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Ceftazidime-avibactam stands up to CRE, but resistance a problem
Intravenous ceftazidime-avibactam successfully treated 59% of carbapenem-resistant Enterobacteriaceae (CRE) infections, and 76% of patients remained alive at 30 days, according to a retrospective cohort study published in Clinical Infectious Diseases.
Those rates resemble previous reports of treatment with in vitro active agents, while the rate of acute kidney injury was about a third lower, said Ryan K. Shields, PharmD, of the University of Pittsburgh, and his associates. But 8% of CRE infections developed ceftazidime-avibactam resistance, which accounted for about a third of microbiological failures, the researchers said. “It is incumbent upon health care providers to share their clinical experiences with ceftazidime-avibactam and other new beta-lactamase inhibitors, so these agents can be used most effectively for the longest period of time,” they added.
Ceftazidime-avibactam (Avycaz) is a novel beta-lactam/beta-lactamase inhibitor combination approved by the Food and Drug Administration in 2015 for complicated intra-abdominal and urinary tract infections. It was hoped that the newly approved combination would prove safer and more effective than previously developed agents that showed in vitro activity against CRE, such as colistin, gentamicin, and tigecycline, the researchers noted.
They described CRE-infected patients treated with ceftazidime-avibactam (median, 14 days; range, 4-71 days) between April 2015 and February 2016. The average age of the patients was 64 years (range 26-78 years), and 57% were men. Infections included ventilator or health care–associated pneumonia, primary bacteremia, intra-abdominal infection, skin and soft tissue infections, pyelonephritis, mediastinitis, subdural empyema/ventriculitis, and purulent tracheobronchitis. All the CRE isolates were susceptible to ceftazidime-avibactam at baseline. In all, 70% of patients received ceftazidime-avibactam as monotherapy, while 30% received it in combination with intravenous or inhaled gentamicin, intravenous or intrathecal colistin, or tigecycline (Clin Infect Dis. 2016 Sep 13. doi: 10.1093/cid/ciw636).
A total of 28 (76%) patients were alive at 30 days and 62% were alive at 90 days, the investigators said. They calculated a 59% rate of clinical success, defined as absence of recurrence within 30 days of onset, resolution of signs and symptoms, and sterilization of site-specific cultures within 7 days of treatment. Combination therapy did not improve the chances of clinical success, they noted. Among the 15 clinical failures, 9 patients died, 4 developed recurrent CRE infections, and 2 did not clinically improve. Clinical success was less likely when patients needed continuous renal replacement therapy (17% vs. 68% for other patients; P = .03) or had higher Sequential Organ Failure Assessment (SOFA) scores (average, 5.2 in clinical successes vs. 8.8 in clinical failures; P = .047). In addition, 10% of patients developed acute kidney injury within 7 days of starting treatment, which was “considerably lower than the approximately 30% rate we previously reported with carbapenem-colistin or aminoglycoside-based combinations,” the investigators said.
The sample size was too small to definitively answer questions about whether combination regimens can overcome resistance, improve outcomes, or effectively treat specific types of CRE infection, the researchers noted. “Nevertheless, we can conclude that ceftazidime-avibactam offers an important advance in the treatment of CRE infections,” they wrote. “The development of resistance after as few as 10 days of therapy is troubling, and treatment failures and deaths in a significant minority of patients highlight the need for more agents with activity against CRE.”
The University of Pittsburgh Medical Center and the National Institutes of Health provided funding. One coauthor disclosed ties to Meiji, Shionogi, Tetraphase, Achaogen, Merck, and The Medicines Company. The other authors had no disclosures.
In the movie “Jaws,” after confidently setting out with an experienced shark hunter, upon catching his first glimpse of the predator, Chief Brody famously uttered, “We’re gonna need a bigger boat.” Similarly, we rejoiced at our triumph when ceftazidime-avibactam became available to treat our patients infected with [Klebsiella pneumoniae carbapenemase]-producing bacteria, and confidently set out to combat this killer. But like Chief Brody, we appear to have underestimated our foe; we too need a “bigger boat.”
We must not let the past repeat itself; hubris about the sudden availability of effective antibiotics has led to overconfidence and complacency among the medical and microbiological communities on several prior occasions in the last 80 years, with serious societal consequences. Shields and colleagues have provided us with a sobering reminder that there is no endpoint in our struggle against microbes. They will never stop adapting to what we conceive of to combat them, and in turn we must never stop conceiving of new ways to stay one step ahead.
Brad Spellberg, MD, is at Los Angeles County–USC Medical Center in Los Angeles. He disclosed ties to Cempra, The Medicines Company, MedImmune/AstraZeneca, PTC Therapeutics, Entasis, Tetraphase, Merck, Genentech, Dipexium, Motif, BioAIM, and Synthetic Biologics. He has received grants from AstraZeneca, Merck, Melinta, Steris, NIH, and Veterans Affairs Merit Review. These comments are from an editorial (Clin Infect Dis. 2016 Sept 13. doi: 10.1093/cid/ciw639).
In the movie “Jaws,” after confidently setting out with an experienced shark hunter, upon catching his first glimpse of the predator, Chief Brody famously uttered, “We’re gonna need a bigger boat.” Similarly, we rejoiced at our triumph when ceftazidime-avibactam became available to treat our patients infected with [Klebsiella pneumoniae carbapenemase]-producing bacteria, and confidently set out to combat this killer. But like Chief Brody, we appear to have underestimated our foe; we too need a “bigger boat.”
We must not let the past repeat itself; hubris about the sudden availability of effective antibiotics has led to overconfidence and complacency among the medical and microbiological communities on several prior occasions in the last 80 years, with serious societal consequences. Shields and colleagues have provided us with a sobering reminder that there is no endpoint in our struggle against microbes. They will never stop adapting to what we conceive of to combat them, and in turn we must never stop conceiving of new ways to stay one step ahead.
Brad Spellberg, MD, is at Los Angeles County–USC Medical Center in Los Angeles. He disclosed ties to Cempra, The Medicines Company, MedImmune/AstraZeneca, PTC Therapeutics, Entasis, Tetraphase, Merck, Genentech, Dipexium, Motif, BioAIM, and Synthetic Biologics. He has received grants from AstraZeneca, Merck, Melinta, Steris, NIH, and Veterans Affairs Merit Review. These comments are from an editorial (Clin Infect Dis. 2016 Sept 13. doi: 10.1093/cid/ciw639).
In the movie “Jaws,” after confidently setting out with an experienced shark hunter, upon catching his first glimpse of the predator, Chief Brody famously uttered, “We’re gonna need a bigger boat.” Similarly, we rejoiced at our triumph when ceftazidime-avibactam became available to treat our patients infected with [Klebsiella pneumoniae carbapenemase]-producing bacteria, and confidently set out to combat this killer. But like Chief Brody, we appear to have underestimated our foe; we too need a “bigger boat.”
We must not let the past repeat itself; hubris about the sudden availability of effective antibiotics has led to overconfidence and complacency among the medical and microbiological communities on several prior occasions in the last 80 years, with serious societal consequences. Shields and colleagues have provided us with a sobering reminder that there is no endpoint in our struggle against microbes. They will never stop adapting to what we conceive of to combat them, and in turn we must never stop conceiving of new ways to stay one step ahead.
Brad Spellberg, MD, is at Los Angeles County–USC Medical Center in Los Angeles. He disclosed ties to Cempra, The Medicines Company, MedImmune/AstraZeneca, PTC Therapeutics, Entasis, Tetraphase, Merck, Genentech, Dipexium, Motif, BioAIM, and Synthetic Biologics. He has received grants from AstraZeneca, Merck, Melinta, Steris, NIH, and Veterans Affairs Merit Review. These comments are from an editorial (Clin Infect Dis. 2016 Sept 13. doi: 10.1093/cid/ciw639).
Intravenous ceftazidime-avibactam successfully treated 59% of carbapenem-resistant Enterobacteriaceae (CRE) infections, and 76% of patients remained alive at 30 days, according to a retrospective cohort study published in Clinical Infectious Diseases.
Those rates resemble previous reports of treatment with in vitro active agents, while the rate of acute kidney injury was about a third lower, said Ryan K. Shields, PharmD, of the University of Pittsburgh, and his associates. But 8% of CRE infections developed ceftazidime-avibactam resistance, which accounted for about a third of microbiological failures, the researchers said. “It is incumbent upon health care providers to share their clinical experiences with ceftazidime-avibactam and other new beta-lactamase inhibitors, so these agents can be used most effectively for the longest period of time,” they added.
Ceftazidime-avibactam (Avycaz) is a novel beta-lactam/beta-lactamase inhibitor combination approved by the Food and Drug Administration in 2015 for complicated intra-abdominal and urinary tract infections. It was hoped that the newly approved combination would prove safer and more effective than previously developed agents that showed in vitro activity against CRE, such as colistin, gentamicin, and tigecycline, the researchers noted.
They described CRE-infected patients treated with ceftazidime-avibactam (median, 14 days; range, 4-71 days) between April 2015 and February 2016. The average age of the patients was 64 years (range 26-78 years), and 57% were men. Infections included ventilator or health care–associated pneumonia, primary bacteremia, intra-abdominal infection, skin and soft tissue infections, pyelonephritis, mediastinitis, subdural empyema/ventriculitis, and purulent tracheobronchitis. All the CRE isolates were susceptible to ceftazidime-avibactam at baseline. In all, 70% of patients received ceftazidime-avibactam as monotherapy, while 30% received it in combination with intravenous or inhaled gentamicin, intravenous or intrathecal colistin, or tigecycline (Clin Infect Dis. 2016 Sep 13. doi: 10.1093/cid/ciw636).
