Presenters

Samir Shah, MD, MSCE

Session summary

Antibiotic stewardship is more than narrowing coverage once susceptibilities are available. It also means conversion of antibiotics to oral therapy when clinically appropriate.

Previously, many childhood infections were treated with IV therapy due to severity or concern that oral absorption delayed or limited response. Multiple studies have shown that early conversion is not only safe, but safer than prolonging IV therapy. At HM 17, we had the opportunity to hear from Samir Shah, MD, about the current literature that supports safe transitions to oral therapy, including the “when” and the “how.”

Terminology for conversion to oral therapy should not state that it is “step-down” therapy, but rather switch therapy or sequential therapy. This conversion reduces likelihood of treatment complications, reduces length of hospital stay, reduces nursing and pharmacy time, decreases discomfort for the patient, and reduces cost.

Antibiotics such as levofloxacin, clindamycin, ciprofloxacin, and metronidazole have excellent bioavailability when taken orally. Other commonly used IV medications such as ampicillin, ampicillin-sulbactam, and cefazolin can be substituted with amoxicillin, amoxicillin-clavulanate, and cephalexin, which have similar penetration characteristics.

In general, unless there are serious complications, such as endocarditis and meningitis, most patients should be switched to oral therapy as soon as clinically warranted to complete therapy. For example, the incidence of meningitis in patients less than 1 month of age with UTI is 1%-2% and the incidence of meningitis in those 1-2 months of age is 0.3%-0.5%. Therefore, these patients can be treated with oral therapy earlier in their course when meningitis is not suspected. The likelihood of endocarditis in a pediatric patient without a known heart lesion is very low, even in patients with repeat positive blood cultures, unlike our adult colleagues who have much higher incidence of endocarditis in bacteremic patients.

Further studies are emerging to help reduce total length of therapy for many bacterial infections. For example, good evidence now exists that skin and soft tissue infections can now be treated safely with 5-day courses.

Key takeaways for HM

• Transition to oral therapy earlier in the hospital course is justified and much safer than IV therapy.

• Conversion to oral antibiotic therapy reduces the likelihood of treatment complications, length of hospital stay, nursing time, pharmacy time, discomfort to the patient, and costs.

• Do not use the term “step-down” when referencing a transition to oral therapy.

• Oral therapy is effective in most bacterial infections in children except for meningitis and endocarditis.

• Levofloxacin, clindamycin, ciprofloxacin, and metronidazole have excellent bioavailability when taken orally and can be easily swapped for IV therapy.

Dr. Schwenk is a pediatric hospitalist at Norton Children’s Hospital and associate professor of pediatrics at the University of Louisville (Ky.), and a member of the Pediatrics Committee for SHM.

Presenters

Samir Shah, MD, MSCE

Session summary

Antibiotic stewardship is more than narrowing coverage once susceptibilities are available. It also means conversion of antibiotics to oral therapy when clinically appropriate.

Previously, many childhood infections were treated with IV therapy due to severity or concern that oral absorption delayed or limited response. Multiple studies have shown that early conversion is not only safe, but safer than prolonging IV therapy. At HM 17, we had the opportunity to hear from Samir Shah, MD, about the current literature that supports safe transitions to oral therapy, including the “when” and the “how.”

Terminology for conversion to oral therapy should not state that it is “step-down” therapy, but rather switch therapy or sequential therapy. This conversion reduces likelihood of treatment complications, reduces length of hospital stay, reduces nursing and pharmacy time, decreases discomfort for the patient, and reduces cost.

Antibiotics such as levofloxacin, clindamycin, ciprofloxacin, and metronidazole have excellent bioavailability when taken orally. Other commonly used IV medications such as ampicillin, ampicillin-sulbactam, and cefazolin can be substituted with amoxicillin, amoxicillin-clavulanate, and cephalexin, which have similar penetration characteristics.

In general, unless there are serious complications, such as endocarditis and meningitis, most patients should be switched to oral therapy as soon as clinically warranted to complete therapy. For example, the incidence of meningitis in patients less than 1 month of age with UTI is 1%-2% and the incidence of meningitis in those 1-2 months of age is 0.3%-0.5%. Therefore, these patients can be treated with oral therapy earlier in their course when meningitis is not suspected. The likelihood of endocarditis in a pediatric patient without a known heart lesion is very low, even in patients with repeat positive blood cultures, unlike our adult colleagues who have much higher incidence of endocarditis in bacteremic patients.

Further studies are emerging to help reduce total length of therapy for many bacterial infections. For example, good evidence now exists that skin and soft tissue infections can now be treated safely with 5-day courses.

Key takeaways for HM

• Transition to oral therapy earlier in the hospital course is justified and much safer than IV therapy.

• Conversion to oral antibiotic therapy reduces the likelihood of treatment complications, length of hospital stay, nursing time, pharmacy time, discomfort to the patient, and costs.

• Do not use the term “step-down” when referencing a transition to oral therapy.

• Oral therapy is effective in most bacterial infections in children except for meningitis and endocarditis.

• Levofloxacin, clindamycin, ciprofloxacin, and metronidazole have excellent bioavailability when taken orally and can be easily swapped for IV therapy.

Dr. Schwenk is a pediatric hospitalist at Norton Children’s Hospital and associate professor of pediatrics at the University of Louisville (Ky.), and a member of the Pediatrics Committee for SHM.

Presenters

Samir Shah, MD, MSCE

Session summary

Antibiotic stewardship is more than narrowing coverage once susceptibilities are available. It also means conversion of antibiotics to oral therapy when clinically appropriate.

Previously, many childhood infections were treated with IV therapy due to severity or concern that oral absorption delayed or limited response. Multiple studies have shown that early conversion is not only safe, but safer than prolonging IV therapy. At HM 17, we had the opportunity to hear from Samir Shah, MD, about the current literature that supports safe transitions to oral therapy, including the “when” and the “how.”

Terminology for conversion to oral therapy should not state that it is “step-down” therapy, but rather switch therapy or sequential therapy. This conversion reduces likelihood of treatment complications, reduces length of hospital stay, reduces nursing and pharmacy time, decreases discomfort for the patient, and reduces cost.

Antibiotics such as levofloxacin, clindamycin, ciprofloxacin, and metronidazole have excellent bioavailability when taken orally. Other commonly used IV medications such as ampicillin, ampicillin-sulbactam, and cefazolin can be substituted with amoxicillin, amoxicillin-clavulanate, and cephalexin, which have similar penetration characteristics.

In general, unless there are serious complications, such as endocarditis and meningitis, most patients should be switched to oral therapy as soon as clinically warranted to complete therapy. For example, the incidence of meningitis in patients less than 1 month of age with UTI is 1%-2% and the incidence of meningitis in those 1-2 months of age is 0.3%-0.5%. Therefore, these patients can be treated with oral therapy earlier in their course when meningitis is not suspected. The likelihood of endocarditis in a pediatric patient without a known heart lesion is very low, even in patients with repeat positive blood cultures, unlike our adult colleagues who have much higher incidence of endocarditis in bacteremic patients.

Further studies are emerging to help reduce total length of therapy for many bacterial infections. For example, good evidence now exists that skin and soft tissue infections can now be treated safely with 5-day courses.

Key takeaways for HM

• Transition to oral therapy earlier in the hospital course is justified and much safer than IV therapy.

• Conversion to oral antibiotic therapy reduces the likelihood of treatment complications, length of hospital stay, nursing time, pharmacy time, discomfort to the patient, and costs.

• Do not use the term “step-down” when referencing a transition to oral therapy.

• Oral therapy is effective in most bacterial infections in children except for meningitis and endocarditis.

• Levofloxacin, clindamycin, ciprofloxacin, and metronidazole have excellent bioavailability when taken orally and can be easily swapped for IV therapy.

Dr. Schwenk is a pediatric hospitalist at Norton Children’s Hospital and associate professor of pediatrics at the University of Louisville (Ky.), and a member of the Pediatrics Committee for SHM.

High intake of myristic acid approximately tripled the odds of relapse in patients with ulcerative colitis (UC), compared with low intake, according to the results of a 12-month multicenter, prospective, observational study reported in the September 2017 issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2016.12.036).

Relapsers consumed an average of 2.2 g of this saturated fatty acid daily from sources such as palm and coconut oils, as well as dairy fats, reported Edward L. Barnes, MD, MPH, and his associates at Brigham and Women’s Hospital, Boston, on behalf of the DREAM (Diet’s Role in Exacerbations of Mesalamine Maintenance) investigators. Nonrelapsers averaged 1.4 g/day. “Our broader goal is to determine how alterations in diet can improve the care of people with IBD [inflammatory bowel disease],” the researchers wrote. “These findings can help design interventional dietary studies to determine if supplementation or avoidance of certain compounds might reduce the risk of a flare for patients with ulcerative colitis in remission.”

