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Fentanyl analogs nearly double their overdose death toll
, according to preliminary data from 10 states.
During July 2016 to December 2016, there were 764 opioid overdose deaths that tested positive for any fentanyl analog, with carfentanil being the most common (421 deaths). From January 2017 to June 2017, the respective numbers increased by 98% (1,511) and 94% (815), wrote Julie O’Donnell, PhD, and her associates at the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control. The report was published in the Morbidity and Mortality Weekly Report.
“The increasing array of fentanyl analogs highlights the need to build forensic toxicological testing capabilities to identify and report emerging threats, and to enhance capacity to rapidly respond to evolving drug trends,” Dr. O’Donnell and her associates said.
Along with carfentanil, 13 other analogs were detected in decedents during the 12-month period: 3-methylfentanyl, 4-fluorobutyrfentanyl, 4-fluorofentanyl, 4-fluoroisobutyrfentanyl, acetylfentanyl, acrylfentanyl, butyrylfentanyl, cyclopropylfentanyl, cyclopentylfentanyl, furanylethylfentanyl, furanylfentanyl, isobutyrylfentanyl, and tetrahydrofuranylfentanyl. Deaths may have involved “more than one analog, as well as ... other opioid and nonopioid substances,” they noted.
The 10 states reporting data to the State Unintentional Drug Overdose Reporting System (SUDORS) were Kentucky, Maine, Massachusetts, New Hampshire, New Mexico, Ohio, Oklahoma, Rhode Island, West Virginia, and Wisconsin. Two other SUDORS-reporting states – Missouri and Pennsylvania – did not have their data ready in time to be included in this analysis.
The increasing availability of fentanyl analogs hit Ohio especially hard: More deaths occurred there than in the other 10 states combined. Of the 421 carfentanil-related deaths in July 2016 to December 2016, nearly 400 were in Ohio, and there were 218 Ohio deaths in April 2017 alone. A look at the bigger picture shows that 3 of the 10 states reported carfentanil-related overdose deaths in the second half of 2016, compared with 7 in the first half of 2017, the investigators said.
Carfentanil, which is the most potent of the 14 fentanyl analogs that have been detected so far, “is intended for sedation of large animals, and is estimated to have 10,000 times the potency of morphine,” Dr. O’Donnell and her associates wrote.
SOURCE: O’Donnell J et al. MMWR. 2018 Jul 13;67(27):767-8.
, according to preliminary data from 10 states.
During July 2016 to December 2016, there were 764 opioid overdose deaths that tested positive for any fentanyl analog, with carfentanil being the most common (421 deaths). From January 2017 to June 2017, the respective numbers increased by 98% (1,511) and 94% (815), wrote Julie O’Donnell, PhD, and her associates at the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control. The report was published in the Morbidity and Mortality Weekly Report.
“The increasing array of fentanyl analogs highlights the need to build forensic toxicological testing capabilities to identify and report emerging threats, and to enhance capacity to rapidly respond to evolving drug trends,” Dr. O’Donnell and her associates said.
Along with carfentanil, 13 other analogs were detected in decedents during the 12-month period: 3-methylfentanyl, 4-fluorobutyrfentanyl, 4-fluorofentanyl, 4-fluoroisobutyrfentanyl, acetylfentanyl, acrylfentanyl, butyrylfentanyl, cyclopropylfentanyl, cyclopentylfentanyl, furanylethylfentanyl, furanylfentanyl, isobutyrylfentanyl, and tetrahydrofuranylfentanyl. Deaths may have involved “more than one analog, as well as ... other opioid and nonopioid substances,” they noted.
The 10 states reporting data to the State Unintentional Drug Overdose Reporting System (SUDORS) were Kentucky, Maine, Massachusetts, New Hampshire, New Mexico, Ohio, Oklahoma, Rhode Island, West Virginia, and Wisconsin. Two other SUDORS-reporting states – Missouri and Pennsylvania – did not have their data ready in time to be included in this analysis.
The increasing availability of fentanyl analogs hit Ohio especially hard: More deaths occurred there than in the other 10 states combined. Of the 421 carfentanil-related deaths in July 2016 to December 2016, nearly 400 were in Ohio, and there were 218 Ohio deaths in April 2017 alone. A look at the bigger picture shows that 3 of the 10 states reported carfentanil-related overdose deaths in the second half of 2016, compared with 7 in the first half of 2017, the investigators said.
Carfentanil, which is the most potent of the 14 fentanyl analogs that have been detected so far, “is intended for sedation of large animals, and is estimated to have 10,000 times the potency of morphine,” Dr. O’Donnell and her associates wrote.
SOURCE: O’Donnell J et al. MMWR. 2018 Jul 13;67(27):767-8.
, according to preliminary data from 10 states.
During July 2016 to December 2016, there were 764 opioid overdose deaths that tested positive for any fentanyl analog, with carfentanil being the most common (421 deaths). From January 2017 to June 2017, the respective numbers increased by 98% (1,511) and 94% (815), wrote Julie O’Donnell, PhD, and her associates at the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control. The report was published in the Morbidity and Mortality Weekly Report.
“The increasing array of fentanyl analogs highlights the need to build forensic toxicological testing capabilities to identify and report emerging threats, and to enhance capacity to rapidly respond to evolving drug trends,” Dr. O’Donnell and her associates said.
Along with carfentanil, 13 other analogs were detected in decedents during the 12-month period: 3-methylfentanyl, 4-fluorobutyrfentanyl, 4-fluorofentanyl, 4-fluoroisobutyrfentanyl, acetylfentanyl, acrylfentanyl, butyrylfentanyl, cyclopropylfentanyl, cyclopentylfentanyl, furanylethylfentanyl, furanylfentanyl, isobutyrylfentanyl, and tetrahydrofuranylfentanyl. Deaths may have involved “more than one analog, as well as ... other opioid and nonopioid substances,” they noted.
The 10 states reporting data to the State Unintentional Drug Overdose Reporting System (SUDORS) were Kentucky, Maine, Massachusetts, New Hampshire, New Mexico, Ohio, Oklahoma, Rhode Island, West Virginia, and Wisconsin. Two other SUDORS-reporting states – Missouri and Pennsylvania – did not have their data ready in time to be included in this analysis.
The increasing availability of fentanyl analogs hit Ohio especially hard: More deaths occurred there than in the other 10 states combined. Of the 421 carfentanil-related deaths in July 2016 to December 2016, nearly 400 were in Ohio, and there were 218 Ohio deaths in April 2017 alone. A look at the bigger picture shows that 3 of the 10 states reported carfentanil-related overdose deaths in the second half of 2016, compared with 7 in the first half of 2017, the investigators said.
Carfentanil, which is the most potent of the 14 fentanyl analogs that have been detected so far, “is intended for sedation of large animals, and is estimated to have 10,000 times the potency of morphine,” Dr. O’Donnell and her associates wrote.
SOURCE: O’Donnell J et al. MMWR. 2018 Jul 13;67(27):767-8.
FROM MMWR
New guideline for managing MCL
Rituximab should be included in first-line chemotherapy when treating mantle cell lymphoma, according to a new management guideline from the British Society for Haematology.
The best outcome data is for the R-CHOP regimen (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone) followed by maintenance treatment with rituximab, wrote Pamela McKay, MD, of Beatson West of Scotland Cancer Centre in Glasgow, and her colleagues. The report was published in the British Journal of Haematology. But the combination of rituximab and bendamustine is also effective and a more favorable safety profile, according to the guideline. Single agent rituximab is not recommended.
At relapse, the guideline calls on physicians to take an individualized approach based on age, comorbidities, performance status, and response to prior therapy. Some options to consider include ibrutinib as a single agent or rituximab plus chemotherapy. The authors cautioned that there is little evidence to support maintenance rituximab after relapse treatment.
The guideline also explores the role of autologous stem cell transplantation (ASCT) and allogeneic SCT (alloSCT). The authors recommend that ASCT be considered as consolidation of first-line therapy for patients who are fit for intensive therapy. AlloSCT is a viable option in second remission among fit patients who have an appropriate donor and it may also be effective as a rescue therapy for patients who relapse after ASCT. But alloSCT is appropriate only as a first-line therapy for high-risk patients and is best used as part of a clinical trial, according to the recommendations.
The British Society of Haematology previously issued guidance on mantle cell lymphoma in 2012, but the updated document includes new drug therapeutic options and transplant data. The guideline includes a therapeutic algorithm to assist physicians in choosing first-line therapy, options after first relapse, and management in the case of higher relapse.
The guideline authors reported having no conflicts of interest.
SOURCE: McKay P et al. Br J Haematol. 2018 Jul;182(1):46-62.
Rituximab should be included in first-line chemotherapy when treating mantle cell lymphoma, according to a new management guideline from the British Society for Haematology.
The best outcome data is for the R-CHOP regimen (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone) followed by maintenance treatment with rituximab, wrote Pamela McKay, MD, of Beatson West of Scotland Cancer Centre in Glasgow, and her colleagues. The report was published in the British Journal of Haematology. But the combination of rituximab and bendamustine is also effective and a more favorable safety profile, according to the guideline. Single agent rituximab is not recommended.
At relapse, the guideline calls on physicians to take an individualized approach based on age, comorbidities, performance status, and response to prior therapy. Some options to consider include ibrutinib as a single agent or rituximab plus chemotherapy. The authors cautioned that there is little evidence to support maintenance rituximab after relapse treatment.
The guideline also explores the role of autologous stem cell transplantation (ASCT) and allogeneic SCT (alloSCT). The authors recommend that ASCT be considered as consolidation of first-line therapy for patients who are fit for intensive therapy. AlloSCT is a viable option in second remission among fit patients who have an appropriate donor and it may also be effective as a rescue therapy for patients who relapse after ASCT. But alloSCT is appropriate only as a first-line therapy for high-risk patients and is best used as part of a clinical trial, according to the recommendations.
