SVS members, please encourage medical or pre-med students interested in vascular surgery to apply for scholarship to attend the 2018 Vascular Annual Meeting.

VAM will be held June 20 to 23, 2018, in Boston. (Plenaries are June 21-23 and exhibits are open June 21-22.)  The Society for Vascular Surgery offers travel awards, including complimentary VAM registration, to be used toward the cost of travel, housing and meals.

Two awards are available, the General Surgery Resident/Medical Student Travel Scholarship and the Diversity Medical Student Travel Scholarship. Recipients become part of the hugely popular scholarship program, designed to let residents and students explore their interest in vascular surgery.

The SVS Foundation seeks applicants for its Student Research Fellowship awards, designed to stimulate laboratory and clinical vascular research by undergraduate college students and medical students attending universities in the United States and Canada.

Urge students you know with an interest in research to apply today.

SVS members, please encourage medical or pre-med students interested in vascular surgery to apply for scholarship to attend the 2018 Vascular Annual Meeting.

VAM will be held June 20 to 23, 2018, in Boston. (Plenaries are June 21-23 and exhibits are open June 21-22.)  The Society for Vascular Surgery offers travel awards, including complimentary VAM registration, to be used toward the cost of travel, housing and meals.

Two awards are available, the General Surgery Resident/Medical Student Travel Scholarship and the Diversity Medical Student Travel Scholarship. Recipients become part of the hugely popular scholarship program, designed to let residents and students explore their interest in vascular surgery.

The SVS Foundation seeks applicants for its Student Research Fellowship awards, designed to stimulate laboratory and clinical vascular research by undergraduate college students and medical students attending universities in the United States and Canada.

Urge students you know with an interest in research to apply today.

SVS members, please encourage medical or pre-med students interested in vascular surgery to apply for scholarship to attend the 2018 Vascular Annual Meeting.

VAM will be held June 20 to 23, 2018, in Boston. (Plenaries are June 21-23 and exhibits are open June 21-22.)  The Society for Vascular Surgery offers travel awards, including complimentary VAM registration, to be used toward the cost of travel, housing and meals.

Two awards are available, the General Surgery Resident/Medical Student Travel Scholarship and the Diversity Medical Student Travel Scholarship. Recipients become part of the hugely popular scholarship program, designed to let residents and students explore their interest in vascular surgery.

The SVS Foundation seeks applicants for its Student Research Fellowship awards, designed to stimulate laboratory and clinical vascular research by undergraduate college students and medical students attending universities in the United States and Canada.

Urge students you know with an interest in research to apply today.

Q2. CORRECT ANSWER: C

RATIONALE
In a population study of U.S. veterans infected with hepatitis C (n = 110,484), a cox proportional hazards model was used to determine risk of developing cirrhosis and hepatocellular carcinoma for genotypes 1-4, after adjusting for age, period of service, race, sex, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment. Despite genotype 3 patients being younger, their risk of developing cirrhosis was highest with hazard ratio = 1.30 (1.22, 1.39), compared to genotype 1 (reference, HR 1.0), genotype 2 with HR = 0.68 (0.64, 0.73), and genotype 4 with HR = 0.94 (0.78, 1.14). Likewise, the risk of development of HCC was highest for genotype 3 HCV with HR = 1.80 (1.60, 2.03), compared to a genotype 2 (HR = 0.55; 0.47, 0.63), and genotype 4 (0.99; 0.68, 1.45).
It is speculated that the hepatic steatosis that is a direct result of genotype 3 HCV may contribute to the accelerated progression to cirrhosis and HCC, but this has not been proven and was not evaluated in this Veteran Affairs study.

REFERENCE
1. Kanwal F., Kramer J.R., Ilyas J., et al. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98-105.

Q2. CORRECT ANSWER: C

RATIONALE
In a population study of U.S. veterans infected with hepatitis C (n = 110,484), a cox proportional hazards model was used to determine risk of developing cirrhosis and hepatocellular carcinoma for genotypes 1-4, after adjusting for age, period of service, race, sex, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment. Despite genotype 3 patients being younger, their risk of developing cirrhosis was highest with hazard ratio = 1.30 (1.22, 1.39), compared to genotype 1 (reference, HR 1.0), genotype 2 with HR = 0.68 (0.64, 0.73), and genotype 4 with HR = 0.94 (0.78, 1.14). Likewise, the risk of development of HCC was highest for genotype 3 HCV with HR = 1.80 (1.60, 2.03), compared to a genotype 2 (HR = 0.55; 0.47, 0.63), and genotype 4 (0.99; 0.68, 1.45).
It is speculated that the hepatic steatosis that is a direct result of genotype 3 HCV may contribute to the accelerated progression to cirrhosis and HCC, but this has not been proven and was not evaluated in this Veteran Affairs study.

REFERENCE
1. Kanwal F., Kramer J.R., Ilyas J., et al. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98-105.

Q2. CORRECT ANSWER: C

RATIONALE
In a population study of U.S. veterans infected with hepatitis C (n = 110,484), a cox proportional hazards model was used to determine risk of developing cirrhosis and hepatocellular carcinoma for genotypes 1-4, after adjusting for age, period of service, race, sex, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment. Despite genotype 3 patients being younger, their risk of developing cirrhosis was highest with hazard ratio = 1.30 (1.22, 1.39), compared to genotype 1 (reference, HR 1.0), genotype 2 with HR = 0.68 (0.64, 0.73), and genotype 4 with HR = 0.94 (0.78, 1.14). Likewise, the risk of development of HCC was highest for genotype 3 HCV with HR = 1.80 (1.60, 2.03), compared to a genotype 2 (HR = 0.55; 0.47, 0.63), and genotype 4 (0.99; 0.68, 1.45).
It is speculated that the hepatic steatosis that is a direct result of genotype 3 HCV may contribute to the accelerated progression to cirrhosis and HCC, but this has not been proven and was not evaluated in this Veteran Affairs study.

REFERENCE
1. Kanwal F., Kramer J.R., Ilyas J., et al. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98-105.

If you haven’t started reporting quality data for the Merit-Based Incentive Payment System (MIPS), there’s still time to avoid a 4% cut to your Medicare payments.

Under the Pick Your Pace approach being offered this year, the Centers for Medicare & Medicaid Services allows clinicians to test the system by reporting on one quality measure for one patient through paper-based claims. Be sure to append a Quality Data Code (QDC) to the claim form for care provided up to Dec. 31, 2017, in order to avoid a penalty in payment year 2019.

Consider this measure:

Measure #134: Preventive Care and Screening: Screening for Depression and Follow-Up Plan

This measure aims to capture the percentage of patients aged 12 years and older who have been screened for depression and have a documented follow-up plan of care, if appropriate.

What you need to do: Use an age-appropriate, standardized tool to screen patients for depression during the visit. If they screen positive, develop a follow-up plan during the visit and document it.