Dietary factors are thought to underlie relapse in ulcerative colitis, but specific culprits are poorly defined, the investigators said. Therefore, the DREAM study prospectively tracked dietary intake and flares among a homogeneous group of 412 patients with UC from 25 academic and community gastroenterology practices in the United States. Between 2007 and 2014, patients were interviewed by telephone every 3 months for 1 year or until they reported a flare, defined as a Simple Clinical Colitis Activity Index score of at least 5 or a change in disease activity that entailed a change in medication.

Source: American Gastroenterological Association

A total of 34 patients were lost to follow-up, and 45 (11% of those remaining) flared within a year of study enrollment. “When analyzed in tertiles, increasing intake of multiple fatty acids was associated with increasing odds of relapse,” the researchers wrote. Predictors of flare in the univariate analysis included high intake of myristic acid, oleic acid, eicosenoic acid, palmitelaidic acid, total translinoleic acid, saturated fat, monounsaturated fat, and omega-3 fatty acids. These predictors also included moderate or high intake of alpha-linolenic acid. Only high intake of myristic acid maintained a significant dose-response relationship in the multivariable analysis (odds ratio, 3.0; 95% confidence interval, 1.2-7.7; P = .02 for high vs. low intake). Moderate intake of alpha-linolenic acid predicted flare (OR, 5.5; CI, 95%, 1.6-19.3; P = .001) in the multivariable analysis, but high intake did not (OR, 1.3; CI, 95%, 0.3-7.0; P = .4). “Other foods previously implicated in flares of UC, such as processed meat, alcohol, and foods high in sulfur, were not associated with an increased risk of flare,” the researchers wrote.

Study participants were generally in their mid- to late 40s, white, and not current smokers. More than half were male. Most had proctitis or left-sided colitis, not pancolitis. Relapsers averaged 2.4 flares in the 18 months before enrollment (standard deviation, 1.9), compared with 1.8 flares for nonrelapsers (SD, 2.4; P = .003).

This observational study not only was subject to unmeasured confounding, but also excluded many types of patients. Among those excluded were anyone with a history of allergy to salicylates, aminosalicylates, or mesalamine tablets. Also excluded were those who had recent exposure to NSAIDs, oral or parenteral antibiotics, antidiarrheals, antispasmodics, immunosuppressives, biologics, or corticosteroids (except budesonide). Requiring monotherapy with an aminosalicylate might limit the generalizability of the findings, the investigators noted. Patients also were on variable doses of aminosalicylates, and higher doses might have helped inhibit flares.

Actavis and the National Institutes of Health provided funding. The investigators reported having no relevant financial conflicts.

High intake of myristic acid approximately tripled the odds of relapse in patients with ulcerative colitis (UC), compared with low intake, according to the results of a 12-month multicenter, prospective, observational study reported in the September 2017 issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2016.12.036).

Relapsers consumed an average of 2.2 g of this saturated fatty acid daily from sources such as palm and coconut oils, as well as dairy fats, reported Edward L. Barnes, MD, MPH, and his associates at Brigham and Women’s Hospital, Boston, on behalf of the DREAM (Diet’s Role in Exacerbations of Mesalamine Maintenance) investigators. Nonrelapsers averaged 1.4 g/day. “Our broader goal is to determine how alterations in diet can improve the care of people with IBD [inflammatory bowel disease],” the researchers wrote. “These findings can help design interventional dietary studies to determine if supplementation or avoidance of certain compounds might reduce the risk of a flare for patients with ulcerative colitis in remission.”

Dietary factors are thought to underlie relapse in ulcerative colitis, but specific culprits are poorly defined, the investigators said. Therefore, the DREAM study prospectively tracked dietary intake and flares among a homogeneous group of 412 patients with UC from 25 academic and community gastroenterology practices in the United States. Between 2007 and 2014, patients were interviewed by telephone every 3 months for 1 year or until they reported a flare, defined as a Simple Clinical Colitis Activity Index score of at least 5 or a change in disease activity that entailed a change in medication.

Source: American Gastroenterological Association

A total of 34 patients were lost to follow-up, and 45 (11% of those remaining) flared within a year of study enrollment. “When analyzed in tertiles, increasing intake of multiple fatty acids was associated with increasing odds of relapse,” the researchers wrote. Predictors of flare in the univariate analysis included high intake of myristic acid, oleic acid, eicosenoic acid, palmitelaidic acid, total translinoleic acid, saturated fat, monounsaturated fat, and omega-3 fatty acids. These predictors also included moderate or high intake of alpha-linolenic acid. Only high intake of myristic acid maintained a significant dose-response relationship in the multivariable analysis (odds ratio, 3.0; 95% confidence interval, 1.2-7.7; P = .02 for high vs. low intake). Moderate intake of alpha-linolenic acid predicted flare (OR, 5.5; CI, 95%, 1.6-19.3; P = .001) in the multivariable analysis, but high intake did not (OR, 1.3; CI, 95%, 0.3-7.0; P = .4). “Other foods previously implicated in flares of UC, such as processed meat, alcohol, and foods high in sulfur, were not associated with an increased risk of flare,” the researchers wrote.

Study participants were generally in their mid- to late 40s, white, and not current smokers. More than half were male. Most had proctitis or left-sided colitis, not pancolitis. Relapsers averaged 2.4 flares in the 18 months before enrollment (standard deviation, 1.9), compared with 1.8 flares for nonrelapsers (SD, 2.4; P = .003).

This observational study not only was subject to unmeasured confounding, but also excluded many types of patients. Among those excluded were anyone with a history of allergy to salicylates, aminosalicylates, or mesalamine tablets. Also excluded were those who had recent exposure to NSAIDs, oral or parenteral antibiotics, antidiarrheals, antispasmodics, immunosuppressives, biologics, or corticosteroids (except budesonide). Requiring monotherapy with an aminosalicylate might limit the generalizability of the findings, the investigators noted. Patients also were on variable doses of aminosalicylates, and higher doses might have helped inhibit flares.

Actavis and the National Institutes of Health provided funding. The investigators reported having no relevant financial conflicts.

High intake of myristic acid approximately tripled the odds of relapse in patients with ulcerative colitis (UC), compared with low intake, according to the results of a 12-month multicenter, prospective, observational study reported in the September 2017 issue of Clinical Gastroenterology and Hepatology (doi: 10.1016/j.cgh.2016.12.036).

Relapsers consumed an average of 2.2 g of this saturated fatty acid daily from sources such as palm and coconut oils, as well as dairy fats, reported Edward L. Barnes, MD, MPH, and his associates at Brigham and Women’s Hospital, Boston, on behalf of the DREAM (Diet’s Role in Exacerbations of Mesalamine Maintenance) investigators. Nonrelapsers averaged 1.4 g/day. “Our broader goal is to determine how alterations in diet can improve the care of people with IBD [inflammatory bowel disease],” the researchers wrote. “These findings can help design interventional dietary studies to determine if supplementation or avoidance of certain compounds might reduce the risk of a flare for patients with ulcerative colitis in remission.”

Dietary factors are thought to underlie relapse in ulcerative colitis, but specific culprits are poorly defined, the investigators said. Therefore, the DREAM study prospectively tracked dietary intake and flares among a homogeneous group of 412 patients with UC from 25 academic and community gastroenterology practices in the United States. Between 2007 and 2014, patients were interviewed by telephone every 3 months for 1 year or until they reported a flare, defined as a Simple Clinical Colitis Activity Index score of at least 5 or a change in disease activity that entailed a change in medication.

Source: American Gastroenterological Association

A total of 34 patients were lost to follow-up, and 45 (11% of those remaining) flared within a year of study enrollment. “When analyzed in tertiles, increasing intake of multiple fatty acids was associated with increasing odds of relapse,” the researchers wrote. Predictors of flare in the univariate analysis included high intake of myristic acid, oleic acid, eicosenoic acid, palmitelaidic acid, total translinoleic acid, saturated fat, monounsaturated fat, and omega-3 fatty acids. These predictors also included moderate or high intake of alpha-linolenic acid. Only high intake of myristic acid maintained a significant dose-response relationship in the multivariable analysis (odds ratio, 3.0; 95% confidence interval, 1.2-7.7; P = .02 for high vs. low intake). Moderate intake of alpha-linolenic acid predicted flare (OR, 5.5; CI, 95%, 1.6-19.3; P = .001) in the multivariable analysis, but high intake did not (OR, 1.3; CI, 95%, 0.3-7.0; P = .4). “Other foods previously implicated in flares of UC, such as processed meat, alcohol, and foods high in sulfur, were not associated with an increased risk of flare,” the researchers wrote.