The British Society of Haematology previously issued guidance on mantle cell lymphoma in 2012, but the updated document includes new drug therapeutic options and transplant data. The guideline includes a therapeutic algorithm to assist physicians in choosing first-line therapy, options after first relapse, and management in the case of higher relapse.
The guideline authors reported having no conflicts of interest.
SOURCE: McKay P et al. Br J Haematol. 2018 Jul;182(1):46-62.
Rituximab should be included in first-line chemotherapy when treating mantle cell lymphoma, according to a new management guideline from the British Society for Haematology.
The best outcome data is for the R-CHOP regimen (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone) followed by maintenance treatment with rituximab, wrote Pamela McKay, MD, of Beatson West of Scotland Cancer Centre in Glasgow, and her colleagues. The report was published in the British Journal of Haematology. But the combination of rituximab and bendamustine is also effective and a more favorable safety profile, according to the guideline. Single agent rituximab is not recommended.
At relapse, the guideline calls on physicians to take an individualized approach based on age, comorbidities, performance status, and response to prior therapy. Some options to consider include ibrutinib as a single agent or rituximab plus chemotherapy. The authors cautioned that there is little evidence to support maintenance rituximab after relapse treatment.
The guideline also explores the role of autologous stem cell transplantation (ASCT) and allogeneic SCT (alloSCT). The authors recommend that ASCT be considered as consolidation of first-line therapy for patients who are fit for intensive therapy. AlloSCT is a viable option in second remission among fit patients who have an appropriate donor and it may also be effective as a rescue therapy for patients who relapse after ASCT. But alloSCT is appropriate only as a first-line therapy for high-risk patients and is best used as part of a clinical trial, according to the recommendations.
The British Society of Haematology previously issued guidance on mantle cell lymphoma in 2012, but the updated document includes new drug therapeutic options and transplant data. The guideline includes a therapeutic algorithm to assist physicians in choosing first-line therapy, options after first relapse, and management in the case of higher relapse.
The guideline authors reported having no conflicts of interest.
SOURCE: McKay P et al. Br J Haematol. 2018 Jul;182(1):46-62.
FROM THE BRITISH JOURNAL OF HAEMATOLOGY
Immunogenicity of two-dose Gardasil 9 persists at 36 months
MALMO, SWEDEN – Robust human papillomavirus antibody responses persist through 36 months in boys and girls who received two doses of the 9-valent HPV vaccine known as Gardasil 9 at age 9-14 years, according to an open-label randomized immunogenicity study conducted in 15 countries.
This is reassuring news supportive of regulatory decisions made in 2016/2017 to license the more convenient two-dose schedule in the United States, European Union, Canada, and other countries, Rosybel Drury, PhD, observed in reporting the results at the annual meeting of the European Society for Paediatric Infectious Diseases.
Moreover, HPV type-specific antibody levels at 36 months post vaccination in boys and girls who received two doses were similar to or greater than in the 36-month follow-up of adolescent and young adult females who received three doses at ages 16-26 years.
“This result supports the bridging of efficacy findings in young women receiving three doses to girls and boys receiving two doses,” according to Dr. Drury, a vaccine scientist at Merck Sharp & Dohme in Lyon, France.
She presented an update of a five-cohort study including roughly 1,500 recipients of either two doses of the 9-valent HPV vaccine given 6 or 12 months apart or three doses administered at 0, 2, and 6 months. Four cohorts were composed of 9- to 14-year-olds. The fifth consisted of adolescent girls and young women who got three doses of Gardasil 9 over the course of 6 months at ages 16-26 years. The previous report from this major study provided only short-term data based upon measurements of immunogenicity obtained 1 month after the last dose of vaccine (JAMA. 2016 Dec. 13;316(22):2411-21).
Anti-HPV geometric mean titers were highest 1 month after completing a two- or three-dose series, dropped off sharply during the next 6-12 months, then declined more slowly through 36 months.
While the demonstration of persistent immunogenicity over 3 years of follow-up was reassuring overall, there was a potential hitch: Significantly lower antibody levels for some HPV types were observed in girls who received two doses of the vaccine than in those who got three. Specifically, levels of anti-HPV antibodies to HPV types 18, 31, 45, and 52 were significantly lower in the girls who got two doses of the 9-valent HPV vaccine than in those who got three doses at the same age. Antibody levels directed against HPV types 6, 11, 16, 33, and 58 were similar in the two patient populations.
“The clinical significance of this finding remains unknown,” Dr. Drury said.
Challenged as to why the study didn’t include a single-dose vaccine arm, which would be the preferred preventive strategy in low-income countries where the burden of anogenital cancers and warts due to HPV is greatest, she replied that while there is great interest in this approach, and some modeling studies suggest it would be beneficial, the study she presented was designed to evaluate immunogenicity over time, not clinical efficacy, which needs to be assessed before single-dose public health programs are implemented.
The study was funded by Merck and presented by a company employee.
MALMO, SWEDEN – Robust human papillomavirus antibody responses persist through 36 months in boys and girls who received two doses of the 9-valent HPV vaccine known as Gardasil 9 at age 9-14 years, according to an open-label randomized immunogenicity study conducted in 15 countries.
This is reassuring news supportive of regulatory decisions made in 2016/2017 to license the more convenient two-dose schedule in the United States, European Union, Canada, and other countries, Rosybel Drury, PhD, observed in reporting the results at the annual meeting of the European Society for Paediatric Infectious Diseases.
Moreover, HPV type-specific antibody levels at 36 months post vaccination in boys and girls who received two doses were similar to or greater than in the 36-month follow-up of adolescent and young adult females who received three doses at ages 16-26 years.
“This result supports the bridging of efficacy findings in young women receiving three doses to girls and boys receiving two doses,” according to Dr. Drury, a vaccine scientist at Merck Sharp & Dohme in Lyon, France.
She presented an update of a five-cohort study including roughly 1,500 recipients of either two doses of the 9-valent HPV vaccine given 6 or 12 months apart or three doses administered at 0, 2, and 6 months. Four cohorts were composed of 9- to 14-year-olds. The fifth consisted of adolescent girls and young women who got three doses of Gardasil 9 over the course of 6 months at ages 16-26 years. The previous report from this major study provided only short-term data based upon measurements of immunogenicity obtained 1 month after the last dose of vaccine (JAMA. 2016 Dec. 13;316(22):2411-21).
Anti-HPV geometric mean titers were highest 1 month after completing a two- or three-dose series, dropped off sharply during the next 6-12 months, then declined more slowly through 36 months.
While the demonstration of persistent immunogenicity over 3 years of follow-up was reassuring overall, there was a potential hitch: Significantly lower antibody levels for some HPV types were observed in girls who received two doses of the vaccine than in those who got three. Specifically, levels of anti-HPV antibodies to HPV types 18, 31, 45, and 52 were significantly lower in the girls who got two doses of the 9-valent HPV vaccine than in those who got three doses at the same age. Antibody levels directed against HPV types 6, 11, 16, 33, and 58 were similar in the two patient populations.
“The clinical significance of this finding remains unknown,” Dr. Drury said.
Challenged as to why the study didn’t include a single-dose vaccine arm, which would be the preferred preventive strategy in low-income countries where the burden of anogenital cancers and warts due to HPV is greatest, she replied that while there is great interest in this approach, and some modeling studies suggest it would be beneficial, the study she presented was designed to evaluate immunogenicity over time, not clinical efficacy, which needs to be assessed before single-dose public health programs are implemented.
The study was funded by Merck and presented by a company employee.
MALMO, SWEDEN – Robust human papillomavirus antibody responses persist through 36 months in boys and girls who received two doses of the 9-valent HPV vaccine known as Gardasil 9 at age 9-14 years, according to an open-label randomized immunogenicity study conducted in 15 countries.
This is reassuring news supportive of regulatory decisions made in 2016/2017 to license the more convenient two-dose schedule in the United States, European Union, Canada, and other countries, Rosybel Drury, PhD, observed in reporting the results at the annual meeting of the European Society for Paediatric Infectious Diseases.
Moreover, HPV type-specific antibody levels at 36 months post vaccination in boys and girls who received two doses were similar to or greater than in the 36-month follow-up of adolescent and young adult females who received three doses at ages 16-26 years.
“This result supports the bridging of efficacy findings in young women receiving three doses to girls and boys receiving two doses,” according to Dr. Drury, a vaccine scientist at Merck Sharp & Dohme in Lyon, France.
She presented an update of a five-cohort study including roughly 1,500 recipients of either two doses of the 9-valent HPV vaccine given 6 or 12 months apart or three doses administered at 0, 2, and 6 months. Four cohorts were composed of 9- to 14-year-olds. The fifth consisted of adolescent girls and young women who got three doses of Gardasil 9 over the course of 6 months at ages 16-26 years. The previous report from this major study provided only short-term data based upon measurements of immunogenicity obtained 1 month after the last dose of vaccine (JAMA. 2016 Dec. 13;316(22):2411-21).
Anti-HPV geometric mean titers were highest 1 month after completing a two- or three-dose series, dropped off sharply during the next 6-12 months, then declined more slowly through 36 months.
While the demonstration of persistent immunogenicity over 3 years of follow-up was reassuring overall, there was a potential hitch: Significantly lower antibody levels for some HPV types were observed in girls who received two doses of the vaccine than in those who got three. Specifically, levels of anti-HPV antibodies to HPV types 18, 31, 45, and 52 were significantly lower in the girls who got two doses of the 9-valent HPV vaccine than in those who got three doses at the same age. Antibody levels directed against HPV types 6, 11, 16, 33, and 58 were similar in the two patient populations.
“The clinical significance of this finding remains unknown,” Dr. Drury said.