Eligible cases include patients who were aged 12 years or older on the date of the encounter and have a patient encounter during the performance period. Applicable codes include (CPT or HCPCS): 90791, 90792, 90832, 90834, 90837, 92625, 96116, 96118, 96150, 96151, 97165, 97166, 97167, 99201, 99202, 99203, 99204, 99205, 99212, 99213, 99214, 99215, G0101, G0402, G0438, G0439, G0444.

To get credit under MIPS, be sure to include a QDC that shows that you successfully performed the measure or had a good reason for not doing so. For instance, G8431 indicates that depression screening was positive and a follow-up plan was documented, while G8510 indicates that the depression screening was negative and a follow-up plan is not required. Use exclusion code G9717 if the patient has an active diagnosis of depression for bipolar disorder.

CMS has a full list measures available for claims-based reporting at qpp.cms.gov. The American Medical Association has also created a step-by-step guide for reporting on one quality measure.

Certain clinicians are exempt from reporting and do not face a penalty under MIPS:

• Those who enrolled in Medicare for the first time during a performance period.
• Those who have Medicare Part B allowed charges of $30,000 or less.
• Those who have 100 or fewer Medicare Part B patients.
• Those who are significantly participating in an Advanced Alternative Payment Model (APM).

If you haven’t started reporting quality data for the Merit-Based Incentive Payment System (MIPS), there’s still time to avoid a 4% cut to your Medicare payments.

Under the Pick Your Pace approach being offered this year, the Centers for Medicare & Medicaid Services allows clinicians to test the system by reporting on one quality measure for one patient through paper-based claims. Be sure to append a Quality Data Code (QDC) to the claim form for care provided up to Dec. 31, 2017, in order to avoid a penalty in payment year 2019.

Consider this measure:

Measure #134: Preventive Care and Screening: Screening for Depression and Follow-Up Plan

This measure aims to capture the percentage of patients aged 12 years and older who have been screened for depression and have a documented follow-up plan of care, if appropriate.

What you need to do: Use an age-appropriate, standardized tool to screen patients for depression during the visit. If they screen positive, develop a follow-up plan during the visit and document it.

Eligible cases include patients who were aged 12 years or older on the date of the encounter and have a patient encounter during the performance period. Applicable codes include (CPT or HCPCS): 90791, 90792, 90832, 90834, 90837, 92625, 96116, 96118, 96150, 96151, 97165, 97166, 97167, 99201, 99202, 99203, 99204, 99205, 99212, 99213, 99214, 99215, G0101, G0402, G0438, G0439, G0444.

To get credit under MIPS, be sure to include a QDC that shows that you successfully performed the measure or had a good reason for not doing so. For instance, G8431 indicates that depression screening was positive and a follow-up plan was documented, while G8510 indicates that the depression screening was negative and a follow-up plan is not required. Use exclusion code G9717 if the patient has an active diagnosis of depression for bipolar disorder.

CMS has a full list measures available for claims-based reporting at qpp.cms.gov. The American Medical Association has also created a step-by-step guide for reporting on one quality measure.

Certain clinicians are exempt from reporting and do not face a penalty under MIPS:

• Those who enrolled in Medicare for the first time during a performance period.
• Those who have Medicare Part B allowed charges of $30,000 or less.
• Those who have 100 or fewer Medicare Part B patients.
• Those who are significantly participating in an Advanced Alternative Payment Model (APM).

If you haven’t started reporting quality data for the Merit-Based Incentive Payment System (MIPS), there’s still time to avoid a 4% cut to your Medicare payments.

Under the Pick Your Pace approach being offered this year, the Centers for Medicare & Medicaid Services allows clinicians to test the system by reporting on one quality measure for one patient through paper-based claims. Be sure to append a Quality Data Code (QDC) to the claim form for care provided up to Dec. 31, 2017, in order to avoid a penalty in payment year 2019.

Consider this measure:

Measure #134: Preventive Care and Screening: Screening for Depression and Follow-Up Plan

This measure aims to capture the percentage of patients aged 12 years and older who have been screened for depression and have a documented follow-up plan of care, if appropriate.

What you need to do: Use an age-appropriate, standardized tool to screen patients for depression during the visit. If they screen positive, develop a follow-up plan during the visit and document it.

Eligible cases include patients who were aged 12 years or older on the date of the encounter and have a patient encounter during the performance period. Applicable codes include (CPT or HCPCS): 90791, 90792, 90832, 90834, 90837, 92625, 96116, 96118, 96150, 96151, 97165, 97166, 97167, 99201, 99202, 99203, 99204, 99205, 99212, 99213, 99214, 99215, G0101, G0402, G0438, G0439, G0444.

To get credit under MIPS, be sure to include a QDC that shows that you successfully performed the measure or had a good reason for not doing so. For instance, G8431 indicates that depression screening was positive and a follow-up plan was documented, while G8510 indicates that the depression screening was negative and a follow-up plan is not required. Use exclusion code G9717 if the patient has an active diagnosis of depression for bipolar disorder.

CMS has a full list measures available for claims-based reporting at qpp.cms.gov. The American Medical Association has also created a step-by-step guide for reporting on one quality measure.

Certain clinicians are exempt from reporting and do not face a penalty under MIPS:

• Those who enrolled in Medicare for the first time during a performance period.
• Those who have Medicare Part B allowed charges of $30,000 or less.
• Those who have 100 or fewer Medicare Part B patients.
• Those who are significantly participating in an Advanced Alternative Payment Model (APM).

Pruritus is a subjective report of itching, which can be caused by dermatologic or systemic conditions. Pruritus accounts for about 5% of all skin adverse drug reactions (ADRs) after administration.¹ Mechanisms by which medication-induced pruritus occurs are still unknown and have been understudied. Treatment modalities also have been understudied; however, the understood method for treatment is cessation of the causative agent.²

Anticoagulants commonly are used in several conditions, including prevention of ischemic cerebrovascular accident (CVA) in patients with atrial fibrillation (AF) as well as for the treatment and prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE).³ Traditionally, warfarin was the gold standard anticoagulant. With the relatively recent approval of several direct oral anticoagulants (DOACs), such as rivaroxaban, apixaban, and dabigatran, the landscape of anticoagulation is changing. One benefit of using DOACs as opposed to warfarin is that they often require less frequent laboratory monitoring. However, rare ADRs not detected during clinical trials have appeared following drug approval.⁴

In a VA anticoagulation clinic that managed more than 60 patients taking DOACs, the authors identified 2 cases of pruritus, possibly associated with DOAC agents. These 2 cases point to a higher incidence rate than the rate reported in the rivaroxaban package insert (2%).⁵ Of note, pruritus is not mentioned in the apixaban package insert.⁶

Patient 1 Case Presentation

Patient 1 was a 69-year-old male with AF who was switched to rivaroxaban after 5 years of warfarin therapy. Past medical history included iron deficiency anemia, hypertension, type 2 diabetes mellitus, systolic heart failure, hyperlipidemia, hepatic steatosis, benign prostatic hyperplasia, and gastroesophageal reflux disease. The patient reported “itching all over” soon after initiation of rivaroxaban and that the itching was intolerable and always began 90 to 120 minutes after each dose of rivaroxaban with no associated rash.

