The number of Zika virus cases continue to rise, with 177 more pregnant women showing laboratory evidence of infection in the United States for the week ending Sept. 29, according to the Centers for Disease Control and Prevention.

The week also included a report of another live-born infant with Zika-related birth defects, bringing the U.S. total to 23 for the year: 22 in the 50 states and District of Columbia and 1 in the territories, the CDC reported Oct. 6. There also have been six Zika-related pregnancy losses reported so far in the states and territories, a number that has not changed since early August.

[email protected]

The number of Zika virus cases continue to rise, with 177 more pregnant women showing laboratory evidence of infection in the United States for the week ending Sept. 29, according to the Centers for Disease Control and Prevention.

The week also included a report of another live-born infant with Zika-related birth defects, bringing the U.S. total to 23 for the year: 22 in the 50 states and District of Columbia and 1 in the territories, the CDC reported Oct. 6. There also have been six Zika-related pregnancy losses reported so far in the states and territories, a number that has not changed since early August.

[email protected]

The number of Zika virus cases continue to rise, with 177 more pregnant women showing laboratory evidence of infection in the United States for the week ending Sept. 29, according to the Centers for Disease Control and Prevention.

The week also included a report of another live-born infant with Zika-related birth defects, bringing the U.S. total to 23 for the year: 22 in the 50 states and District of Columbia and 1 in the territories, the CDC reported Oct. 6. There also have been six Zika-related pregnancy losses reported so far in the states and territories, a number that has not changed since early August.

[email protected]

JoAnn Pinkerton, MD, Professor of Obstetrics and Gynecology at the University of Virginia, Executive Director of the North American Menopause Society (NAMS), and OBG Management Board of Editors Member, revealed the 2016 NAMS position statement on hormone therapy (HT) in Orlando, Florida, on Thursday, October 6, at the NAMS 2016 Annual Scientific Meeting.

The process of consensus among the more than 20 menopause experts who authored the 2016 statement was at times a challenge, indicated Pinkerton, given the variance in views on the significance of published clinical trial findings since the Society’s 2012¹ HT position statement. Over a 9-month period, the experts developed guidelines for clinicians, using levels of evidence to identify strength of the recommendations.

The clearest benefit for HT to treat hot flashes and prevent bone loss was found for women aged younger than 60 years and within 10 years of menopause onset.

According to the 2016 statement presented at NAMS:

Level I US Food and Drug Administration (FDA)-approved indications for HT include:

• as first-line therapy for women with vasomotor symptoms (VMS) of menopause without contraindications
• possible first-line therapy for prevention of bone loss and fracture in postmenopausal women at elevated risk for fracture (primarily for women aged younger than 60 years and within 10 years of menopause onset)
• low-dose vaginal estrogen as first-line treatment for women with isolated genitourinary symptoms caused by menopause (genitourinary syndrome of menopause [GSM]/vulvovaginal atrophy).

Level II FDA-approved indications for HT include:

• at least until age 52 (the median age of menopause onset) for women with early onset menopause (women with hypogonadism, primary ovarian insufficiency, or premature surgical menopause) and no HT contraindications.

Other level II indications, with observational data indicating benefit over risk, for HT include:

• at least until the median age of menopause for women with early onset menopause
• consideration among women with a family history of breast cancer, although family history is one risk among many for breast cancer that should be assessed
• benefit/risk consideration for women with a BRCA gene mutation who have undergone risk-reducing oophorectomy
• consideration of systemic use until the median age of menopause—after appropriate counseling and in the absence of HT contraindications, with longer duration of HT use individualized.

Level III indications for HT include:

• individualized decisions on use after the age of 60. (The position statement authors did not find that the current Beers criteria recommendation to routinely discontinue HT at age 65 was supported by data.)

The 2016 bottom line on HT

Overall, HT has clear benefits for the treatment of VMS and bone loss prevention, according to the presented position statement. These benefits are most favorable among women aged younger than 60 years who are within 10 years of menopause onset and have no contraindications to HT use. Women older than age 60 who initiate HT beyond 10 years of menopause onset appear to have a less favorable benefit-risk ratio because of elevated risks of coronary heart disease, stroke, venous thromboembolism, and dementia.

The risks of HT vary among women depending on the HT type, duration of use, administration route, timing of treatment initiation, and whether a progestogen is needed. (With longer HT use, estrogen therapy is more favorable than estrogen-progestin therapy.) Therefore, HT should be individualized and reevaluated periodically to maximize the benefits as well as minimize the risks of use, according to the position statement.

Nonhormonal therapies for menopausal symptoms

The Society released its position on nonhormonal management of menopause-associated VMS in 2015.² Based on examination of 340 original research articles and 105 systematic reviews, clinical and research experts categorized therapies as recommended, recommended with caution, and not recommended at this time.

Recommended non-HT to reduce VMS include:

• cognitive-behavioral therapy
• clinical hypnosis
• low-dose salt of paroxetine (FDA approved for menopausal VMS management)
• other SSRIs/SNRIs
• gabapentinoids
• clonidine.

Recommended-with-caution non-HT for VMS include:

• weight loss
• stress reduction (mindfulness based)
• S-equol derivatives of soy isoflavones
• stellate ganglion block.

Not recommended non-HT for VMS due to negative, insufficient, or inconclusive data include:

• cooling techniques
• avoidance of triggers
• exercise
• yoga
• paced respiration
• relaxation
• over-the-counter supplements and herbs
• acupuncture
• calibration of neural oscillations
• chiropractic interventions.

Note that the NAMS 2016 Hormone Therapy Position Statement was presented at the 2016 Annual Scientific Meeting of the North American Menopause Society, but the statement is not yet published.

JoAnn Pinkerton, MD, Professor of Obstetrics and Gynecology at the University of Virginia, Executive Director of the North American Menopause Society (NAMS), and OBG Management Board of Editors Member, revealed the 2016 NAMS position statement on hormone therapy (HT) in Orlando, Florida, on Thursday, October 6, at the NAMS 2016 Annual Scientific Meeting.

The process of consensus among the more than 20 menopause experts who authored the 2016 statement was at times a challenge, indicated Pinkerton, given the variance in views on the significance of published clinical trial findings since the Society’s 2012¹ HT position statement. Over a 9-month period, the experts developed guidelines for clinicians, using levels of evidence to identify strength of the recommendations.

The clearest benefit for HT to treat hot flashes and prevent bone loss was found for women aged younger than 60 years and within 10 years of menopause onset.

According to the 2016 statement presented at NAMS:

Level I US Food and Drug Administration (FDA)-approved indications for HT include:

• as first-line therapy for women with vasomotor symptoms (VMS) of menopause without contraindications
• possible first-line therapy for prevention of bone loss and fracture in postmenopausal women at elevated risk for fracture (primarily for women aged younger than 60 years and within 10 years of menopause onset)
• low-dose vaginal estrogen as first-line treatment for women with isolated genitourinary symptoms caused by menopause (genitourinary syndrome of menopause [GSM]/vulvovaginal atrophy).

Level II FDA-approved indications for HT include:

• at least until age 52 (the median age of menopause onset) for women with early onset menopause (women with hypogonadism, primary ovarian insufficiency, or premature surgical menopause) and no HT contraindications.