Challenged as to why the study didn’t include a single-dose vaccine arm, which would be the preferred preventive strategy in low-income countries where the burden of anogenital cancers and warts due to HPV is greatest, she replied that while there is great interest in this approach, and some modeling studies suggest it would be beneficial, the study she presented was designed to evaluate immunogenicity over time, not clinical efficacy, which needs to be assessed before single-dose public health programs are implemented.
The study was funded by Merck and presented by a company employee.
REPORTING FROM ESPID 2018
Key clinical point:
Major finding: HPV type-specific antibody responses to two doses given at age 9-14 years were as good as or better than in 16- to 26-year-olds who got three doses.
Study details: This prospective open-label immunogenicity study included roughly 1,500 subjects in 15 countries who received either two or three doses of the 9-valent HPV vaccine.
Disclosures: The study was funded by Merck and presented by a company employee.
AGA Clinical Practice Update: Statins are safe, effective, and important for most patients with liver disease and dyslipidemia
The medications are only contraindicated in patients with decompensated cirrhosis and statin-induced liver injury, Elizabeth Speliotes, MD, PhD, MPH, and her colleagues wrote in an expert review published in Clinical Gastroenterology and Hepatology. In these patients, statin treatment can compound liver damage and should be avoided, wrote Dr. Speliotes and her coauthors.
Because the liver plays a central role in cholesterol production, many clinicians shy away from treating hyperlipidemia in patients with liver disease. But studies consistently show that lipid-lowering drugs improve dyslipidemia in these patients, which significantly improves both high- and low-density lipoproteins and thereby reduces the long-term risk of cardiovascular disease, the authors wrote.
“Furthermore, the liver plays a role in the metabolism of many drugs, including those that are used to treat dyslipidemia,” wrote Dr. Speliotes of the University of Michigan, Ann Arbor. “It is not surprising, therefore, that many practitioners are hesitant to prescribe medicines to treat dyslipidemia in the setting of liver disease.”
Cholesterol targets described in the 2013 American College of Cardiology/American Heart Association guidelines can safely be applied to patients with liver disease. “The guidelines recommend that adults with cardiovascular disease or LDL of 190 mg/dL or higher be treated with high-intensity statins with the goal of reducing LDL levels by 50%,” they said. Patients whose LDL is 189 mg/dL or lower will benefit from moderate-intensity statins, with a target of a 30%-50% decrease in LDL.
The authors described best practice advice for dyslipidemia treatment in six liver diseases: drug-induced liver injury (DILI), nonalcoholic fatty liver disease (NAFLD), viral hepatitis B and C (HBV and HCV), primary biliary cholangitis (PBC), cirrhosis, and posttransplant dyslipidemia.
DILI
DILI is characterized by elevations of threefold or more in serum alanine aminotransferase (ALT) or aspartate aminotransferase and at least a doubling of total serum bilirubin with no other identifiable cause of these aberrations except the suspect drug. Statins rarely cause a DILI (1 in 100,000 patients), but can cause transient, benign ALT elevations. Statins should be discontinued if ALT or aspartate aminotransferase levels exceed a tripling of the upper limit of normal with concomitant bilirubin elevations. They should not be prescribed to patients with acute liver failure or decompensated liver disease, but otherwise they are safe for most patients with liver disease.
NAFLD
Many patients with NAFLD also have dyslipidemia. All NAFLD patients have an increased risk of cardiovascular disease, although NAFLD and nonalcoholic steatohepatitis are not traditional cardiovascular risk factors. Nevertheless, statins and the accompanying improvement in dyslipidemia have been shown to decrease cardiovascular mortality in these patients. The IDEAL study, for example, showed that moderate statin treatment with 80 mg atorvastatin was associated with a 44% decreased risk in secondary cardiovascular events. Other studies show similar results.
NAFLD patients with elevated LDL may benefit from ezetimibe as primary or add-on therapy. However, none of the drugs used to treat dyslipidemia will improve NAFLD or nonalcoholic steatohepatitis histology.
Viral hepatitis
Hepatitis C virus
Patients with HCV infection often experience decreased serum LDL and total cholesterol. However, these are virally mediated and don’t confer cardiovascular protection. In fact, HCV infections are associated with an increased risk of myocardial infarction. If the patient spontaneously clears the virus, lipids may rebound, so levels should be regularly monitored even if the patient does not need statin therapy.
Hepatitis B virus
HBV also interacts with lipid metabolism and can lead to hyperlipidemia. The American College of Cardiology/American Heart Association guidelines for cardiovascular risk assessment and statin therapy apply to these patients. Statins are safe in patients with either HCV or HBV, who tolerate them well.
PBC
PBC is a chronic autoimmune inflammatory cholestatic disease that is associated with dyslipidemia. These patients exhibit increased serum triglyceride and HDL levels that vary according to PBC stage. About 10% have a significant risk of cardiovascular disease. PBC patients with compensated liver disease can safely tolerate statin treatment, but the drugs should not be given to PBC patients with decompensated liver disease.
Obeticholic acid (OCA) is sometimes used as second-line therapy for PBC; it affects genes that regulate bile acid synthesis, transport, and action. However, the POISE study showed that, while OCA improved PBC symptoms, it was associated with an increase in LDL and total cholesterol and a decrease in HDL. No follow-up studies have determined cardiovascular implications of that change, but OCA should be avoided in patients with active cardiovascular disease or with cardiovascular risk factors.
Cirrhosis
Recent work suggests that patients with cirrhosis may face a higher risk of coronary artery disease than was previously thought, although that risk varies widely according to the etiology of the cirrhosis.
Statins are safe and effective in patients with Child-Pugh class A cirrhosis; there are few data on their safety in patients with decompensated cirrhosis. Some guidance for these patients exists in the 2014 recommendations of the Liver Expert Panel, which advised against statin use in patients with Child-Pugh class B or C cirrhosis.
There’s some evidence that statins reduce portal pressure and may reduce the risk of decompensation in patients whose cirrhosis is caused by HCV or HBV infections, but they should not be used for this purpose.
Posttransplant dyslipidemia
After liver transplant, more than 60% of patients will develop dyslipidemia; these patients often have obesity or diabetes.
Statins are safe for patients with liver transplant. Concomitant use of calcineurin inhibitors and statins that are metabolized by cytochrome P450 may increase the risk of statin-associated myopathy. Pravastatin and fluvastatin are preferable, because they are metabolized by cytochrome P450 34A.
Neither Dr. Speliotes nor her coauthors had any financial disclosures.
SOURCE: Speliotes EK et al. Clin Gastroenterol Hepatol. 2018 Apr 21. doi: 10.1016/j.cgh.2018.04.023.
The medications are only contraindicated in patients with decompensated cirrhosis and statin-induced liver injury, Elizabeth Speliotes, MD, PhD, MPH, and her colleagues wrote in an expert review published in Clinical Gastroenterology and Hepatology. In these patients, statin treatment can compound liver damage and should be avoided, wrote Dr. Speliotes and her coauthors.
Because the liver plays a central role in cholesterol production, many clinicians shy away from treating hyperlipidemia in patients with liver disease. But studies consistently show that lipid-lowering drugs improve dyslipidemia in these patients, which significantly improves both high- and low-density lipoproteins and thereby reduces the long-term risk of cardiovascular disease, the authors wrote.
“Furthermore, the liver plays a role in the metabolism of many drugs, including those that are used to treat dyslipidemia,” wrote Dr. Speliotes of the University of Michigan, Ann Arbor. “It is not surprising, therefore, that many practitioners are hesitant to prescribe medicines to treat dyslipidemia in the setting of liver disease.”
Cholesterol targets described in the 2013 American College of Cardiology/American Heart Association guidelines can safely be applied to patients with liver disease. “The guidelines recommend that adults with cardiovascular disease or LDL of 190 mg/dL or higher be treated with high-intensity statins with the goal of reducing LDL levels by 50%,” they said. Patients whose LDL is 189 mg/dL or lower will benefit from moderate-intensity statins, with a target of a 30%-50% decrease in LDL.
The authors described best practice advice for dyslipidemia treatment in six liver diseases: drug-induced liver injury (DILI), nonalcoholic fatty liver disease (NAFLD), viral hepatitis B and C (HBV and HCV), primary biliary cholangitis (PBC), cirrhosis, and posttransplant dyslipidemia.
DILI
DILI is characterized by elevations of threefold or more in serum alanine aminotransferase (ALT) or aspartate aminotransferase and at least a doubling of total serum bilirubin with no other identifiable cause of these aberrations except the suspect drug. Statins rarely cause a DILI (1 in 100,000 patients), but can cause transient, benign ALT elevations. Statins should be discontinued if ALT or aspartate aminotransferase levels exceed a tripling of the upper limit of normal with concomitant bilirubin elevations. They should not be prescribed to patients with acute liver failure or decompensated liver disease, but otherwise they are safe for most patients with liver disease.
NAFLD
Many patients with NAFLD also have dyslipidemia. All NAFLD patients have an increased risk of cardiovascular disease, although NAFLD and nonalcoholic steatohepatitis are not traditional cardiovascular risk factors. Nevertheless, statins and the accompanying improvement in dyslipidemia have been shown to decrease cardiovascular mortality in these patients. The IDEAL study, for example, showed that moderate statin treatment with 80 mg atorvastatin was associated with a 44% decreased risk in secondary cardiovascular events. Other studies show similar results.
NAFLD patients with elevated LDL may benefit from ezetimibe as primary or add-on therapy. However, none of the drugs used to treat dyslipidemia will improve NAFLD or nonalcoholic steatohepatitis histology.
Viral hepatitis
Hepatitis C virus
Patients with HCV infection often experience decreased serum LDL and total cholesterol. However, these are virally mediated and don’t confer cardiovascular protection. In fact, HCV infections are associated with an increased risk of myocardial infarction. If the patient spontaneously clears the virus, lipids may rebound, so levels should be regularly monitored even if the patient does not need statin therapy.