After about 6 months of treatment with rivaroxaban, the patient was switched to apixaban; however, the pruritus persisted even after the switch. The onset of itching had similar timing with regard to the apixaban doses. When apixaban was initiated, the patient also was started on amiodarone and tamsulosin. A full pharmacotherapy review of the patient’s medication list for the incidence of pruritus was conducted. Regarding amiodarone and tamsulosin, incidence of pruritus was < 1%.^7,8 Neither agent had yet been started during the rivaroxaban therapy; therefore, it was unlikely that either of these 2 medications were the causative agent of the pruritic ADR.

In response to the itching, the patient was given diphenhydramine 25 mg twice daily, taken with each dose of apixaban. Shortly thereafter, the patient reported that diphenhydramine lessened the severity of the pruritus. He was switched to loratadine 10 mg twice daily with each dose of apixaban, to avoid drowsiness as well as the increased anticholinergic ADRs of first-generation antihistamines. The patient reported that the itching was tolerable.

Patient 2 Case Presentation

Patient 2 was a 63-year-old male with AF and hypertension who was initially started on rivaroxaban and reported pruritus after about 1 month. Despite the uncomfortable itch, the patient elected to continue therapy and began diphenhydramine 25 mg daily with each dose of rivaroxaban. Diphenhydramine seemed to improve the pruritus but did not completely alleviate it. While on rivaroxaban, the patient experienced an acute drop in hemoglobin; however, no source of bleeding was found. Although the pruritus was largely resolved, he was switched to apixaban due to its favorable bleeding profile.⁹ The patient continued to have pruritus on apixaban; however, he reported that pruritus was less severe than it had been while taking rivaroxaban. The patient restarted on diphenhydramine twice daily with each dose of apixaban and reported cessation of pruritus.

Discussion

After observing both cases in relation to the timing between the administration of a DOAC and onset of pruritus, it seemed likely that the causative agent could be the DOAC. A Naranjo Nomogram was used to determine the likeliness of each drug to be the causative agent of the ADR.¹⁰ This nomogram is scaled from a low score of -4 to a high score of 13. Patients 1 and 2 had a score of 4, which is reflective of a possible ADR (score 1-4). Using the nomogram as well as the subjective information provided by the patients, it is reasonable to conclude that the pruritus was possibly associated with the use of the DOACs. Nonadherence to anticoagulants may lead to potentially fatal adverse outcomes, such as stroke. Medication-associated pruritus could lead to medication nonadherence if left unaddressed. It is notable that prescribing an antihistamine that is taken at the time of the anticoagulant dose allowed these patients with possible DOAC-associated pruritus to continue therapy with the selected anticoagulant. Further research on this topic is needed.

Pruritus is a subjective report of itching, which can be caused by dermatologic or systemic conditions. Pruritus accounts for about 5% of all skin adverse drug reactions (ADRs) after administration.¹ Mechanisms by which medication-induced pruritus occurs are still unknown and have been understudied. Treatment modalities also have been understudied; however, the understood method for treatment is cessation of the causative agent.²

Anticoagulants commonly are used in several conditions, including prevention of ischemic cerebrovascular accident (CVA) in patients with atrial fibrillation (AF) as well as for the treatment and prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE).³ Traditionally, warfarin was the gold standard anticoagulant. With the relatively recent approval of several direct oral anticoagulants (DOACs), such as rivaroxaban, apixaban, and dabigatran, the landscape of anticoagulation is changing. One benefit of using DOACs as opposed to warfarin is that they often require less frequent laboratory monitoring. However, rare ADRs not detected during clinical trials have appeared following drug approval.⁴

In a VA anticoagulation clinic that managed more than 60 patients taking DOACs, the authors identified 2 cases of pruritus, possibly associated with DOAC agents. These 2 cases point to a higher incidence rate than the rate reported in the rivaroxaban package insert (2%).⁵ Of note, pruritus is not mentioned in the apixaban package insert.⁶

Patient 1 Case Presentation

Patient 1 was a 69-year-old male with AF who was switched to rivaroxaban after 5 years of warfarin therapy. Past medical history included iron deficiency anemia, hypertension, type 2 diabetes mellitus, systolic heart failure, hyperlipidemia, hepatic steatosis, benign prostatic hyperplasia, and gastroesophageal reflux disease. The patient reported “itching all over” soon after initiation of rivaroxaban and that the itching was intolerable and always began 90 to 120 minutes after each dose of rivaroxaban with no associated rash.

After about 6 months of treatment with rivaroxaban, the patient was switched to apixaban; however, the pruritus persisted even after the switch. The onset of itching had similar timing with regard to the apixaban doses. When apixaban was initiated, the patient also was started on amiodarone and tamsulosin. A full pharmacotherapy review of the patient’s medication list for the incidence of pruritus was conducted. Regarding amiodarone and tamsulosin, incidence of pruritus was < 1%.^7,8 Neither agent had yet been started during the rivaroxaban therapy; therefore, it was unlikely that either of these 2 medications were the causative agent of the pruritic ADR.

In response to the itching, the patient was given diphenhydramine 25 mg twice daily, taken with each dose of apixaban. Shortly thereafter, the patient reported that diphenhydramine lessened the severity of the pruritus. He was switched to loratadine 10 mg twice daily with each dose of apixaban, to avoid drowsiness as well as the increased anticholinergic ADRs of first-generation antihistamines. The patient reported that the itching was tolerable.

Patient 2 Case Presentation

Patient 2 was a 63-year-old male with AF and hypertension who was initially started on rivaroxaban and reported pruritus after about 1 month. Despite the uncomfortable itch, the patient elected to continue therapy and began diphenhydramine 25 mg daily with each dose of rivaroxaban. Diphenhydramine seemed to improve the pruritus but did not completely alleviate it. While on rivaroxaban, the patient experienced an acute drop in hemoglobin; however, no source of bleeding was found. Although the pruritus was largely resolved, he was switched to apixaban due to its favorable bleeding profile.⁹ The patient continued to have pruritus on apixaban; however, he reported that pruritus was less severe than it had been while taking rivaroxaban. The patient restarted on diphenhydramine twice daily with each dose of apixaban and reported cessation of pruritus.

Discussion

After observing both cases in relation to the timing between the administration of a DOAC and onset of pruritus, it seemed likely that the causative agent could be the DOAC. A Naranjo Nomogram was used to determine the likeliness of each drug to be the causative agent of the ADR.¹⁰ This nomogram is scaled from a low score of -4 to a high score of 13. Patients 1 and 2 had a score of 4, which is reflective of a possible ADR (score 1-4). Using the nomogram as well as the subjective information provided by the patients, it is reasonable to conclude that the pruritus was possibly associated with the use of the DOACs. Nonadherence to anticoagulants may lead to potentially fatal adverse outcomes, such as stroke. Medication-associated pruritus could lead to medication nonadherence if left unaddressed. It is notable that prescribing an antihistamine that is taken at the time of the anticoagulant dose allowed these patients with possible DOAC-associated pruritus to continue therapy with the selected anticoagulant. Further research on this topic is needed.