Other level II indications, with observational data indicating benefit over risk, for HT include:

• at least until the median age of menopause for women with early onset menopause
• consideration among women with a family history of breast cancer, although family history is one risk among many for breast cancer that should be assessed
• benefit/risk consideration for women with a BRCA gene mutation who have undergone risk-reducing oophorectomy
• consideration of systemic use until the median age of menopause—after appropriate counseling and in the absence of HT contraindications, with longer duration of HT use individualized.

Level III indications for HT include:

• individualized decisions on use after the age of 60. (The position statement authors did not find that the current Beers criteria recommendation to routinely discontinue HT at age 65 was supported by data.)

The 2016 bottom line on HT

Overall, HT has clear benefits for the treatment of VMS and bone loss prevention, according to the presented position statement. These benefits are most favorable among women aged younger than 60 years who are within 10 years of menopause onset and have no contraindications to HT use. Women older than age 60 who initiate HT beyond 10 years of menopause onset appear to have a less favorable benefit-risk ratio because of elevated risks of coronary heart disease, stroke, venous thromboembolism, and dementia.

The risks of HT vary among women depending on the HT type, duration of use, administration route, timing of treatment initiation, and whether a progestogen is needed. (With longer HT use, estrogen therapy is more favorable than estrogen-progestin therapy.) Therefore, HT should be individualized and reevaluated periodically to maximize the benefits as well as minimize the risks of use, according to the position statement.

Nonhormonal therapies for menopausal symptoms

The Society released its position on nonhormonal management of menopause-associated VMS in 2015.² Based on examination of 340 original research articles and 105 systematic reviews, clinical and research experts categorized therapies as recommended, recommended with caution, and not recommended at this time.

Recommended non-HT to reduce VMS include:

• cognitive-behavioral therapy
• clinical hypnosis
• low-dose salt of paroxetine (FDA approved for menopausal VMS management)
• other SSRIs/SNRIs
• gabapentinoids
• clonidine.

Recommended-with-caution non-HT for VMS include:

• weight loss
• stress reduction (mindfulness based)
• S-equol derivatives of soy isoflavones
• stellate ganglion block.

Not recommended non-HT for VMS due to negative, insufficient, or inconclusive data include:

• cooling techniques
• avoidance of triggers
• exercise
• yoga
• paced respiration
• relaxation
• over-the-counter supplements and herbs
• acupuncture
• calibration of neural oscillations
• chiropractic interventions.

Note that the NAMS 2016 Hormone Therapy Position Statement was presented at the 2016 Annual Scientific Meeting of the North American Menopause Society, but the statement is not yet published.

JoAnn Pinkerton, MD, Professor of Obstetrics and Gynecology at the University of Virginia, Executive Director of the North American Menopause Society (NAMS), and OBG Management Board of Editors Member, revealed the 2016 NAMS position statement on hormone therapy (HT) in Orlando, Florida, on Thursday, October 6, at the NAMS 2016 Annual Scientific Meeting.

The process of consensus among the more than 20 menopause experts who authored the 2016 statement was at times a challenge, indicated Pinkerton, given the variance in views on the significance of published clinical trial findings since the Society’s 2012¹ HT position statement. Over a 9-month period, the experts developed guidelines for clinicians, using levels of evidence to identify strength of the recommendations.

The clearest benefit for HT to treat hot flashes and prevent bone loss was found for women aged younger than 60 years and within 10 years of menopause onset.

According to the 2016 statement presented at NAMS:

Level I US Food and Drug Administration (FDA)-approved indications for HT include:

• as first-line therapy for women with vasomotor symptoms (VMS) of menopause without contraindications
• possible first-line therapy for prevention of bone loss and fracture in postmenopausal women at elevated risk for fracture (primarily for women aged younger than 60 years and within 10 years of menopause onset)
• low-dose vaginal estrogen as first-line treatment for women with isolated genitourinary symptoms caused by menopause (genitourinary syndrome of menopause [GSM]/vulvovaginal atrophy).

Level II FDA-approved indications for HT include:

• at least until age 52 (the median age of menopause onset) for women with early onset menopause (women with hypogonadism, primary ovarian insufficiency, or premature surgical menopause) and no HT contraindications.

Other level II indications, with observational data indicating benefit over risk, for HT include:

• at least until the median age of menopause for women with early onset menopause
• consideration among women with a family history of breast cancer, although family history is one risk among many for breast cancer that should be assessed
• benefit/risk consideration for women with a BRCA gene mutation who have undergone risk-reducing oophorectomy
• consideration of systemic use until the median age of menopause—after appropriate counseling and in the absence of HT contraindications, with longer duration of HT use individualized.

Level III indications for HT include:

• individualized decisions on use after the age of 60. (The position statement authors did not find that the current Beers criteria recommendation to routinely discontinue HT at age 65 was supported by data.)

The 2016 bottom line on HT

Overall, HT has clear benefits for the treatment of VMS and bone loss prevention, according to the presented position statement. These benefits are most favorable among women aged younger than 60 years who are within 10 years of menopause onset and have no contraindications to HT use. Women older than age 60 who initiate HT beyond 10 years of menopause onset appear to have a less favorable benefit-risk ratio because of elevated risks of coronary heart disease, stroke, venous thromboembolism, and dementia.

The risks of HT vary among women depending on the HT type, duration of use, administration route, timing of treatment initiation, and whether a progestogen is needed. (With longer HT use, estrogen therapy is more favorable than estrogen-progestin therapy.) Therefore, HT should be individualized and reevaluated periodically to maximize the benefits as well as minimize the risks of use, according to the position statement.

Nonhormonal therapies for menopausal symptoms

The Society released its position on nonhormonal management of menopause-associated VMS in 2015.² Based on examination of 340 original research articles and 105 systematic reviews, clinical and research experts categorized therapies as recommended, recommended with caution, and not recommended at this time.

Recommended non-HT to reduce VMS include:

• cognitive-behavioral therapy
• clinical hypnosis
• low-dose salt of paroxetine (FDA approved for menopausal VMS management)
• other SSRIs/SNRIs
• gabapentinoids
• clonidine.

Recommended-with-caution non-HT for VMS include:

• weight loss
• stress reduction (mindfulness based)
• S-equol derivatives of soy isoflavones
• stellate ganglion block.

Not recommended non-HT for VMS due to negative, insufficient, or inconclusive data include:

• cooling techniques
• avoidance of triggers
• exercise
• yoga
• paced respiration
• relaxation
• over-the-counter supplements and herbs
• acupuncture
• calibration of neural oscillations
• chiropractic interventions.

Note that the NAMS 2016 Hormone Therapy Position Statement was presented at the 2016 Annual Scientific Meeting of the North American Menopause Society, but the statement is not yet published.

Nearly a third of Medicare beneficiaries with chronic myeloid leukemia (CML) did not initiate tyrosine kinase inhibitor therapy within 6 months of diagnosis, according to a review of SEER-Medicare data.

The findings suggest that out-of-pocket costs might be a barrier to timely initiation of tyrosine kinase inhibitor (TKI) therapy in CML patients, Aaron N. Winn of the University of North Carolina at Chapel Hill and his colleagues reported online ahead of print in the Journal of Clinical Oncology.