A total of 28 (76%) patients were alive at 30 days and 62% were alive at 90 days, the investigators said. They calculated a 59% rate of clinical success, defined as absence of recurrence within 30 days of onset, resolution of signs and symptoms, and sterilization of site-specific cultures within 7 days of treatment. Combination therapy did not improve the chances of clinical success, they noted. Among the 15 clinical failures, 9 patients died, 4 developed recurrent CRE infections, and 2 did not clinically improve. Clinical success was less likely when patients needed continuous renal replacement therapy (17% vs. 68% for other patients; P = .03) or had higher Sequential Organ Failure Assessment (SOFA) scores (average, 5.2 in clinical successes vs. 8.8 in clinical failures; P = .047). In addition, 10% of patients developed acute kidney injury within 7 days of starting treatment, which was “considerably lower than the approximately 30% rate we previously reported with carbapenem-colistin or aminoglycoside-based combinations,” the investigators said.
The sample size was too small to definitively answer questions about whether combination regimens can overcome resistance, improve outcomes, or effectively treat specific types of CRE infection, the researchers noted. “Nevertheless, we can conclude that ceftazidime-avibactam offers an important advance in the treatment of CRE infections,” they wrote. “The development of resistance after as few as 10 days of therapy is troubling, and treatment failures and deaths in a significant minority of patients highlight the need for more agents with activity against CRE.”
The University of Pittsburgh Medical Center and the National Institutes of Health provided funding. One coauthor disclosed ties to Meiji, Shionogi, Tetraphase, Achaogen, Merck, and The Medicines Company. The other authors had no disclosures.
Intravenous ceftazidime-avibactam successfully treated 59% of carbapenem-resistant Enterobacteriaceae (CRE) infections, and 76% of patients remained alive at 30 days, according to a retrospective cohort study published in Clinical Infectious Diseases.
Those rates resemble previous reports of treatment with in vitro active agents, while the rate of acute kidney injury was about a third lower, said Ryan K. Shields, PharmD, of the University of Pittsburgh, and his associates. But 8% of CRE infections developed ceftazidime-avibactam resistance, which accounted for about a third of microbiological failures, the researchers said. “It is incumbent upon health care providers to share their clinical experiences with ceftazidime-avibactam and other new beta-lactamase inhibitors, so these agents can be used most effectively for the longest period of time,” they added.
Ceftazidime-avibactam (Avycaz) is a novel beta-lactam/beta-lactamase inhibitor combination approved by the Food and Drug Administration in 2015 for complicated intra-abdominal and urinary tract infections. It was hoped that the newly approved combination would prove safer and more effective than previously developed agents that showed in vitro activity against CRE, such as colistin, gentamicin, and tigecycline, the researchers noted.
They described CRE-infected patients treated with ceftazidime-avibactam (median, 14 days; range, 4-71 days) between April 2015 and February 2016. The average age of the patients was 64 years (range 26-78 years), and 57% were men. Infections included ventilator or health care–associated pneumonia, primary bacteremia, intra-abdominal infection, skin and soft tissue infections, pyelonephritis, mediastinitis, subdural empyema/ventriculitis, and purulent tracheobronchitis. All the CRE isolates were susceptible to ceftazidime-avibactam at baseline. In all, 70% of patients received ceftazidime-avibactam as monotherapy, while 30% received it in combination with intravenous or inhaled gentamicin, intravenous or intrathecal colistin, or tigecycline (Clin Infect Dis. 2016 Sep 13. doi: 10.1093/cid/ciw636).
A total of 28 (76%) patients were alive at 30 days and 62% were alive at 90 days, the investigators said. They calculated a 59% rate of clinical success, defined as absence of recurrence within 30 days of onset, resolution of signs and symptoms, and sterilization of site-specific cultures within 7 days of treatment. Combination therapy did not improve the chances of clinical success, they noted. Among the 15 clinical failures, 9 patients died, 4 developed recurrent CRE infections, and 2 did not clinically improve. Clinical success was less likely when patients needed continuous renal replacement therapy (17% vs. 68% for other patients; P = .03) or had higher Sequential Organ Failure Assessment (SOFA) scores (average, 5.2 in clinical successes vs. 8.8 in clinical failures; P = .047). In addition, 10% of patients developed acute kidney injury within 7 days of starting treatment, which was “considerably lower than the approximately 30% rate we previously reported with carbapenem-colistin or aminoglycoside-based combinations,” the investigators said.
The sample size was too small to definitively answer questions about whether combination regimens can overcome resistance, improve outcomes, or effectively treat specific types of CRE infection, the researchers noted. “Nevertheless, we can conclude that ceftazidime-avibactam offers an important advance in the treatment of CRE infections,” they wrote. “The development of resistance after as few as 10 days of therapy is troubling, and treatment failures and deaths in a significant minority of patients highlight the need for more agents with activity against CRE.”
The University of Pittsburgh Medical Center and the National Institutes of Health provided funding. One coauthor disclosed ties to Meiji, Shionogi, Tetraphase, Achaogen, Merck, and The Medicines Company. The other authors had no disclosures.
FROM CLINICAL INFECTIOUS DISEASES
Key clinical point: Ceftazidime-avibactam effectively treated carbapenem-resistant Enterobacteriaceae (CRE) infections, but resistance emerged rapidly and in some cases led to microbiological failure.
Major finding: The rate of clinical success was 59%; 10% of patients developed acute kidney injury within 7 days of starting treatment; 8% developed resistance.
Data source: A single-center retrospective study of 37 patients with carbapenem-resistant Enterobacteriaceae infections treated with ceftazidime-avibactam.
Disclosures: The University of Pittsburgh Medical Center and the National Institutes of Health provided funding. A coauthor disclosed ties to Meiji, Shionogi, Tetraphase, Achaogen, Merck, and The Medicines Company. The other authors had no disclosures.
Targeted HCV patients improve on sofosbuvir/daclatasvir combination
A combination of sofosbuvir/daclatasvir yielded sustained virological responses at 12 weeks after the last treatment in 95% of hepatitis C virus–infected patients with genotype 1.
“Real-life results of the sofosbuvir + ribavirin or sofosbuvir + simeprevir combination have been extensively reported, but there are few data regarding the sofosbuvir + daclatasvir combination in genotype 1–infected patients,” wrote Stanislas Pol, MD, of Hôpital Cochin, Institut Pasteur, Paris, and his colleagues.
To assess the effectiveness of the combination, researchers reviewed data from 768 patients with HCV genotype 1 who began treatments of 400 mg/day sofosbuvir and 60 mg/day daclatasvir prior to Oct. 1, 2014 (J Hepatol. 2016. doi: 10.1016/j.jhep.2016.08.021). Patients were treated for 12 or 24 weeks, and the primary endpoint was sustained virological response 12 weeks after the last treatment (SVR12).
A total of 92% of patients treated for 12 weeks and 99% of patients treated for 24 weeks with the combination met the primary endpoint of SVR12, for an average of 95% overall. Treatment duration and the presence or absence of ribavirin had no significant impact on the treatment responses in noncirrhotic patients. However, the SVR12 rate was significantly higher among cirrhotic patients in the 24-week treatment group than in the 12-week group (95% vs. 88%).
One patient died from cerebral hemorrhage 6 weeks after beginning treatment, and the death was considered possibly related to the combination treatment; two deaths from septic shock and two deaths from end-stage liver disease were not considered treatment related. Other serious adverse events were reported in 10% of patients independent of treatment duration or use of ribavirin. The six serious adverse events possibly related to treatment included three cardiac disorders. The most common adverse events included insomnia, headache, and asthenia, reported in at least 10% of patients.
Only decompensated cirrhosis and a prothrombin time greater than 70% were independently associated with serious adverse events.
The study was limited by several factors, including its observational nature and relatively low number of patients treated with ribavirin in the 12-week group, the researchers noted. However, the results suggest that “in real life, the sofosbuvir + daclatasvir combination in difficult-to-treat patients with HCV genotype 1 infection was associated with a high rate of SVR12,” they said.
Inserm-ANRS supported the study. The researchers disclosed funding from government organizations and pharmaceutical companies including MSD, Janssen, Gilead, AbbVie, BMS, and Roche.
A combination of sofosbuvir/daclatasvir yielded sustained virological responses at 12 weeks after the last treatment in 95% of hepatitis C virus–infected patients with genotype 1.
“Real-life results of the sofosbuvir + ribavirin or sofosbuvir + simeprevir combination have been extensively reported, but there are few data regarding the sofosbuvir + daclatasvir combination in genotype 1–infected patients,” wrote Stanislas Pol, MD, of Hôpital Cochin, Institut Pasteur, Paris, and his colleagues.
To assess the effectiveness of the combination, researchers reviewed data from 768 patients with HCV genotype 1 who began treatments of 400 mg/day sofosbuvir and 60 mg/day daclatasvir prior to Oct. 1, 2014 (J Hepatol. 2016. doi: 10.1016/j.jhep.2016.08.021). Patients were treated for 12 or 24 weeks, and the primary endpoint was sustained virological response 12 weeks after the last treatment (SVR12).