Pruritus is a subjective report of itching, which can be caused by dermatologic or systemic conditions. Pruritus accounts for about 5% of all skin adverse drug reactions (ADRs) after administration.¹ Mechanisms by which medication-induced pruritus occurs are still unknown and have been understudied. Treatment modalities also have been understudied; however, the understood method for treatment is cessation of the causative agent.²

Anticoagulants commonly are used in several conditions, including prevention of ischemic cerebrovascular accident (CVA) in patients with atrial fibrillation (AF) as well as for the treatment and prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE).³ Traditionally, warfarin was the gold standard anticoagulant. With the relatively recent approval of several direct oral anticoagulants (DOACs), such as rivaroxaban, apixaban, and dabigatran, the landscape of anticoagulation is changing. One benefit of using DOACs as opposed to warfarin is that they often require less frequent laboratory monitoring. However, rare ADRs not detected during clinical trials have appeared following drug approval.⁴

In a VA anticoagulation clinic that managed more than 60 patients taking DOACs, the authors identified 2 cases of pruritus, possibly associated with DOAC agents. These 2 cases point to a higher incidence rate than the rate reported in the rivaroxaban package insert (2%).⁵ Of note, pruritus is not mentioned in the apixaban package insert.⁶

Patient 1 Case Presentation

Patient 1 was a 69-year-old male with AF who was switched to rivaroxaban after 5 years of warfarin therapy. Past medical history included iron deficiency anemia, hypertension, type 2 diabetes mellitus, systolic heart failure, hyperlipidemia, hepatic steatosis, benign prostatic hyperplasia, and gastroesophageal reflux disease. The patient reported “itching all over” soon after initiation of rivaroxaban and that the itching was intolerable and always began 90 to 120 minutes after each dose of rivaroxaban with no associated rash.

After about 6 months of treatment with rivaroxaban, the patient was switched to apixaban; however, the pruritus persisted even after the switch. The onset of itching had similar timing with regard to the apixaban doses. When apixaban was initiated, the patient also was started on amiodarone and tamsulosin. A full pharmacotherapy review of the patient’s medication list for the incidence of pruritus was conducted. Regarding amiodarone and tamsulosin, incidence of pruritus was < 1%.^7,8 Neither agent had yet been started during the rivaroxaban therapy; therefore, it was unlikely that either of these 2 medications were the causative agent of the pruritic ADR.

In response to the itching, the patient was given diphenhydramine 25 mg twice daily, taken with each dose of apixaban. Shortly thereafter, the patient reported that diphenhydramine lessened the severity of the pruritus. He was switched to loratadine 10 mg twice daily with each dose of apixaban, to avoid drowsiness as well as the increased anticholinergic ADRs of first-generation antihistamines. The patient reported that the itching was tolerable.

Patient 2 Case Presentation

Patient 2 was a 63-year-old male with AF and hypertension who was initially started on rivaroxaban and reported pruritus after about 1 month. Despite the uncomfortable itch, the patient elected to continue therapy and began diphenhydramine 25 mg daily with each dose of rivaroxaban. Diphenhydramine seemed to improve the pruritus but did not completely alleviate it. While on rivaroxaban, the patient experienced an acute drop in hemoglobin; however, no source of bleeding was found. Although the pruritus was largely resolved, he was switched to apixaban due to its favorable bleeding profile.⁹ The patient continued to have pruritus on apixaban; however, he reported that pruritus was less severe than it had been while taking rivaroxaban. The patient restarted on diphenhydramine twice daily with each dose of apixaban and reported cessation of pruritus.

Discussion

After observing both cases in relation to the timing between the administration of a DOAC and onset of pruritus, it seemed likely that the causative agent could be the DOAC. A Naranjo Nomogram was used to determine the likeliness of each drug to be the causative agent of the ADR.¹⁰ This nomogram is scaled from a low score of -4 to a high score of 13. Patients 1 and 2 had a score of 4, which is reflective of a possible ADR (score 1-4). Using the nomogram as well as the subjective information provided by the patients, it is reasonable to conclude that the pruritus was possibly associated with the use of the DOACs. Nonadherence to anticoagulants may lead to potentially fatal adverse outcomes, such as stroke. Medication-associated pruritus could lead to medication nonadherence if left unaddressed. It is notable that prescribing an antihistamine that is taken at the time of the anticoagulant dose allowed these patients with possible DOAC-associated pruritus to continue therapy with the selected anticoagulant. Further research on this topic is needed.

Annual Meeting

ATLANTA—A new study suggests the JAK2 inhibitor ruxolitinib has the potential to significantly improve survival in patients who have chronic phase (CP) myelofibrosis (MF), with or without elevated blasts.

In this retrospective study, researchers found evidence to suggest that MF patients in CP with elevated blasts (CP-e) should be considered a high-risk group.

However, ruxolitinib significantly improved overall survival (OS) in CP-e patients—who had 5% to 9% blasts in the bone marrow or peripheral blood—and in patients with CP and less than 5% blasts.

On the other hand, ruxolitinib had no impact on the rate of progression to acute myeloid leukemia (AML) in CP or CP-e patients.

Lucia Masarova, MD, of The University of Texas MD Anderson Cancer Center in Houston, presented these findings at the 2017 ASH Annual Meeting (abstract 201).

Clinical characteristics of MF CP-e patients are not well described, and the outcome of available therapy in this population is largely unknown. Therefore, Dr Masarova and her colleagues set out to evaluate the effects of ruxolitinib on CP-e patients.

The team conducted a retrospective chart review of 1199 MF patients, 832 with primary MF, 169 with post-essential thrombocythemia MF, and 198 with post-polycythemia vera MF. About two-thirds of the patients were newly diagnosed.

The majority of patients (85%, n=1020) were in CP with less than 5% blasts, 10% (n=123) were in CP-e, and 5% (n=56) were in accelerated phase (AP, 10% to 19% blasts).

CP-e patients had similar clinical characteristics as patients in AP. Both groups had higher white blood cell counts; lower hemoglobin and platelets; and more frequent splenomegaly, systemic symptoms, and presence of abnormal and unfavorable karyotype than CP patients.

Among the 1030 treated patients, ruxolitinib was used in 30% (n=328), including 28% of CP patients (n=289), 27% of CP-e patients (n=33), and 11% of AP patients (n=6). The median treatment duration was about 22 months in the CP and CP-e groups.

After a median follow-up of 27 months, half the patients studied had died.

“Patients in the [CP-e] group had similar OS as those in AP, which was inferior to patients in CP,” Dr Masarova said.

The median OS was 48 months for the entire cohort, 56 months in the CP group, 34 months in the CP-e group, and 23 months in the AP group.

One-year OS rates were 86% for the CP group, 73% for the CP-e group, and 65% for the AP group. Five-year OS rates were 46%, 24%, and 21%, respectively.

CP and CP-e patients had superior OS if they had received ruxolitinib.

Among CP patients, the median OS was 61 months in those who received ruxolitinib and 54 months in those who did not (hazard ratio=0.85, P=0.002).

Among CP-e patients, the median OS was 54 months in those who received ruxolitinib and 27 months in those who did not (hazard ratio=0.50, P=0.001).

