS, Poon RW, Chau S, et al. Development of conventional and real-time quantitative PCR assays for diagnosis and monitoring of scabies. J Clin Microbiol. 2015;53:2095-2102.
  6. Kearns TM, Speare R, Cheng AC, et al. Impact of an ivermectin mass drug administration on scabies prevalence in a remote Australian aboriginal community. PLoS Negl Trop Dis. 2015;9:e0004151.
  7. Gilmore SJ. Control strategies for endemic childhood scabies. PLoS One. 2011;6:e15990.
  8. Hay RJ, Steer AC, Engelman D, Walton S. Scabies in the developing world—its prevalence, complications, and management. Clin Microbiol Infect. 2012;18:313-323.
  9. Hoy WE, White AV, Dowling A, et al. Post-streptococcal glomerulonephritis is a strong risk factor for chronic kidney disease in later life. Kidney Int. 2012;81:1026-1032.
  10. Mika A, Reynolds SL, Pickering D, et al. Complement inhibitors from scabies mites promote streptococcal growth—a novel mechanism in infected epidermis? PLoS Negl Trop Dis. 2012;6:e1563.
  11. McLean FE. The elimination of scabies: a task for our generation. Int J Dermatol. 2013;52:1215-1223.
  12. Hengge UR, Currie BJ, Jäger G, et al. Scabies: a ubiquitous neglected skin disease. Lancet Infect Dis. 2006;6:769-779.
  13. Heukelbach J, Feldmeier H. Scabies. Lancet. 2006;367:1767-1774.
  14. Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ. 2005;331:619-622.
  15. Yeoh DK, Bowen AC, Carapetis JR. Impetigo and scabies—disease burden and modern treatment strategies [published online May 11, 2016]. J Infect. 2016;(72 suppl):S61-S67.
  16. Bowen AC, Mahé A, Hay RJ, et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma. PLoS One. 2015;10:e0136789.
  17. Bowen AC, Tong SY, Chatfield MD, et al. The microbiology of impetigo in indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus, scabies, and nasal carriage. BMC Infect Dis. 2014;14:727.
  18. Sesso R, Pinto SW. Five-year follow-up of patients with epidemic glomerulonephritis due to Streptococcus zooepidemicus. Nephrol Dial Transplant. 2005;20:1808-1812.
  19. Singh GR. Glomerulonephritis and managing the risks of chronic renal disease. Pediatr Clin North Am. 2009;56:1363-1382.
  20. La Vincente S, Kearns T, Connors C, et al. Community management of endemic scabies in remote aboriginal communities of northern Australia: low treatment uptake and high ongoing acquisition. PLoS Negl Trop Dis. 2009;3:e444.
  21. Clucas DB, Carville KS, Connors C, et al. Disease burden and health-care clinic attendances for young children in remote aboriginal communities of northern Australia. Bull World Health Organ. 2008;86:275-281.
  22. Stanton B, Khanam S, Nazrul H, et al. Scabies in urban Bangladesh. J Trop Med Hyg. 1987;90:219-226.
  23. Heukelbach J, de Oliveira FA, Feldmeier H. Ecoparasitoses and public health in Brazil: challenges for control [in Portuguese]. Cad Saude Publica. 2003;19:1535-1540.
  24. Edison L, Beaudoin A, Goh L, et al. Scabies and bacterial superinfection among American Samoan children, 2011-2012. PLoS One. 2015;10:e0139336.
  25. Steer AC, Jenney AW, Kado J, et al. High burden of impetigo and scabies in a tropical country. PLoS Negl Trop Dis. 2009;3:e467.
  26. Romani L, Steer AC, Whitfeld MJ, et al. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet Infect Dis. 2015;15:960-967.
  27. Romani L, Koroivueta J, Steer AC, et al. Scabies and impetigo prevalence and risk factors in Fiji: a national survey. PLoS Negl Trop Dis. 2015;9:e0003452.
  28. Micali G, Lacarrubba F, Verzì AE, et al. Low-cost equipment for diagnosis and management of endemic scabies outbreaks in underserved populations. Clin Infect Dis. 2015;60:327-329.
  29. Pasay C, Walton S, Fischer K, et al. PCR-based assay to survey for knockdown resistance to pyrethroid acaricides in human scabies mites (Sarcoptes scabiei var hominis). Am J Trop Med Hyg. 2006;74:649-657.
  30. Heukelbach J, van Haeff E, Rump B, et al. Parasitic skin diseases: health care-seeking in a slum in north-east Brazil. Trop Med Int Health. 2003;8:368-373.
  31. Potter EV, Mayon-White R, Poon-King T, et al. Acute glomerulonephritis as a complication of scabies. In: Orkin M, Maibach HI, eds. Cutaneous Infestations and Insect Bites. New York, NY: Marcel Dekker; 1985.
  32. Mahé A. Mass drug administration for scabies control. N Engl J Med. 2016;374:1689.
  33. Steer AC, Romani L, Kaldor JM. Mass drug administration for scabies control. N Engl J Med. 2016;374:1690.
  34. Mounsey KE, Holt DC, McCarthy JS, et al. Longitudinal evidence of increasing in vitro tolerance of scabies mites to ivermectin in scabies-endemic communities. Arch Dermatol. 2009;145:840-841.
  35. Currie BJ. Scabies and global control of neglected tropical diseases. N Engl J Med. 2015;373:2371-2372.
  36. O’Donnell V, Morris S, Ward J. Mass drug administration for scabies control. N Engl J Med. 2016;374:1689-1690.
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The authors report no conflict of interest.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, MSC 578, 135 Rutledge Ave, 11th Floor, Charleston, SC 29425-5780 ([email protected]).