A total of 92% of patients treated for 12 weeks and 99% of patients treated for 24 weeks with the combination met the primary endpoint of SVR12, for an average of 95% overall. Treatment duration and the presence or absence of ribavirin had no significant impact on the treatment responses in noncirrhotic patients. However, the SVR12 rate was significantly higher among cirrhotic patients in the 24-week treatment group than in the 12-week group (95% vs. 88%).
One patient died from cerebral hemorrhage 6 weeks after beginning treatment, and the death was considered possibly related to the combination treatment; two deaths from septic shock and two deaths from end-stage liver disease were not considered treatment related. Other serious adverse events were reported in 10% of patients independent of treatment duration or use of ribavirin. The six serious adverse events possibly related to treatment included three cardiac disorders. The most common adverse events included insomnia, headache, and asthenia, reported in at least 10% of patients.
Only decompensated cirrhosis and a prothrombin time greater than 70% were independently associated with serious adverse events.
The study was limited by several factors, including its observational nature and relatively low number of patients treated with ribavirin in the 12-week group, the researchers noted. However, the results suggest that “in real life, the sofosbuvir + daclatasvir combination in difficult-to-treat patients with HCV genotype 1 infection was associated with a high rate of SVR12,” they said.
Inserm-ANRS supported the study. The researchers disclosed funding from government organizations and pharmaceutical companies including MSD, Janssen, Gilead, AbbVie, BMS, and Roche.
A combination of sofosbuvir/daclatasvir yielded sustained virological responses at 12 weeks after the last treatment in 95% of hepatitis C virus–infected patients with genotype 1.
“Real-life results of the sofosbuvir + ribavirin or sofosbuvir + simeprevir combination have been extensively reported, but there are few data regarding the sofosbuvir + daclatasvir combination in genotype 1–infected patients,” wrote Stanislas Pol, MD, of Hôpital Cochin, Institut Pasteur, Paris, and his colleagues.
To assess the effectiveness of the combination, researchers reviewed data from 768 patients with HCV genotype 1 who began treatments of 400 mg/day sofosbuvir and 60 mg/day daclatasvir prior to Oct. 1, 2014 (J Hepatol. 2016. doi: 10.1016/j.jhep.2016.08.021). Patients were treated for 12 or 24 weeks, and the primary endpoint was sustained virological response 12 weeks after the last treatment (SVR12).
A total of 92% of patients treated for 12 weeks and 99% of patients treated for 24 weeks with the combination met the primary endpoint of SVR12, for an average of 95% overall. Treatment duration and the presence or absence of ribavirin had no significant impact on the treatment responses in noncirrhotic patients. However, the SVR12 rate was significantly higher among cirrhotic patients in the 24-week treatment group than in the 12-week group (95% vs. 88%).
One patient died from cerebral hemorrhage 6 weeks after beginning treatment, and the death was considered possibly related to the combination treatment; two deaths from septic shock and two deaths from end-stage liver disease were not considered treatment related. Other serious adverse events were reported in 10% of patients independent of treatment duration or use of ribavirin. The six serious adverse events possibly related to treatment included three cardiac disorders. The most common adverse events included insomnia, headache, and asthenia, reported in at least 10% of patients.
Only decompensated cirrhosis and a prothrombin time greater than 70% were independently associated with serious adverse events.
The study was limited by several factors, including its observational nature and relatively low number of patients treated with ribavirin in the 12-week group, the researchers noted. However, the results suggest that “in real life, the sofosbuvir + daclatasvir combination in difficult-to-treat patients with HCV genotype 1 infection was associated with a high rate of SVR12,” they said.
Inserm-ANRS supported the study. The researchers disclosed funding from government organizations and pharmaceutical companies including MSD, Janssen, Gilead, AbbVie, BMS, and Roche.
FROM THE JOURNAL OF HEPATOLOGY
Key clinical point: A sofosbuvir/daclatasvir combination was effective in most patients with HCV genotype 1, independent of an addition of ribavirin.
Major finding: Sustained virological response at 12 weeks after the last treatment occurred in 95% of patients treated with a combination of sofosbuvir and daclatasvir.
Data source: A selection of 768 patients with a HCV genotype 1 who were part of a ongoing multicenter, observational cohort study.
Disclosures: Inserm-ANRS supported the study. The researchers disclosed funding from government organizations and pharmaceutical companies including MSD, Janssen, Gilead, AbbVie, BMS, and Roche.
Hot flashes and sleep disruption contribute independently to depression in menopause
Hot flashes and sleep disruption contribute independently to the development of depression in menopause, judging from the findings of a recent study.
In that study, 29 premenopausal women, aged 18-45 years, received a single dose of the GnRH agonist leuprolide in order to induce hypoestrogenism and ovarian suppression for the study period. The women in the study had no history of primary sleep disturbances, low estrogen levels, or depression, according to Hadine Joffe, MD, director of the Women’s Hormone and Aging Research Program at Harvard Medical School, in Boston, and her associates.
All the study participants underwent baseline mood evaluation using both the Montgomery-Asberg Depression Rating Scale (MADRS) and the Beck Depression Inventory (BDI). Existing sleep disturbances were ruled out at baseline with sleep diaries, questionnaires, and two ambulatory screening polysomnography (PSG) studies.
After 4 weeks of administration of leuprolide, depressive symptoms had developed among most of the women in the study. The mean MADRS score was 4.1, and overall, it was 3.1 points higher than it had been at baseline. One woman had a 15-point increase in her score, suggesting significant depression. The MADRS score increased by at least 5 points in 24% of the women and remained unchanged in 38%, reflecting variability among the women on the impact of leuprolide on depressive symptoms, the investigators reported (J Clin Endocrinol Metab. 2016 Sep 20. doi: 10.1210/jc.2016-2348).
Leuprolide universally suppressed estradiol to postmenopausal levels in the women within 2 weeks. Hot flashes developed in 20 (69%) women, with a median of 3.6 hot flashes during the day and 3.8 at night. The median number of objectively measured nighttime hot flashes per night was 3.
Changes to sleep patterns varied widely for each woman; for example, wake time after sleep onset ranged from an additional 140 minutes to 23 fewer minutes for one woman. There was a correlation between the number of subjectively reported nighttime hot flashes with increased sleep fragmentation as measured by PSG. The number of reported nighttime hot flashes was associated with an increase in depressive symptoms that was disproportionate to the number of nighttime hot flashes reported, according to the findings of a univariate analysis. The number of daytime hot flashes had no such effect.
In light of these findings, Dr. Joffe and her associates urged clinicians to screen women who report nighttime hot flashes and sleep interruption for mood disturbance. “Treatment of those with menopause-related depressive symptoms should encompass therapies that improve sleep interruption as well as nocturnal [hot flashes],” they wrote.
The study was sponsored by the National Institute of Mental Health. Dr. Joffe has received grant support from Merck and has served as a consultant/adviser for Merck, Mitsubishi Tanabe, NeRRe Therapeutics, and Noven.
Hot flashes and sleep disruption contribute independently to the development of depression in menopause, judging from the findings of a recent study.
In that study, 29 premenopausal women, aged 18-45 years, received a single dose of the GnRH agonist leuprolide in order to induce hypoestrogenism and ovarian suppression for the study period. The women in the study had no history of primary sleep disturbances, low estrogen levels, or depression, according to Hadine Joffe, MD, director of the Women’s Hormone and Aging Research Program at Harvard Medical School, in Boston, and her associates.
All the study participants underwent baseline mood evaluation using both the Montgomery-Asberg Depression Rating Scale (MADRS) and the Beck Depression Inventory (BDI). Existing sleep disturbances were ruled out at baseline with sleep diaries, questionnaires, and two ambulatory screening polysomnography (PSG) studies.
After 4 weeks of administration of leuprolide, depressive symptoms had developed among most of the women in the study. The mean MADRS score was 4.1, and overall, it was 3.1 points higher than it had been at baseline. One woman had a 15-point increase in her score, suggesting significant depression. The MADRS score increased by at least 5 points in 24% of the women and remained unchanged in 38%, reflecting variability among the women on the impact of leuprolide on depressive symptoms, the investigators reported (J Clin Endocrinol Metab. 2016 Sep 20. doi: 10.1210/jc.2016-2348).
Leuprolide universally suppressed estradiol to postmenopausal levels in the women within 2 weeks. Hot flashes developed in 20 (69%) women, with a median of 3.6 hot flashes during the day and 3.8 at night. The median number of objectively measured nighttime hot flashes per night was 3.
Changes to sleep patterns varied widely for each woman; for example, wake time after sleep onset ranged from an additional 140 minutes to 23 fewer minutes for one woman. There was a correlation between the number of subjectively reported nighttime hot flashes with increased sleep fragmentation as measured by PSG. The number of reported nighttime hot flashes was associated with an increase in depressive symptoms that was disproportionate to the number of nighttime hot flashes reported, according to the findings of a univariate analysis. The number of daytime hot flashes had no such effect.
In light of these findings, Dr. Joffe and her associates urged clinicians to screen women who report nighttime hot flashes and sleep interruption for mood disturbance. “Treatment of those with menopause-related depressive symptoms should encompass therapies that improve sleep interruption as well as nocturnal [hot flashes],” they wrote.
The study was sponsored by the National Institute of Mental Health. Dr. Joffe has received grant support from Merck and has served as a consultant/adviser for Merck, Mitsubishi Tanabe, NeRRe Therapeutics, and Noven.
Hot flashes and sleep disruption contribute independently to the development of depression in menopause, judging from the findings of a recent study.