Ruxolitinib had no impact on OS in AP patients, which was 23 months with or without the drug. However, Dr Masarova noted that the AP patient numbers were small.

Progression to AML occurred in 9% of patients overall (n=139), 9% in the CP group, 20% in the CP-e group, and 39% in the AP group.

Ruxolitinib had no impact on the rate of AML progression, which was 9% in CP patients, with and without the drug.

In CP-e patients, AML progression occurred in 22% of those who received ruxolitinib and 18% of those who did not.

“The [CP-e] patients are similar to AP patients, with adverse clinical characteristics, inferior OS, and a 20% to 40% AML rate,” Dr Masarova said. “Ruxolitinib improves survival of [CP-e] patients, which is similar to CP patients on the drug.”

CP-e patients should be considered a high-risk population, she said, adding “we need to find new, better treatments for these patients.”

Dr Masarova had no disclosures.

Annual Meeting

ATLANTA—A new study suggests the JAK2 inhibitor ruxolitinib has the potential to significantly improve survival in patients who have chronic phase (CP) myelofibrosis (MF), with or without elevated blasts.

In this retrospective study, researchers found evidence to suggest that MF patients in CP with elevated blasts (CP-e) should be considered a high-risk group.

However, ruxolitinib significantly improved overall survival (OS) in CP-e patients—who had 5% to 9% blasts in the bone marrow or peripheral blood—and in patients with CP and less than 5% blasts.

On the other hand, ruxolitinib had no impact on the rate of progression to acute myeloid leukemia (AML) in CP or CP-e patients.

Lucia Masarova, MD, of The University of Texas MD Anderson Cancer Center in Houston, presented these findings at the 2017 ASH Annual Meeting (abstract 201).

Clinical characteristics of MF CP-e patients are not well described, and the outcome of available therapy in this population is largely unknown. Therefore, Dr Masarova and her colleagues set out to evaluate the effects of ruxolitinib on CP-e patients.

The team conducted a retrospective chart review of 1199 MF patients, 832 with primary MF, 169 with post-essential thrombocythemia MF, and 198 with post-polycythemia vera MF. About two-thirds of the patients were newly diagnosed.

The majority of patients (85%, n=1020) were in CP with less than 5% blasts, 10% (n=123) were in CP-e, and 5% (n=56) were in accelerated phase (AP, 10% to 19% blasts).

CP-e patients had similar clinical characteristics as patients in AP. Both groups had higher white blood cell counts; lower hemoglobin and platelets; and more frequent splenomegaly, systemic symptoms, and presence of abnormal and unfavorable karyotype than CP patients.

Among the 1030 treated patients, ruxolitinib was used in 30% (n=328), including 28% of CP patients (n=289), 27% of CP-e patients (n=33), and 11% of AP patients (n=6). The median treatment duration was about 22 months in the CP and CP-e groups.

After a median follow-up of 27 months, half the patients studied had died.

“Patients in the [CP-e] group had similar OS as those in AP, which was inferior to patients in CP,” Dr Masarova said.

The median OS was 48 months for the entire cohort, 56 months in the CP group, 34 months in the CP-e group, and 23 months in the AP group.

One-year OS rates were 86% for the CP group, 73% for the CP-e group, and 65% for the AP group. Five-year OS rates were 46%, 24%, and 21%, respectively.

CP and CP-e patients had superior OS if they had received ruxolitinib.

Among CP patients, the median OS was 61 months in those who received ruxolitinib and 54 months in those who did not (hazard ratio=0.85, P=0.002).

Among CP-e patients, the median OS was 54 months in those who received ruxolitinib and 27 months in those who did not (hazard ratio=0.50, P=0.001).

Ruxolitinib had no impact on OS in AP patients, which was 23 months with or without the drug. However, Dr Masarova noted that the AP patient numbers were small.

Progression to AML occurred in 9% of patients overall (n=139), 9% in the CP group, 20% in the CP-e group, and 39% in the AP group.

Ruxolitinib had no impact on the rate of AML progression, which was 9% in CP patients, with and without the drug.

In CP-e patients, AML progression occurred in 22% of those who received ruxolitinib and 18% of those who did not.

“The [CP-e] patients are similar to AP patients, with adverse clinical characteristics, inferior OS, and a 20% to 40% AML rate,” Dr Masarova said. “Ruxolitinib improves survival of [CP-e] patients, which is similar to CP patients on the drug.”

CP-e patients should be considered a high-risk population, she said, adding “we need to find new, better treatments for these patients.”

Dr Masarova had no disclosures.

Annual Meeting

ATLANTA—A new study suggests the JAK2 inhibitor ruxolitinib has the potential to significantly improve survival in patients who have chronic phase (CP) myelofibrosis (MF), with or without elevated blasts.

In this retrospective study, researchers found evidence to suggest that MF patients in CP with elevated blasts (CP-e) should be considered a high-risk group.

However, ruxolitinib significantly improved overall survival (OS) in CP-e patients—who had 5% to 9% blasts in the bone marrow or peripheral blood—and in patients with CP and less than 5% blasts.

On the other hand, ruxolitinib had no impact on the rate of progression to acute myeloid leukemia (AML) in CP or CP-e patients.

Lucia Masarova, MD, of The University of Texas MD Anderson Cancer Center in Houston, presented these findings at the 2017 ASH Annual Meeting (abstract 201).

Clinical characteristics of MF CP-e patients are not well described, and the outcome of available therapy in this population is largely unknown. Therefore, Dr Masarova and her colleagues set out to evaluate the effects of ruxolitinib on CP-e patients.

The team conducted a retrospective chart review of 1199 MF patients, 832 with primary MF, 169 with post-essential thrombocythemia MF, and 198 with post-polycythemia vera MF. About two-thirds of the patients were newly diagnosed.

The majority of patients (85%, n=1020) were in CP with less than 5% blasts, 10% (n=123) were in CP-e, and 5% (n=56) were in accelerated phase (AP, 10% to 19% blasts).

CP-e patients had similar clinical characteristics as patients in AP. Both groups had higher white blood cell counts; lower hemoglobin and platelets; and more frequent splenomegaly, systemic symptoms, and presence of abnormal and unfavorable karyotype than CP patients.

Among the 1030 treated patients, ruxolitinib was used in 30% (n=328), including 28% of CP patients (n=289), 27% of CP-e patients (n=33), and 11% of AP patients (n=6). The median treatment duration was about 22 months in the CP and CP-e groups.

After a median follow-up of 27 months, half the patients studied had died.

“Patients in the [CP-e] group had similar OS as those in AP, which was inferior to patients in CP,” Dr Masarova said.

The median OS was 48 months for the entire cohort, 56 months in the CP group, 34 months in the CP-e group, and 23 months in the AP group.

One-year OS rates were 86% for the CP group, 73% for the CP-e group, and 65% for the AP group. Five-year OS rates were 46%, 24%, and 21%, respectively.

CP and CP-e patients had superior OS if they had received ruxolitinib.