Hepatitis B virus
HBV also interacts with lipid metabolism and can lead to hyperlipidemia. The American College of Cardiology/American Heart Association guidelines for cardiovascular risk assessment and statin therapy apply to these patients. Statins are safe in patients with either HCV or HBV, who tolerate them well.
PBC
PBC is a chronic autoimmune inflammatory cholestatic disease that is associated with dyslipidemia. These patients exhibit increased serum triglyceride and HDL levels that vary according to PBC stage. About 10% have a significant risk of cardiovascular disease. PBC patients with compensated liver disease can safely tolerate statin treatment, but the drugs should not be given to PBC patients with decompensated liver disease.
Obeticholic acid (OCA) is sometimes used as second-line therapy for PBC; it affects genes that regulate bile acid synthesis, transport, and action. However, the POISE study showed that, while OCA improved PBC symptoms, it was associated with an increase in LDL and total cholesterol and a decrease in HDL. No follow-up studies have determined cardiovascular implications of that change, but OCA should be avoided in patients with active cardiovascular disease or with cardiovascular risk factors.
Cirrhosis
Recent work suggests that patients with cirrhosis may face a higher risk of coronary artery disease than was previously thought, although that risk varies widely according to the etiology of the cirrhosis.
Statins are safe and effective in patients with Child-Pugh class A cirrhosis; there are few data on their safety in patients with decompensated cirrhosis. Some guidance for these patients exists in the 2014 recommendations of the Liver Expert Panel, which advised against statin use in patients with Child-Pugh class B or C cirrhosis.
There’s some evidence that statins reduce portal pressure and may reduce the risk of decompensation in patients whose cirrhosis is caused by HCV or HBV infections, but they should not be used for this purpose.
Posttransplant dyslipidemia
After liver transplant, more than 60% of patients will develop dyslipidemia; these patients often have obesity or diabetes.
Statins are safe for patients with liver transplant. Concomitant use of calcineurin inhibitors and statins that are metabolized by cytochrome P450 may increase the risk of statin-associated myopathy. Pravastatin and fluvastatin are preferable, because they are metabolized by cytochrome P450 34A.
Neither Dr. Speliotes nor her coauthors had any financial disclosures.
SOURCE: Speliotes EK et al. Clin Gastroenterol Hepatol. 2018 Apr 21. doi: 10.1016/j.cgh.2018.04.023.
The medications are only contraindicated in patients with decompensated cirrhosis and statin-induced liver injury, Elizabeth Speliotes, MD, PhD, MPH, and her colleagues wrote in an expert review published in Clinical Gastroenterology and Hepatology. In these patients, statin treatment can compound liver damage and should be avoided, wrote Dr. Speliotes and her coauthors.
Because the liver plays a central role in cholesterol production, many clinicians shy away from treating hyperlipidemia in patients with liver disease. But studies consistently show that lipid-lowering drugs improve dyslipidemia in these patients, which significantly improves both high- and low-density lipoproteins and thereby reduces the long-term risk of cardiovascular disease, the authors wrote.
“Furthermore, the liver plays a role in the metabolism of many drugs, including those that are used to treat dyslipidemia,” wrote Dr. Speliotes of the University of Michigan, Ann Arbor. “It is not surprising, therefore, that many practitioners are hesitant to prescribe medicines to treat dyslipidemia in the setting of liver disease.”
Cholesterol targets described in the 2013 American College of Cardiology/American Heart Association guidelines can safely be applied to patients with liver disease. “The guidelines recommend that adults with cardiovascular disease or LDL of 190 mg/dL or higher be treated with high-intensity statins with the goal of reducing LDL levels by 50%,” they said. Patients whose LDL is 189 mg/dL or lower will benefit from moderate-intensity statins, with a target of a 30%-50% decrease in LDL.
The authors described best practice advice for dyslipidemia treatment in six liver diseases: drug-induced liver injury (DILI), nonalcoholic fatty liver disease (NAFLD), viral hepatitis B and C (HBV and HCV), primary biliary cholangitis (PBC), cirrhosis, and posttransplant dyslipidemia.
DILI
DILI is characterized by elevations of threefold or more in serum alanine aminotransferase (ALT) or aspartate aminotransferase and at least a doubling of total serum bilirubin with no other identifiable cause of these aberrations except the suspect drug. Statins rarely cause a DILI (1 in 100,000 patients), but can cause transient, benign ALT elevations. Statins should be discontinued if ALT or aspartate aminotransferase levels exceed a tripling of the upper limit of normal with concomitant bilirubin elevations. They should not be prescribed to patients with acute liver failure or decompensated liver disease, but otherwise they are safe for most patients with liver disease.
NAFLD
Many patients with NAFLD also have dyslipidemia. All NAFLD patients have an increased risk of cardiovascular disease, although NAFLD and nonalcoholic steatohepatitis are not traditional cardiovascular risk factors. Nevertheless, statins and the accompanying improvement in dyslipidemia have been shown to decrease cardiovascular mortality in these patients. The IDEAL study, for example, showed that moderate statin treatment with 80 mg atorvastatin was associated with a 44% decreased risk in secondary cardiovascular events. Other studies show similar results.
NAFLD patients with elevated LDL may benefit from ezetimibe as primary or add-on therapy. However, none of the drugs used to treat dyslipidemia will improve NAFLD or nonalcoholic steatohepatitis histology.
Viral hepatitis
Hepatitis C virus
Patients with HCV infection often experience decreased serum LDL and total cholesterol. However, these are virally mediated and don’t confer cardiovascular protection. In fact, HCV infections are associated with an increased risk of myocardial infarction. If the patient spontaneously clears the virus, lipids may rebound, so levels should be regularly monitored even if the patient does not need statin therapy.
Hepatitis B virus
HBV also interacts with lipid metabolism and can lead to hyperlipidemia. The American College of Cardiology/American Heart Association guidelines for cardiovascular risk assessment and statin therapy apply to these patients. Statins are safe in patients with either HCV or HBV, who tolerate them well.
PBC
PBC is a chronic autoimmune inflammatory cholestatic disease that is associated with dyslipidemia. These patients exhibit increased serum triglyceride and HDL levels that vary according to PBC stage. About 10% have a significant risk of cardiovascular disease. PBC patients with compensated liver disease can safely tolerate statin treatment, but the drugs should not be given to PBC patients with decompensated liver disease.
Obeticholic acid (OCA) is sometimes used as second-line therapy for PBC; it affects genes that regulate bile acid synthesis, transport, and action. However, the POISE study showed that, while OCA improved PBC symptoms, it was associated with an increase in LDL and total cholesterol and a decrease in HDL. No follow-up studies have determined cardiovascular implications of that change, but OCA should be avoided in patients with active cardiovascular disease or with cardiovascular risk factors.
Cirrhosis
Recent work suggests that patients with cirrhosis may face a higher risk of coronary artery disease than was previously thought, although that risk varies widely according to the etiology of the cirrhosis.
Statins are safe and effective in patients with Child-Pugh class A cirrhosis; there are few data on their safety in patients with decompensated cirrhosis. Some guidance for these patients exists in the 2014 recommendations of the Liver Expert Panel, which advised against statin use in patients with Child-Pugh class B or C cirrhosis.
There’s some evidence that statins reduce portal pressure and may reduce the risk of decompensation in patients whose cirrhosis is caused by HCV or HBV infections, but they should not be used for this purpose.
Posttransplant dyslipidemia
After liver transplant, more than 60% of patients will develop dyslipidemia; these patients often have obesity or diabetes.
Statins are safe for patients with liver transplant. Concomitant use of calcineurin inhibitors and statins that are metabolized by cytochrome P450 may increase the risk of statin-associated myopathy. Pravastatin and fluvastatin are preferable, because they are metabolized by cytochrome P450 34A.
Neither Dr. Speliotes nor her coauthors had any financial disclosures.
SOURCE: Speliotes EK et al. Clin Gastroenterol Hepatol. 2018 Apr 21. doi: 10.1016/j.cgh.2018.04.023.
EXPERT ANALYSIS FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Spironolactone effectively treats acne in adolescent females
LAKE TAHOE, CALIF. –
In an interview at the annual meeting of the Society for Pediatric Dermatology, study author Erin Roberts, MD, said that while spironolactone is widely used in dermatology for treating acne vulgaris in women, it is not approved by the Food and Drug Administration for the treatment of acne, likely because published data are lacking. In addition, she said, less is known about its use, safety, and efficacy in the pediatric population.
Dr. Roberts, a resident in the department of dermatology at the Mayo Clinic, Rochester, Minn., and her associates retrospectively reviewed 80 female patients younger than 21 years of age who were treated with spironolactone and topical therapies alone, or with spironolactone plus oral antibiotics and/or contraceptive pills. All patients were seen by clinicians at the Mayo department of dermatology and were followed for a mean of 11.2 months.
The mean age of patients was 19 years and 71.3% had acne flares with their menstrual cycles, 67.5% had acne located on the jawline, 58.8% had concomitant use of an estrogen-containing oral contraceptive, and 93.8% were unresponsive to other oral treatments prior to using spironolactone.
The median spironolactone daily dose was 100 mg, and ranged between 25 mg and 200 mg. Following acne score assessments, the researchers observed that 64 of the 80 patients (80%) experienced improvement of acne on treatment with spironolactone, while 16 (20%) did not respond and were subsequently escalated to oral isotretinoin therapy. Three patients (3.8%) experienced side effects, most commonly lightheadedness, headache, and fatigue, while five patients stopped taking the medication because of adverse effects, cost, or personal preference.