Study participants were generally in their mid- to late 40s, white, and not current smokers. More than half were male. Most had proctitis or left-sided colitis, not pancolitis. Relapsers averaged 2.4 flares in the 18 months before enrollment (standard deviation, 1.9), compared with 1.8 flares for nonrelapsers (SD, 2.4; P = .003).

This observational study not only was subject to unmeasured confounding, but also excluded many types of patients. Among those excluded were anyone with a history of allergy to salicylates, aminosalicylates, or mesalamine tablets. Also excluded were those who had recent exposure to NSAIDs, oral or parenteral antibiotics, antidiarrheals, antispasmodics, immunosuppressives, biologics, or corticosteroids (except budesonide). Requiring monotherapy with an aminosalicylate might limit the generalizability of the findings, the investigators noted. Patients also were on variable doses of aminosalicylates, and higher doses might have helped inhibit flares.

Actavis and the National Institutes of Health provided funding. The investigators reported having no relevant financial conflicts.

Stand Up To Cancer (SU2C) is supporting a new translational research team to explore how chimeric antigen receptor T-cell (CAR T-cell) therapy can be applied to pancreatic cancer.

The Stand Up To Cancer–Lustgarten Foundation CAR T Translational Research Team will be directed by three investigators at the University of Pennsylvania’s Perelman School of Medicine who have been pioneers in CAR T-cell therapy development: Carl H. June, MD, the Richard W. Vague professor in immunotherapy; Shelley L. Berger, PhD, the Daniel S. Och university professor; and E. John Wherry, PhD, Richard and Barbara Schiffrin president’s distinguished professor of microbiology, and director, Institute for Immunology, according to a press release from the American Association for Cancer Research, SU2C’s Scientific Partner.

The team, which will receive a total of $2 million in funding from both SU2C and the Lustgarten Foundation for Pancreatic Cancer Research, will focus on epigenetics; a phase 1 trial will help identify epigenetic changes that are common to patients who don’t respond to immunotherapy, compared to those who do.

The team will also explore the use of CAR T cells to target mesothelin, a protein that is overexpressed in pancreatic cancer, according to the press release.

The Food and Drug Administration’s Oncologic Drugs Advisory Committee recently gave a thumbs up to a version of CAR T-cell therapy for the treatment of advanced acute lymphoblastic leukemia.This new SU2C translational research team will meet twice a year with the three other SU2C-sponsored research teams addressing pancreatic cancer to share progress and data.

Stand Up To Cancer (SU2C) is supporting a new translational research team to explore how chimeric antigen receptor T-cell (CAR T-cell) therapy can be applied to pancreatic cancer.

The Stand Up To Cancer–Lustgarten Foundation CAR T Translational Research Team will be directed by three investigators at the University of Pennsylvania’s Perelman School of Medicine who have been pioneers in CAR T-cell therapy development: Carl H. June, MD, the Richard W. Vague professor in immunotherapy; Shelley L. Berger, PhD, the Daniel S. Och university professor; and E. John Wherry, PhD, Richard and Barbara Schiffrin president’s distinguished professor of microbiology, and director, Institute for Immunology, according to a press release from the American Association for Cancer Research, SU2C’s Scientific Partner.

The team, which will receive a total of $2 million in funding from both SU2C and the Lustgarten Foundation for Pancreatic Cancer Research, will focus on epigenetics; a phase 1 trial will help identify epigenetic changes that are common to patients who don’t respond to immunotherapy, compared to those who do.

The team will also explore the use of CAR T cells to target mesothelin, a protein that is overexpressed in pancreatic cancer, according to the press release.

The Food and Drug Administration’s Oncologic Drugs Advisory Committee recently gave a thumbs up to a version of CAR T-cell therapy for the treatment of advanced acute lymphoblastic leukemia.This new SU2C translational research team will meet twice a year with the three other SU2C-sponsored research teams addressing pancreatic cancer to share progress and data.

Stand Up To Cancer (SU2C) is supporting a new translational research team to explore how chimeric antigen receptor T-cell (CAR T-cell) therapy can be applied to pancreatic cancer.

The Stand Up To Cancer–Lustgarten Foundation CAR T Translational Research Team will be directed by three investigators at the University of Pennsylvania’s Perelman School of Medicine who have been pioneers in CAR T-cell therapy development: Carl H. June, MD, the Richard W. Vague professor in immunotherapy; Shelley L. Berger, PhD, the Daniel S. Och university professor; and E. John Wherry, PhD, Richard and Barbara Schiffrin president’s distinguished professor of microbiology, and director, Institute for Immunology, according to a press release from the American Association for Cancer Research, SU2C’s Scientific Partner.

The team, which will receive a total of $2 million in funding from both SU2C and the Lustgarten Foundation for Pancreatic Cancer Research, will focus on epigenetics; a phase 1 trial will help identify epigenetic changes that are common to patients who don’t respond to immunotherapy, compared to those who do.

The team will also explore the use of CAR T cells to target mesothelin, a protein that is overexpressed in pancreatic cancer, according to the press release.

The Food and Drug Administration’s Oncologic Drugs Advisory Committee recently gave a thumbs up to a version of CAR T-cell therapy for the treatment of advanced acute lymphoblastic leukemia.This new SU2C translational research team will meet twice a year with the three other SU2C-sponsored research teams addressing pancreatic cancer to share progress and data.

BOSTON—Compared with intermediate sleep duration, shorter sleep is associated with greater brain atrophy among community-dwelling older adults, according to a study presented at the 31st Annual Meeting of the Associated Professional Sleep Societies. Sleep duration appears to have no association with hippocampal volume, however.

More than 80% of older adults have sleep complaints, and research indicating an association between disturbed sleep and poor cognitive outcomes is accumulating. Sleep could be a crucial modifiable risk factor for cognitive outcomes, but few studies have examined the association between nonrespiratory sleep measures and brain volume, said Adam Spira, PhD, Associate Professor of Mental Health at Johns Hopkins Bloomberg School of Public Health in Baltimore.

Participants Underwent MRI and Actigraphy

Dr. Spira and his colleagues at the National Institute on Aging Intramural Research Program and Johns Hopkins University studied adults without dementia enrolled in the ongoing Baltimore Longitudinal Study of Aging. To be eligible for the study, participants could not have cognitive impairment, functional limitations, or chronic medical conditions besides controlled hypertension.

Dr. Spira and colleagues examined the 183 participants for whom wrist actigraphy and MRI data from the same study visit were available. The sample’s mean age was 75. About 57% of the sample was female, and 28% were racial or ethnic minorities (mostly African American). Approximately 84% of the sample had 16 or more years of education.

Participants completed an average of 6.8 nights of actigraphy. The actigraph unit was worn on the nondominant wrist. The study’s primary actigraphy variables were total sleep time (TST), wake after sleep onset (WASO), and average wake bout length. Participants also underwent 3-T MRI, and the researchers’ main imaging variables were ventricular volume and hippocampal volume. Dr. Spira and colleagues adjusted their analyses for age, sex, education, race, depressive symptomatology, and the log of the intracranial volume.

Links Between Sleep and Brain Volumes

The population’s mean TST was 6.6 hours, and the investigators divided the TST data into tertiles. The mean TST for tertile 1 was 5.4 hours, the mean TST for tertile 2 was 6.6 hours, and the mean TST for tertile 3 was 7.7 hours. Mean WASO was 53 minutes, and mean wake bout length was 2.5 minutes.

Dr. Spira’s group found a statistically significant 0.17-unit increase in ventricular volume in tertile 1, compared with tertile 2. They also found a 0.12-unit increase in ventricular volume in tertile 3, compared with tertile 2, but the difference did not reach statistical significance. WASO was not associated with ventricular volume, but the investigators found a statistically significant 0.06-unit increase in ventricular volume for every standard deviation increase in average wake bout length.

There was no significant association between TST and hippocampal volume. Every standard deviation increase in WASO, however, was associated with decrease in hippocampal volume that was not statistically significant. Wake bout length was not associated with hippocampal volume.