Among CP patients, the median OS was 61 months in those who received ruxolitinib and 54 months in those who did not (hazard ratio=0.85, P=0.002).

Among CP-e patients, the median OS was 54 months in those who received ruxolitinib and 27 months in those who did not (hazard ratio=0.50, P=0.001).

Ruxolitinib had no impact on OS in AP patients, which was 23 months with or without the drug. However, Dr Masarova noted that the AP patient numbers were small.

Progression to AML occurred in 9% of patients overall (n=139), 9% in the CP group, 20% in the CP-e group, and 39% in the AP group.

Ruxolitinib had no impact on the rate of AML progression, which was 9% in CP patients, with and without the drug.

In CP-e patients, AML progression occurred in 22% of those who received ruxolitinib and 18% of those who did not.

“The [CP-e] patients are similar to AP patients, with adverse clinical characteristics, inferior OS, and a 20% to 40% AML rate,” Dr Masarova said. “Ruxolitinib improves survival of [CP-e] patients, which is similar to CP patients on the drug.”

CP-e patients should be considered a high-risk population, she said, adding “we need to find new, better treatments for these patients.”

Dr Masarova had no disclosures.

Nonmedical vaccine exemptions for children in Washington State decreased by 40% after the implementation of a law requiring parent counseling and a signed form from a medical provider, based on data from a regression analysis of kindergarten students during time periods before and after the law took effect.

gpointstudio/Thinkstock

SOURCE: Omer, SB et al. Pediatrics. 2018;141(1):e20172364.

Nonmedical vaccine exemptions for children in Washington State decreased by 40% after the implementation of a law requiring parent counseling and a signed form from a medical provider, based on data from a regression analysis of kindergarten students during time periods before and after the law took effect.

gpointstudio/Thinkstock

SOURCE: Omer, SB et al. Pediatrics. 2018;141(1):e20172364.

Nonmedical vaccine exemptions for children in Washington State decreased by 40% after the implementation of a law requiring parent counseling and a signed form from a medical provider, based on data from a regression analysis of kindergarten students during time periods before and after the law took effect.

gpointstudio/Thinkstock

SOURCE: Omer, SB et al. Pediatrics. 2018;141(1):e20172364.

Q) How do you know if a neurologic symptom is due to a relapse of neuromyelitis optica spectrum disorder? And how should a confirmed relapse be treated?

Neuromyelitis optica spectrum disorder (NMOSD) is a severe, relapsing autoimmune disease of the central nervous system (CNS) that targets the optic nerves and spinal cord, leading to blindness and paralysis.^1,2 Whereas multiple sclerosis (MS) is characterized by demyelination, NMOSD is associated with astrocytic damage and tissue necrosis.³ Because longitudinally extensive inflammatory lesions are typical with NMOSD, permanent CNS damage is common with each relapse.⁴

Health care providers first need to determine whether a patient with NMOSD who presents with new or worsening symptoms is having a relapse. A relapse is caused by a breach of the blood-brain barrier by the peripheral immune system, which leads to inflammation and damage to the CNS.⁵ This causes neurologic symptoms that depend on the anatomic location. Once damage has occurred, symptoms may result either from a new relapse in the same location as a previous inflammatory event or from a pseudorelapse.⁶

Pseudorelapses are triggered by a systemic metabolic imbalance; they exacerbate symptoms from previous CNS damage. Differentiating between a true relapse and a pseudorelapse can be a diagnostic challenge for even the most seasoned of health care providers. Kessler et al retrospectively examined which clinical factors can distinguish relapses from pseudorelapses.⁶ Their findings suggest that while clinical examination alone may be effective in events involving vision loss, MRI may be necessary when signs and symptoms are attributable to a spinal cord lesion.

In fact, they found that the degree of clinical worsening in patients with spinal cord symptoms caused by a pseudorelapse was similar to that of a true relapse. The most common causes of pseudorelapse included infection, dysautonomia, metabolic abnormalities, and changes to medication regimens. Interestingly, the presence of infection did not rule out a relapse, as patients experiencing relapses were equally likely as those with pseudorelapse to have a urinary tract infection. The authors concluded, based on their data, that an MRI is warranted to verify a relapse in patients who experience worsening of symptoms localized to the spinal cord but is not necessary to rule out a pseudorelapse of optic neuritis if visual acuity is reduced compared to baseline.⁶

In contrast to MS, a progressive phase is not believed to be associated with NMOSD.⁷ Instead, accrual of disability occurs with each relapse. The majority of patients with NMOSD do not return to baseline following an untreated relapse, making it especially important that patients receive adequate acute treatment to mitigate the damage.⁸

Currently, there are no medications approved by the FDA for the acute or preventive treatment of NMOSD. However, off-label use of immunotherapies, including rituximab, mycophenolate mofetil, azathioprine, prednisone, methotrexate, tocilizumab, and mitoxantrone, have been studied for relapse prevention.² In addition, there are three ongoing phase III trials investigating eculizumab (C5 complement inhibitor), inebilizumab (CD19 monoclonal antibody), and SA237 (IL6R blocker); results from these studies could potentially widen the landscape of immunotherapy use in NMOSD.²

Less investigation into appropriate acute treatment of new relapses has been conducted, however, leaving clinicians and patients uncertain about how to manage a new inflammatory event. Traditionally, firstline treatment for acute NMOSD relapses has been the same as for MS relapses—high-dose methylprednisolone. However, due to the severity of NMOSD relapses and the relative lack of response to steroids alone, methylprednisolone is commonly followed by plasma exchange (PLEX).²

Most data to guide clinical decision-making suggest that patients with NMOSD relapses recover better when PLEX is added to steroid treatment. Abboud et al found that 65% of patients who received both PLEX and methylprednisolone recovered to their prerelapse baseline, compared to 35% of those who received methylprednisolone alone.⁹ These findings were supported by a larger retrospective investigation by Kleiter et al, which found improved recovery with treatment escalation in their cohort.⁸ These data support the recommendation to use PLEX as an adjunct therapy in acute relapses—particularly in relapses with severe presentations.

Because diagnosis and treatment of relapses involve many factors, ranging from accrual of disability, long-term immunotherapy decisions, and medical costs, diligence in provider decision-making is essential when caring for patients with NMOSD. -MAM

Maureen A. Mealy, BSN, MSCN
Neuromyelitis Optica Research Program Manager, Senior Research Nurse of the Transverse Myelitis & Multiple Sclerosis Centers, PhD candidate at Johns Hopkins School of Nursing in Baltimore

Q) How do you know if a neurologic symptom is due to a relapse of neuromyelitis optica spectrum disorder? And how should a confirmed relapse be treated?