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Dr. Salgado is from the Department of Dermatology and Pathology, Rutgers New Jersey Medical School, Newark. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, MSC 578, 135 Rutledge Ave, 11th Floor, Charleston, SC 29425-5780 ([email protected]).

Author and Disclosure Information

Dr. Salgado is from the Department of Dermatology and Pathology, Rutgers New Jersey Medical School, Newark. Dr. Elston is from the Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, Charleston.

The authors report no conflict of interest.

Correspondence: Dirk M. Elston, MD, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina, MSC 578, 135 Rutledge Ave, 11th Floor, Charleston, SC 29425-5780 ([email protected]).

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Related Articles

Scabies is caused by the mite Sarcoptes scabiei var hominis.1 It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.2 Historically, scabies was first described in the Old Testament and by Aristotle,2 but the causative organism was not identified until 1687 using a light microscope.3 Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.1 It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.8 Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.10 As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.12 They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.2 The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,2 in skin burrows within the stratum granulosum.12 Maturation from larva to adult takes 10 to 14 days.12 A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Figure 1. Sarcoptes scabiei mite (A), ova (B) and scybala (fecal material)(C).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.13

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.14 However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.13 Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.12 In adults, sexual contact is an important method of transmission,12 and patients with scabies should be screened for other sexually transmitted diseases.8

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).12 The scalp, face, and neck frequently are involved in infants and children,2 and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.12 Itching is characteristically worse at night.8 In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.15,16 Mika et al10 suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).18 In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).19 Scabies skin infestations and infections are endemic in many remote aboriginal communities20 where 70% of children younger than 2 years have chronic scabies and skin sores.21 In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.22 In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.23 Edison et al24 reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al25 found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al26 concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.27

Figure 2. Scabies rash in an infant with burrows and erythematous papules.

 

 

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al28 found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,13 whereas permethrin cream 5% is the standard treatment in the developed world.29 Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.30 Drug shortages also can contribute to a high prevalence of scabies infestation in the community.31 Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.8 However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.34 Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.35

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.20 Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.34,36

Scabies is caused by the mite Sarcoptes scabiei var hominis.1 It is in the arthropod class Arachnida, subclass Acari, and family Sarcoptidae.2 Historically, scabies was first described in the Old Testament and by Aristotle,2 but the causative organism was not identified until 1687 using a light microscope.3 Scabies affects all age groups, races, and social classes and is globally widespread. It is most prevalent in developing tropical countries.1 It is estimated that 300 million individuals worldwide are infested with scabies mites annually, with the highest burden in young children.4-7 In industrialized societies, infections often are seen in young adults and in institutional settings such as nursing homes.8 Scabies disproportionately impacts impoverished communities with crowded living conditions, poor hygiene and nutrition, and substandard housing.5,9 Controlling the spread of the disease in these communities presents challenges but is important because of the connection between scabies and chronic kidney disease.10 As such, scabies represents a major health problem in the developing world and has been the focus of major health initiatives.1,11