Of 393 individuals diagnosed with CML between 2007 and 2011, only 68% initiated TKI therapy within 180 days (median, 75 days), and 61% of those patients were adherent. Earlier treatment initiation was associated with receipt of cost-sharing subsidies (hazard ratio, 1.35), more-recent diagnosis (HR, 1.14), and living in a big metropolitan area (HR, 1.80) or metropolitan area vs. an urban area (HR, 1.84), while later treatment initiation was associated with higher levels of comorbidity (HR, 0.81) and age older than 80 years vs. age younger than 70 years (HR, 0.53)

Multivariate analysis showed that therapy initiation within 180 days was significantly more likely among those with more-recent diagnosis (relative risk, 1.06) and those living in a large metropolitan area vs. an urban area (RR, 1.57), and was significantly less likely among those older than age 80 years vs. those younger than age 70 years (RR, 0.71). Adherence within 180 days of therapy initiation was higher for those diagnosed in more-recent years (RR, 1.07) and lower for patients aged 80 years or older vs. 66-69 years (RR, 0.74), the investigators found (J Clin Oncol. 2016 Oct 3. doi: 10/1200/JCO.2016.67.4184).

“Our findings highlight important gaps in TKI use among Medicare beneficiaries with CML and suggest that high cost sharing may result in delays in initiation of these life-saving medications,” they concluded.

This study was supported by a University of North Carolina Clinical and Translational Science award, the UNC School of Medicine, the Royster Society of Fellows at UNC Chapel Hill, and by grants from the National Institutes of Health, North Carolina Translational and Clinical Sciences Institute, and the National Cancer Institute. The authors reported having no disclosures.

[email protected]

Nearly a third of Medicare beneficiaries with chronic myeloid leukemia (CML) did not initiate tyrosine kinase inhibitor therapy within 6 months of diagnosis, according to a review of SEER-Medicare data.

The findings suggest that out-of-pocket costs might be a barrier to timely initiation of tyrosine kinase inhibitor (TKI) therapy in CML patients, Aaron N. Winn of the University of North Carolina at Chapel Hill and his colleagues reported online ahead of print in the Journal of Clinical Oncology.

Of 393 individuals diagnosed with CML between 2007 and 2011, only 68% initiated TKI therapy within 180 days (median, 75 days), and 61% of those patients were adherent. Earlier treatment initiation was associated with receipt of cost-sharing subsidies (hazard ratio, 1.35), more-recent diagnosis (HR, 1.14), and living in a big metropolitan area (HR, 1.80) or metropolitan area vs. an urban area (HR, 1.84), while later treatment initiation was associated with higher levels of comorbidity (HR, 0.81) and age older than 80 years vs. age younger than 70 years (HR, 0.53)

Multivariate analysis showed that therapy initiation within 180 days was significantly more likely among those with more-recent diagnosis (relative risk, 1.06) and those living in a large metropolitan area vs. an urban area (RR, 1.57), and was significantly less likely among those older than age 80 years vs. those younger than age 70 years (RR, 0.71). Adherence within 180 days of therapy initiation was higher for those diagnosed in more-recent years (RR, 1.07) and lower for patients aged 80 years or older vs. 66-69 years (RR, 0.74), the investigators found (J Clin Oncol. 2016 Oct 3. doi: 10/1200/JCO.2016.67.4184).

“Our findings highlight important gaps in TKI use among Medicare beneficiaries with CML and suggest that high cost sharing may result in delays in initiation of these life-saving medications,” they concluded.

This study was supported by a University of North Carolina Clinical and Translational Science award, the UNC School of Medicine, the Royster Society of Fellows at UNC Chapel Hill, and by grants from the National Institutes of Health, North Carolina Translational and Clinical Sciences Institute, and the National Cancer Institute. The authors reported having no disclosures.

[email protected]

Nearly a third of Medicare beneficiaries with chronic myeloid leukemia (CML) did not initiate tyrosine kinase inhibitor therapy within 6 months of diagnosis, according to a review of SEER-Medicare data.

The findings suggest that out-of-pocket costs might be a barrier to timely initiation of tyrosine kinase inhibitor (TKI) therapy in CML patients, Aaron N. Winn of the University of North Carolina at Chapel Hill and his colleagues reported online ahead of print in the Journal of Clinical Oncology.

Of 393 individuals diagnosed with CML between 2007 and 2011, only 68% initiated TKI therapy within 180 days (median, 75 days), and 61% of those patients were adherent. Earlier treatment initiation was associated with receipt of cost-sharing subsidies (hazard ratio, 1.35), more-recent diagnosis (HR, 1.14), and living in a big metropolitan area (HR, 1.80) or metropolitan area vs. an urban area (HR, 1.84), while later treatment initiation was associated with higher levels of comorbidity (HR, 0.81) and age older than 80 years vs. age younger than 70 years (HR, 0.53)

Multivariate analysis showed that therapy initiation within 180 days was significantly more likely among those with more-recent diagnosis (relative risk, 1.06) and those living in a large metropolitan area vs. an urban area (RR, 1.57), and was significantly less likely among those older than age 80 years vs. those younger than age 70 years (RR, 0.71). Adherence within 180 days of therapy initiation was higher for those diagnosed in more-recent years (RR, 1.07) and lower for patients aged 80 years or older vs. 66-69 years (RR, 0.74), the investigators found (J Clin Oncol. 2016 Oct 3. doi: 10/1200/JCO.2016.67.4184).

“Our findings highlight important gaps in TKI use among Medicare beneficiaries with CML and suggest that high cost sharing may result in delays in initiation of these life-saving medications,” they concluded.

This study was supported by a University of North Carolina Clinical and Translational Science award, the UNC School of Medicine, the Royster Society of Fellows at UNC Chapel Hill, and by grants from the National Institutes of Health, North Carolina Translational and Clinical Sciences Institute, and the National Cancer Institute. The authors reported having no disclosures.

[email protected]

Longitudinal results of a prospective study of women with and without breast arterial calcifications showed that women with the calcifications were significantly more likely to have atherosclerotic cardiovascular events than were women without them.

In a 10-year follow-up of a cohort of women receiving screening mammograms, women who did not have cardiovascular disease at baseline and were positive for breast arterial calcifications (BACs) were three times more likely to develop atherosclerotic cardiovascular disease (ASCVD) as those who were BAC negative at baseline (9.8% vs. 3.3%; P = .001).

These results paralleled those found 5 years previously among the cohort. At that point, 6.3% of the BAC-positive group developed ASCVD, compared with 2.3% of the BAC-negative group (P = .003). At 10 years, “multiple logistic regression analysis found BAC to be strongly associated with ASCVD events, with an odds ratio of 2.29,” senior investigator Peter Schnatz, DO, said in an interview.

Based on these results, Dr. Schnatz and his coinvestigators are suggesting that BACs be routinely reported on mammograms and viewed as a marker for the development of cardiovascular disease.

Presenting the unpublished 10-year findings at the annual meeting of the North American Menopause Society, Dr. Schnatz, the society’s 2015-2016 president, said that the BAC-positive group was also more likely to develop risk factors for ASCVD (86.8% vs. 76.3; P = .01).

These risk factors were age, hypertension, hypercholesterolemia, diabetes, and menopause. The other results were significant after the investigators controlled for age, so the increased risk was not merely caused by the passage of time and the normal aging process.

The prospective study compared age-matched controls with and without BACs to determine whether BACs seen on routine mammography can predict the development of ASCVD, by tracking the presence of BACs and gathering information about ASCVD risk factors and events via patient self-report in an annual questionnaire. The events that were considered ASCVD markers were angina, myocardial infarction, an abnormal angiogram, coronary artery bypass grafting, and stroke.