“It was nice to see that spironolactone did improve acne,” Dr. Roberts said. “We think of it as something to use for patients in their 20s, but not as much for patients in their teens. I think it could be a good option for them.” She also recommended starting patients on a dose of 100 mg daily. “We saw that it does have a dose response,” Dr. Roberts said. “It wasn’t until patients got to 100 mg daily that we started to see significant improvement.”
She reported having no financial disclosures.
LAKE TAHOE, CALIF. –
In an interview at the annual meeting of the Society for Pediatric Dermatology, study author Erin Roberts, MD, said that while spironolactone is widely used in dermatology for treating acne vulgaris in women, it is not approved by the Food and Drug Administration for the treatment of acne, likely because published data are lacking. In addition, she said, less is known about its use, safety, and efficacy in the pediatric population.
Dr. Roberts, a resident in the department of dermatology at the Mayo Clinic, Rochester, Minn., and her associates retrospectively reviewed 80 female patients younger than 21 years of age who were treated with spironolactone and topical therapies alone, or with spironolactone plus oral antibiotics and/or contraceptive pills. All patients were seen by clinicians at the Mayo department of dermatology and were followed for a mean of 11.2 months.
The mean age of patients was 19 years and 71.3% had acne flares with their menstrual cycles, 67.5% had acne located on the jawline, 58.8% had concomitant use of an estrogen-containing oral contraceptive, and 93.8% were unresponsive to other oral treatments prior to using spironolactone.
The median spironolactone daily dose was 100 mg, and ranged between 25 mg and 200 mg. Following acne score assessments, the researchers observed that 64 of the 80 patients (80%) experienced improvement of acne on treatment with spironolactone, while 16 (20%) did not respond and were subsequently escalated to oral isotretinoin therapy. Three patients (3.8%) experienced side effects, most commonly lightheadedness, headache, and fatigue, while five patients stopped taking the medication because of adverse effects, cost, or personal preference.
“It was nice to see that spironolactone did improve acne,” Dr. Roberts said. “We think of it as something to use for patients in their 20s, but not as much for patients in their teens. I think it could be a good option for them.” She also recommended starting patients on a dose of 100 mg daily. “We saw that it does have a dose response,” Dr. Roberts said. “It wasn’t until patients got to 100 mg daily that we started to see significant improvement.”
She reported having no financial disclosures.
LAKE TAHOE, CALIF. –
In an interview at the annual meeting of the Society for Pediatric Dermatology, study author Erin Roberts, MD, said that while spironolactone is widely used in dermatology for treating acne vulgaris in women, it is not approved by the Food and Drug Administration for the treatment of acne, likely because published data are lacking. In addition, she said, less is known about its use, safety, and efficacy in the pediatric population.
Dr. Roberts, a resident in the department of dermatology at the Mayo Clinic, Rochester, Minn., and her associates retrospectively reviewed 80 female patients younger than 21 years of age who were treated with spironolactone and topical therapies alone, or with spironolactone plus oral antibiotics and/or contraceptive pills. All patients were seen by clinicians at the Mayo department of dermatology and were followed for a mean of 11.2 months.
The mean age of patients was 19 years and 71.3% had acne flares with their menstrual cycles, 67.5% had acne located on the jawline, 58.8% had concomitant use of an estrogen-containing oral contraceptive, and 93.8% were unresponsive to other oral treatments prior to using spironolactone.
The median spironolactone daily dose was 100 mg, and ranged between 25 mg and 200 mg. Following acne score assessments, the researchers observed that 64 of the 80 patients (80%) experienced improvement of acne on treatment with spironolactone, while 16 (20%) did not respond and were subsequently escalated to oral isotretinoin therapy. Three patients (3.8%) experienced side effects, most commonly lightheadedness, headache, and fatigue, while five patients stopped taking the medication because of adverse effects, cost, or personal preference.
“It was nice to see that spironolactone did improve acne,” Dr. Roberts said. “We think of it as something to use for patients in their 20s, but not as much for patients in their teens. I think it could be a good option for them.” She also recommended starting patients on a dose of 100 mg daily. “We saw that it does have a dose response,” Dr. Roberts said. “It wasn’t until patients got to 100 mg daily that we started to see significant improvement.”
She reported having no financial disclosures.
AT SPD 2018
Key clinical point: Use of spironolactone for acne may be limited by side effects of lightheadedness, headache, and fatigue.
Major finding: Following acne score assessments, the researchers observed that 64 of the 80 patients (80%) experienced improvement of acne on treatment with spironolactone.
Study details: A retrospective review of 80 adolescent females who were treated with spironolactone and topical therapies alone, or with spironolactone plus oral antibiotics and/or contraceptive pills.
Disclosures: Dr. Roberts reported having no financial disclosures.
Maternal lifestyle affects child obesity
A study published in the British Medical Journal found that women who practiced five healthy habits had children who when they reached adolescence were 75% less likely to be overweight, compared with women who practiced none of the those healthy habits.
The healthy habits were maintaining a healthy weight, eating a nutritious diet, exercising regularly, not smoking, and consuming no more than a moderate amount of alcohol (BMJ 2018;362:k2486). I suspect you aren’t surprised by the core finding of this study of 16,945 female nurses and their 24,289 children. You’ve seen it scores of times. Mothers who lead unhealthy lifestyles seem to have children who are more likely to be obese. Now you have some numbers to support your decades of anecdotal observations. But the question is, what are we supposed to do with this new data? When and with whom should we share this unfortunate truth?
Evidence from previous studies makes it clear that by the time a child enters grade school the die is cast. Baby fat is neither cute nor temporary. This means that our target audience must be mothers-to-be and women whose children are infants and toddlers. On the other hand, telling the mother of an overweight teenager that her own unhealthy habits have probably contributed to her child’s weight problem is cruel and a waste of time. The mother already may have suspected her culpability. She also may feel that it is too late to do anything about it. While there have been some studies looking for an association between paternal body mass index and offspring BMI, I was unable to find any addressing paternal lifestyle and adolescent obesity.
This new study doesn’t address the unusual situation in which a mother of a teenager sheds all five of her unhealthy habits. I guess there may be examples in which a mother’s positive lifestyle change has helped reverse her adolescent child’s path to obesity. But I suspect these cases are rare.
So on one hand but on the other we must be careful to avoid playing the blame game and giving other mothers a one-way ticket on the guilt train. This is just one more example of the tightrope that we have been walking for generations. Every day in our offices we see children whose health is endangered by their parents’ behaviors and lifestyles. In cases in which the parental behavior is creating a serious short-term risk, such as failing to use an appropriate motor vehicle safety restraint system, we have no qualms about speaking out. We aren’t afraid to do a little shaming in hopes of sparing a family a serious guilt trip. When the threat to the child is more abstract and less dramatic – such as vaccine refusal – shaming and education don’t seem to be effective in changing parental behavior.
Obesity presents its own collection of complexities. It is like a car wreck seen in slow motion as the plots on the growth chart accumulate pound by pound. Unfortunately, parents often are among the last to notice or accept the reality. This new study doesn’t tell us whether we can make a difference. But it does suggest that when we first see the warning signs on the growth chart that we should engage the parents in a discussion of their lifestyle and its possible association with the child’s weight gain. The challenge, of course, is how one can cast the discussion without sounding judgmental.
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.” Email him at [email protected].
A study published in the British Medical Journal found that women who practiced five healthy habits had children who when they reached adolescence were 75% less likely to be overweight, compared with women who practiced none of the those healthy habits.
The healthy habits were maintaining a healthy weight, eating a nutritious diet, exercising regularly, not smoking, and consuming no more than a moderate amount of alcohol (BMJ 2018;362:k2486). I suspect you aren’t surprised by the core finding of this study of 16,945 female nurses and their 24,289 children. You’ve seen it scores of times. Mothers who lead unhealthy lifestyles seem to have children who are more likely to be obese. Now you have some numbers to support your decades of anecdotal observations. But the question is, what are we supposed to do with this new data? When and with whom should we share this unfortunate truth?
Evidence from previous studies makes it clear that by the time a child enters grade school the die is cast. Baby fat is neither cute nor temporary. This means that our target audience must be mothers-to-be and women whose children are infants and toddlers. On the other hand, telling the mother of an overweight teenager that her own unhealthy habits have probably contributed to her child’s weight problem is cruel and a waste of time. The mother already may have suspected her culpability. She also may feel that it is too late to do anything about it. While there have been some studies looking for an association between paternal body mass index and offspring BMI, I was unable to find any addressing paternal lifestyle and adolescent obesity.
This new study doesn’t address the unusual situation in which a mother of a teenager sheds all five of her unhealthy habits. I guess there may be examples in which a mother’s positive lifestyle change has helped reverse her adolescent child’s path to obesity. But I suspect these cases are rare.
So on one hand but on the other we must be careful to avoid playing the blame game and giving other mothers a one-way ticket on the guilt train. This is just one more example of the tightrope that we have been walking for generations. Every day in our offices we see children whose health is endangered by their parents’ behaviors and lifestyles. In cases in which the parental behavior is creating a serious short-term risk, such as failing to use an appropriate motor vehicle safety restraint system, we have no qualms about speaking out. We aren’t afraid to do a little shaming in hopes of sparing a family a serious guilt trip. When the threat to the child is more abstract and less dramatic – such as vaccine refusal – shaming and education don’t seem to be effective in changing parental behavior.
Obesity presents its own collection of complexities. It is like a car wreck seen in slow motion as the plots on the growth chart accumulate pound by pound. Unfortunately, parents often are among the last to notice or accept the reality. This new study doesn’t tell us whether we can make a difference. But it does suggest that when we first see the warning signs on the growth chart that we should engage the parents in a discussion of their lifestyle and its possible association with the child’s weight gain. The challenge, of course, is how one can cast the discussion without sounding judgmental.