In that study, 29 premenopausal women, aged 18-45 years, received a single dose of the GnRH agonist leuprolide in order to induce hypoestrogenism and ovarian suppression for the study period. The women in the study had no history of primary sleep disturbances, low estrogen levels, or depression, according to Hadine Joffe, MD, director of the Women’s Hormone and Aging Research Program at Harvard Medical School, in Boston, and her associates.
All the study participants underwent baseline mood evaluation using both the Montgomery-Asberg Depression Rating Scale (MADRS) and the Beck Depression Inventory (BDI). Existing sleep disturbances were ruled out at baseline with sleep diaries, questionnaires, and two ambulatory screening polysomnography (PSG) studies.
After 4 weeks of administration of leuprolide, depressive symptoms had developed among most of the women in the study. The mean MADRS score was 4.1, and overall, it was 3.1 points higher than it had been at baseline. One woman had a 15-point increase in her score, suggesting significant depression. The MADRS score increased by at least 5 points in 24% of the women and remained unchanged in 38%, reflecting variability among the women on the impact of leuprolide on depressive symptoms, the investigators reported (J Clin Endocrinol Metab. 2016 Sep 20. doi: 10.1210/jc.2016-2348).
Leuprolide universally suppressed estradiol to postmenopausal levels in the women within 2 weeks. Hot flashes developed in 20 (69%) women, with a median of 3.6 hot flashes during the day and 3.8 at night. The median number of objectively measured nighttime hot flashes per night was 3.
Changes to sleep patterns varied widely for each woman; for example, wake time after sleep onset ranged from an additional 140 minutes to 23 fewer minutes for one woman. There was a correlation between the number of subjectively reported nighttime hot flashes with increased sleep fragmentation as measured by PSG. The number of reported nighttime hot flashes was associated with an increase in depressive symptoms that was disproportionate to the number of nighttime hot flashes reported, according to the findings of a univariate analysis. The number of daytime hot flashes had no such effect.
In light of these findings, Dr. Joffe and her associates urged clinicians to screen women who report nighttime hot flashes and sleep interruption for mood disturbance. “Treatment of those with menopause-related depressive symptoms should encompass therapies that improve sleep interruption as well as nocturnal [hot flashes],” they wrote.
The study was sponsored by the National Institute of Mental Health. Dr. Joffe has received grant support from Merck and has served as a consultant/adviser for Merck, Mitsubishi Tanabe, NeRRe Therapeutics, and Noven.
FROM THE JOURNAL OF ENDOCRINOLOGY & METABOLISM
Key clinical point: Hot flashes and sleep disruption contribute independently to the development of depression in menopause.
Major finding: Depression scores increased by 3 points on the MADRS after 4 weeks on GnRH agonist leuprolide. Sleep disruption was also common among the women in the study. Depression developed among many, but not all the women, with univariate analysis showing that hot flashes and sleep disruption contributed independently to their mood changes.
Data source: A prospective study in which 29 young women without depression were subjected to rapid, premature, and reversible menopause with one open-label dose of leuprolide in an experimental model.
Disclosures: The study was sponsored by the National Institute of Mental Health. Dr. Hadine Joffe has received grant support from Merck and has served as a consultant/adviser for Merck, Mitsubishi Tanabe, NeRRe Therapeutics, and Noven.
Congress sends Zika funding bill to President
In a move that narrowly avoids a government shutdown, Congress has passed a long-awaited bill that keeps the government afloat and provides $1.1 billion in funding to combat the Zika virus.
The House cleared H.R. 5325 late Sept. 28 by a 342-85 tally, following a 72-26 vote by the Senate earlier in the day. The final package, which keeps the government operating through Dec. 9, also includes $37 million for opioid addiction and $500 million for flooding in Louisiana. The White House has indicated that President Obama will sign the bill into law.
The American Congress of Obstetricians and Gynecologists praised Congress for passing the long-delayed comprehensive Zika funding package.
“Congress has finally treated Zika like the emergency it is and shown the American people that it is capable of rising above partisanship for the health of its citizens,” Thomas Gellhaus, MD, ACOG president, said in a statement. “ACOG stands with peer organizations and government agencies in the fight to prevent and respond to the Zika virus and support the care and treatment of all people affected by it. ... The fight against the spread of Zika cannot be won without the resources to support responsive and proactive solutions. This comprehensive funding package is essential to our success and the health of women and babies.”
The bill’s passage caps months of fiery debate within Congress over what to include in the measure. The bill stalled earlier this week largely over whether to direct funds to Flint, Mich., to deal with the crisis over lead-tainted water. Leaders agreed to provide aid to Flint residents in a separate water projects bill. Legislators will address final approval of the Flint measure in December.
Of the $1.1 billion included in the final package to fight Zika, $15 million would go to Florida and $60 million to the territory of Puerto Rico to respond to Zika outbreaks in those areas. The remainder of the funding would be used to prevent, prepare for, and respond to Zika; health conditions related to such virus; and other vector-borne diseases, domestically and internationally.
If signed by the President, the money would also go toward developing necessary countermeasures and vaccines, including the development and purchase of vaccines, therapeutics, diagnostics, and necessary medical supplies. Additionally, the funding would aid research on the virology, natural history, and pathogenesis of the Zika virus infection and preclinical and clinical development of vaccines and other medical countermeasures for the Zika virus.
The American Medical Association expressed relief that Congress had finally taken action to provide resources for fighting Zika.
“It has been clear over the past several months that the U.S. has needed additional resources to combat the Zika virus,” AMA president Andrew W. Gurman, MD, said in a statement. “With the threat of the virus continuing to loom, this funding will help protect more people – particularly pregnant women and their children – from the virus’s lasting negative health effects.”
On Twitter @legal_med
In a move that narrowly avoids a government shutdown, Congress has passed a long-awaited bill that keeps the government afloat and provides $1.1 billion in funding to combat the Zika virus.
The House cleared H.R. 5325 late Sept. 28 by a 342-85 tally, following a 72-26 vote by the Senate earlier in the day. The final package, which keeps the government operating through Dec. 9, also includes $37 million for opioid addiction and $500 million for flooding in Louisiana. The White House has indicated that President Obama will sign the bill into law.
The American Congress of Obstetricians and Gynecologists praised Congress for passing the long-delayed comprehensive Zika funding package.
“Congress has finally treated Zika like the emergency it is and shown the American people that it is capable of rising above partisanship for the health of its citizens,” Thomas Gellhaus, MD, ACOG president, said in a statement. “ACOG stands with peer organizations and government agencies in the fight to prevent and respond to the Zika virus and support the care and treatment of all people affected by it. ... The fight against the spread of Zika cannot be won without the resources to support responsive and proactive solutions. This comprehensive funding package is essential to our success and the health of women and babies.”
The bill’s passage caps months of fiery debate within Congress over what to include in the measure. The bill stalled earlier this week largely over whether to direct funds to Flint, Mich., to deal with the crisis over lead-tainted water. Leaders agreed to provide aid to Flint residents in a separate water projects bill. Legislators will address final approval of the Flint measure in December.
Of the $1.1 billion included in the final package to fight Zika, $15 million would go to Florida and $60 million to the territory of Puerto Rico to respond to Zika outbreaks in those areas. The remainder of the funding would be used to prevent, prepare for, and respond to Zika; health conditions related to such virus; and other vector-borne diseases, domestically and internationally.
If signed by the President, the money would also go toward developing necessary countermeasures and vaccines, including the development and purchase of vaccines, therapeutics, diagnostics, and necessary medical supplies. Additionally, the funding would aid research on the virology, natural history, and pathogenesis of the Zika virus infection and preclinical and clinical development of vaccines and other medical countermeasures for the Zika virus.
The American Medical Association expressed relief that Congress had finally taken action to provide resources for fighting Zika.
“It has been clear over the past several months that the U.S. has needed additional resources to combat the Zika virus,” AMA president Andrew W. Gurman, MD, said in a statement. “With the threat of the virus continuing to loom, this funding will help protect more people – particularly pregnant women and their children – from the virus’s lasting negative health effects.”
On Twitter @legal_med
In a move that narrowly avoids a government shutdown, Congress has passed a long-awaited bill that keeps the government afloat and provides $1.1 billion in funding to combat the Zika virus.
The House cleared H.R. 5325 late Sept. 28 by a 342-85 tally, following a 72-26 vote by the Senate earlier in the day. The final package, which keeps the government operating through Dec. 9, also includes $37 million for opioid addiction and $500 million for flooding in Louisiana. The White House has indicated that President Obama will sign the bill into law.
The American Congress of Obstetricians and Gynecologists praised Congress for passing the long-delayed comprehensive Zika funding package.
“Congress has finally treated Zika like the emergency it is and shown the American people that it is capable of rising above partisanship for the health of its citizens,” Thomas Gellhaus, MD, ACOG president, said in a statement. “ACOG stands with peer organizations and government agencies in the fight to prevent and respond to the Zika virus and support the care and treatment of all people affected by it. ... The fight against the spread of Zika cannot be won without the resources to support responsive and proactive solutions. This comprehensive funding package is essential to our success and the health of women and babies.”
The bill’s passage caps months of fiery debate within Congress over what to include in the measure. The bill stalled earlier this week largely over whether to direct funds to Flint, Mich., to deal with the crisis over lead-tainted water. Leaders agreed to provide aid to Flint residents in a separate water projects bill. Legislators will address final approval of the Flint measure in December.