The initial baseline study upon which the longitudinal prospective studies are based gathered data from 1,919 women with a median age of 56, plus or minus 12.7 years (range, 25-96), to determine whether women with BAC had an increased frequency of cardiovascular disease risk factors, and of ASCVD. Baseline findings showed an independent association of BAC with multiple risk factors and with ASCVD events, even after age was controlled for.

Dr. Schnatz, who is a professor of ob.gyn. and internal medicine at Thomas Jefferson University, Philadelphia, said in his presentation that BACs “appear to be a risk indicator of the presence of ASCVD. More importantly, in this first prospective analysis of BAC as a risk predictor, BAC appears to be a risk predictor for the future development of ASCVD.”

Patients were considered BAC positive if their mammograms showed BAC on at least one of two standard views of either or both breasts. The screening mammograms were read in a uniform fashion by 1 of 21 radiologists, who used identical and well-accepted criteria for BACs. Overall, 268 women (14%) were BAC positive, in line with the 9%-17.5% prevalence reported in the literature, Dr. Schnatz said.

BACs are diffuse calcifications of the arterial tunica media, which are common but often unreported by radiologists who find them on screening mammograms, though they are seen in up to 17.5% of mammograms.

Medial arterial calcifications, such as BACs, are fine-grained deposits seen in small- to medium-sized muscular arteries. Though they have been observed for some time, their significance has been unknown, and they are often seen as part of the normal aging process, Dr. Schnatz said. With the advent of newer mammography technology in the 2000s, much smaller calcifications could be seen, and research into the significance of BACs detected on screening mammogram was revived and refined, he said.

“If BAC has value as a marker for coronary artery disease, then mammograms could be a practical tool for detecting CAD risk in women,” Dr. Schnatz said. “This might contribute to earlier detection of vascular damage, especially important in women at high risk of CAD or with unrecognized heart disease.”

Dr. Schnatz said he plans to incorporate BAC status into validated cardiovascular risk predictors, and see how a prediction model that includes BAC fares.

Dr. Schnatz reported having no relevant financial disclosures.

[email protected]

On Twitter @karioakes

Longitudinal results of a prospective study of women with and without breast arterial calcifications showed that women with the calcifications were significantly more likely to have atherosclerotic cardiovascular events than were women without them.

In a 10-year follow-up of a cohort of women receiving screening mammograms, women who did not have cardiovascular disease at baseline and were positive for breast arterial calcifications (BACs) were three times more likely to develop atherosclerotic cardiovascular disease (ASCVD) as those who were BAC negative at baseline (9.8% vs. 3.3%; P = .001).

These results paralleled those found 5 years previously among the cohort. At that point, 6.3% of the BAC-positive group developed ASCVD, compared with 2.3% of the BAC-negative group (P = .003). At 10 years, “multiple logistic regression analysis found BAC to be strongly associated with ASCVD events, with an odds ratio of 2.29,” senior investigator Peter Schnatz, DO, said in an interview.

Based on these results, Dr. Schnatz and his coinvestigators are suggesting that BACs be routinely reported on mammograms and viewed as a marker for the development of cardiovascular disease.

Presenting the unpublished 10-year findings at the annual meeting of the North American Menopause Society, Dr. Schnatz, the society’s 2015-2016 president, said that the BAC-positive group was also more likely to develop risk factors for ASCVD (86.8% vs. 76.3; P = .01).

These risk factors were age, hypertension, hypercholesterolemia, diabetes, and menopause. The other results were significant after the investigators controlled for age, so the increased risk was not merely caused by the passage of time and the normal aging process.

The prospective study compared age-matched controls with and without BACs to determine whether BACs seen on routine mammography can predict the development of ASCVD, by tracking the presence of BACs and gathering information about ASCVD risk factors and events via patient self-report in an annual questionnaire. The events that were considered ASCVD markers were angina, myocardial infarction, an abnormal angiogram, coronary artery bypass grafting, and stroke.

The initial baseline study upon which the longitudinal prospective studies are based gathered data from 1,919 women with a median age of 56, plus or minus 12.7 years (range, 25-96), to determine whether women with BAC had an increased frequency of cardiovascular disease risk factors, and of ASCVD. Baseline findings showed an independent association of BAC with multiple risk factors and with ASCVD events, even after age was controlled for.

Dr. Schnatz, who is a professor of ob.gyn. and internal medicine at Thomas Jefferson University, Philadelphia, said in his presentation that BACs “appear to be a risk indicator of the presence of ASCVD. More importantly, in this first prospective analysis of BAC as a risk predictor, BAC appears to be a risk predictor for the future development of ASCVD.”

Patients were considered BAC positive if their mammograms showed BAC on at least one of two standard views of either or both breasts. The screening mammograms were read in a uniform fashion by 1 of 21 radiologists, who used identical and well-accepted criteria for BACs. Overall, 268 women (14%) were BAC positive, in line with the 9%-17.5% prevalence reported in the literature, Dr. Schnatz said.

BACs are diffuse calcifications of the arterial tunica media, which are common but often unreported by radiologists who find them on screening mammograms, though they are seen in up to 17.5% of mammograms.

Medial arterial calcifications, such as BACs, are fine-grained deposits seen in small- to medium-sized muscular arteries. Though they have been observed for some time, their significance has been unknown, and they are often seen as part of the normal aging process, Dr. Schnatz said. With the advent of newer mammography technology in the 2000s, much smaller calcifications could be seen, and research into the significance of BACs detected on screening mammogram was revived and refined, he said.

“If BAC has value as a marker for coronary artery disease, then mammograms could be a practical tool for detecting CAD risk in women,” Dr. Schnatz said. “This might contribute to earlier detection of vascular damage, especially important in women at high risk of CAD or with unrecognized heart disease.”

Dr. Schnatz said he plans to incorporate BAC status into validated cardiovascular risk predictors, and see how a prediction model that includes BAC fares.

Dr. Schnatz reported having no relevant financial disclosures.

[email protected]

On Twitter @karioakes

Longitudinal results of a prospective study of women with and without breast arterial calcifications showed that women with the calcifications were significantly more likely to have atherosclerotic cardiovascular events than were women without them.

In a 10-year follow-up of a cohort of women receiving screening mammograms, women who did not have cardiovascular disease at baseline and were positive for breast arterial calcifications (BACs) were three times more likely to develop atherosclerotic cardiovascular disease (ASCVD) as those who were BAC negative at baseline (9.8% vs. 3.3%; P = .001).

These results paralleled those found 5 years previously among the cohort. At that point, 6.3% of the BAC-positive group developed ASCVD, compared with 2.3% of the BAC-negative group (P = .003). At 10 years, “multiple logistic regression analysis found BAC to be strongly associated with ASCVD events, with an odds ratio of 2.29,” senior investigator Peter Schnatz, DO, said in an interview.

Based on these results, Dr. Schnatz and his coinvestigators are suggesting that BACs be routinely reported on mammograms and viewed as a marker for the development of cardiovascular disease.

Presenting the unpublished 10-year findings at the annual meeting of the North American Menopause Society, Dr. Schnatz, the society’s 2015-2016 president, said that the BAC-positive group was also more likely to develop risk factors for ASCVD (86.8% vs. 76.3; P = .01).