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.” Email him at [email protected].
A study published in the British Medical Journal found that women who practiced five healthy habits had children who when they reached adolescence were 75% less likely to be overweight, compared with women who practiced none of the those healthy habits.
The healthy habits were maintaining a healthy weight, eating a nutritious diet, exercising regularly, not smoking, and consuming no more than a moderate amount of alcohol (BMJ 2018;362:k2486). I suspect you aren’t surprised by the core finding of this study of 16,945 female nurses and their 24,289 children. You’ve seen it scores of times. Mothers who lead unhealthy lifestyles seem to have children who are more likely to be obese. Now you have some numbers to support your decades of anecdotal observations. But the question is, what are we supposed to do with this new data? When and with whom should we share this unfortunate truth?
Evidence from previous studies makes it clear that by the time a child enters grade school the die is cast. Baby fat is neither cute nor temporary. This means that our target audience must be mothers-to-be and women whose children are infants and toddlers. On the other hand, telling the mother of an overweight teenager that her own unhealthy habits have probably contributed to her child’s weight problem is cruel and a waste of time. The mother already may have suspected her culpability. She also may feel that it is too late to do anything about it. While there have been some studies looking for an association between paternal body mass index and offspring BMI, I was unable to find any addressing paternal lifestyle and adolescent obesity.
This new study doesn’t address the unusual situation in which a mother of a teenager sheds all five of her unhealthy habits. I guess there may be examples in which a mother’s positive lifestyle change has helped reverse her adolescent child’s path to obesity. But I suspect these cases are rare.
So on one hand but on the other we must be careful to avoid playing the blame game and giving other mothers a one-way ticket on the guilt train. This is just one more example of the tightrope that we have been walking for generations. Every day in our offices we see children whose health is endangered by their parents’ behaviors and lifestyles. In cases in which the parental behavior is creating a serious short-term risk, such as failing to use an appropriate motor vehicle safety restraint system, we have no qualms about speaking out. We aren’t afraid to do a little shaming in hopes of sparing a family a serious guilt trip. When the threat to the child is more abstract and less dramatic – such as vaccine refusal – shaming and education don’t seem to be effective in changing parental behavior.
Obesity presents its own collection of complexities. It is like a car wreck seen in slow motion as the plots on the growth chart accumulate pound by pound. Unfortunately, parents often are among the last to notice or accept the reality. This new study doesn’t tell us whether we can make a difference. But it does suggest that when we first see the warning signs on the growth chart that we should engage the parents in a discussion of their lifestyle and its possible association with the child’s weight gain. The challenge, of course, is how one can cast the discussion without sounding judgmental.
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.” Email him at [email protected].
AHRQ National Guideline Clearinghouse shutting down
The Agency for Healthcare Research and Quality has announced that after July 16, 2018, its National Guideline Clearinghouse (NGC) website (guideline.gov) will no longer be available because its federal funding will be discontinued. According to the NGC website, its mission is to provide “an accessible mechanism for obtaining objective, detailed information on clinical practice guidelines and to further their dissemination, implementation, and use.”
Its services, all free to use, included providing summaries of each guideline, side-by-side comparisons of two or more guidelines, and syntheses of guidelines covering similar topics, highlighting areas of similarity and difference.
Update, July 17, 2018: Now that the guidelines are no longer available on the government site, ECRI Institute, the independent nonprofit that developed and maintained the National Guidelines Clearinghouse since its inception 20 years ago, “announced plans to continue providing this critical service to the healthcare community.” The ECRI Institute stated that they will launch an interim website this Fall “with many additional features planned for the near future.” Participating guideline developers will be able to access and contribute to the website free of charge, according to the company, while others will be charged a fee. In addition, as a temporary stop-gap, Fred Trotter, founder and CTO of CareSet Systems, a Medicare data use site, voluntarily cloned the complete guidelines before the government site shut down and made them available for public use here: https://github.com/CareSet/AHRQ_search_clone.
The Agency for Healthcare Research and Quality has announced that after July 16, 2018, its National Guideline Clearinghouse (NGC) website (guideline.gov) will no longer be available because its federal funding will be discontinued. According to the NGC website, its mission is to provide “an accessible mechanism for obtaining objective, detailed information on clinical practice guidelines and to further their dissemination, implementation, and use.”
Its services, all free to use, included providing summaries of each guideline, side-by-side comparisons of two or more guidelines, and syntheses of guidelines covering similar topics, highlighting areas of similarity and difference.
Update, July 17, 2018: Now that the guidelines are no longer available on the government site, ECRI Institute, the independent nonprofit that developed and maintained the National Guidelines Clearinghouse since its inception 20 years ago, “announced plans to continue providing this critical service to the healthcare community.” The ECRI Institute stated that they will launch an interim website this Fall “with many additional features planned for the near future.” Participating guideline developers will be able to access and contribute to the website free of charge, according to the company, while others will be charged a fee. In addition, as a temporary stop-gap, Fred Trotter, founder and CTO of CareSet Systems, a Medicare data use site, voluntarily cloned the complete guidelines before the government site shut down and made them available for public use here: https://github.com/CareSet/AHRQ_search_clone.
The Agency for Healthcare Research and Quality has announced that after July 16, 2018, its National Guideline Clearinghouse (NGC) website (guideline.gov) will no longer be available because its federal funding will be discontinued. According to the NGC website, its mission is to provide “an accessible mechanism for obtaining objective, detailed information on clinical practice guidelines and to further their dissemination, implementation, and use.”
Its services, all free to use, included providing summaries of each guideline, side-by-side comparisons of two or more guidelines, and syntheses of guidelines covering similar topics, highlighting areas of similarity and difference.
Update, July 17, 2018: Now that the guidelines are no longer available on the government site, ECRI Institute, the independent nonprofit that developed and maintained the National Guidelines Clearinghouse since its inception 20 years ago, “announced plans to continue providing this critical service to the healthcare community.” The ECRI Institute stated that they will launch an interim website this Fall “with many additional features planned for the near future.” Participating guideline developers will be able to access and contribute to the website free of charge, according to the company, while others will be charged a fee. In addition, as a temporary stop-gap, Fred Trotter, founder and CTO of CareSet Systems, a Medicare data use site, voluntarily cloned the complete guidelines before the government site shut down and made them available for public use here: https://github.com/CareSet/AHRQ_search_clone.
Credit cards FAQ
After my last column on credit cards, I was (as usual) inundated with questions, comments, and requests for copies of the letter we give to patients explaining our credit card policy.
at www.mdedge.com/edermatologynews. If you have a question not addressed here, feel free to ask, either on the website or via email ([email protected]).
How do you safeguard the credit information you keep on file?
The same way we do medical information; it’s all covered by the same HIPAA rules. If you have an EHR, it can go in the chart with everything else; if not, I suggest a separate portable file that can be locked up each night.
How do you keep the info current, as cards do expire?
We check expiration dates at each visit, and ask for a new number or date if the card has expired or is close.
Don’t your patients object to signing, in effect, a blank check?
They’re not “signing a blank check.” All credit card contracts give cardholders the right to challenge any charge against their account.
There were some initial objections, mostly from devotees of the financial “old school.” But when we explain that we’re doing nothing different than a hotel does at each check-in, and that it will work to their advantage as well, by decreasing the bills they will receive and the checks they must write, most come around.
How do you handle patients who refuse to hand over a number, particularly those who say they have no credit cards?
We used to let refusers slide, but now we’ve made the policy mandatory. Patients who refuse without a good reason are asked, like any patient who refuses to cooperate with any standard office policy, to go elsewhere. Life’s too short. And “I don’t have any credit cards” does not count as a good reason. Nearly everyone has credit cards in this day and age. For the occasional patient who does not have a credit card, my office manager does have authority to make exceptions on a case-by-case basis, however.
One cosmetic surgeon I know asks “no credit card” patients to pay a lawyer-style “retainer,” which is held in escrow, and used to pay receivable amounts as they come due. When presented with that alternative, he told me, most of them suddenly remember that they do have a credit card after all.
What’s the difference between this and “balance billing”?
All the difference in the world. “Balance billing” is billing patients for the difference between your normal fee and the insurer’s authorized payment. If your office has contracted to accept that particular insurance, you can’t do that; but you can bill for the portion of the insurer-determined payment not paid by the insurer. (Many contracts stipulate that you must do so.) For example, your normal fee is $200; the insurer approves $100, and pays 80% of that. The other $20 is the patient’s responsibility, and that is what you charge to the credit card – instead of sending out a statement for that amount.
Since we instituted this policy, one patient has called to ask if it is legal, and one insurance company has inquired about it. How do you respond to such queries?
Of course it’s legal; you are entitled to collect what is owed to you. Ask those patients if they question the legality every time they check into a hotel or rent a car.
We have had no inquiries from insurers, but my response would be that it’s none of their business. Again, you have every right to bill for the patient-owed portion of your fees – in fact, Medicare and many private insurers consider it an illegal “inducement” if you don’t – and third parties have no right to dictate how you can or cannot collect it.
In the past, another popular practice management columnist advised against adopting this policy.
Despite multiple requests from me and others, that columnist – who owns a medical billing company – has never, to my knowledge, offered a single convincing argument in support of that position.
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].
After my last column on credit cards, I was (as usual) inundated with questions, comments, and requests for copies of the letter we give to patients explaining our credit card policy.
at www.mdedge.com/edermatologynews. If you have a question not addressed here, feel free to ask, either on the website or via email ([email protected]).
How do you safeguard the credit information you keep on file?
The same way we do medical information; it’s all covered by the same HIPAA rules. If you have an EHR, it can go in the chart with everything else; if not, I suggest a separate portable file that can be locked up each night.
How do you keep the info current, as cards do expire?
We check expiration dates at each visit, and ask for a new number or date if the card has expired or is close.