Because it is a cross sectional study, the researchers cannot examine the temporal associations that would support the possibility of a causal effect of sleep on brain atrophy, said Dr. Spira. “It could also be that brain atrophy is linked to disturbed sleep,” he added. The investigators did not screen participants for sleep apnea or adjust the data for BMI.

The findings are consistent, however, with longitudinal results of studies with self-report measures of sleep duration or quality, and with cross sectional associations between actigraphic fragmentation indices and lower brain volumes.

“Longitudinal studies with larger samples are needed,” said Dr. Spira. “Ultimately, trials will be needed to examine the effects of optimizing sleep on cognitive and neuroimaging outcomes.”

—Erik Greb

Suggested Reading

Branger P, Arenaza-Urquijo EM, Tomadesso C, et al. Relationships between sleep quality and brain volume, metabolism, and amyloid deposition in late adulthood. Neurobiol Aging. 2016;41:107-114.

Koo DL, Shin JH, Lim JS, et al. Changes in subcortical shape and cognitive function in patients with chronic insomnia. Sleep Med. 2017;35:23-26.

BOSTON—Compared with intermediate sleep duration, shorter sleep is associated with greater brain atrophy among community-dwelling older adults, according to a study presented at the 31st Annual Meeting of the Associated Professional Sleep Societies. Sleep duration appears to have no association with hippocampal volume, however.

More than 80% of older adults have sleep complaints, and research indicating an association between disturbed sleep and poor cognitive outcomes is accumulating. Sleep could be a crucial modifiable risk factor for cognitive outcomes, but few studies have examined the association between nonrespiratory sleep measures and brain volume, said Adam Spira, PhD, Associate Professor of Mental Health at Johns Hopkins Bloomberg School of Public Health in Baltimore.

Participants Underwent MRI and Actigraphy

Dr. Spira and his colleagues at the National Institute on Aging Intramural Research Program and Johns Hopkins University studied adults without dementia enrolled in the ongoing Baltimore Longitudinal Study of Aging. To be eligible for the study, participants could not have cognitive impairment, functional limitations, or chronic medical conditions besides controlled hypertension.

Dr. Spira and colleagues examined the 183 participants for whom wrist actigraphy and MRI data from the same study visit were available. The sample’s mean age was 75. About 57% of the sample was female, and 28% were racial or ethnic minorities (mostly African American). Approximately 84% of the sample had 16 or more years of education.

Participants completed an average of 6.8 nights of actigraphy. The actigraph unit was worn on the nondominant wrist. The study’s primary actigraphy variables were total sleep time (TST), wake after sleep onset (WASO), and average wake bout length. Participants also underwent 3-T MRI, and the researchers’ main imaging variables were ventricular volume and hippocampal volume. Dr. Spira and colleagues adjusted their analyses for age, sex, education, race, depressive symptomatology, and the log of the intracranial volume.

Links Between Sleep and Brain Volumes

The population’s mean TST was 6.6 hours, and the investigators divided the TST data into tertiles. The mean TST for tertile 1 was 5.4 hours, the mean TST for tertile 2 was 6.6 hours, and the mean TST for tertile 3 was 7.7 hours. Mean WASO was 53 minutes, and mean wake bout length was 2.5 minutes.

Dr. Spira’s group found a statistically significant 0.17-unit increase in ventricular volume in tertile 1, compared with tertile 2. They also found a 0.12-unit increase in ventricular volume in tertile 3, compared with tertile 2, but the difference did not reach statistical significance. WASO was not associated with ventricular volume, but the investigators found a statistically significant 0.06-unit increase in ventricular volume for every standard deviation increase in average wake bout length.

There was no significant association between TST and hippocampal volume. Every standard deviation increase in WASO, however, was associated with decrease in hippocampal volume that was not statistically significant. Wake bout length was not associated with hippocampal volume.

Because it is a cross sectional study, the researchers cannot examine the temporal associations that would support the possibility of a causal effect of sleep on brain atrophy, said Dr. Spira. “It could also be that brain atrophy is linked to disturbed sleep,” he added. The investigators did not screen participants for sleep apnea or adjust the data for BMI.

The findings are consistent, however, with longitudinal results of studies with self-report measures of sleep duration or quality, and with cross sectional associations between actigraphic fragmentation indices and lower brain volumes.

“Longitudinal studies with larger samples are needed,” said Dr. Spira. “Ultimately, trials will be needed to examine the effects of optimizing sleep on cognitive and neuroimaging outcomes.”

—Erik Greb

Suggested Reading

Branger P, Arenaza-Urquijo EM, Tomadesso C, et al. Relationships between sleep quality and brain volume, metabolism, and amyloid deposition in late adulthood. Neurobiol Aging. 2016;41:107-114.

Koo DL, Shin JH, Lim JS, et al. Changes in subcortical shape and cognitive function in patients with chronic insomnia. Sleep Med. 2017;35:23-26.

BOSTON—Compared with intermediate sleep duration, shorter sleep is associated with greater brain atrophy among community-dwelling older adults, according to a study presented at the 31st Annual Meeting of the Associated Professional Sleep Societies. Sleep duration appears to have no association with hippocampal volume, however.

More than 80% of older adults have sleep complaints, and research indicating an association between disturbed sleep and poor cognitive outcomes is accumulating. Sleep could be a crucial modifiable risk factor for cognitive outcomes, but few studies have examined the association between nonrespiratory sleep measures and brain volume, said Adam Spira, PhD, Associate Professor of Mental Health at Johns Hopkins Bloomberg School of Public Health in Baltimore.

Participants Underwent MRI and Actigraphy

Dr. Spira and his colleagues at the National Institute on Aging Intramural Research Program and Johns Hopkins University studied adults without dementia enrolled in the ongoing Baltimore Longitudinal Study of Aging. To be eligible for the study, participants could not have cognitive impairment, functional limitations, or chronic medical conditions besides controlled hypertension.

Dr. Spira and colleagues examined the 183 participants for whom wrist actigraphy and MRI data from the same study visit were available. The sample’s mean age was 75. About 57% of the sample was female, and 28% were racial or ethnic minorities (mostly African American). Approximately 84% of the sample had 16 or more years of education.

Participants completed an average of 6.8 nights of actigraphy. The actigraph unit was worn on the nondominant wrist. The study’s primary actigraphy variables were total sleep time (TST), wake after sleep onset (WASO), and average wake bout length. Participants also underwent 3-T MRI, and the researchers’ main imaging variables were ventricular volume and hippocampal volume. Dr. Spira and colleagues adjusted their analyses for age, sex, education, race, depressive symptomatology, and the log of the intracranial volume.

Links Between Sleep and Brain Volumes

The population’s mean TST was 6.6 hours, and the investigators divided the TST data into tertiles. The mean TST for tertile 1 was 5.4 hours, the mean TST for tertile 2 was 6.6 hours, and the mean TST for tertile 3 was 7.7 hours. Mean WASO was 53 minutes, and mean wake bout length was 2.5 minutes.

Dr. Spira’s group found a statistically significant 0.17-unit increase in ventricular volume in tertile 1, compared with tertile 2. They also found a 0.12-unit increase in ventricular volume in tertile 3, compared with tertile 2, but the difference did not reach statistical significance. WASO was not associated with ventricular volume, but the investigators found a statistically significant 0.06-unit increase in ventricular volume for every standard deviation increase in average wake bout length.

There was no significant association between TST and hippocampal volume. Every standard deviation increase in WASO, however, was associated with decrease in hippocampal volume that was not statistically significant. Wake bout length was not associated with hippocampal volume.

Because it is a cross sectional study, the researchers cannot examine the temporal associations that would support the possibility of a causal effect of sleep on brain atrophy, said Dr. Spira. “It could also be that brain atrophy is linked to disturbed sleep,” he added. The investigators did not screen participants for sleep apnea or adjust the data for BMI.

The findings are consistent, however, with longitudinal results of studies with self-report measures of sleep duration or quality, and with cross sectional associations between actigraphic fragmentation indices and lower brain volumes.

“Longitudinal studies with larger samples are needed,” said Dr. Spira. “Ultimately, trials will be needed to examine the effects of optimizing sleep on cognitive and neuroimaging outcomes.”

—Erik Greb

Suggested Reading

Branger P, Arenaza-Urquijo EM, Tomadesso C, et al. Relationships between sleep quality and brain volume, metabolism, and amyloid deposition in late adulthood. Neurobiol Aging. 2016;41:107-114.

Koo DL, Shin JH, Lim JS, et al. Changes in subcortical shape and cognitive function in patients with chronic insomnia. Sleep Med. 2017;35:23-26.