These risk factors were age, hypertension, hypercholesterolemia, diabetes, and menopause. The other results were significant after the investigators controlled for age, so the increased risk was not merely caused by the passage of time and the normal aging process.

The prospective study compared age-matched controls with and without BACs to determine whether BACs seen on routine mammography can predict the development of ASCVD, by tracking the presence of BACs and gathering information about ASCVD risk factors and events via patient self-report in an annual questionnaire. The events that were considered ASCVD markers were angina, myocardial infarction, an abnormal angiogram, coronary artery bypass grafting, and stroke.

The initial baseline study upon which the longitudinal prospective studies are based gathered data from 1,919 women with a median age of 56, plus or minus 12.7 years (range, 25-96), to determine whether women with BAC had an increased frequency of cardiovascular disease risk factors, and of ASCVD. Baseline findings showed an independent association of BAC with multiple risk factors and with ASCVD events, even after age was controlled for.

Dr. Schnatz, who is a professor of ob.gyn. and internal medicine at Thomas Jefferson University, Philadelphia, said in his presentation that BACs “appear to be a risk indicator of the presence of ASCVD. More importantly, in this first prospective analysis of BAC as a risk predictor, BAC appears to be a risk predictor for the future development of ASCVD.”

Patients were considered BAC positive if their mammograms showed BAC on at least one of two standard views of either or both breasts. The screening mammograms were read in a uniform fashion by 1 of 21 radiologists, who used identical and well-accepted criteria for BACs. Overall, 268 women (14%) were BAC positive, in line with the 9%-17.5% prevalence reported in the literature, Dr. Schnatz said.

BACs are diffuse calcifications of the arterial tunica media, which are common but often unreported by radiologists who find them on screening mammograms, though they are seen in up to 17.5% of mammograms.

Medial arterial calcifications, such as BACs, are fine-grained deposits seen in small- to medium-sized muscular arteries. Though they have been observed for some time, their significance has been unknown, and they are often seen as part of the normal aging process, Dr. Schnatz said. With the advent of newer mammography technology in the 2000s, much smaller calcifications could be seen, and research into the significance of BACs detected on screening mammogram was revived and refined, he said.

“If BAC has value as a marker for coronary artery disease, then mammograms could be a practical tool for detecting CAD risk in women,” Dr. Schnatz said. “This might contribute to earlier detection of vascular damage, especially important in women at high risk of CAD or with unrecognized heart disease.”

Dr. Schnatz said he plans to incorporate BAC status into validated cardiovascular risk predictors, and see how a prediction model that includes BAC fares.

Dr. Schnatz reported having no relevant financial disclosures.

[email protected]

On Twitter @karioakes

DURBAN, SOUTH AFRICA – Children exposed to HIV in utero but uninfected at birth have neurodevelopmental test scores at age 24 months that are comparable with those of unexposed children, based on a study conducted in Botswana and presented by Jean Leidner at the 21st International AIDS Conference.

“These results provide reassurance regarding the potential effects of in-utero HIV and antiretroviral exposure,” declared Ms. Leidner, CEO of Goodtables Data Consulting in Norman, Okla., and the Botswana Harvard AIDS Institute Partnership.

Bruce Jancin/Frontline Medical News

[email protected]

DURBAN, SOUTH AFRICA – Children exposed to HIV in utero but uninfected at birth have neurodevelopmental test scores at age 24 months that are comparable with those of unexposed children, based on a study conducted in Botswana and presented by Jean Leidner at the 21st International AIDS Conference.

“These results provide reassurance regarding the potential effects of in-utero HIV and antiretroviral exposure,” declared Ms. Leidner, CEO of Goodtables Data Consulting in Norman, Okla., and the Botswana Harvard AIDS Institute Partnership.

Bruce Jancin/Frontline Medical News

[email protected]

DURBAN, SOUTH AFRICA – Children exposed to HIV in utero but uninfected at birth have neurodevelopmental test scores at age 24 months that are comparable with those of unexposed children, based on a study conducted in Botswana and presented by Jean Leidner at the 21st International AIDS Conference.

“These results provide reassurance regarding the potential effects of in-utero HIV and antiretroviral exposure,” declared Ms. Leidner, CEO of Goodtables Data Consulting in Norman, Okla., and the Botswana Harvard AIDS Institute Partnership.

Bruce Jancin/Frontline Medical News

[email protected]

Carbapenem-resistant Enterobacteriaceae (CRE) are extremely drug-resistant organisms. According to the Centers for Disease Control and Prevention’s National Healthcare Safety Network, in 2014 in the United States, 3.6% of Enterobacteriaceae causing hospital-acquired infections were resistant to carbapenems.¹ Antibiotic treatment options for CRE infections are severely limited, and mortality for invasive infections can be as high as 40%-50%.²

Resistance to carbapenems can be mediated by several mechanisms. From an epidemiologic standpoint, production of carbapenemases is the most-threatening mechanism because Enterobacteriaceae-harboring carbapenemases are highly transmissible.

Carbapenemase-producing CRE (CP-CRE) have caused large outbreaks throughout the world. Israel experienced a nationwide outbreak of CP-CRE, primarily Klebsiella pneumoniae carbapenemase–producing Klebsiella pneumoniae, in the mid-2000s. At the peak of the outbreak in 2007, there were 185 new cases per month (55.5/100,000 patient-days). A successful intervention at the national level dramatically decreased the incidence to 4.8/100,000 patient days in 2012.³

One component of the intervention (which is still ongoing) is active surveillance of high-risk groups using rectal swabs. Upon admission to the hospital, we screen patients who were recently in other hospitals or long-term care facilities. In addition, when a patient is newly diagnosed with CP-CRE (either asymptomatic carriage or clinical infection), we screen patients who had contact with that index case before isolation measures were implemented.

We recently published a study in Infection Control and Hospital Epidemiology that draws on our experience with CP-CRE screening of contacts at Tel Aviv Sourasky Medical Center.⁴ Both Israeli and International guidelines do not precisely define which contacts of a CP-CRE index case warrant screening. For example, should only roommates of index cases be screened or should we screen all patients on the same ward as the index case? Likewise, is there a minimum time of contact that should trigger screening?

Identifying which contacts are at high risk of acquiring CP-CRE is important for two reasons: We want to detect contacts who acquired CP-CRE so that they can be isolated before further transmission occurs, and we don’t want to waste resources and screen those at low risk. In our hospital, the criteria for being a contact are staying in the same ward and being treated by the same nursing staff as a newly identified CP-CRE patient.

This strategy appears to lead to overscreening, as we found that from October 2008 to June 2012, 3,158 screening tests were performed to detect 53 positive contacts (a yield of less than 2%). In order to screen more efficiently, our study aimed to determine risk factors for CP-CRE acquisition among patients exposed to a CP-CRE index patient.

We used a matched case-control design. The case group consisted of the 53 contacts who screened positive for CP-CRE. For each case we chose 2 controls: contacts who screened negative for CP-CRE. The basis for matching between the case and the 2 controls was that they were exposed to the same index patient. The benefit of matching this way was that it eliminated the question of whether a contact became positive because the index patient was more likely to transmit CP-CRE (e.g., because of diarrhea), and not because of characteristics of the contact patients themselves.

We found three factors that increased the risk that a contact would screen positive:

• Contact period of at least 3 days with the index case.

• Being on mechanical ventilation.