Neuromyelitis optica spectrum disorder (NMOSD) is a severe, relapsing autoimmune disease of the central nervous system (CNS) that targets the optic nerves and spinal cord, leading to blindness and paralysis.^1,2 Whereas multiple sclerosis (MS) is characterized by demyelination, NMOSD is associated with astrocytic damage and tissue necrosis.³ Because longitudinally extensive inflammatory lesions are typical with NMOSD, permanent CNS damage is common with each relapse.⁴

Health care providers first need to determine whether a patient with NMOSD who presents with new or worsening symptoms is having a relapse. A relapse is caused by a breach of the blood-brain barrier by the peripheral immune system, which leads to inflammation and damage to the CNS.⁵ This causes neurologic symptoms that depend on the anatomic location. Once damage has occurred, symptoms may result either from a new relapse in the same location as a previous inflammatory event or from a pseudorelapse.⁶

Pseudorelapses are triggered by a systemic metabolic imbalance; they exacerbate symptoms from previous CNS damage. Differentiating between a true relapse and a pseudorelapse can be a diagnostic challenge for even the most seasoned of health care providers. Kessler et al retrospectively examined which clinical factors can distinguish relapses from pseudorelapses.⁶ Their findings suggest that while clinical examination alone may be effective in events involving vision loss, MRI may be necessary when signs and symptoms are attributable to a spinal cord lesion.

In fact, they found that the degree of clinical worsening in patients with spinal cord symptoms caused by a pseudorelapse was similar to that of a true relapse. The most common causes of pseudorelapse included infection, dysautonomia, metabolic abnormalities, and changes to medication regimens. Interestingly, the presence of infection did not rule out a relapse, as patients experiencing relapses were equally likely as those with pseudorelapse to have a urinary tract infection. The authors concluded, based on their data, that an MRI is warranted to verify a relapse in patients who experience worsening of symptoms localized to the spinal cord but is not necessary to rule out a pseudorelapse of optic neuritis if visual acuity is reduced compared to baseline.⁶

In contrast to MS, a progressive phase is not believed to be associated with NMOSD.⁷ Instead, accrual of disability occurs with each relapse. The majority of patients with NMOSD do not return to baseline following an untreated relapse, making it especially important that patients receive adequate acute treatment to mitigate the damage.⁸

Currently, there are no medications approved by the FDA for the acute or preventive treatment of NMOSD. However, off-label use of immunotherapies, including rituximab, mycophenolate mofetil, azathioprine, prednisone, methotrexate, tocilizumab, and mitoxantrone, have been studied for relapse prevention.² In addition, there are three ongoing phase III trials investigating eculizumab (C5 complement inhibitor), inebilizumab (CD19 monoclonal antibody), and SA237 (IL6R blocker); results from these studies could potentially widen the landscape of immunotherapy use in NMOSD.²

Less investigation into appropriate acute treatment of new relapses has been conducted, however, leaving clinicians and patients uncertain about how to manage a new inflammatory event. Traditionally, firstline treatment for acute NMOSD relapses has been the same as for MS relapses—high-dose methylprednisolone. However, due to the severity of NMOSD relapses and the relative lack of response to steroids alone, methylprednisolone is commonly followed by plasma exchange (PLEX).²

Most data to guide clinical decision-making suggest that patients with NMOSD relapses recover better when PLEX is added to steroid treatment. Abboud et al found that 65% of patients who received both PLEX and methylprednisolone recovered to their prerelapse baseline, compared to 35% of those who received methylprednisolone alone.⁹ These findings were supported by a larger retrospective investigation by Kleiter et al, which found improved recovery with treatment escalation in their cohort.⁸ These data support the recommendation to use PLEX as an adjunct therapy in acute relapses—particularly in relapses with severe presentations.

Because diagnosis and treatment of relapses involve many factors, ranging from accrual of disability, long-term immunotherapy decisions, and medical costs, diligence in provider decision-making is essential when caring for patients with NMOSD. -MAM

Maureen A. Mealy, BSN, MSCN
Neuromyelitis Optica Research Program Manager, Senior Research Nurse of the Transverse Myelitis & Multiple Sclerosis Centers, PhD candidate at Johns Hopkins School of Nursing in Baltimore

Q) How do you know if a neurologic symptom is due to a relapse of neuromyelitis optica spectrum disorder? And how should a confirmed relapse be treated?

Neuromyelitis optica spectrum disorder (NMOSD) is a severe, relapsing autoimmune disease of the central nervous system (CNS) that targets the optic nerves and spinal cord, leading to blindness and paralysis.^1,2 Whereas multiple sclerosis (MS) is characterized by demyelination, NMOSD is associated with astrocytic damage and tissue necrosis.³ Because longitudinally extensive inflammatory lesions are typical with NMOSD, permanent CNS damage is common with each relapse.⁴

Health care providers first need to determine whether a patient with NMOSD who presents with new or worsening symptoms is having a relapse. A relapse is caused by a breach of the blood-brain barrier by the peripheral immune system, which leads to inflammation and damage to the CNS.⁵ This causes neurologic symptoms that depend on the anatomic location. Once damage has occurred, symptoms may result either from a new relapse in the same location as a previous inflammatory event or from a pseudorelapse.⁶

Pseudorelapses are triggered by a systemic metabolic imbalance; they exacerbate symptoms from previous CNS damage. Differentiating between a true relapse and a pseudorelapse can be a diagnostic challenge for even the most seasoned of health care providers. Kessler et al retrospectively examined which clinical factors can distinguish relapses from pseudorelapses.⁶ Their findings suggest that while clinical examination alone may be effective in events involving vision loss, MRI may be necessary when signs and symptoms are attributable to a spinal cord lesion.

In fact, they found that the degree of clinical worsening in patients with spinal cord symptoms caused by a pseudorelapse was similar to that of a true relapse. The most common causes of pseudorelapse included infection, dysautonomia, metabolic abnormalities, and changes to medication regimens. Interestingly, the presence of infection did not rule out a relapse, as patients experiencing relapses were equally likely as those with pseudorelapse to have a urinary tract infection. The authors concluded, based on their data, that an MRI is warranted to verify a relapse in patients who experience worsening of symptoms localized to the spinal cord but is not necessary to rule out a pseudorelapse of optic neuritis if visual acuity is reduced compared to baseline.⁶

In contrast to MS, a progressive phase is not believed to be associated with NMOSD.⁷ Instead, accrual of disability occurs with each relapse. The majority of patients with NMOSD do not return to baseline following an untreated relapse, making it especially important that patients receive adequate acute treatment to mitigate the damage.⁸

Currently, there are no medications approved by the FDA for the acute or preventive treatment of NMOSD. However, off-label use of immunotherapies, including rituximab, mycophenolate mofetil, azathioprine, prednisone, methotrexate, tocilizumab, and mitoxantrone, have been studied for relapse prevention.² In addition, there are three ongoing phase III trials investigating eculizumab (C5 complement inhibitor), inebilizumab (CD19 monoclonal antibody), and SA237 (IL6R blocker); results from these studies could potentially widen the landscape of immunotherapy use in NMOSD.²

Less investigation into appropriate acute treatment of new relapses has been conducted, however, leaving clinicians and patients uncertain about how to manage a new inflammatory event. Traditionally, firstline treatment for acute NMOSD relapses has been the same as for MS relapses—high-dose methylprednisolone. However, due to the severity of NMOSD relapses and the relative lack of response to steroids alone, methylprednisolone is commonly followed by plasma exchange (PLEX).²

Most data to guide clinical decision-making suggest that patients with NMOSD relapses recover better when PLEX is added to steroid treatment. Abboud et al found that 65% of patients who received both PLEX and methylprednisolone recovered to their prerelapse baseline, compared to 35% of those who received methylprednisolone alone.⁹ These findings were supported by a larger retrospective investigation by Kleiter et al, which found improved recovery with treatment escalation in their cohort.⁸ These data support the recommendation to use PLEX as an adjunct therapy in acute relapses—particularly in relapses with severe presentations.