Identifying Characteristics

Adult females are 0.4-mm long and 0.3-mm wide, with males being smaller. Adult nymphs have 8 legs and larvae have 6 legs. Scabies mites are distinguishable from other arachnids by the position of a distinct gnathosoma and the lack of a division between the abdomen and cephalothorax.12 They are ovoid with a small anterior cephalic and caudal thoracoabdominal portion with hairlike projections coming off from the rudimentary legs. They can crawl as fast as 2.5 cm per minute on warm skin.2 The life cycle of the mite begins after mating: the male mite dies, and the female lays up to 3 eggs per day, which hatch in 3 to 4 days,2 in skin burrows within the stratum granulosum.12 Maturation from larva to adult takes 10 to 14 days.12 A female mite can live for 4 to 6 weeks and can produce up to 40 ova (Figure 1).

Figure 1. Sarcoptes scabiei mite (A), ova (B) and scybala (fecal material)(C).

Disease Transmission

Without a host, mites are able to survive and remain capable of infestation for 24 to 36 hours at 21°C and 40% to 80% relative humidity. Lower temperatures and higher humidity prolong survival, but infectivity decreases the longer they are without a host.13

An adult human with ordinary scabies will have an average of 12 adult female mites on the body surface at a given time.14 However, hundreds of mites can be found in neglected children in underprivileged communities and millions in patients with crusted scabies.13 Transmission of typical scabies requires close direct skin-to-skin contact for 15 to 20 minutes.2,8 Transmission from clothing or fomites are an unlikely source of infestation with the exception of patients who are heavily infested such as in crusted scabies.12 In adults, sexual contact is an important method of transmission,12 and patients with scabies should be screened for other sexually transmitted diseases.8

Clinical Manifestations

Signs of scabies on the skin include burrows, erythematous papules, and generalized pruritus (Figure 2).12 The scalp, face, and neck frequently are involved in infants and children,2 and the hands, wrists, elbows, genitalia, axillae, umbilicus, belt line, nipples, and buttocks commonly are involved in adults.12 Itching is characteristically worse at night.8 In tropical climates, patients with scabies are predisposed to secondary bacterial skin infections, particularly Streptococcus pyogenes (group A streptococci). The association between scabies and pyoderma caused by group A streptococci has been well established.15,16 Mika et al10 suggested that local complement inhibition plays an important role in the development of pyoderma in scabies-infested skin. A relationship between scabies and poststreptococcal glomerulonephritis (PSGN) has been established.11,17 An outbreak of PSGN in Brazil following an epidemic of Streptococcus zooepidemicus resulted in a high prevalence of renal abnormalities (mean follow-up, 5.4 years).18 In an aboriginal population with high rates of end-stage renal disease, follow-up in children 6 to 18 years after an epidemic of PSGN (mean follow-up, 14.6 years) showed that risk for overt proteinuria was more than 6 times greater than in healthy controls (95% confidence interval, 2.2-16.9).19 Scabies skin infestations and infections are endemic in many remote aboriginal communities20 where 70% of children younger than 2 years have chronic scabies and skin sores.21 In Dhaka, an urban slum in Bangladesh, the incidence of at least one scabies infection in children younger than 6 years was 952 per 1000 per year. In urban settlements in Dhaka, 49% (288/589) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed due to restricted access to health care.22 In Brazil, scabies is hyperendemic in many poor communities and slums and is commonly associated with considerable morbidity.23 Edison et al24 reported that scabies and bacterial superinfections cause substantial morbidity among American Samoan children, with superinfections present in 53% (604/1139) of children diagnosed with scabies. Steer et al25 found that impetigo and scabies had been underestimated in Fiji where 25.6% and 18.5% of primary school children and 12.2% and 14.0% of infants had impetigo and scabies, respectively. In a systematic review of scabies and impetigo prevalence, Romani et al26 concluded that scabies and associated impetigo are common problems in the developing world that disproportionately affect children and communities in underprivileged areas and tropical countries, with the Pacific and Latin American regions having the highest prevalence of scabies. Scabies represents a major health concern worldwide due to the strong relationship between scabies and secondary infection.27

Figure 2. Scabies rash in an infant with burrows and erythematous papules.