Mauricio Tohen, MD, DrPH, MBA 
Professor and Chair
Department of Psychiatry and Behavioral Sciences
University of New Mexico School of Medicine
Albuquerque, New Mexico 

Claudia Baldassano, MD 
Associate Professor of Psychiatry
Department of Psychiatry
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania 

Vladimir Maletic, MD, MS 
Clinical Professor of Neuropsychiatry and Behavioral Science
University of South Carolina School of Medicine
Greenville, South Carolina

Consulting Associate
Division of Child and Adolescent Psychiatry Department of Psychiatry
Duke University
Durham, North Carolina

Click here to read the supplement

After reading, visit https://MERdepression.cvent.com to complete the posttest and evaluation for CME/CE credit.

Mauricio Tohen, MD, DrPH, MBA 
Professor and Chair
Department of Psychiatry and Behavioral Sciences
University of New Mexico School of Medicine
Albuquerque, New Mexico 

Claudia Baldassano, MD 
Associate Professor of Psychiatry
Department of Psychiatry
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania 

Vladimir Maletic, MD, MS 
Clinical Professor of Neuropsychiatry and Behavioral Science
University of South Carolina School of Medicine
Greenville, South Carolina

Consulting Associate
Division of Child and Adolescent Psychiatry Department of Psychiatry
Duke University
Durham, North Carolina

Click here to read the supplement

After reading, visit https://MERdepression.cvent.com to complete the posttest and evaluation for CME/CE credit.

Mauricio Tohen, MD, DrPH, MBA 
Professor and Chair
Department of Psychiatry and Behavioral Sciences
University of New Mexico School of Medicine
Albuquerque, New Mexico 

Claudia Baldassano, MD 
Associate Professor of Psychiatry
Department of Psychiatry
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania 

Vladimir Maletic, MD, MS 
Clinical Professor of Neuropsychiatry and Behavioral Science
University of South Carolina School of Medicine
Greenville, South Carolina

Consulting Associate
Division of Child and Adolescent Psychiatry Department of Psychiatry
Duke University
Durham, North Carolina

Click here to read the supplement

After reading, visit https://MERdepression.cvent.com to complete the posttest and evaluation for CME/CE credit.

Delay in delivery--mother and child die: $1.4M settlement

ESTATE'S CLAIM:

The standard of care for placenta accreta requires delivery between 34 and 36 weeks of gestation. The mother died from a placental abruption and amniotic fluid embolism. Placenta accreta increases the risk of catastrophic hemorrhage. If delivery had occurred on January 14, both the mother and child would be alive.

DEFENDANTS' DEFENSE:

The case settled before trial.

VERDICT:

A $1.425 million Georgia settlement was reached. The settlement amount was limited by a damages cap unique to the defendant hospital.

Placental abruption not detected: $6.2M settlement

At 24 weeks of gestation, a mother presented to the hospital with premature contractions that subsided after her arrival. She was discharged from the hospital. The woman gave birth in her bathtub several hours later. The baby was 10 weeks premature. He suffered profound brain damage and has significant physical defects.

PARENT'S CLAIM:

Neither the ObGyn nor the hospital staff appreciated that the mother was experiencing placental abruption. If diagnosed, treatment could have prevented fetal injury.

DEFENDANTS' DEFENSE:

The case was settled prior to trial.

VERDICT:

A $6.2 million New York settlement was reached.

Child has brachial plexus injury: $2M award

A woman was admitted to the hospital for elective induction of labor. She gained a significant amount of weight while pregnant. During delivery, her family practitioner (FP) determined that vacuum extraction was needed but he was not qualified to use the device. An in-house ObGyn was called in to use the vacuum extractor. The FP delivered the baby's shoulders. The infant was born with a floppy right arm and later diagnosed with rupture injuries to the C-5 and C-6 vertebrae and permanent brachial plexus damage. She has limited range of motion in her right arm and shoulder.

PARENT'S CLAIM:

The FP was relatively inexperienced in labor and delivery. He should not have ordered vacuum extraction because of risk factors including the mother's small stature, her significant weight gain during pregnancy, the use of epidural anesthesia, and induction of labor. Using vacuum extraction increases the risk of shoulder dystocia.

The FP improperly applied excessive downward traction on the fetus causing the infant to sustain a brachial plexus injury.

The FP did not notify the parents of the child's injury immediately after birth; he told them about the injury just before discharge.

DEFENDANTS' DEFENSE:

There is no evidence in the medical records of a shoulder dystocia; "no shoulder dystocia" was charted shortly after delivery. No one in the delivery room testified to a delay in delivering the infant's shoulders. The mother's internal contractions caused the injury. The baby was not injured to the extent claimed.

VERDICT:

The ObGyn who used the vacuum extractor settled before the trial for $300,000. A $2 million Illinois verdict was returned against the FP.

Delay in treating infant in respiratory distress: $7.27M settlement

A child was delivered by a certified nurse midwife at a birthing center. At birth, the baby had a heart rate of 60 bpm and was in respiratory distress but there was no one at the clinic qualified to intubate the infant. Emergency personnel were called but the infant remained in respiratory distress for 8 minutes. The baby experienced birth asphyxia with hypoxic ischemic encephalopathy resulting in severe cerebral palsy.

PARENT'S CLAIM:

The birthing center was poorly staffed and unprepared to treat an emergency situation.

DEFENDANTS' DEFENSE:

The defendants denied all allegations of negligence. The case was settled during trial.

VERDICT:

A $7.27 million Pennsylvania settlement was reached.

Was the spinal block given at wrong level?

A MOTHER WENT TO THE HOSPITAL in labor. Prior to cesarean delivery, she underwent an anesthetic spinal block administered by a CRNA. Initially, the patient reported pain shortly after the injection was performed until the block worked. The baby's delivery was uneventful.

In recovery a few hours later, the patient reported intense and uncontrollable pain in her legs. Magnetic resonance imaging revealed a fluid pocket on her spinal cord at the L1-L2 level. The patient has permanent pain, numbness, and tingling in in both legs.

PATIENT'S CLAIM:

The CRNA failed to insert the spinal block needle in the proper location.

DEFENDANTS' DEFENSE:

The CRNA contended that he complied with the standard of care. He claimed that the patient had an unusual spinal cord anatomy: it was tethered down to the L3-L4 level.

VERDICT:

A $509,152 Kentucky verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Delay in delivery--mother and child die: $1.4M settlement

ESTATE'S CLAIM:

The standard of care for placenta accreta requires delivery between 34 and 36 weeks of gestation. The mother died from a placental abruption and amniotic fluid embolism. Placenta accreta increases the risk of catastrophic hemorrhage. If delivery had occurred on January 14, both the mother and child would be alive.

DEFENDANTS' DEFENSE:

The case settled before trial.

VERDICT:

A $1.425 million Georgia settlement was reached. The settlement amount was limited by a damages cap unique to the defendant hospital.

Placental abruption not detected: $6.2M settlement

At 24 weeks of gestation, a mother presented to the hospital with premature contractions that subsided after her arrival. She was discharged from the hospital. The woman gave birth in her bathtub several hours later. The baby was 10 weeks premature. He suffered profound brain damage and has significant physical defects.

PARENT'S CLAIM:

Neither the ObGyn nor the hospital staff appreciated that the mother was experiencing placental abruption. If diagnosed, treatment could have prevented fetal injury.

DEFENDANTS' DEFENSE:

The case was settled prior to trial.

VERDICT:

A $6.2 million New York settlement was reached.

Child has brachial plexus injury: $2M award

A woman was admitted to the hospital for elective induction of labor. She gained a significant amount of weight while pregnant. During delivery, her family practitioner (FP) determined that vacuum extraction was needed but he was not qualified to use the device. An in-house ObGyn was called in to use the vacuum extractor. The FP delivered the baby's shoulders. The infant was born with a floppy right arm and later diagnosed with rupture injuries to the C-5 and C-6 vertebrae and permanent brachial plexus damage. She has limited range of motion in her right arm and shoulder.

PARENT'S CLAIM:

The FP was relatively inexperienced in labor and delivery. He should not have ordered vacuum extraction because of risk factors including the mother's small stature, her significant weight gain during pregnancy, the use of epidural anesthesia, and induction of labor. Using vacuum extraction increases the risk of shoulder dystocia.

The FP improperly applied excessive downward traction on the fetus causing the infant to sustain a brachial plexus injury.

The FP did not notify the parents of the child's injury immediately after birth; he told them about the injury just before discharge.