Of the $1.1 billion included in the final package to fight Zika, $15 million would go to Florida and $60 million to the territory of Puerto Rico to respond to Zika outbreaks in those areas. The remainder of the funding would be used to prevent, prepare for, and respond to Zika; health conditions related to such virus; and other vector-borne diseases, domestically and internationally.
If signed by the President, the money would also go toward developing necessary countermeasures and vaccines, including the development and purchase of vaccines, therapeutics, diagnostics, and necessary medical supplies. Additionally, the funding would aid research on the virology, natural history, and pathogenesis of the Zika virus infection and preclinical and clinical development of vaccines and other medical countermeasures for the Zika virus.
The American Medical Association expressed relief that Congress had finally taken action to provide resources for fighting Zika.
“It has been clear over the past several months that the U.S. has needed additional resources to combat the Zika virus,” AMA president Andrew W. Gurman, MD, said in a statement. “With the threat of the virus continuing to loom, this funding will help protect more people – particularly pregnant women and their children – from the virus’s lasting negative health effects.”
On Twitter @legal_med
AATS Mitral Conclave Call for Abstracts & Videos
AATS welcomes you to submit your abstracts and videos to the 2017 Mitral Conclave.
AATS Mitral Conclave
April 27-28, 2017
New York, NY
Submission Deadline:
Sunday, January 8, 2017 @ 11.59 pm EST
Share:
AATS welcomes you to submit your abstracts and videos to the 2017 Mitral Conclave.
AATS Mitral Conclave
April 27-28, 2017
New York, NY
Submission Deadline:
Sunday, January 8, 2017 @ 11.59 pm EST
Share:
AATS welcomes you to submit your abstracts and videos to the 2017 Mitral Conclave.
AATS Mitral Conclave
April 27-28, 2017
New York, NY
Submission Deadline:
Sunday, January 8, 2017 @ 11.59 pm EST
Share:
The choice in November could not be more important
Editor’s note: For the last five presidential elections, this news organization has offered the Republican and Democrat presidential candidate the opportunity to present their ideas directly to U.S. physicians via side-by-side Guest Editorials. The candidates – or their proxies – have used these pages to reach out to you, our readers, with their views on medicine, health care, and other issues. We have taken pride in the ability to offer you a balanced view in the weeks leading up to the general election. This year, we cannot provide you with that balanced view. Despite repeated efforts via every medium at our disposal – telephone calls, emails, Twitter, LinkedIn, and more – the Donald J. Trump for President organization has not responded to our request for a contribution. Here we present the contribution from Secretary Hillary Clinton’s proxy.
Guest Editorial
As physicians, we have the unique privilege of serving patients, often at their most vulnerable moments. We also bear witness to how our health care system works – and too often, where it falls short – through our patients’ eyes.
That view could change dramatically depending on the outcome of this year’s presidential election. Hillary Clinton has a long track record of expanding affordable health care, and wants to accelerate the march toward universal access to high-quality care. Her opponent, Donald Trump, wants to roll back the progress we’ve made, with a plan that takes health insurance away from more than 20 million Americans.
Secretary Clinton’s career demonstrates her commitment to the ideal of health care as a human right. For example, she was instrumental in the bipartisan effort to pass the Children’s Health Insurance Program. Despite recent gains in health coverage, too many Americans still struggle to access the care they need – where and when they need it. Secretary Clinton’s plan for health care would expand access to care by building on the Affordable Care Act – with more relief for high premiums and out-of-pocket costs, particularly for prescription drugs; by working with states to expand Medicaid and give people the choice of a “public option” health plan. She also worked with Sen. Bernie Sanders (I-Vt.) on a plan to double funding for community health centers and substantially expand our commitment to the National Health Service Corps – so that millions more Americans have access to primary care, especially in rural and medically underserved urban areas, and so that we can offer more loan repayment and scholarships to early-career physicians.
Anyone taking care of patients today knows that improving access to care is only the first step. We must improve the way we deliver care, refocusing around the patient-doctor relationship. Too often there are barriers – regulations, paperwork, or insurance restrictions – to taking care of patients in the way that they deserve. Secretary Clinton wants to ensure an advanced and coordinated health care system that supports patient-doctor relationships instead of getting in the way. She wants to spur delivery system reform to reward value and quality. She was one of the first elected officials to call for modernizing health information technology, reaching across the aisle to work with physician and then-Sen. Bill Frist (R-Tenn.). And she’s offered plans to address major contemporary challenges, such as preventing and better treating Alzheimer’s disease, destigmatizing mental illness, and improving care for substance use disorders.
In addition to improving our health care system, Secretary Clinton believes we must take a number of proactive steps so that all Americans – regardless of location, income, or history – have the opportunity to live full, healthy lives. She believes we must invest in our public health infrastructure to ensure preparedness for emerging threats like Zika at home and abroad; to prevent illness and injury in communities; and to promote health equity. Of course, some of the most important determinants of well-being lie outside the walls of our clinics and hospitals. Secretary Clinton also will move us forward on these fundamental issues, such as women’s rights, criminal justice reform, and climate change.
Meanwhile, Donald Trump offers a very different vision for health care in the United States. His proposals would repeal the Affordable Care Act, instantly stripping millions of people of lifesaving health insurance. He would cut Medicaid through block grants, leaving millions of the poorest Americans without a safety net. And he would once again allow insurers to discriminate, based on preexisting conditions.
The choice in November could not be more important, for our patients and for the practice of medicine. Secretary Clinton’s long track record of fighting for universal, high-quality, affordable health care speaks for itself. With so much more left to do to improve health in our country, she brings the thoughtful leadership and steely determination needed to get the job done.
Dr. Chokshi practices internal medicine at Bellevue Hospital in New York and is a health policy adviser to Hillary for America.
Editor’s note: For the last five presidential elections, this news organization has offered the Republican and Democrat presidential candidate the opportunity to present their ideas directly to U.S. physicians via side-by-side Guest Editorials. The candidates – or their proxies – have used these pages to reach out to you, our readers, with their views on medicine, health care, and other issues. We have taken pride in the ability to offer you a balanced view in the weeks leading up to the general election. This year, we cannot provide you with that balanced view. Despite repeated efforts via every medium at our disposal – telephone calls, emails, Twitter, LinkedIn, and more – the Donald J. Trump for President organization has not responded to our request for a contribution. Here we present the contribution from Secretary Hillary Clinton’s proxy.
Guest Editorial
As physicians, we have the unique privilege of serving patients, often at their most vulnerable moments. We also bear witness to how our health care system works – and too often, where it falls short – through our patients’ eyes.
That view could change dramatically depending on the outcome of this year’s presidential election. Hillary Clinton has a long track record of expanding affordable health care, and wants to accelerate the march toward universal access to high-quality care. Her opponent, Donald Trump, wants to roll back the progress we’ve made, with a plan that takes health insurance away from more than 20 million Americans.
Secretary Clinton’s career demonstrates her commitment to the ideal of health care as a human right. For example, she was instrumental in the bipartisan effort to pass the Children’s Health Insurance Program. Despite recent gains in health coverage, too many Americans still struggle to access the care they need – where and when they need it. Secretary Clinton’s plan for health care would expand access to care by building on the Affordable Care Act – with more relief for high premiums and out-of-pocket costs, particularly for prescription drugs; by working with states to expand Medicaid and give people the choice of a “public option” health plan. She also worked with Sen. Bernie Sanders (I-Vt.) on a plan to double funding for community health centers and substantially expand our commitment to the National Health Service Corps – so that millions more Americans have access to primary care, especially in rural and medically underserved urban areas, and so that we can offer more loan repayment and scholarships to early-career physicians.
Anyone taking care of patients today knows that improving access to care is only the first step. We must improve the way we deliver care, refocusing around the patient-doctor relationship. Too often there are barriers – regulations, paperwork, or insurance restrictions – to taking care of patients in the way that they deserve. Secretary Clinton wants to ensure an advanced and coordinated health care system that supports patient-doctor relationships instead of getting in the way. She wants to spur delivery system reform to reward value and quality. She was one of the first elected officials to call for modernizing health information technology, reaching across the aisle to work with physician and then-Sen. Bill Frist (R-Tenn.). And she’s offered plans to address major contemporary challenges, such as preventing and better treating Alzheimer’s disease, destigmatizing mental illness, and improving care for substance use disorders.
In addition to improving our health care system, Secretary Clinton believes we must take a number of proactive steps so that all Americans – regardless of location, income, or history – have the opportunity to live full, healthy lives. She believes we must invest in our public health infrastructure to ensure preparedness for emerging threats like Zika at home and abroad; to prevent illness and injury in communities; and to promote health equity. Of course, some of the most important determinants of well-being lie outside the walls of our clinics and hospitals. Secretary Clinton also will move us forward on these fundamental issues, such as women’s rights, criminal justice reform, and climate change.
Meanwhile, Donald Trump offers a very different vision for health care in the United States. His proposals would repeal the Affordable Care Act, instantly stripping millions of people of lifesaving health insurance. He would cut Medicaid through block grants, leaving millions of the poorest Americans without a safety net. And he would once again allow insurers to discriminate, based on preexisting conditions.
The choice in November could not be more important, for our patients and for the practice of medicine. Secretary Clinton’s long track record of fighting for universal, high-quality, affordable health care speaks for itself. With so much more left to do to improve health in our country, she brings the thoughtful leadership and steely determination needed to get the job done.
Dr. Chokshi practices internal medicine at Bellevue Hospital in New York and is a health policy adviser to Hillary for America.