• Having a history of carriage or infection with another multidrug-resistant organism (such as methicillin-resistant Staphylococcus aureus).

Unexpectedly, sharing a room with the index patient or being debilitated did not significantly increase the risk of acquiring CP-CRE.

Many studies have identified antibiotic use as a risk factor for acquiring CP-CRE. In our study, no class of antibiotic increased the risk of CP-CRE acquisition, probably because only a small number of patients received each class. We were surprised to find that contacts who had taken cephalosporins were less likely to acquire CP-CRE. On further examination, when we compared patients who received only cephalosporins with patients who received no antibiotic, this protective effect disappeared. Nevertheless, compared with other antibiotics, it appears that cephalosporins might pose less of a risk for CP-CRE acquisition. More studies are needed to confirm our findings.

Our findings have practical implications for infection control. Using the risk factors we identified could help us to avoid excessive screening. We calculated that selective screening, based on our three risk factors, would have decreased the number of contacts screened by 30%, but 2 out of 53 positive contacts would have been missed. Institutions need to decide whether that is a trade-off they are willing to make.

Another way to apply our findings could be to add an additional layer of infection control by preemptively implementing contact precautions for patients at highest risk, for example, those with more than one risk factor.
 

1. Weiner LM, Fridkin SK, Aponte-Torres Z, Avery L, Coffin N, Dudeck MA, Edwards JR, Jernigan JA, Konnor R, Soe MM, Peterson K, Clifford McDonald L. Vital signs: preventing antibiotic-resistant infections in hospitals - United States, 2014. Am J Transplant. 2016 Jul;16(7):2224-30.

2. Centers for Disease Control and Prevention. Facility guidance for control of carbapenem-resistant Enterobacteriaceae (CRE): November 2015 update – CRE Toolkit.

3. Schwaber MJ, Carmeli Y. An ongoing national intervention to contain the spread of carbapenem-resistant enterobacteriaceae. Clin Infect Dis. 2014 Mar;58(5):697-703.

Schwartz-Neiderman A, Braun T, Fallach N, Schwartz D, Carmeli Y, Schechner V. Risk factors for carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) acquisition among contacts of newly diagnosed CP-CRE patients. Infect Control Hosp Epidemiol. 2016 Jul 25:1-7.
 

Vered Schechner, MD, MSc, is an infection control physician in the department of epidemiology at Tel Aviv Sourasky Medical Center.

Carbapenem-resistant Enterobacteriaceae (CRE) are extremely drug-resistant organisms. According to the Centers for Disease Control and Prevention’s National Healthcare Safety Network, in 2014 in the United States, 3.6% of Enterobacteriaceae causing hospital-acquired infections were resistant to carbapenems.¹ Antibiotic treatment options for CRE infections are severely limited, and mortality for invasive infections can be as high as 40%-50%.²

Resistance to carbapenems can be mediated by several mechanisms. From an epidemiologic standpoint, production of carbapenemases is the most-threatening mechanism because Enterobacteriaceae-harboring carbapenemases are highly transmissible.

Carbapenemase-producing CRE (CP-CRE) have caused large outbreaks throughout the world. Israel experienced a nationwide outbreak of CP-CRE, primarily Klebsiella pneumoniae carbapenemase–producing Klebsiella pneumoniae, in the mid-2000s. At the peak of the outbreak in 2007, there were 185 new cases per month (55.5/100,000 patient-days). A successful intervention at the national level dramatically decreased the incidence to 4.8/100,000 patient days in 2012.³

One component of the intervention (which is still ongoing) is active surveillance of high-risk groups using rectal swabs. Upon admission to the hospital, we screen patients who were recently in other hospitals or long-term care facilities. In addition, when a patient is newly diagnosed with CP-CRE (either asymptomatic carriage or clinical infection), we screen patients who had contact with that index case before isolation measures were implemented.

We recently published a study in Infection Control and Hospital Epidemiology that draws on our experience with CP-CRE screening of contacts at Tel Aviv Sourasky Medical Center.⁴ Both Israeli and International guidelines do not precisely define which contacts of a CP-CRE index case warrant screening. For example, should only roommates of index cases be screened or should we screen all patients on the same ward as the index case? Likewise, is there a minimum time of contact that should trigger screening?

Identifying which contacts are at high risk of acquiring CP-CRE is important for two reasons: We want to detect contacts who acquired CP-CRE so that they can be isolated before further transmission occurs, and we don’t want to waste resources and screen those at low risk. In our hospital, the criteria for being a contact are staying in the same ward and being treated by the same nursing staff as a newly identified CP-CRE patient.

This strategy appears to lead to overscreening, as we found that from October 2008 to June 2012, 3,158 screening tests were performed to detect 53 positive contacts (a yield of less than 2%). In order to screen more efficiently, our study aimed to determine risk factors for CP-CRE acquisition among patients exposed to a CP-CRE index patient.

We used a matched case-control design. The case group consisted of the 53 contacts who screened positive for CP-CRE. For each case we chose 2 controls: contacts who screened negative for CP-CRE. The basis for matching between the case and the 2 controls was that they were exposed to the same index patient. The benefit of matching this way was that it eliminated the question of whether a contact became positive because the index patient was more likely to transmit CP-CRE (e.g., because of diarrhea), and not because of characteristics of the contact patients themselves.

We found three factors that increased the risk that a contact would screen positive:

• Contact period of at least 3 days with the index case.

• Being on mechanical ventilation.

• Having a history of carriage or infection with another multidrug-resistant organism (such as methicillin-resistant Staphylococcus aureus).

Unexpectedly, sharing a room with the index patient or being debilitated did not significantly increase the risk of acquiring CP-CRE.

Many studies have identified antibiotic use as a risk factor for acquiring CP-CRE. In our study, no class of antibiotic increased the risk of CP-CRE acquisition, probably because only a small number of patients received each class. We were surprised to find that contacts who had taken cephalosporins were less likely to acquire CP-CRE. On further examination, when we compared patients who received only cephalosporins with patients who received no antibiotic, this protective effect disappeared. Nevertheless, compared with other antibiotics, it appears that cephalosporins might pose less of a risk for CP-CRE acquisition. More studies are needed to confirm our findings.

Our findings have practical implications for infection control. Using the risk factors we identified could help us to avoid excessive screening. We calculated that selective screening, based on our three risk factors, would have decreased the number of contacts screened by 30%, but 2 out of 53 positive contacts would have been missed. Institutions need to decide whether that is a trade-off they are willing to make.

Another way to apply our findings could be to add an additional layer of infection control by preemptively implementing contact precautions for patients at highest risk, for example, those with more than one risk factor.
 

1. Weiner LM, Fridkin SK, Aponte-Torres Z, Avery L, Coffin N, Dudeck MA, Edwards JR, Jernigan JA, Konnor R, Soe MM, Peterson K, Clifford McDonald L. Vital signs: preventing antibiotic-resistant infections in hospitals - United States, 2014. Am J Transplant. 2016 Jul;16(7):2224-30.

2. Centers for Disease Control and Prevention. Facility guidance for control of carbapenem-resistant Enterobacteriaceae (CRE): November 2015 update – CRE Toolkit.

3. Schwaber MJ, Carmeli Y. An ongoing national intervention to contain the spread of carbapenem-resistant enterobacteriaceae. Clin Infect Dis. 2014 Mar;58(5):697-703.