DEFENDANTS' DEFENSE:

There is no evidence in the medical records of a shoulder dystocia; "no shoulder dystocia" was charted shortly after delivery. No one in the delivery room testified to a delay in delivering the infant's shoulders. The mother's internal contractions caused the injury. The baby was not injured to the extent claimed.

VERDICT:

The ObGyn who used the vacuum extractor settled before the trial for $300,000. A $2 million Illinois verdict was returned against the FP.

Delay in treating infant in respiratory distress: $7.27M settlement

A child was delivered by a certified nurse midwife at a birthing center. At birth, the baby had a heart rate of 60 bpm and was in respiratory distress but there was no one at the clinic qualified to intubate the infant. Emergency personnel were called but the infant remained in respiratory distress for 8 minutes. The baby experienced birth asphyxia with hypoxic ischemic encephalopathy resulting in severe cerebral palsy.

PARENT'S CLAIM:

The birthing center was poorly staffed and unprepared to treat an emergency situation.

DEFENDANTS' DEFENSE:

The defendants denied all allegations of negligence. The case was settled during trial.

VERDICT:

A $7.27 million Pennsylvania settlement was reached.

Was the spinal block given at wrong level?

A MOTHER WENT TO THE HOSPITAL in labor. Prior to cesarean delivery, she underwent an anesthetic spinal block administered by a CRNA. Initially, the patient reported pain shortly after the injection was performed until the block worked. The baby's delivery was uneventful.

In recovery a few hours later, the patient reported intense and uncontrollable pain in her legs. Magnetic resonance imaging revealed a fluid pocket on her spinal cord at the L1-L2 level. The patient has permanent pain, numbness, and tingling in in both legs.

PATIENT'S CLAIM:

The CRNA failed to insert the spinal block needle in the proper location.

DEFENDANTS' DEFENSE:

The CRNA contended that he complied with the standard of care. He claimed that the patient had an unusual spinal cord anatomy: it was tethered down to the L3-L4 level.

VERDICT:

A $509,152 Kentucky verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Delay in delivery--mother and child die: $1.4M settlement

ESTATE'S CLAIM:

The standard of care for placenta accreta requires delivery between 34 and 36 weeks of gestation. The mother died from a placental abruption and amniotic fluid embolism. Placenta accreta increases the risk of catastrophic hemorrhage. If delivery had occurred on January 14, both the mother and child would be alive.

DEFENDANTS' DEFENSE:

The case settled before trial.

VERDICT:

A $1.425 million Georgia settlement was reached. The settlement amount was limited by a damages cap unique to the defendant hospital.

Placental abruption not detected: $6.2M settlement

At 24 weeks of gestation, a mother presented to the hospital with premature contractions that subsided after her arrival. She was discharged from the hospital. The woman gave birth in her bathtub several hours later. The baby was 10 weeks premature. He suffered profound brain damage and has significant physical defects.

PARENT'S CLAIM:

Neither the ObGyn nor the hospital staff appreciated that the mother was experiencing placental abruption. If diagnosed, treatment could have prevented fetal injury.

DEFENDANTS' DEFENSE:

The case was settled prior to trial.

VERDICT:

A $6.2 million New York settlement was reached.

Child has brachial plexus injury: $2M award

A woman was admitted to the hospital for elective induction of labor. She gained a significant amount of weight while pregnant. During delivery, her family practitioner (FP) determined that vacuum extraction was needed but he was not qualified to use the device. An in-house ObGyn was called in to use the vacuum extractor. The FP delivered the baby's shoulders. The infant was born with a floppy right arm and later diagnosed with rupture injuries to the C-5 and C-6 vertebrae and permanent brachial plexus damage. She has limited range of motion in her right arm and shoulder.

PARENT'S CLAIM:

The FP was relatively inexperienced in labor and delivery. He should not have ordered vacuum extraction because of risk factors including the mother's small stature, her significant weight gain during pregnancy, the use of epidural anesthesia, and induction of labor. Using vacuum extraction increases the risk of shoulder dystocia.

The FP improperly applied excessive downward traction on the fetus causing the infant to sustain a brachial plexus injury.

The FP did not notify the parents of the child's injury immediately after birth; he told them about the injury just before discharge.

DEFENDANTS' DEFENSE:

There is no evidence in the medical records of a shoulder dystocia; "no shoulder dystocia" was charted shortly after delivery. No one in the delivery room testified to a delay in delivering the infant's shoulders. The mother's internal contractions caused the injury. The baby was not injured to the extent claimed.

VERDICT:

The ObGyn who used the vacuum extractor settled before the trial for $300,000. A $2 million Illinois verdict was returned against the FP.

Delay in treating infant in respiratory distress: $7.27M settlement

A child was delivered by a certified nurse midwife at a birthing center. At birth, the baby had a heart rate of 60 bpm and was in respiratory distress but there was no one at the clinic qualified to intubate the infant. Emergency personnel were called but the infant remained in respiratory distress for 8 minutes. The baby experienced birth asphyxia with hypoxic ischemic encephalopathy resulting in severe cerebral palsy.

PARENT'S CLAIM:

The birthing center was poorly staffed and unprepared to treat an emergency situation.

DEFENDANTS' DEFENSE:

The defendants denied all allegations of negligence. The case was settled during trial.

VERDICT:

A $7.27 million Pennsylvania settlement was reached.

Was the spinal block given at wrong level?

A MOTHER WENT TO THE HOSPITAL in labor. Prior to cesarean delivery, she underwent an anesthetic spinal block administered by a CRNA. Initially, the patient reported pain shortly after the injection was performed until the block worked. The baby's delivery was uneventful.

In recovery a few hours later, the patient reported intense and uncontrollable pain in her legs. Magnetic resonance imaging revealed a fluid pocket on her spinal cord at the L1-L2 level. The patient has permanent pain, numbness, and tingling in in both legs.

PATIENT'S CLAIM:

The CRNA failed to insert the spinal block needle in the proper location.

DEFENDANTS' DEFENSE:

The CRNA contended that he complied with the standard of care. He claimed that the patient had an unusual spinal cord anatomy: it was tethered down to the L3-L4 level.

VERDICT:

A $509,152 Kentucky verdict was returned.

These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Vidyard Video

Vidyard Video

Vidyard Video

Release Date: August 1, 2017
Expiration Date: July 31, 2018

Note: This activity is no longer available for credit.

Agenda

Developing New Strategic Goals in PTCL (duration 27:00)
Andrei R. Shustov, MD
University of Washington School of Medicine
Fred Hutchinson Cancer Research Center
Seattle, WA, USA

PTCL as a Rare Disease: A Case of Overall Survival (duration 19:00)
Owen A. O’Connor, MD, PhD
Columbia University Medical Center
The New York Presbyterian Hospital
New York, NY, USA

Why Might Response Rates Differ Between the East and West? (duration 17:00)
Kensei Tobinai, MD, PhD
National Cancer Center Hospital
Tokyo, Japan

Provided by:

Original activity supported by an educational grant from:

Spectrum Pharmaceuticals

Learning Objectives

At the end of the activity, participants should be able to:

• Explain why progression-free survival is important when treating patients with PTCL
• Determine when overall survival is possible
• Describe the challenges of using matched control analysis in PTCL clinical trials
• Discuss why different response rates to therapy for PTCL may be seen in Asian patients versus North American or European patients and define the possible contributing factors

Target Audience

Hematologists, oncologists, and other clinicians and scientists with an interest in T-cell lymphoma

Statement of Need

This activity explores clinical endpoints in PTCL, the importance of choosing the appropriate ones and the possibility of achieving them. Global and regional differences in PTCL are also explored as they relate to response rates. The presentations highlight the challenges physicians face in treating PTCL patients and recent developments are discussed to help practitioners evaluate the utility of these endpoints in choosing appropriate treatments to improve outcomes in their patients with PTCL.