Don’t your patients object to signing, in effect, a blank check?
They’re not “signing a blank check.” All credit card contracts give cardholders the right to challenge any charge against their account.
There were some initial objections, mostly from devotees of the financial “old school.” But when we explain that we’re doing nothing different than a hotel does at each check-in, and that it will work to their advantage as well, by decreasing the bills they will receive and the checks they must write, most come around.
How do you handle patients who refuse to hand over a number, particularly those who say they have no credit cards?
We used to let refusers slide, but now we’ve made the policy mandatory. Patients who refuse without a good reason are asked, like any patient who refuses to cooperate with any standard office policy, to go elsewhere. Life’s too short. And “I don’t have any credit cards” does not count as a good reason. Nearly everyone has credit cards in this day and age. For the occasional patient who does not have a credit card, my office manager does have authority to make exceptions on a case-by-case basis, however.
One cosmetic surgeon I know asks “no credit card” patients to pay a lawyer-style “retainer,” which is held in escrow, and used to pay receivable amounts as they come due. When presented with that alternative, he told me, most of them suddenly remember that they do have a credit card after all.
What’s the difference between this and “balance billing”?
All the difference in the world. “Balance billing” is billing patients for the difference between your normal fee and the insurer’s authorized payment. If your office has contracted to accept that particular insurance, you can’t do that; but you can bill for the portion of the insurer-determined payment not paid by the insurer. (Many contracts stipulate that you must do so.) For example, your normal fee is $200; the insurer approves $100, and pays 80% of that. The other $20 is the patient’s responsibility, and that is what you charge to the credit card – instead of sending out a statement for that amount.
Since we instituted this policy, one patient has called to ask if it is legal, and one insurance company has inquired about it. How do you respond to such queries?
Of course it’s legal; you are entitled to collect what is owed to you. Ask those patients if they question the legality every time they check into a hotel or rent a car.
We have had no inquiries from insurers, but my response would be that it’s none of their business. Again, you have every right to bill for the patient-owed portion of your fees – in fact, Medicare and many private insurers consider it an illegal “inducement” if you don’t – and third parties have no right to dictate how you can or cannot collect it.
In the past, another popular practice management columnist advised against adopting this policy.
Despite multiple requests from me and others, that columnist – who owns a medical billing company – has never, to my knowledge, offered a single convincing argument in support of that position.
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].
After my last column on credit cards, I was (as usual) inundated with questions, comments, and requests for copies of the letter we give to patients explaining our credit card policy.
at www.mdedge.com/edermatologynews. If you have a question not addressed here, feel free to ask, either on the website or via email ([email protected]).
How do you safeguard the credit information you keep on file?
The same way we do medical information; it’s all covered by the same HIPAA rules. If you have an EHR, it can go in the chart with everything else; if not, I suggest a separate portable file that can be locked up each night.
How do you keep the info current, as cards do expire?
We check expiration dates at each visit, and ask for a new number or date if the card has expired or is close.
Don’t your patients object to signing, in effect, a blank check?
They’re not “signing a blank check.” All credit card contracts give cardholders the right to challenge any charge against their account.
There were some initial objections, mostly from devotees of the financial “old school.” But when we explain that we’re doing nothing different than a hotel does at each check-in, and that it will work to their advantage as well, by decreasing the bills they will receive and the checks they must write, most come around.
How do you handle patients who refuse to hand over a number, particularly those who say they have no credit cards?
We used to let refusers slide, but now we’ve made the policy mandatory. Patients who refuse without a good reason are asked, like any patient who refuses to cooperate with any standard office policy, to go elsewhere. Life’s too short. And “I don’t have any credit cards” does not count as a good reason. Nearly everyone has credit cards in this day and age. For the occasional patient who does not have a credit card, my office manager does have authority to make exceptions on a case-by-case basis, however.
One cosmetic surgeon I know asks “no credit card” patients to pay a lawyer-style “retainer,” which is held in escrow, and used to pay receivable amounts as they come due. When presented with that alternative, he told me, most of them suddenly remember that they do have a credit card after all.
What’s the difference between this and “balance billing”?
All the difference in the world. “Balance billing” is billing patients for the difference between your normal fee and the insurer’s authorized payment. If your office has contracted to accept that particular insurance, you can’t do that; but you can bill for the portion of the insurer-determined payment not paid by the insurer. (Many contracts stipulate that you must do so.) For example, your normal fee is $200; the insurer approves $100, and pays 80% of that. The other $20 is the patient’s responsibility, and that is what you charge to the credit card – instead of sending out a statement for that amount.
Since we instituted this policy, one patient has called to ask if it is legal, and one insurance company has inquired about it. How do you respond to such queries?
Of course it’s legal; you are entitled to collect what is owed to you. Ask those patients if they question the legality every time they check into a hotel or rent a car.
We have had no inquiries from insurers, but my response would be that it’s none of their business. Again, you have every right to bill for the patient-owed portion of your fees – in fact, Medicare and many private insurers consider it an illegal “inducement” if you don’t – and third parties have no right to dictate how you can or cannot collect it.
In the past, another popular practice management columnist advised against adopting this policy.
Despite multiple requests from me and others, that columnist – who owns a medical billing company – has never, to my knowledge, offered a single convincing argument in support of that position.
Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].
Pediatric inpatient seizures treated quickly with new intervention
TORONTO – Researchers at UCSF Benioff Children’s Hospital in San Francisco implemented a novel intervention that leveraged existing in-room technology to expedite antiepileptic drug administration to inpatients having a seizure.
With the quality initiative, they were able to decrease median time from seizure onset to benzodiazepine (BZD) administration from 7 minutes (preintervention) to 2 minutes (post intervention) and reduce the median time from order to administration of second-phase non-BZDs from 28 minutes to 11 minutes.
“Leveraging existing patient room technology to mobilize pharmacy to the bedside expedited non-BZD administration by 60%,” reported principal investigator Arpi Bekmezian, MD, a pediatric hospitalist and medical director of quality and safety at Benioff Children’s Hospital. She presented the findings at the Pediatric Academic Societies annual meeting.
“Furthermore, the rapid-response seizure rescue process may have created an increased sense of urgency helping to expedite initial BZD administration by 70%. ... This may have prevented the need for second-phase therapy and progression to status epilepticus, potentially minimizing the risk of neuronal injury, and all without the additional resources of a Code team.”
Early and rapid escalation of treatment is critical to prevent neuronal injury in patients with status epilepticus. Guidelines recommend initial antiepileptic therapy at 5 minutes, with rapid escalation to second-phase therapy if the seizure persists.
Preintervention baseline data from UCSF Benioff Children’s indicated a 7-minute lag time from seizure onset to BZD therapy and a 28-minute lag from order to administration of non-BZDs (phenobarbital, phenytoin, levetiracetam, valproic acid). Other studies have shown significantly greater delays to antiepileptic treatment.
“That was just too long, and it matched our clinical experience of being at the bedside of a seizing patient and wondering why the medication was taking so long to arrive from the pharmacy.”
The researchers set out to reduce time to BZD administration from 7 minutes to 5 minutes or less and to reduce time to second-phase non-BZD administration to less than 10 minutes. To accomplish this, a multidisciplinary team that included leadership from physicians, pharmacy, and nursing defined primary and secondary drivers of efficiency, with interventions targeting both team communication and medication delivery.
The intervention period lasted 16 months, during which time there were 61 seizure events requiring urgent antiepileptic treatment. Complete data were available for 57 seizures.
Among the interventions they implemented was to stock all medication-dispensing stations with intranasal/buccal BZD available on “nursing override” for easy access and administration.
Because non-BZDs require pharmacy compounding, and the main pharmacy receives many STAT orders with competing priorities, they developed a hospitalwide “seizure rescue” (SR) process by using patient-room staff terminals to activate a dedicated individual from the pharmacy, who would then report to the bedside with a backpack stocked with non-BZDs ready to compound. Nurses were trained to press the SR button for any seizure that may require urgent therapy.
“We didn’t want nurses to waste time on the phone [calling pharmacy], and we considered calling a Code, but we couldn’t really justify the resource utilization as most of these patients didn’t have respiratory compromise, and they didn’t need the whole Code team,” said Dr. Bekmezian. She noted that her hospital strongly discourages bedside compounding by nursing staff.
Instead, they realized they could easily reprogram the patient-room electronic staff terminals to have a dedicated SR button that would directly alert a dedicated pharmacist carrying the SR phone. The pharmacist could then swipe and confirm that they received the alert and let the nurse know they were on the way, “and this would free up the nurse to go ahead and obtain the benzodiazepines and administer them as pharmacy made their way to the room.”
“To our knowledge, this is the first study to report expediting antiepileptic drug delivery to patients in the hospital,” said Dr. Bekmezian. She noted that less than 50% of cases actually required pharmacist response, “but the pharmacy staff chose to be activated earlier in the management algorithm to avoid delays in treatment.”
UCSF Children’s Hospital San Francisco campus is a 183-bed, tertiary care, teaching children’s hospital that has pediatric, neonatal, and cardiac intensive care units and set-down units. They provide liver, bone marrow, kidney, and cardiac transplantation and have more than 10,000 annual admissions.
The investigators reported no conflicts of interest.
SOURCE: Bekmezian A et al. PAS 2018. Abstract 3545.3.
TORONTO – Researchers at UCSF Benioff Children’s Hospital in San Francisco implemented a novel intervention that leveraged existing in-room technology to expedite antiepileptic drug administration to inpatients having a seizure.
With the quality initiative, they were able to decrease median time from seizure onset to benzodiazepine (BZD) administration from 7 minutes (preintervention) to 2 minutes (post intervention) and reduce the median time from order to administration of second-phase non-BZDs from 28 minutes to 11 minutes.