Because diagnosis and treatment of relapses involve many factors, ranging from accrual of disability, long-term immunotherapy decisions, and medical costs, diligence in provider decision-making is essential when caring for patients with NMOSD. -MAM

Maureen A. Mealy, BSN, MSCN
Neuromyelitis Optica Research Program Manager, Senior Research Nurse of the Transverse Myelitis & Multiple Sclerosis Centers, PhD candidate at Johns Hopkins School of Nursing in Baltimore

Clinical question: In patients with sleep apnea, does using positive airway pressure (PAP) treatment prevent adverse cardiovascular events and death?

Background: Previous observational studies have suggested that untreated sleep apnea is a factor in cardiopulmonary morbidity as well as cerebrovascular events. Guidelines advise its use for prevention of cerebrovascular events. However, not enough is known from trials about its impact on prevention of cardiovascular events.

Dr. Sata is a medical instructor, Duke University Hospital.

Clinical question: In patients with sleep apnea, does using positive airway pressure (PAP) treatment prevent adverse cardiovascular events and death?

Background: Previous observational studies have suggested that untreated sleep apnea is a factor in cardiopulmonary morbidity as well as cerebrovascular events. Guidelines advise its use for prevention of cerebrovascular events. However, not enough is known from trials about its impact on prevention of cardiovascular events.

Dr. Sata is a medical instructor, Duke University Hospital.

Clinical question: In patients with sleep apnea, does using positive airway pressure (PAP) treatment prevent adverse cardiovascular events and death?

Background: Previous observational studies have suggested that untreated sleep apnea is a factor in cardiopulmonary morbidity as well as cerebrovascular events. Guidelines advise its use for prevention of cerebrovascular events. However, not enough is known from trials about its impact on prevention of cardiovascular events.

Dr. Sata is a medical instructor, Duke University Hospital.

Frontline Medical Communications today announced that its journal, Clinician Reviews (CR), dedicated to nurse practitioners and physician assistants, has been named recipient of the 2018 Nostradamus Award.

Annually, National Kidney Foundation’s Council of Advanced Practitioners (CAP) presents this award to an individual, group, or organization that, through forethought and vision, recognizes, supports, and promotes the contributions of Advance Practitioners in nephrology. Clinician Reviews is being recognized for its Q&A feature Renal Consult, which provides expert advice to help clinicians address the complexities of renal diseases.

“Clinician Reviews joins a list of outstanding winners, including nephrologists, a United States senator, and others who have recognized CAP’s worth and supported its advancement,” said Karen Clemments, Editorial Director of clinical publications and Editor of Clinician Reviews. She continued, “We are excited to be among an esteemed group of past recipients for our ongoing endeavors to educate advanced practitioners in support of their clinical, professional needs in preventing, diagnosing, and treating kidney diseases.”

In announcing the award, Ms. Clemments noted that Renal Consult aligns with CAP’s goal to improve patient outcomes by enhancing advanced practitioners’ knowledge base and skills that will have a direct impact on clinical practice in a variety of settings. Renal Consult appears quarterly in print and online in CR’s robust, interactive website, digital edition, and mobile app.

The National Kidney Foundation is the leading organization in the United States dedicated to the awareness, prevention, and treatment of kidney disease for hundreds of thousands of healthcare professionals, millions of patients and their families, and tens of millions of Americans at risk. Clinician Reviews will be recognized during an awards luncheon at the NKF 2018 Spring Clinical Meeting in April.

Frontline Medical Communications today announced that its journal, Clinician Reviews (CR), dedicated to nurse practitioners and physician assistants, has been named recipient of the 2018 Nostradamus Award.

Annually, National Kidney Foundation’s Council of Advanced Practitioners (CAP) presents this award to an individual, group, or organization that, through forethought and vision, recognizes, supports, and promotes the contributions of Advance Practitioners in nephrology. Clinician Reviews is being recognized for its Q&A feature Renal Consult, which provides expert advice to help clinicians address the complexities of renal diseases.

“Clinician Reviews joins a list of outstanding winners, including nephrologists, a United States senator, and others who have recognized CAP’s worth and supported its advancement,” said Karen Clemments, Editorial Director of clinical publications and Editor of Clinician Reviews. She continued, “We are excited to be among an esteemed group of past recipients for our ongoing endeavors to educate advanced practitioners in support of their clinical, professional needs in preventing, diagnosing, and treating kidney diseases.”

In announcing the award, Ms. Clemments noted that Renal Consult aligns with CAP’s goal to improve patient outcomes by enhancing advanced practitioners’ knowledge base and skills that will have a direct impact on clinical practice in a variety of settings. Renal Consult appears quarterly in print and online in CR’s robust, interactive website, digital edition, and mobile app.

The National Kidney Foundation is the leading organization in the United States dedicated to the awareness, prevention, and treatment of kidney disease for hundreds of thousands of healthcare professionals, millions of patients and their families, and tens of millions of Americans at risk. Clinician Reviews will be recognized during an awards luncheon at the NKF 2018 Spring Clinical Meeting in April.

Frontline Medical Communications today announced that its journal, Clinician Reviews (CR), dedicated to nurse practitioners and physician assistants, has been named recipient of the 2018 Nostradamus Award.

Annually, National Kidney Foundation’s Council of Advanced Practitioners (CAP) presents this award to an individual, group, or organization that, through forethought and vision, recognizes, supports, and promotes the contributions of Advance Practitioners in nephrology. Clinician Reviews is being recognized for its Q&A feature Renal Consult, which provides expert advice to help clinicians address the complexities of renal diseases.

“Clinician Reviews joins a list of outstanding winners, including nephrologists, a United States senator, and others who have recognized CAP’s worth and supported its advancement,” said Karen Clemments, Editorial Director of clinical publications and Editor of Clinician Reviews. She continued, “We are excited to be among an esteemed group of past recipients for our ongoing endeavors to educate advanced practitioners in support of their clinical, professional needs in preventing, diagnosing, and treating kidney diseases.”

In announcing the award, Ms. Clemments noted that Renal Consult aligns with CAP’s goal to improve patient outcomes by enhancing advanced practitioners’ knowledge base and skills that will have a direct impact on clinical practice in a variety of settings. Renal Consult appears quarterly in print and online in CR’s robust, interactive website, digital edition, and mobile app.

The National Kidney Foundation is the leading organization in the United States dedicated to the awareness, prevention, and treatment of kidney disease for hundreds of thousands of healthcare professionals, millions of patients and their families, and tens of millions of Americans at risk. Clinician Reviews will be recognized during an awards luncheon at the NKF 2018 Spring Clinical Meeting in April.