Editor’s note: For the last five presidential elections, this news organization has offered the Republican and Democrat presidential candidate the opportunity to present their ideas directly to U.S. physicians via side-by-side Guest Editorials. The candidates – or their proxies – have used these pages to reach out to you, our readers, with their views on medicine, health care, and other issues. We have taken pride in the ability to offer you a balanced view in the weeks leading up to the general election. This year, we cannot provide you with that balanced view. Despite repeated efforts via every medium at our disposal – telephone calls, emails, Twitter, LinkedIn, and more – the Donald J. Trump for President organization has not responded to our request for a contribution. Here we present the contribution from Secretary Hillary Clinton’s proxy.
Guest Editorial
As physicians, we have the unique privilege of serving patients, often at their most vulnerable moments. We also bear witness to how our health care system works – and too often, where it falls short – through our patients’ eyes.
That view could change dramatically depending on the outcome of this year’s presidential election. Hillary Clinton has a long track record of expanding affordable health care, and wants to accelerate the march toward universal access to high-quality care. Her opponent, Donald Trump, wants to roll back the progress we’ve made, with a plan that takes health insurance away from more than 20 million Americans.
Secretary Clinton’s career demonstrates her commitment to the ideal of health care as a human right. For example, she was instrumental in the bipartisan effort to pass the Children’s Health Insurance Program. Despite recent gains in health coverage, too many Americans still struggle to access the care they need – where and when they need it. Secretary Clinton’s plan for health care would expand access to care by building on the Affordable Care Act – with more relief for high premiums and out-of-pocket costs, particularly for prescription drugs; by working with states to expand Medicaid and give people the choice of a “public option” health plan. She also worked with Sen. Bernie Sanders (I-Vt.) on a plan to double funding for community health centers and substantially expand our commitment to the National Health Service Corps – so that millions more Americans have access to primary care, especially in rural and medically underserved urban areas, and so that we can offer more loan repayment and scholarships to early-career physicians.
Anyone taking care of patients today knows that improving access to care is only the first step. We must improve the way we deliver care, refocusing around the patient-doctor relationship. Too often there are barriers – regulations, paperwork, or insurance restrictions – to taking care of patients in the way that they deserve. Secretary Clinton wants to ensure an advanced and coordinated health care system that supports patient-doctor relationships instead of getting in the way. She wants to spur delivery system reform to reward value and quality. She was one of the first elected officials to call for modernizing health information technology, reaching across the aisle to work with physician and then-Sen. Bill Frist (R-Tenn.). And she’s offered plans to address major contemporary challenges, such as preventing and better treating Alzheimer’s disease, destigmatizing mental illness, and improving care for substance use disorders.
In addition to improving our health care system, Secretary Clinton believes we must take a number of proactive steps so that all Americans – regardless of location, income, or history – have the opportunity to live full, healthy lives. She believes we must invest in our public health infrastructure to ensure preparedness for emerging threats like Zika at home and abroad; to prevent illness and injury in communities; and to promote health equity. Of course, some of the most important determinants of well-being lie outside the walls of our clinics and hospitals. Secretary Clinton also will move us forward on these fundamental issues, such as women’s rights, criminal justice reform, and climate change.
Meanwhile, Donald Trump offers a very different vision for health care in the United States. His proposals would repeal the Affordable Care Act, instantly stripping millions of people of lifesaving health insurance. He would cut Medicaid through block grants, leaving millions of the poorest Americans without a safety net. And he would once again allow insurers to discriminate, based on preexisting conditions.
The choice in November could not be more important, for our patients and for the practice of medicine. Secretary Clinton’s long track record of fighting for universal, high-quality, affordable health care speaks for itself. With so much more left to do to improve health in our country, she brings the thoughtful leadership and steely determination needed to get the job done.
Dr. Chokshi practices internal medicine at Bellevue Hospital in New York and is a health policy adviser to Hillary for America.
Applications Open for AATS Leadership Academy
Current and future CT surgery division chiefs/department chairs are invited to apply for the AATS Leadership Academy Program.
Friday, April 28, 2017
AATS Centennial
Boston, MA
This intensive, didactic and interactive program brings together up to 20 international surgeons who have demonstrated significant promise as potential future division chiefs or have recent assumed that role. The program provides participants with administrative, interpersonal, mentoring and negotiating skills, as well as the opportunity to network with well-known thoracic surgeon leaders and potential mentors.
Deadline: November 30, 2016
Current and future CT surgery division chiefs/department chairs are invited to apply for the AATS Leadership Academy Program.
Friday, April 28, 2017
AATS Centennial
Boston, MA
This intensive, didactic and interactive program brings together up to 20 international surgeons who have demonstrated significant promise as potential future division chiefs or have recent assumed that role. The program provides participants with administrative, interpersonal, mentoring and negotiating skills, as well as the opportunity to network with well-known thoracic surgeon leaders and potential mentors.
Deadline: November 30, 2016
Current and future CT surgery division chiefs/department chairs are invited to apply for the AATS Leadership Academy Program.
Friday, April 28, 2017
AATS Centennial
Boston, MA
This intensive, didactic and interactive program brings together up to 20 international surgeons who have demonstrated significant promise as potential future division chiefs or have recent assumed that role. The program provides participants with administrative, interpersonal, mentoring and negotiating skills, as well as the opportunity to network with well-known thoracic surgeon leaders and potential mentors.
Deadline: November 30, 2016
Nonsexual secondary Zika virus case confirmed in Utah
The first case of nonsexual secondary Zika virus transmission has occurred in the United States, according to a research letter published by the New England Journal of Medicine.
“We report a rapidly progressive, fatal [Zika virus] infection acquired outside the United States and secondary local transmission in the absence of known risk factors,” wrote the authors of the report, led by Sankar Swaminathan, MD, of the University of Utah in Salt Lake City.
The individual infected via secondary transmission, dubbed Patient Two in the report, is suspected to have contracted the disease from Patient One, a 73-year-old man who visited the southwestern coast of Mexico – a known hotbed of Zika virus – for a 3-week trip before returning to the United States. Eight days after returning, Patient One was admitted to a Salt Lake City hospital with symptoms consistent with a flavivirus infection and told doctors that he had been bitten by mosquitoes during his trip (N Engl J Med. 2016 Sep 28. doi: 10.1056/NEJMc1610613).
After undergoing tourniquet and laboratory testing, a diagnosis of dengue shock syndrome was made, but Patient One’s condition continued to deteriorate rapidly. Patient One died 4 days after initial hospitalization; real-time PCR assay confirmed Zika virus infection shortly thereafter.
Patient Two came into contact with Patient One during the latter’s hospitalization, reporting that he “assisted a nurse in repositioning Patient One in bed without using gloves,” according to the report. Patient Two began experiencing conjunctivitis, fever, myalgia, and a maculopapular rash on his face 5 days after Patient One died. The rash resolved itself after 7 days, and while PCR analysis of Patient Two’s serum was negative for Zika, his urinalysis was positive.
Because Patient Two had not traveled to a Zika-endemic area within 9 months of experiencing Zika-like symptoms and had not engaged in sexual intercourse with anyone who traveled to a Zika-endemic area, the authors conclude that he contracted the disease from contact with Patient One. The authors posit that, given the high levels of viremia in Patient One, the Zika virus could have been transmitted to Patient Two via sweat or tears, which Patient Two came into contact with while not wearing gloves. Local transmission via Aedis aegypti mosquito bite was highly unlikely to be the cause of transmission because of the lack of such mosquitoes in the Salt Lake City area.
“These two cases illustrate several important points,” the authors concluded. “The spectrum of those at risk for fulminant [Zika virus] infection may be broader than previously recognized, and those who are not severely immunocompromised or chronically ill may nevertheless be at risk for fatal infection.”
The first case of nonsexual secondary Zika virus transmission has occurred in the United States, according to a research letter published by the New England Journal of Medicine.
“We report a rapidly progressive, fatal [Zika virus] infection acquired outside the United States and secondary local transmission in the absence of known risk factors,” wrote the authors of the report, led by Sankar Swaminathan, MD, of the University of Utah in Salt Lake City.
The individual infected via secondary transmission, dubbed Patient Two in the report, is suspected to have contracted the disease from Patient One, a 73-year-old man who visited the southwestern coast of Mexico – a known hotbed of Zika virus – for a 3-week trip before returning to the United States. Eight days after returning, Patient One was admitted to a Salt Lake City hospital with symptoms consistent with a flavivirus infection and told doctors that he had been bitten by mosquitoes during his trip (N Engl J Med. 2016 Sep 28. doi: 10.1056/NEJMc1610613).
After undergoing tourniquet and laboratory testing, a diagnosis of dengue shock syndrome was made, but Patient One’s condition continued to deteriorate rapidly. Patient One died 4 days after initial hospitalization; real-time PCR assay confirmed Zika virus infection shortly thereafter.
Patient Two came into contact with Patient One during the latter’s hospitalization, reporting that he “assisted a nurse in repositioning Patient One in bed without using gloves,” according to the report. Patient Two began experiencing conjunctivitis, fever, myalgia, and a maculopapular rash on his face 5 days after Patient One died. The rash resolved itself after 7 days, and while PCR analysis of Patient Two’s serum was negative for Zika, his urinalysis was positive.