“Leveraging existing patient room technology to mobilize pharmacy to the bedside expedited non-BZD administration by 60%,” reported principal investigator Arpi Bekmezian, MD, a pediatric hospitalist and medical director of quality and safety at Benioff Children’s Hospital. She presented the findings at the Pediatric Academic Societies annual meeting.
“Furthermore, the rapid-response seizure rescue process may have created an increased sense of urgency helping to expedite initial BZD administration by 70%. ... This may have prevented the need for second-phase therapy and progression to status epilepticus, potentially minimizing the risk of neuronal injury, and all without the additional resources of a Code team.”
Early and rapid escalation of treatment is critical to prevent neuronal injury in patients with status epilepticus. Guidelines recommend initial antiepileptic therapy at 5 minutes, with rapid escalation to second-phase therapy if the seizure persists.
Preintervention baseline data from UCSF Benioff Children’s indicated a 7-minute lag time from seizure onset to BZD therapy and a 28-minute lag from order to administration of non-BZDs (phenobarbital, phenytoin, levetiracetam, valproic acid). Other studies have shown significantly greater delays to antiepileptic treatment.
“That was just too long, and it matched our clinical experience of being at the bedside of a seizing patient and wondering why the medication was taking so long to arrive from the pharmacy.”
The researchers set out to reduce time to BZD administration from 7 minutes to 5 minutes or less and to reduce time to second-phase non-BZD administration to less than 10 minutes. To accomplish this, a multidisciplinary team that included leadership from physicians, pharmacy, and nursing defined primary and secondary drivers of efficiency, with interventions targeting both team communication and medication delivery.
The intervention period lasted 16 months, during which time there were 61 seizure events requiring urgent antiepileptic treatment. Complete data were available for 57 seizures.
Among the interventions they implemented was to stock all medication-dispensing stations with intranasal/buccal BZD available on “nursing override” for easy access and administration.
Because non-BZDs require pharmacy compounding, and the main pharmacy receives many STAT orders with competing priorities, they developed a hospitalwide “seizure rescue” (SR) process by using patient-room staff terminals to activate a dedicated individual from the pharmacy, who would then report to the bedside with a backpack stocked with non-BZDs ready to compound. Nurses were trained to press the SR button for any seizure that may require urgent therapy.
“We didn’t want nurses to waste time on the phone [calling pharmacy], and we considered calling a Code, but we couldn’t really justify the resource utilization as most of these patients didn’t have respiratory compromise, and they didn’t need the whole Code team,” said Dr. Bekmezian. She noted that her hospital strongly discourages bedside compounding by nursing staff.
Instead, they realized they could easily reprogram the patient-room electronic staff terminals to have a dedicated SR button that would directly alert a dedicated pharmacist carrying the SR phone. The pharmacist could then swipe and confirm that they received the alert and let the nurse know they were on the way, “and this would free up the nurse to go ahead and obtain the benzodiazepines and administer them as pharmacy made their way to the room.”
“To our knowledge, this is the first study to report expediting antiepileptic drug delivery to patients in the hospital,” said Dr. Bekmezian. She noted that less than 50% of cases actually required pharmacist response, “but the pharmacy staff chose to be activated earlier in the management algorithm to avoid delays in treatment.”
UCSF Children’s Hospital San Francisco campus is a 183-bed, tertiary care, teaching children’s hospital that has pediatric, neonatal, and cardiac intensive care units and set-down units. They provide liver, bone marrow, kidney, and cardiac transplantation and have more than 10,000 annual admissions.
The investigators reported no conflicts of interest.
SOURCE: Bekmezian A et al. PAS 2018. Abstract 3545.3.
TORONTO – Researchers at UCSF Benioff Children’s Hospital in San Francisco implemented a novel intervention that leveraged existing in-room technology to expedite antiepileptic drug administration to inpatients having a seizure.
With the quality initiative, they were able to decrease median time from seizure onset to benzodiazepine (BZD) administration from 7 minutes (preintervention) to 2 minutes (post intervention) and reduce the median time from order to administration of second-phase non-BZDs from 28 minutes to 11 minutes.
“Leveraging existing patient room technology to mobilize pharmacy to the bedside expedited non-BZD administration by 60%,” reported principal investigator Arpi Bekmezian, MD, a pediatric hospitalist and medical director of quality and safety at Benioff Children’s Hospital. She presented the findings at the Pediatric Academic Societies annual meeting.
“Furthermore, the rapid-response seizure rescue process may have created an increased sense of urgency helping to expedite initial BZD administration by 70%. ... This may have prevented the need for second-phase therapy and progression to status epilepticus, potentially minimizing the risk of neuronal injury, and all without the additional resources of a Code team.”
Early and rapid escalation of treatment is critical to prevent neuronal injury in patients with status epilepticus. Guidelines recommend initial antiepileptic therapy at 5 minutes, with rapid escalation to second-phase therapy if the seizure persists.
Preintervention baseline data from UCSF Benioff Children’s indicated a 7-minute lag time from seizure onset to BZD therapy and a 28-minute lag from order to administration of non-BZDs (phenobarbital, phenytoin, levetiracetam, valproic acid). Other studies have shown significantly greater delays to antiepileptic treatment.
“That was just too long, and it matched our clinical experience of being at the bedside of a seizing patient and wondering why the medication was taking so long to arrive from the pharmacy.”
The researchers set out to reduce time to BZD administration from 7 minutes to 5 minutes or less and to reduce time to second-phase non-BZD administration to less than 10 minutes. To accomplish this, a multidisciplinary team that included leadership from physicians, pharmacy, and nursing defined primary and secondary drivers of efficiency, with interventions targeting both team communication and medication delivery.
The intervention period lasted 16 months, during which time there were 61 seizure events requiring urgent antiepileptic treatment. Complete data were available for 57 seizures.
Among the interventions they implemented was to stock all medication-dispensing stations with intranasal/buccal BZD available on “nursing override” for easy access and administration.
Because non-BZDs require pharmacy compounding, and the main pharmacy receives many STAT orders with competing priorities, they developed a hospitalwide “seizure rescue” (SR) process by using patient-room staff terminals to activate a dedicated individual from the pharmacy, who would then report to the bedside with a backpack stocked with non-BZDs ready to compound. Nurses were trained to press the SR button for any seizure that may require urgent therapy.
“We didn’t want nurses to waste time on the phone [calling pharmacy], and we considered calling a Code, but we couldn’t really justify the resource utilization as most of these patients didn’t have respiratory compromise, and they didn’t need the whole Code team,” said Dr. Bekmezian. She noted that her hospital strongly discourages bedside compounding by nursing staff.
Instead, they realized they could easily reprogram the patient-room electronic staff terminals to have a dedicated SR button that would directly alert a dedicated pharmacist carrying the SR phone. The pharmacist could then swipe and confirm that they received the alert and let the nurse know they were on the way, “and this would free up the nurse to go ahead and obtain the benzodiazepines and administer them as pharmacy made their way to the room.”
“To our knowledge, this is the first study to report expediting antiepileptic drug delivery to patients in the hospital,” said Dr. Bekmezian. She noted that less than 50% of cases actually required pharmacist response, “but the pharmacy staff chose to be activated earlier in the management algorithm to avoid delays in treatment.”
UCSF Children’s Hospital San Francisco campus is a 183-bed, tertiary care, teaching children’s hospital that has pediatric, neonatal, and cardiac intensive care units and set-down units. They provide liver, bone marrow, kidney, and cardiac transplantation and have more than 10,000 annual admissions.
The investigators reported no conflicts of interest.
SOURCE: Bekmezian A et al. PAS 2018. Abstract 3545.3.
AT PAS 2018
Key clinical point: An intervention to speed delivery of antiepileptic drugs significantly reduced time to treatment.
Major finding: Median time from seizure onset to benzodiazepine (BZD) administration fell from 7 minutes preintervention to 2 minutes post intervention, and median time from order to administration of non-BZDs dropped from 28 minutes to 11 minutes.
Study details: A prospective, multicenter study of 57 seizure events during a 16-month period.
Disclosures: The investigators reported no conflicts of interest.
Source: Bekmezian A et al. PAS 2018. Abstract 3545.3.
CDC releases website for ME/CFS information
The Centers for Disease Control and Prevention has released a website for health care providers about myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
The website is designed to help clinicians by offering information about how they can better assess and help their patients manage the illness. The website includes information about the presentation and clinical course of ME/CFS, diagnosis, clinical care, understanding historical case definitions and criteria, and free continuing education.
The website’s resource section includes the National Academy of Medicine report published in 2015, as well as primers and clinical practice guidelines.
Currently, it is estimated that 836,000 to 2.5 million Americans have ME/CFS. Roughly 90% of people who have ME/CFS have not been diagnosed.
The Centers for Disease Control and Prevention has released a website for health care providers about myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
The website is designed to help clinicians by offering information about how they can better assess and help their patients manage the illness. The website includes information about the presentation and clinical course of ME/CFS, diagnosis, clinical care, understanding historical case definitions and criteria, and free continuing education.
The website’s resource section includes the National Academy of Medicine report published in 2015, as well as primers and clinical practice guidelines.
Currently, it is estimated that 836,000 to 2.5 million Americans have ME/CFS. Roughly 90% of people who have ME/CFS have not been diagnosed.
The Centers for Disease Control and Prevention has released a website for health care providers about myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
The website is designed to help clinicians by offering information about how they can better assess and help their patients manage the illness. The website includes information about the presentation and clinical course of ME/CFS, diagnosis, clinical care, understanding historical case definitions and criteria, and free continuing education.
The website’s resource section includes the National Academy of Medicine report published in 2015, as well as primers and clinical practice guidelines.
Currently, it is estimated that 836,000 to 2.5 million Americans have ME/CFS. Roughly 90% of people who have ME/CFS have not been diagnosed.