 

 

Prevention and Control in the Developing World

Low-cost diagnostic equipment can play a key role in the definitive diagnosis and management of scabies outbreaks in the developing world. Micali et al28 found that a $30 videomicroscope was as effective in scabies diagnosis as a $20,000 videodermatoscope. Because of the low cost of benzyl benzoate, it is commonly used as a first-line drug in many parts of the world,13 whereas permethrin cream 5% is the standard treatment in the developed world.29 Recognition of the role of scabies in patients with pyoderma is key, and one study indicated clinically apparent scabies went unnoticed by physicians in 52% of patients presenting with skin lesions.30 Drug shortages also can contribute to a high prevalence of scabies infestation in the community.31 Mass treatment with ivermectin has proven to be an effective means of reducing the prevalence of many parasitic diseases,1,32,33 and it shows great promise for crusted scabies, institutional outbreaks, and mass administration in highly endemic communites.8 However, there is evidence of ivermectin tolerance among mites, which could undermine the success of mass drug administration.34 Another important consideration is population mobility and the risk for rapid reintroduction of scabies infection across regions.35

Complicating disease control are the socioeconomic factors associated with scabies in the developing world. Families with scabies infestation typically do not own their homes, are less likely to have constant electricity, have a lower monthly income, and live in substandard housing.20 Families can spend a substantial part of their household income on treatment, impacting what they can spend on food.8,11 In addition to medication, control of scabies requires community education and involvement, along with access to primary care and attention to living conditions and environmental factors.34,36