FACULTY

Faculty

Andrei R. Shustov, MD
Disclosures: Consulting fee: Celgene; BMS

Owen O’Connor, MD, PhD
Disclosures: Consulting fees: Mundipharma; Celgene; Contracted Research: Mundipharma; Spectrum; Celgene; Seattle Genetics; TG Therapeutics; ADCT; Trillium

Kensei Tobinai, MD, PhD
Disclosures: Honoraria: Eisai; HUYA Bioscience International; Janssen; Mundipharma; Takeda; Zenyaku Kogyo; Contracted research: Abbvie; Celgene; Chugai Pharma; Eisai; GlaxoSmithKline; Janssen; Kyowa Hakko Kirin; Mundipharma; Ono Pharmaceutical; SERVIER; Takeda

Permissions

Andrei Shustov presentation

• Slide 7: PTCL Prognosis Is Indicative of Diverse Biology
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 8: PTCL: Global Epidemiology
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 9: PTCL: USA Epidemiology (top half)
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 9: PTCL: USA Epidemiology (bottom half)
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slide 10: PTCL Prognosis: Histology x Race (USA)
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slide 12: PTCL Prognosis: Clinical Features (top right side)
  • Reprinted with permission. © 2013 American Society of Clinical Oncology. All rights reserved.
• Slide 14: PTCL Prognosis: Molecular Classifiers (left side)
  • Republished with permission of the American Society of Hematology, from Parilla Castellar ER, et al. Blood 2014;124:1473-1480
• Slide 14: PTCL Prognosis: Molecular Classifiers (right side)
  • Republished with permission of the American Society of Hematology, from Iqbal J, et al. Blood 2014;123:2915-2923
• Slide 17: US Epidemiology of PTCL
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slides 18-19: Romidepsin in Relapsed/Refractory PTCL
  • Reprinted with permission. © 2012 American Society of Clinical Oncology. All rights reserved.
• Slides 20-22, 25: Romidepsin in Elderly Patients
  • Shustov A, et al. Romidepsin is effective and well tolerated in older patients with peripheral T-cell lymphoma: analysis of two phase II trials. Leuk Lymphoma 2017 [Epub ahead of print]. Reprinted by permission of Taylor & Francis Ltd, http://www.tandfonline.com
• Slides 27-28: Belinostat in Relapsed/Refractory PTCL
  • Reprinted with permission. © 2015 American Society of Clinical Oncology. All rights reserved.

Kensei Tobinai presentation

• Slide 7: Overall Survival of ATL Pts in JCOG 9801
  • Reprinted with permission. © 2007 American Society of Clinical Oncology. All rights reserved.

Disclaimer

The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of Hemedicus, the supporter, or Frontline Medical Communications. This material is prepared based upon a review of multiple sources of information, but it is not exhaustive of the subject matter. Therefore, healthcare professionals and other individuals should review and consider other publications and materials on the subject matter before relying solely upon the information contained within this educational activity.

Vidyard Video

Vidyard Video

Vidyard Video

Release Date: August 1, 2017
Expiration Date: July 31, 2018

Note: This activity is no longer available for credit.

Agenda

Developing New Strategic Goals in PTCL (duration 27:00)
Andrei R. Shustov, MD
University of Washington School of Medicine
Fred Hutchinson Cancer Research Center
Seattle, WA, USA

PTCL as a Rare Disease: A Case of Overall Survival (duration 19:00)
Owen A. O’Connor, MD, PhD
Columbia University Medical Center
The New York Presbyterian Hospital
New York, NY, USA

Why Might Response Rates Differ Between the East and West? (duration 17:00)
Kensei Tobinai, MD, PhD
National Cancer Center Hospital
Tokyo, Japan

Provided by:

Original activity supported by an educational grant from:

Spectrum Pharmaceuticals

Learning Objectives

At the end of the activity, participants should be able to:

• Explain why progression-free survival is important when treating patients with PTCL
• Determine when overall survival is possible
• Describe the challenges of using matched control analysis in PTCL clinical trials
• Discuss why different response rates to therapy for PTCL may be seen in Asian patients versus North American or European patients and define the possible contributing factors

Target Audience

Hematologists, oncologists, and other clinicians and scientists with an interest in T-cell lymphoma

Statement of Need

This activity explores clinical endpoints in PTCL, the importance of choosing the appropriate ones and the possibility of achieving them. Global and regional differences in PTCL are also explored as they relate to response rates. The presentations highlight the challenges physicians face in treating PTCL patients and recent developments are discussed to help practitioners evaluate the utility of these endpoints in choosing appropriate treatments to improve outcomes in their patients with PTCL.

FACULTY

Faculty

Andrei R. Shustov, MD
Disclosures: Consulting fee: Celgene; BMS

Owen O’Connor, MD, PhD
Disclosures: Consulting fees: Mundipharma; Celgene; Contracted Research: Mundipharma; Spectrum; Celgene; Seattle Genetics; TG Therapeutics; ADCT; Trillium

Kensei Tobinai, MD, PhD
Disclosures: Honoraria: Eisai; HUYA Bioscience International; Janssen; Mundipharma; Takeda; Zenyaku Kogyo; Contracted research: Abbvie; Celgene; Chugai Pharma; Eisai; GlaxoSmithKline; Janssen; Kyowa Hakko Kirin; Mundipharma; Ono Pharmaceutical; SERVIER; Takeda

Permissions

Andrei Shustov presentation

• Slide 7: PTCL Prognosis Is Indicative of Diverse Biology
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 8: PTCL: Global Epidemiology
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 9: PTCL: USA Epidemiology (top half)
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 9: PTCL: USA Epidemiology (bottom half)
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slide 10: PTCL Prognosis: Histology x Race (USA)
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slide 12: PTCL Prognosis: Clinical Features (top right side)
  • Reprinted with permission. © 2013 American Society of Clinical Oncology. All rights reserved.
• Slide 14: PTCL Prognosis: Molecular Classifiers (left side)
  • Republished with permission of the American Society of Hematology, from Parilla Castellar ER, et al. Blood 2014;124:1473-1480
• Slide 14: PTCL Prognosis: Molecular Classifiers (right side)
  • Republished with permission of the American Society of Hematology, from Iqbal J, et al. Blood 2014;123:2915-2923
• Slide 17: US Epidemiology of PTCL
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slides 18-19: Romidepsin in Relapsed/Refractory PTCL
  • Reprinted with permission. © 2012 American Society of Clinical Oncology. All rights reserved.
• Slides 20-22, 25: Romidepsin in Elderly Patients
  • Shustov A, et al. Romidepsin is effective and well tolerated in older patients with peripheral T-cell lymphoma: analysis of two phase II trials. Leuk Lymphoma 2017 [Epub ahead of print]. Reprinted by permission of Taylor & Francis Ltd, http://www.tandfonline.com
• Slides 27-28: Belinostat in Relapsed/Refractory PTCL
  • Reprinted with permission. © 2015 American Society of Clinical Oncology. All rights reserved.

Kensei Tobinai presentation

• Slide 7: Overall Survival of ATL Pts in JCOG 9801
  • Reprinted with permission. © 2007 American Society of Clinical Oncology. All rights reserved.

Disclaimer

The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of Hemedicus, the supporter, or Frontline Medical Communications. This material is prepared based upon a review of multiple sources of information, but it is not exhaustive of the subject matter. Therefore, healthcare professionals and other individuals should review and consider other publications and materials on the subject matter before relying solely upon the information contained within this educational activity.

Vidyard Video

Vidyard Video

Vidyard Video

Release Date: August 1, 2017
Expiration Date: July 31, 2018

Note: This activity is no longer available for credit.

Agenda

Developing New Strategic Goals in PTCL (duration 27:00)
Andrei R. Shustov, MD
University of Washington School of Medicine
Fred Hutchinson Cancer Research Center
Seattle, WA, USA

PTCL as a Rare Disease: A Case of Overall Survival (duration 19:00)
Owen A. O’Connor, MD, PhD
Columbia University Medical Center
The New York Presbyterian Hospital
New York, NY, USA

Why Might Response Rates Differ Between the East and West? (duration 17:00)
Kensei Tobinai, MD, PhD
National Cancer Center Hospital
Tokyo, Japan

Provided by:

Original activity supported by an educational grant from:

Spectrum Pharmaceuticals

Learning Objectives

At the end of the activity, participants should be able to:

• Explain why progression-free survival is important when treating patients with PTCL
• Determine when overall survival is possible
• Describe the challenges of using matched control analysis in PTCL clinical trials
• Discuss why different response rates to therapy for PTCL may be seen in Asian patients versus North American or European patients and define the possible contributing factors

Target Audience

Hematologists, oncologists, and other clinicians and scientists with an interest in T-cell lymphoma

Statement of Need

This activity explores clinical endpoints in PTCL, the importance of choosing the appropriate ones and the possibility of achieving them. Global and regional differences in PTCL are also explored as they relate to response rates. The presentations highlight the challenges physicians face in treating PTCL patients and recent developments are discussed to help practitioners evaluate the utility of these endpoints in choosing appropriate treatments to improve outcomes in their patients with PTCL.