Because Patient Two had not traveled to a Zika-endemic area within 9 months of experiencing Zika-like symptoms and had not engaged in sexual intercourse with anyone who traveled to a Zika-endemic area, the authors conclude that he contracted the disease from contact with Patient One. The authors posit that, given the high levels of viremia in Patient One, the Zika virus could have been transmitted to Patient Two via sweat or tears, which Patient Two came into contact with while not wearing gloves. Local transmission via Aedis aegypti mosquito bite was highly unlikely to be the cause of transmission because of the lack of such mosquitoes in the Salt Lake City area.
“These two cases illustrate several important points,” the authors concluded. “The spectrum of those at risk for fulminant [Zika virus] infection may be broader than previously recognized, and those who are not severely immunocompromised or chronically ill may nevertheless be at risk for fatal infection.”
The first case of nonsexual secondary Zika virus transmission has occurred in the United States, according to a research letter published by the New England Journal of Medicine.
“We report a rapidly progressive, fatal [Zika virus] infection acquired outside the United States and secondary local transmission in the absence of known risk factors,” wrote the authors of the report, led by Sankar Swaminathan, MD, of the University of Utah in Salt Lake City.
The individual infected via secondary transmission, dubbed Patient Two in the report, is suspected to have contracted the disease from Patient One, a 73-year-old man who visited the southwestern coast of Mexico – a known hotbed of Zika virus – for a 3-week trip before returning to the United States. Eight days after returning, Patient One was admitted to a Salt Lake City hospital with symptoms consistent with a flavivirus infection and told doctors that he had been bitten by mosquitoes during his trip (N Engl J Med. 2016 Sep 28. doi: 10.1056/NEJMc1610613).
After undergoing tourniquet and laboratory testing, a diagnosis of dengue shock syndrome was made, but Patient One’s condition continued to deteriorate rapidly. Patient One died 4 days after initial hospitalization; real-time PCR assay confirmed Zika virus infection shortly thereafter.
Patient Two came into contact with Patient One during the latter’s hospitalization, reporting that he “assisted a nurse in repositioning Patient One in bed without using gloves,” according to the report. Patient Two began experiencing conjunctivitis, fever, myalgia, and a maculopapular rash on his face 5 days after Patient One died. The rash resolved itself after 7 days, and while PCR analysis of Patient Two’s serum was negative for Zika, his urinalysis was positive.
Because Patient Two had not traveled to a Zika-endemic area within 9 months of experiencing Zika-like symptoms and had not engaged in sexual intercourse with anyone who traveled to a Zika-endemic area, the authors conclude that he contracted the disease from contact with Patient One. The authors posit that, given the high levels of viremia in Patient One, the Zika virus could have been transmitted to Patient Two via sweat or tears, which Patient Two came into contact with while not wearing gloves. Local transmission via Aedis aegypti mosquito bite was highly unlikely to be the cause of transmission because of the lack of such mosquitoes in the Salt Lake City area.
“These two cases illustrate several important points,” the authors concluded. “The spectrum of those at risk for fulminant [Zika virus] infection may be broader than previously recognized, and those who are not severely immunocompromised or chronically ill may nevertheless be at risk for fatal infection.”
FROM NEW ENGLAND JOURNAL OF MEDICINE
Rise in HPV vaccination spurs CIN drop
As human papillomavirus vaccination rates climbed in New Mexico, all grades of cervical intraepithelial neoplasia declined in females aged 15-19 years, and grade 2 neoplasia fell among those who were aged 20-24 years, according to an analysis published online Sept. 29 in JAMA Oncology.
In the 15- to 19-year-old group, the annual incidence of cervical intraepithelial neoplasia (CIN) 1 dropped from 3,468 cases per 100,000 individuals screened in 2007 to 1,591 in 2014, an annual percentage change (APC) of –9.0.
CIN2 cases fell from 896 to 415 (APC, –10.5), and CIN3 from 240 to 0 (APC, –41.3). Among women aged 20-24 years, CIN2 annual incidence fell from 1,028 to 627 cases per 100,000 women screened (APC, –6.3).
The reductions were greater than expected, given that only 40% of females aged 13-17 years had received all three doses in 2014, up from 17% in 2008. It’s likely that herd immunity, benefit from even partial vaccination, and cross-protection against HPV strains not in vaccines contributed to the success, reported Vicki B. Benard, PhD, of the Centers for Disease Control and Prevention, and her colleagues (JAMA Oncol. 2016 Sept. 29. doi: 10.1001/jamaoncol.2016.3609).
The investigators adjusted their findings to account for trends towards longer intervals between cervical screenings and later initiation of screening. Otherwise, the effect of the vaccine would have been overestimated.
The ultimate goal “is a rational integration of HPV vaccination and cervical screening,” they wrote. Current cervical cancer screening guidelines do not differentiate between women who have been vaccinated and those who have not, but this should be reevaluated in light of the study findings, the researchers noted.
“Our data demonstrate that clinical outcomes of CIN will be reduced among cohorts [even] partially vaccinated for HPV,” which will reduce the cost-effectiveness of screening. “A later starting age for cervical screening among partially vaccinated populations of young women ... may be prudent given the already infrequent incidence of invasive cervical cancer for women younger than 25 years” even before the HPV vaccine was introduced in 2007, the investigators wrote.
The study focuses on data from New Mexico because it is the only state that has captured population-based estimates of both screening prevalence and CIN since the introduction of the vaccine.
The National Institute of Allergy and Infectious Diseases funded the work. Dr. Benard reported having no financial disclosures, but other investigators reported ties with HPV vaccine makers Merck and GSK, among other companies.
As human papillomavirus vaccination rates climbed in New Mexico, all grades of cervical intraepithelial neoplasia declined in females aged 15-19 years, and grade 2 neoplasia fell among those who were aged 20-24 years, according to an analysis published online Sept. 29 in JAMA Oncology.
In the 15- to 19-year-old group, the annual incidence of cervical intraepithelial neoplasia (CIN) 1 dropped from 3,468 cases per 100,000 individuals screened in 2007 to 1,591 in 2014, an annual percentage change (APC) of –9.0.
CIN2 cases fell from 896 to 415 (APC, –10.5), and CIN3 from 240 to 0 (APC, –41.3). Among women aged 20-24 years, CIN2 annual incidence fell from 1,028 to 627 cases per 100,000 women screened (APC, –6.3).
The reductions were greater than expected, given that only 40% of females aged 13-17 years had received all three doses in 2014, up from 17% in 2008. It’s likely that herd immunity, benefit from even partial vaccination, and cross-protection against HPV strains not in vaccines contributed to the success, reported Vicki B. Benard, PhD, of the Centers for Disease Control and Prevention, and her colleagues (JAMA Oncol. 2016 Sept. 29. doi: 10.1001/jamaoncol.2016.3609).
The investigators adjusted their findings to account for trends towards longer intervals between cervical screenings and later initiation of screening. Otherwise, the effect of the vaccine would have been overestimated.
The ultimate goal “is a rational integration of HPV vaccination and cervical screening,” they wrote. Current cervical cancer screening guidelines do not differentiate between women who have been vaccinated and those who have not, but this should be reevaluated in light of the study findings, the researchers noted.
“Our data demonstrate that clinical outcomes of CIN will be reduced among cohorts [even] partially vaccinated for HPV,” which will reduce the cost-effectiveness of screening. “A later starting age for cervical screening among partially vaccinated populations of young women ... may be prudent given the already infrequent incidence of invasive cervical cancer for women younger than 25 years” even before the HPV vaccine was introduced in 2007, the investigators wrote.
The study focuses on data from New Mexico because it is the only state that has captured population-based estimates of both screening prevalence and CIN since the introduction of the vaccine.
The National Institute of Allergy and Infectious Diseases funded the work. Dr. Benard reported having no financial disclosures, but other investigators reported ties with HPV vaccine makers Merck and GSK, among other companies.
As human papillomavirus vaccination rates climbed in New Mexico, all grades of cervical intraepithelial neoplasia declined in females aged 15-19 years, and grade 2 neoplasia fell among those who were aged 20-24 years, according to an analysis published online Sept. 29 in JAMA Oncology.
In the 15- to 19-year-old group, the annual incidence of cervical intraepithelial neoplasia (CIN) 1 dropped from 3,468 cases per 100,000 individuals screened in 2007 to 1,591 in 2014, an annual percentage change (APC) of –9.0.
CIN2 cases fell from 896 to 415 (APC, –10.5), and CIN3 from 240 to 0 (APC, –41.3). Among women aged 20-24 years, CIN2 annual incidence fell from 1,028 to 627 cases per 100,000 women screened (APC, –6.3).
The reductions were greater than expected, given that only 40% of females aged 13-17 years had received all three doses in 2014, up from 17% in 2008. It’s likely that herd immunity, benefit from even partial vaccination, and cross-protection against HPV strains not in vaccines contributed to the success, reported Vicki B. Benard, PhD, of the Centers for Disease Control and Prevention, and her colleagues (JAMA Oncol. 2016 Sept. 29. doi: 10.1001/jamaoncol.2016.3609).
The investigators adjusted their findings to account for trends towards longer intervals between cervical screenings and later initiation of screening. Otherwise, the effect of the vaccine would have been overestimated.
The ultimate goal “is a rational integration of HPV vaccination and cervical screening,” they wrote. Current cervical cancer screening guidelines do not differentiate between women who have been vaccinated and those who have not, but this should be reevaluated in light of the study findings, the researchers noted.