References
  1. Romani L, Whitfeld MJ, Koroivueta J, et al. Mass drug administration for scabies control in a population with endemic disease. N Engl J Med. 2015;373:2305-2313.
  2. Hicks MI, Elston DM. Scabies. Dermatol Ther. 2009;22:279-292.
  3. Ramos-e-Silva M. Giovan Cosimo Bonomo (1663-1696): discoverer of the etiology of scabies. Int J Dermatol. 1998;37:625-630.
  4. Chung SD, Wang KH, Huang CC, et al. Scabies increased the risk of chronic kidney disease: a 5-year follow-up study. J Eur Acad Dermatol Venereol. 2014;28:286-292.
  5. Wong SS, Poon RW, Chau S, et al. Development of conventional and real-time quantitative PCR assays for diagnosis and monitoring of scabies. J Clin Microbiol. 2015;53:2095-2102.
  6. Kearns TM, Speare R, Cheng AC, et al. Impact of an ivermectin mass drug administration on scabies prevalence in a remote Australian aboriginal community. PLoS Negl Trop Dis. 2015;9:e0004151.
  7. Gilmore SJ. Control strategies for endemic childhood scabies. PLoS One. 2011;6:e15990.
  8. Hay RJ, Steer AC, Engelman D, Walton S. Scabies in the developing world—its prevalence, complications, and management. Clin Microbiol Infect. 2012;18:313-323.
  9. Hoy WE, White AV, Dowling A, et al. Post-streptococcal glomerulonephritis is a strong risk factor for chronic kidney disease in later life. Kidney Int. 2012;81:1026-1032.
  10. Mika A, Reynolds SL, Pickering D, et al. Complement inhibitors from scabies mites promote streptococcal growth—a novel mechanism in infected epidermis? PLoS Negl Trop Dis. 2012;6:e1563.
  11. McLean FE. The elimination of scabies: a task for our generation. Int J Dermatol. 2013;52:1215-1223.
  12. Hengge UR, Currie BJ, Jäger G, et al. Scabies: a ubiquitous neglected skin disease. Lancet Infect Dis. 2006;6:769-779.
  13. Heukelbach J, Feldmeier H. Scabies. Lancet. 2006;367:1767-1774.
  14. Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ. 2005;331:619-622.
  15. Yeoh DK, Bowen AC, Carapetis JR. Impetigo and scabies—disease burden and modern treatment strategies [published online May 11, 2016]. J Infect. 2016;(72 suppl):S61-S67.
  16. Bowen AC, Mahé A, Hay RJ, et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma. PLoS One. 2015;10:e0136789.
  17. Bowen AC, Tong SY, Chatfield MD, et al. The microbiology of impetigo in indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus, scabies, and nasal carriage. BMC Infect Dis. 2014;14:727.
  18. Sesso R, Pinto SW. Five-year follow-up of patients with epidemic glomerulonephritis due to Streptococcus zooepidemicus. Nephrol Dial Transplant. 2005;20:1808-1812.
  19. Singh GR. Glomerulonephritis and managing the risks of chronic renal disease. Pediatr Clin North Am. 2009;56:1363-1382.
  20. La Vincente S, Kearns T, Connors C, et al. Community management of endemic scabies in remote aboriginal communities of northern Australia: low treatment uptake and high ongoing acquisition. PLoS Negl Trop Dis. 2009;3:e444.
  21. Clucas DB, Carville KS, Connors C, et al. Disease burden and health-care clinic attendances for young children in remote aboriginal communities of northern Australia. Bull World Health Organ. 2008;86:275-281.
  22. Stanton B, Khanam S, Nazrul H, et al. Scabies in urban Bangladesh. J Trop Med Hyg. 1987;90:219-226.
  23. Heukelbach J, de Oliveira FA, Feldmeier H. Ecoparasitoses and public health in Brazil: challenges for control [in Portuguese]. Cad Saude Publica. 2003;19:1535-1540.
  24. Edison L, Beaudoin A, Goh L, et al. Scabies and bacterial superinfection among American Samoan children, 2011-2012. PLoS One. 2015;10:e0139336.
  25. Steer AC, Jenney AW, Kado J, et al. High burden of impetigo and scabies in a tropical country. PLoS Negl Trop Dis. 2009;3:e467.
  26. Romani L, Steer AC, Whitfeld MJ, et al. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet Infect Dis. 2015;15:960-967.
  27. Romani L, Koroivueta J, Steer AC, et al. Scabies and impetigo prevalence and risk factors in Fiji: a national survey. PLoS Negl Trop Dis. 2015;9:e0003452.
  28. Micali G, Lacarrubba F, Verzì AE, et al. Low-cost equipment for diagnosis and management of endemic scabies outbreaks in underserved populations. Clin Infect Dis. 2015;60:327-329.
  29. Pasay C, Walton S, Fischer K, et al. PCR-based assay to survey for knockdown resistance to pyrethroid acaricides in human scabies mites (Sarcoptes scabiei var hominis). Am J Trop Med Hyg. 2006;74:649-657.
  30. Heukelbach J, van Haeff E, Rump B, et al. Parasitic skin diseases: health care-seeking in a slum in north-east Brazil. Trop Med Int Health. 2003;8:368-373.
  31. Potter EV, Mayon-White R, Poon-King T, et al. Acute glomerulonephritis as a complication of scabies. In: Orkin M, Maibach HI, eds. Cutaneous Infestations and Insect Bites. New York, NY: Marcel Dekker; 1985.
  32. Mahé A. Mass drug administration for scabies control. N Engl J Med. 2016;374:1689.
  33. Steer AC, Romani L, Kaldor JM. Mass drug administration for scabies control. N Engl J Med. 2016;374:1690.
  34. Mounsey KE, Holt DC, McCarthy JS, et al. Longitudinal evidence of increasing in vitro tolerance of scabies mites to ivermectin in scabies-endemic communities. Arch Dermatol. 2009;145:840-841.
  35. Currie BJ. Scabies and global control of neglected tropical diseases. N Engl J Med. 2015;373:2371-2372.
  36. O’Donnell V, Morris S, Ward J. Mass drug administration for scabies control. N Engl J Med. 2016;374:1689-1690.
References
  1. Romani L, Whitfeld MJ, Koroivueta J, et al. Mass drug administration for scabies control in a population with endemic disease. N Engl J Med. 2015;373:2305-2313.