Schwartz-Neiderman A, Braun T, Fallach N, Schwartz D, Carmeli Y, Schechner V. Risk factors for carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) acquisition among contacts of newly diagnosed CP-CRE patients. Infect Control Hosp Epidemiol. 2016 Jul 25:1-7.
 

Vered Schechner, MD, MSc, is an infection control physician in the department of epidemiology at Tel Aviv Sourasky Medical Center.

Carbapenem-resistant Enterobacteriaceae (CRE) are extremely drug-resistant organisms. According to the Centers for Disease Control and Prevention’s National Healthcare Safety Network, in 2014 in the United States, 3.6% of Enterobacteriaceae causing hospital-acquired infections were resistant to carbapenems.¹ Antibiotic treatment options for CRE infections are severely limited, and mortality for invasive infections can be as high as 40%-50%.²

Resistance to carbapenems can be mediated by several mechanisms. From an epidemiologic standpoint, production of carbapenemases is the most-threatening mechanism because Enterobacteriaceae-harboring carbapenemases are highly transmissible.

Carbapenemase-producing CRE (CP-CRE) have caused large outbreaks throughout the world. Israel experienced a nationwide outbreak of CP-CRE, primarily Klebsiella pneumoniae carbapenemase–producing Klebsiella pneumoniae, in the mid-2000s. At the peak of the outbreak in 2007, there were 185 new cases per month (55.5/100,000 patient-days). A successful intervention at the national level dramatically decreased the incidence to 4.8/100,000 patient days in 2012.³

One component of the intervention (which is still ongoing) is active surveillance of high-risk groups using rectal swabs. Upon admission to the hospital, we screen patients who were recently in other hospitals or long-term care facilities. In addition, when a patient is newly diagnosed with CP-CRE (either asymptomatic carriage or clinical infection), we screen patients who had contact with that index case before isolation measures were implemented.

We recently published a study in Infection Control and Hospital Epidemiology that draws on our experience with CP-CRE screening of contacts at Tel Aviv Sourasky Medical Center.⁴ Both Israeli and International guidelines do not precisely define which contacts of a CP-CRE index case warrant screening. For example, should only roommates of index cases be screened or should we screen all patients on the same ward as the index case? Likewise, is there a minimum time of contact that should trigger screening?

Identifying which contacts are at high risk of acquiring CP-CRE is important for two reasons: We want to detect contacts who acquired CP-CRE so that they can be isolated before further transmission occurs, and we don’t want to waste resources and screen those at low risk. In our hospital, the criteria for being a contact are staying in the same ward and being treated by the same nursing staff as a newly identified CP-CRE patient.

This strategy appears to lead to overscreening, as we found that from October 2008 to June 2012, 3,158 screening tests were performed to detect 53 positive contacts (a yield of less than 2%). In order to screen more efficiently, our study aimed to determine risk factors for CP-CRE acquisition among patients exposed to a CP-CRE index patient.

We used a matched case-control design. The case group consisted of the 53 contacts who screened positive for CP-CRE. For each case we chose 2 controls: contacts who screened negative for CP-CRE. The basis for matching between the case and the 2 controls was that they were exposed to the same index patient. The benefit of matching this way was that it eliminated the question of whether a contact became positive because the index patient was more likely to transmit CP-CRE (e.g., because of diarrhea), and not because of characteristics of the contact patients themselves.

We found three factors that increased the risk that a contact would screen positive:

• Contact period of at least 3 days with the index case.

• Being on mechanical ventilation.

• Having a history of carriage or infection with another multidrug-resistant organism (such as methicillin-resistant Staphylococcus aureus).

Unexpectedly, sharing a room with the index patient or being debilitated did not significantly increase the risk of acquiring CP-CRE.

Many studies have identified antibiotic use as a risk factor for acquiring CP-CRE. In our study, no class of antibiotic increased the risk of CP-CRE acquisition, probably because only a small number of patients received each class. We were surprised to find that contacts who had taken cephalosporins were less likely to acquire CP-CRE. On further examination, when we compared patients who received only cephalosporins with patients who received no antibiotic, this protective effect disappeared. Nevertheless, compared with other antibiotics, it appears that cephalosporins might pose less of a risk for CP-CRE acquisition. More studies are needed to confirm our findings.

Our findings have practical implications for infection control. Using the risk factors we identified could help us to avoid excessive screening. We calculated that selective screening, based on our three risk factors, would have decreased the number of contacts screened by 30%, but 2 out of 53 positive contacts would have been missed. Institutions need to decide whether that is a trade-off they are willing to make.

Another way to apply our findings could be to add an additional layer of infection control by preemptively implementing contact precautions for patients at highest risk, for example, those with more than one risk factor.
 

1. Weiner LM, Fridkin SK, Aponte-Torres Z, Avery L, Coffin N, Dudeck MA, Edwards JR, Jernigan JA, Konnor R, Soe MM, Peterson K, Clifford McDonald L. Vital signs: preventing antibiotic-resistant infections in hospitals - United States, 2014. Am J Transplant. 2016 Jul;16(7):2224-30.

2. Centers for Disease Control and Prevention. Facility guidance for control of carbapenem-resistant Enterobacteriaceae (CRE): November 2015 update – CRE Toolkit.

3. Schwaber MJ, Carmeli Y. An ongoing national intervention to contain the spread of carbapenem-resistant enterobacteriaceae. Clin Infect Dis. 2014 Mar;58(5):697-703.

Schwartz-Neiderman A, Braun T, Fallach N, Schwartz D, Carmeli Y, Schechner V. Risk factors for carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) acquisition among contacts of newly diagnosed CP-CRE patients. Infect Control Hosp Epidemiol. 2016 Jul 25:1-7.
 

Vered Schechner, MD, MSc, is an infection control physician in the department of epidemiology at Tel Aviv Sourasky Medical Center.

Switching between generic versions of the same antiepileptic drug made by different manufacturers does not appear to change the risk of seizure-related events in patients with epilepsy, according to a population-based, case-crossover study of generic antiepileptic drug users.

Instead, the study indicates that delays and complications of the medication refilling process might increase a patient’s risk for a seizure, said first author Aaron Kesselheim, MD, and his associates from Brigham and Women’s Hospital and Harvard Medical School, Boston (Neurology. 2016 Sep 28. doi: 10.1212/WNL.0000000000003259).

The study was not supported by any specific targeted funding. The investigators reported receiving support from various foundations and from programs within Harvard University and grants from the Agency for Healthcare Research and Quality and the Food and Drug Administration; the investigators also disclosed acting in a research support role for and/or receiving financial compensation from several pharmaceutical companies and other organizations.

[email protected]

On Twitter @jessnicolecraig

Switching between generic versions of the same antiepileptic drug made by different manufacturers does not appear to change the risk of seizure-related events in patients with epilepsy, according to a population-based, case-crossover study of generic antiepileptic drug users.

Instead, the study indicates that delays and complications of the medication refilling process might increase a patient’s risk for a seizure, said first author Aaron Kesselheim, MD, and his associates from Brigham and Women’s Hospital and Harvard Medical School, Boston (Neurology. 2016 Sep 28. doi: 10.1212/WNL.0000000000003259).

The study was not supported by any specific targeted funding. The investigators reported receiving support from various foundations and from programs within Harvard University and grants from the Agency for Healthcare Research and Quality and the Food and Drug Administration; the investigators also disclosed acting in a research support role for and/or receiving financial compensation from several pharmaceutical companies and other organizations.