“Our data demonstrate that clinical outcomes of CIN will be reduced among cohorts [even] partially vaccinated for HPV,” which will reduce the cost-effectiveness of screening. “A later starting age for cervical screening among partially vaccinated populations of young women ... may be prudent given the already infrequent incidence of invasive cervical cancer for women younger than 25 years” even before the HPV vaccine was introduced in 2007, the investigators wrote.
The study focuses on data from New Mexico because it is the only state that has captured population-based estimates of both screening prevalence and CIN since the introduction of the vaccine.
The National Institute of Allergy and Infectious Diseases funded the work. Dr. Benard reported having no financial disclosures, but other investigators reported ties with HPV vaccine makers Merck and GSK, among other companies.
FROM JAMA ONCOLOGY
Key clinical point: Future cervical cancer screening guidelines may need to differentiate between those who have been vaccinated against HPV and those who have not.
Major finding: As HPV vaccination rates increased in New Mexico, the annual incidence of CIN1 among 15- to 19-year-old females dropped from 3,468 cases per 100,000 individuals screened in 2007 to 1,591 in 2014, an annual percentage change of –9.0.
Data source: An analysis of the New Mexico HPV Pap Registry of 2007-2014.
Disclosures: The National Institute of Allergy and Infectious Diseases funded the work. The lead investigator had no financial disclosures, but others reported ties with HPV vaccine makers Merck and GSK, among other companies.
A different Thanksgiving
Thanksgiving is at least one time when families sit down and focus on the meal. While the turkey may be the centerpiece, at least in our family we are presented with a variety of vegetables, salads, baked goods, and desserts. Some of the dishes remain on the traditional menu because “Aunt Martha always brings her molded salad,” although if the truth be known, she had fallen out of love with making it years ago. Other selections survive as memorials to long-departed family members: “Remember how much Grampy Stevens loved that pickled watermelon rind” that no one has touched since he died 10 years ago?
And although Thanksgiving may be all about the food, it’s really about sitting down together and celebrating each other over a meal. It should really be a happy meal but not one that comes in a box with a plastic toy. But for the parents of a picky eater, Thanksgiving is often destined to be another stressful dining experience. They know that despite the bountiful spread of food, there isn’t going to be anything on the table their child is going to eat.
They can cope with the situation in one of two ways. They can bring something they know he will eat, such as a can of corn or a microwaveable macaroni and cheese so he won’t “starve.” Or they can cast a pall on the festivities by attempting to badger, coax, and coerce him to eat something, as they do every night at home.
Parents may be assisted in their efforts by other family members who will bring something from the picky eater’s “might eat list.” Or, more likely, they will join in a chorus of old favorites such as “Don’t you want to grow up to be big and strong?” Or “You won’t be able to have any of Grandma’s cookies if you don’t eat some dinner.”
Either approach will be another step toward solidifying the child’s reputation in the family as a picky eater. Rachel is the cousin who plays the piano, and everyone knows that Brandon is going to be a great soccer player. Bobby is the one who won’t eat anything but mac and cheese.
A few years ago I had the thought that instead of allowing Thanksgiving to become an event that highlights and perpetuates the picky eater’s unfortunate habits, why not use the holiday as an opportunity to turn the page and begin a more sensible approach to selective eating?
So for some parents of picky eaters, I have begun to recommend the following: Tell everyone who will be coming to Thanksgiving that the pediatrician says everyone should agree that the event will be all about having a good time and not about who eats or doesn’t eat what’s on the table. And there will be no discussion about the picky eater’s habits – positive or negative.
It might be nice to include on the menu a dish or dessert that the picky eater has eaten in the past. But this is done without ceremony, comment, or preconditions such as “You have to eat some of this to get that.” This silent gesture of kindness also may reassure nervous grandparents who are worried that the child will starve if he doesn’t eat anything for a day despite your reassurance to them that the pediatrician said it was okay.
While I admit that one Thanksgiving with these new rules is unlikely to convert a 6-year-old picky eater into a voracious omnivore, it can be a first step toward helping a family adopt a sensible approach to the child’s eating habits. At least it won’t make things worse and is likely to turn unhappy meals at home into mini feasts that celebrate togetherness.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”
Thanksgiving is at least one time when families sit down and focus on the meal. While the turkey may be the centerpiece, at least in our family we are presented with a variety of vegetables, salads, baked goods, and desserts. Some of the dishes remain on the traditional menu because “Aunt Martha always brings her molded salad,” although if the truth be known, she had fallen out of love with making it years ago. Other selections survive as memorials to long-departed family members: “Remember how much Grampy Stevens loved that pickled watermelon rind” that no one has touched since he died 10 years ago?
And although Thanksgiving may be all about the food, it’s really about sitting down together and celebrating each other over a meal. It should really be a happy meal but not one that comes in a box with a plastic toy. But for the parents of a picky eater, Thanksgiving is often destined to be another stressful dining experience. They know that despite the bountiful spread of food, there isn’t going to be anything on the table their child is going to eat.
They can cope with the situation in one of two ways. They can bring something they know he will eat, such as a can of corn or a microwaveable macaroni and cheese so he won’t “starve.” Or they can cast a pall on the festivities by attempting to badger, coax, and coerce him to eat something, as they do every night at home.
Parents may be assisted in their efforts by other family members who will bring something from the picky eater’s “might eat list.” Or, more likely, they will join in a chorus of old favorites such as “Don’t you want to grow up to be big and strong?” Or “You won’t be able to have any of Grandma’s cookies if you don’t eat some dinner.”
Either approach will be another step toward solidifying the child’s reputation in the family as a picky eater. Rachel is the cousin who plays the piano, and everyone knows that Brandon is going to be a great soccer player. Bobby is the one who won’t eat anything but mac and cheese.
A few years ago I had the thought that instead of allowing Thanksgiving to become an event that highlights and perpetuates the picky eater’s unfortunate habits, why not use the holiday as an opportunity to turn the page and begin a more sensible approach to selective eating?
So for some parents of picky eaters, I have begun to recommend the following: Tell everyone who will be coming to Thanksgiving that the pediatrician says everyone should agree that the event will be all about having a good time and not about who eats or doesn’t eat what’s on the table. And there will be no discussion about the picky eater’s habits – positive or negative.
It might be nice to include on the menu a dish or dessert that the picky eater has eaten in the past. But this is done without ceremony, comment, or preconditions such as “You have to eat some of this to get that.” This silent gesture of kindness also may reassure nervous grandparents who are worried that the child will starve if he doesn’t eat anything for a day despite your reassurance to them that the pediatrician said it was okay.
While I admit that one Thanksgiving with these new rules is unlikely to convert a 6-year-old picky eater into a voracious omnivore, it can be a first step toward helping a family adopt a sensible approach to the child’s eating habits. At least it won’t make things worse and is likely to turn unhappy meals at home into mini feasts that celebrate togetherness.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”
Thanksgiving is at least one time when families sit down and focus on the meal. While the turkey may be the centerpiece, at least in our family we are presented with a variety of vegetables, salads, baked goods, and desserts. Some of the dishes remain on the traditional menu because “Aunt Martha always brings her molded salad,” although if the truth be known, she had fallen out of love with making it years ago. Other selections survive as memorials to long-departed family members: “Remember how much Grampy Stevens loved that pickled watermelon rind” that no one has touched since he died 10 years ago?
And although Thanksgiving may be all about the food, it’s really about sitting down together and celebrating each other over a meal. It should really be a happy meal but not one that comes in a box with a plastic toy. But for the parents of a picky eater, Thanksgiving is often destined to be another stressful dining experience. They know that despite the bountiful spread of food, there isn’t going to be anything on the table their child is going to eat.
They can cope with the situation in one of two ways. They can bring something they know he will eat, such as a can of corn or a microwaveable macaroni and cheese so he won’t “starve.” Or they can cast a pall on the festivities by attempting to badger, coax, and coerce him to eat something, as they do every night at home.
Parents may be assisted in their efforts by other family members who will bring something from the picky eater’s “might eat list.” Or, more likely, they will join in a chorus of old favorites such as “Don’t you want to grow up to be big and strong?” Or “You won’t be able to have any of Grandma’s cookies if you don’t eat some dinner.”
Either approach will be another step toward solidifying the child’s reputation in the family as a picky eater. Rachel is the cousin who plays the piano, and everyone knows that Brandon is going to be a great soccer player. Bobby is the one who won’t eat anything but mac and cheese.
A few years ago I had the thought that instead of allowing Thanksgiving to become an event that highlights and perpetuates the picky eater’s unfortunate habits, why not use the holiday as an opportunity to turn the page and begin a more sensible approach to selective eating?
So for some parents of picky eaters, I have begun to recommend the following: Tell everyone who will be coming to Thanksgiving that the pediatrician says everyone should agree that the event will be all about having a good time and not about who eats or doesn’t eat what’s on the table. And there will be no discussion about the picky eater’s habits – positive or negative.
It might be nice to include on the menu a dish or dessert that the picky eater has eaten in the past. But this is done without ceremony, comment, or preconditions such as “You have to eat some of this to get that.” This silent gesture of kindness also may reassure nervous grandparents who are worried that the child will starve if he doesn’t eat anything for a day despite your reassurance to them that the pediatrician said it was okay.
While I admit that one Thanksgiving with these new rules is unlikely to convert a 6-year-old picky eater into a voracious omnivore, it can be a first step toward helping a family adopt a sensible approach to the child’s eating habits. At least it won’t make things worse and is likely to turn unhappy meals at home into mini feasts that celebrate togetherness.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”