  2. Hicks MI, Elston DM. Scabies. Dermatol Ther. 2009;22:279-292.
  3. Ramos-e-Silva M. Giovan Cosimo Bonomo (1663-1696): discoverer of the etiology of scabies. Int J Dermatol. 1998;37:625-630.
  4. Chung SD, Wang KH, Huang CC, et al. Scabies increased the risk of chronic kidney disease: a 5-year follow-up study. J Eur Acad Dermatol Venereol. 2014;28:286-292.
  5. Wong SS, Poon RW, Chau S, et al. Development of conventional and real-time quantitative PCR assays for diagnosis and monitoring of scabies. J Clin Microbiol. 2015;53:2095-2102.
  6. Kearns TM, Speare R, Cheng AC, et al. Impact of an ivermectin mass drug administration on scabies prevalence in a remote Australian aboriginal community. PLoS Negl Trop Dis. 2015;9:e0004151.
  7. Gilmore SJ. Control strategies for endemic childhood scabies. PLoS One. 2011;6:e15990.
  8. Hay RJ, Steer AC, Engelman D, Walton S. Scabies in the developing world—its prevalence, complications, and management. Clin Microbiol Infect. 2012;18:313-323.
  9. Hoy WE, White AV, Dowling A, et al. Post-streptococcal glomerulonephritis is a strong risk factor for chronic kidney disease in later life. Kidney Int. 2012;81:1026-1032.
  10. Mika A, Reynolds SL, Pickering D, et al. Complement inhibitors from scabies mites promote streptococcal growth—a novel mechanism in infected epidermis? PLoS Negl Trop Dis. 2012;6:e1563.
  11. McLean FE. The elimination of scabies: a task for our generation. Int J Dermatol. 2013;52:1215-1223.
  12. Hengge UR, Currie BJ, Jäger G, et al. Scabies: a ubiquitous neglected skin disease. Lancet Infect Dis. 2006;6:769-779.
  13. Heukelbach J, Feldmeier H. Scabies. Lancet. 2006;367:1767-1774.
  14. Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ. 2005;331:619-622.
  15. Yeoh DK, Bowen AC, Carapetis JR. Impetigo and scabies—disease burden and modern treatment strategies [published online May 11, 2016]. J Infect. 2016;(72 suppl):S61-S67.
  16. Bowen AC, Mahé A, Hay RJ, et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma. PLoS One. 2015;10:e0136789.
  17. Bowen AC, Tong SY, Chatfield MD, et al. The microbiology of impetigo in indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus, scabies, and nasal carriage. BMC Infect Dis. 2014;14:727.
  18. Sesso R, Pinto SW. Five-year follow-up of patients with epidemic glomerulonephritis due to Streptococcus zooepidemicus. Nephrol Dial Transplant. 2005;20:1808-1812.
  19. Singh GR. Glomerulonephritis and managing the risks of chronic renal disease. Pediatr Clin North Am. 2009;56:1363-1382.
  20. La Vincente S, Kearns T, Connors C, et al. Community management of endemic scabies in remote aboriginal communities of northern Australia: low treatment uptake and high ongoing acquisition. PLoS Negl Trop Dis. 2009;3:e444.
  21. Clucas DB, Carville KS, Connors C, et al. Disease burden and health-care clinic attendances for young children in remote aboriginal communities of northern Australia. Bull World Health Organ. 2008;86:275-281.
  22. Stanton B, Khanam S, Nazrul H, et al. Scabies in urban Bangladesh. J Trop Med Hyg. 1987;90:219-226.
  23. Heukelbach J, de Oliveira FA, Feldmeier H. Ecoparasitoses and public health in Brazil: challenges for control [in Portuguese]. Cad Saude Publica. 2003;19:1535-1540.
  24. Edison L, Beaudoin A, Goh L, et al. Scabies and bacterial superinfection among American Samoan children, 2011-2012. PLoS One. 2015;10:e0139336.
  25. Steer AC, Jenney AW, Kado J, et al. High burden of impetigo and scabies in a tropical country. PLoS Negl Trop Dis. 2009;3:e467.
  26. Romani L, Steer AC, Whitfeld MJ, et al. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet Infect Dis. 2015;15:960-967.
  27. Romani L, Koroivueta J, Steer AC, et al. Scabies and impetigo prevalence and risk factors in Fiji: a national survey. PLoS Negl Trop Dis. 2015;9:e0003452.
  28. Micali G, Lacarrubba F, Verzì AE, et al. Low-cost equipment for diagnosis and management of endemic scabies outbreaks in underserved populations. Clin Infect Dis. 2015;60:327-329.
  29. Pasay C, Walton S, Fischer K, et al. PCR-based assay to survey for knockdown resistance to pyrethroid acaricides in human scabies mites (Sarcoptes scabiei var hominis). Am J Trop Med Hyg. 2006;74:649-657.
  30. Heukelbach J, van Haeff E, Rump B, et al. Parasitic skin diseases: health care-seeking in a slum in north-east Brazil. Trop Med Int Health. 2003;8:368-373.
  31. Potter EV, Mayon-White R, Poon-King T, et al. Acute glomerulonephritis as a complication of scabies. In: Orkin M, Maibach HI, eds. Cutaneous Infestations and Insect Bites. New York, NY: Marcel Dekker; 1985.
  32. Mahé A. Mass drug administration for scabies control. N Engl J Med. 2016;374:1689.
  33. Steer AC, Romani L, Kaldor JM. Mass drug administration for scabies control. N Engl J Med. 2016;374:1690.
  34. Mounsey KE, Holt DC, McCarthy JS, et al. Longitudinal evidence of increasing in vitro tolerance of scabies mites to ivermectin in scabies-endemic communities. Arch Dermatol. 2009;145:840-841.
  35. Currie BJ. Scabies and global control of neglected tropical diseases. N Engl J Med. 2015;373:2371-2372.
  36. O’Donnell V, Morris S, Ward J. Mass drug administration for scabies control. N Engl J Med. 2016;374:1689-1690.
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  • Scabies infestation is one of the world’s leading causes of chronic kidney disease.
  • Ivermectin can be used to treat mass infestations, and older topical therapies also are commonly used.
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FDA approves acalabrutinib for second-line treatment of MCL