FACULTY

Faculty

Andrei R. Shustov, MD
Disclosures: Consulting fee: Celgene; BMS

Owen O’Connor, MD, PhD
Disclosures: Consulting fees: Mundipharma; Celgene; Contracted Research: Mundipharma; Spectrum; Celgene; Seattle Genetics; TG Therapeutics; ADCT; Trillium

Kensei Tobinai, MD, PhD
Disclosures: Honoraria: Eisai; HUYA Bioscience International; Janssen; Mundipharma; Takeda; Zenyaku Kogyo; Contracted research: Abbvie; Celgene; Chugai Pharma; Eisai; GlaxoSmithKline; Janssen; Kyowa Hakko Kirin; Mundipharma; Ono Pharmaceutical; SERVIER; Takeda

Permissions

Andrei Shustov presentation

• Slide 7: PTCL Prognosis Is Indicative of Diverse Biology
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 8: PTCL: Global Epidemiology
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 9: PTCL: USA Epidemiology (top half)
  • Reprinted with permission. © 2008 American Society of Clinical Oncology. All rights reserved.
• Slide 9: PTCL: USA Epidemiology (bottom half)
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slide 10: PTCL Prognosis: Histology x Race (USA)
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slide 12: PTCL Prognosis: Clinical Features (top right side)
  • Reprinted with permission. © 2013 American Society of Clinical Oncology. All rights reserved.
• Slide 14: PTCL Prognosis: Molecular Classifiers (left side)
  • Republished with permission of the American Society of Hematology, from Parilla Castellar ER, et al. Blood 2014;124:1473-1480
• Slide 14: PTCL Prognosis: Molecular Classifiers (right side)
  • Republished with permission of the American Society of Hematology, from Iqbal J, et al. Blood 2014;123:2915-2923
• Slide 17: US Epidemiology of PTCL
  • Reprinted with permission. © 2016 American Society of Clinical Oncology. All rights reserved.
• Slides 18-19: Romidepsin in Relapsed/Refractory PTCL
  • Reprinted with permission. © 2012 American Society of Clinical Oncology. All rights reserved.
• Slides 20-22, 25: Romidepsin in Elderly Patients
  • Shustov A, et al. Romidepsin is effective and well tolerated in older patients with peripheral T-cell lymphoma: analysis of two phase II trials. Leuk Lymphoma 2017 [Epub ahead of print]. Reprinted by permission of Taylor & Francis Ltd, http://www.tandfonline.com
• Slides 27-28: Belinostat in Relapsed/Refractory PTCL
  • Reprinted with permission. © 2015 American Society of Clinical Oncology. All rights reserved.

Kensei Tobinai presentation

• Slide 7: Overall Survival of ATL Pts in JCOG 9801
  • Reprinted with permission. © 2007 American Society of Clinical Oncology. All rights reserved.

Disclaimer

The content and views presented in this educational activity are those of the authors and do not necessarily reflect those of Hemedicus, the supporter, or Frontline Medical Communications. This material is prepared based upon a review of multiple sources of information, but it is not exhaustive of the subject matter. Therefore, healthcare professionals and other individuals should review and consider other publications and materials on the subject matter before relying solely upon the information contained within this educational activity.

SAN DIEGO – For middle-aged men with diabetes, odds of erectile dysfunction are 50-50 at 50: By the age of 50, a full half will have the condition.

This isn’t normal for men of that age, according to Hunter B. Wessells, MD.“It’s not just that they’re aging. It’s a 20-year acceleration of the aging process,” he said at the annual scientific sessions of the American Diabetes Association.

That’s not all. In some cases, men with diabetes may experience decreased libido that’s potentially caused by low testosterone, said Dr. Wessells, professor and Wilma Wise Nelson, Ole A. Nelson, and Mabel Wise Nelson Endowed Chair in Urology at the University of Washington, Seattle

SAN DIEGO – For middle-aged men with diabetes, odds of erectile dysfunction are 50-50 at 50: By the age of 50, a full half will have the condition.

This isn’t normal for men of that age, according to Hunter B. Wessells, MD.“It’s not just that they’re aging. It’s a 20-year acceleration of the aging process,” he said at the annual scientific sessions of the American Diabetes Association.

That’s not all. In some cases, men with diabetes may experience decreased libido that’s potentially caused by low testosterone, said Dr. Wessells, professor and Wilma Wise Nelson, Ole A. Nelson, and Mabel Wise Nelson Endowed Chair in Urology at the University of Washington, Seattle

SAN DIEGO – For middle-aged men with diabetes, odds of erectile dysfunction are 50-50 at 50: By the age of 50, a full half will have the condition.

This isn’t normal for men of that age, according to Hunter B. Wessells, MD.“It’s not just that they’re aging. It’s a 20-year acceleration of the aging process,” he said at the annual scientific sessions of the American Diabetes Association.

That’s not all. In some cases, men with diabetes may experience decreased libido that’s potentially caused by low testosterone, said Dr. Wessells, professor and Wilma Wise Nelson, Ole A. Nelson, and Mabel Wise Nelson Endowed Chair in Urology at the University of Washington, Seattle

For the July-August issue of the Journal of Community and Supportive Oncology, the Editor-in-Chief, Dr David Henry, discusses a recap by Howard Burris, MD, of the top presentations at this year’s annual meeting of the American Society for Clinical Oncology, and a selection of articles on some of the key findings reported at the meeting. A number of articles, in keeping with the journal mission of delivering content that can inform or change daily practice in the community setting, provide ‘how-to’ clinical and supportive advice. They include an outline by Thomas J Smith of Johns Hopkins University of how to initiate goals-of-care conversations with patients and their family members; a review of managing polycythemia vera in the community oncology setting; a New Therapies feature on how immunotherapies are shaping the treatment of hematologic malignancies; and research articles on using Onodera’s Prognostic Nutritional Index to predict wound complications in patients with soft tissue sarcoma, and bone remodeling associated with CTLA-4 inhibition. A third research article assesses a multidisciplinary survivorship program in a group of predominantly Hispanic women with breast cancer. Also in the line-up for discussion are Case Reports, one on managing high-grade pleomorphic sarcoma in a patient with colon metastasis and another on intramedullary spinal cord and leptomeningeal metastases presenting as cauda equina syndrome in a patient with melanoma.

Listen to the podcast below.

For the July-August issue of the Journal of Community and Supportive Oncology, the Editor-in-Chief, Dr David Henry, discusses a recap by Howard Burris, MD, of the top presentations at this year’s annual meeting of the American Society for Clinical Oncology, and a selection of articles on some of the key findings reported at the meeting. A number of articles, in keeping with the journal mission of delivering content that can inform or change daily practice in the community setting, provide ‘how-to’ clinical and supportive advice. They include an outline by Thomas J Smith of Johns Hopkins University of how to initiate goals-of-care conversations with patients and their family members; a review of managing polycythemia vera in the community oncology setting; a New Therapies feature on how immunotherapies are shaping the treatment of hematologic malignancies; and research articles on using Onodera’s Prognostic Nutritional Index to predict wound complications in patients with soft tissue sarcoma, and bone remodeling associated with CTLA-4 inhibition. A third research article assesses a multidisciplinary survivorship program in a group of predominantly Hispanic women with breast cancer. Also in the line-up for discussion are Case Reports, one on managing high-grade pleomorphic sarcoma in a patient with colon metastasis and another on intramedullary spinal cord and leptomeningeal metastases presenting as cauda equina syndrome in a patient with melanoma.

Listen to the podcast below.

For the July-August issue of the Journal of Community and Supportive Oncology, the Editor-in-Chief, Dr David Henry, discusses a recap by Howard Burris, MD, of the top presentations at this year’s annual meeting of the American Society for Clinical Oncology, and a selection of articles on some of the key findings reported at the meeting. A number of articles, in keeping with the journal mission of delivering content that can inform or change daily practice in the community setting, provide ‘how-to’ clinical and supportive advice. They include an outline by Thomas J Smith of Johns Hopkins University of how to initiate goals-of-care conversations with patients and their family members; a review of managing polycythemia vera in the community oncology setting; a New Therapies feature on how immunotherapies are shaping the treatment of hematologic malignancies; and research articles on using Onodera’s Prognostic Nutritional Index to predict wound complications in patients with soft tissue sarcoma, and bone remodeling associated with CTLA-4 inhibition. A third research article assesses a multidisciplinary survivorship program in a group of predominantly Hispanic women with breast cancer. Also in the line-up for discussion are Case Reports, one on managing high-grade pleomorphic sarcoma in a patient with colon metastasis and another on intramedullary spinal cord and leptomeningeal metastases presenting as cauda equina syndrome in a patient with melanoma.

Listen to the podcast below.