[email protected]

On Twitter @jessnicolecraig

Switching between generic versions of the same antiepileptic drug made by different manufacturers does not appear to change the risk of seizure-related events in patients with epilepsy, according to a population-based, case-crossover study of generic antiepileptic drug users.

Instead, the study indicates that delays and complications of the medication refilling process might increase a patient’s risk for a seizure, said first author Aaron Kesselheim, MD, and his associates from Brigham and Women’s Hospital and Harvard Medical School, Boston (Neurology. 2016 Sep 28. doi: 10.1212/WNL.0000000000003259).

The study was not supported by any specific targeted funding. The investigators reported receiving support from various foundations and from programs within Harvard University and grants from the Agency for Healthcare Research and Quality and the Food and Drug Administration; the investigators also disclosed acting in a research support role for and/or receiving financial compensation from several pharmaceutical companies and other organizations.

[email protected]

On Twitter @jessnicolecraig

Children with primary hypertension demonstrated significantly lower performance on neurocognitive testing, compared with children without primary hypertension, according to Marc B. Lande, MD, of the University of Rochester (N.Y.), and his associates.

kzenon/Thinkstock

In the study, 75 children with newly diagnosed untreated primary hypertension and 75 normotensive control subjects were examined. Hypertension was linked with worse performances on neurocognitive measures of attention, learning, memory, and fine motor dexterity, compared with the controls. There also was an association between increased disordered sleep and worse executive function. This was more pronounced in children with hypertension than in normotensive children. Hypertension and control groups did not differ significantly in age, sex, maternal education, income, race, ethnicity, obesity, anxiety, depression, cholesterol, glucose, insulin, and C-reactive protein.

“These results suggest that hypertension in youth may have an impact on brain function, and perhaps brain development, in childhood,” the researchers concluded. “Future results from this study will assess the degree to which these effects can be minimized or reversed with antihypertensive therapies.”

Find the full study in the Journal of Pediatrics (2016 Sept 29. doi: 10.1016/j.jpeds.2016.08.076).

[email protected]

Children with primary hypertension demonstrated significantly lower performance on neurocognitive testing, compared with children without primary hypertension, according to Marc B. Lande, MD, of the University of Rochester (N.Y.), and his associates.

kzenon/Thinkstock

In the study, 75 children with newly diagnosed untreated primary hypertension and 75 normotensive control subjects were examined. Hypertension was linked with worse performances on neurocognitive measures of attention, learning, memory, and fine motor dexterity, compared with the controls. There also was an association between increased disordered sleep and worse executive function. This was more pronounced in children with hypertension than in normotensive children. Hypertension and control groups did not differ significantly in age, sex, maternal education, income, race, ethnicity, obesity, anxiety, depression, cholesterol, glucose, insulin, and C-reactive protein.

“These results suggest that hypertension in youth may have an impact on brain function, and perhaps brain development, in childhood,” the researchers concluded. “Future results from this study will assess the degree to which these effects can be minimized or reversed with antihypertensive therapies.”

Find the full study in the Journal of Pediatrics (2016 Sept 29. doi: 10.1016/j.jpeds.2016.08.076).

[email protected]

Children with primary hypertension demonstrated significantly lower performance on neurocognitive testing, compared with children without primary hypertension, according to Marc B. Lande, MD, of the University of Rochester (N.Y.), and his associates.

kzenon/Thinkstock

In the study, 75 children with newly diagnosed untreated primary hypertension and 75 normotensive control subjects were examined. Hypertension was linked with worse performances on neurocognitive measures of attention, learning, memory, and fine motor dexterity, compared with the controls. There also was an association between increased disordered sleep and worse executive function. This was more pronounced in children with hypertension than in normotensive children. Hypertension and control groups did not differ significantly in age, sex, maternal education, income, race, ethnicity, obesity, anxiety, depression, cholesterol, glucose, insulin, and C-reactive protein.

“These results suggest that hypertension in youth may have an impact on brain function, and perhaps brain development, in childhood,” the researchers concluded. “Future results from this study will assess the degree to which these effects can be minimized or reversed with antihypertensive therapies.”

Find the full study in the Journal of Pediatrics (2016 Sept 29. doi: 10.1016/j.jpeds.2016.08.076).

[email protected]

A great volume of HIV and AIDS research enters the medical literature every month. It’s difficult to monitor everything, so here’s a quick look at some notable news items and journal articles published over the past few weeks.

Plasma lopinavir concentrations predicted viral outcomes in HIV-infected children receiving lopinavir-based antiretroviral therapy, a recent study demonstrated. Investigators said their findings support a minimum target concentration of greater than and equal to 1 mg/L of lopinavir to ensure sustained viral suppression.

©alexskopje/ThinkStock.com

[email protected]

On Twitter @richpizzi

A great volume of HIV and AIDS research enters the medical literature every month. It’s difficult to monitor everything, so here’s a quick look at some notable news items and journal articles published over the past few weeks.

Plasma lopinavir concentrations predicted viral outcomes in HIV-infected children receiving lopinavir-based antiretroviral therapy, a recent study demonstrated. Investigators said their findings support a minimum target concentration of greater than and equal to 1 mg/L of lopinavir to ensure sustained viral suppression.

©alexskopje/ThinkStock.com

[email protected]

On Twitter @richpizzi

A great volume of HIV and AIDS research enters the medical literature every month. It’s difficult to monitor everything, so here’s a quick look at some notable news items and journal articles published over the past few weeks.

Plasma lopinavir concentrations predicted viral outcomes in HIV-infected children receiving lopinavir-based antiretroviral therapy, a recent study demonstrated. Investigators said their findings support a minimum target concentration of greater than and equal to 1 mg/L of lopinavir to ensure sustained viral suppression.

©alexskopje/ThinkStock.com

[email protected]

On Twitter @richpizzi

WASHINGTON – The role of ostracism in overall poor health outcomes in service personnel is a growing concern, according to a panel of military experts.

“Think about the primary mechanism of suicide in kids who are bullied: It’s ostracism,” Kate McGraw, PhD, said in an interview at the American Psychiatric Association’s Institute on Psychiatric Services. Dr. McGraw is the interim director of the Deployment Health Clinical Center, a Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury.

Whitney McKnight/Frontline Medical News

[email protected]

On Twitter @whitneymcknight

WASHINGTON – The role of ostracism in overall poor health outcomes in service personnel is a growing concern, according to a panel of military experts.

“Think about the primary mechanism of suicide in kids who are bullied: It’s ostracism,” Kate McGraw, PhD, said in an interview at the American Psychiatric Association’s Institute on Psychiatric Services. Dr. McGraw is the interim director of the Deployment Health Clinical Center, a Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury.

Whitney McKnight/Frontline Medical News

[email protected]

On Twitter @whitneymcknight

WASHINGTON – The role of ostracism in overall poor health outcomes in service personnel is a growing concern, according to a panel of military experts.

“Think about the primary mechanism of suicide in kids who are bullied: It’s ostracism,” Kate McGraw, PhD, said in an interview at the American Psychiatric Association’s Institute on Psychiatric Services. Dr. McGraw is the interim director of the Deployment Health Clinical Center, a Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury.

Whitney McKnight/Frontline Medical News

[email protected]

On Twitter @whitneymcknight