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The Food and Drug Administration has granted accelerated approval to acalabrutinib, a Bruton tyrosine kinase inhibitor, for the treatment of adults with mantle cell lymphoma (MCL) who have received at least one prior therapy.

Approval was based on an 81% overall response rate in a phase 2, single-arm trial (ACE-LY-004) of 124 patients with MCL who had received at least one prior treatment (40% complete response, 41% partial response), the FDA said in a statement.

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Common adverse effects of acalabrutinib include headache, diarrhea, bruising, myalgia, anemia, thrombocytopenia, and neutropenia.

Serious adverse effects include hemorrhage and atrial fibrillation. Second primary malignancies have occurred in some patients, according to the FDA.

Acalabrutinib will be marketed as Calquence by AstraZeneca. The company is currently enrolling patients in a phase 3 trial evaluating acalabrutinib as a first-line treatment for patients with MCL in combination with bendamustine and rituximab.

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The Food and Drug Administration has granted accelerated approval to acalabrutinib, a Bruton tyrosine kinase inhibitor, for the treatment of adults with mantle cell lymphoma (MCL) who have received at least one prior therapy.

Approval was based on an 81% overall response rate in a phase 2, single-arm trial (ACE-LY-004) of 124 patients with MCL who had received at least one prior treatment (40% complete response, 41% partial response), the FDA said in a statement.

Purple FDA logo.
Common adverse effects of acalabrutinib include headache, diarrhea, bruising, myalgia, anemia, thrombocytopenia, and neutropenia.

Serious adverse effects include hemorrhage and atrial fibrillation. Second primary malignancies have occurred in some patients, according to the FDA.

Acalabrutinib will be marketed as Calquence by AstraZeneca. The company is currently enrolling patients in a phase 3 trial evaluating acalabrutinib as a first-line treatment for patients with MCL in combination with bendamustine and rituximab.

 

The Food and Drug Administration has granted accelerated approval to acalabrutinib, a Bruton tyrosine kinase inhibitor, for the treatment of adults with mantle cell lymphoma (MCL) who have received at least one prior therapy.

Approval was based on an 81% overall response rate in a phase 2, single-arm trial (ACE-LY-004) of 124 patients with MCL who had received at least one prior treatment (40% complete response, 41% partial response), the FDA said in a statement.

Purple FDA logo.
Common adverse effects of acalabrutinib include headache, diarrhea, bruising, myalgia, anemia, thrombocytopenia, and neutropenia.

Serious adverse effects include hemorrhage and atrial fibrillation. Second primary malignancies have occurred in some patients, according to the FDA.

Acalabrutinib will be marketed as Calquence by AstraZeneca. The company is currently enrolling patients in a phase 3 trial evaluating acalabrutinib as a first-line treatment for patients with MCL in combination with bendamustine and rituximab.

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