Among adolescents examined in the emergency department, exposure to synthetic cannabinoids is strongly associated with neuropsychiatric morbidity, according to data published online July 8 ahead of print in Pediatrics. The results support a distinct neuropsychiatric profile of acute synthetic cannabinoid toxicity in adolescents, wrote the investigators.

Synthetic cannabinoids have become popular and accessible and primarily are used for recreation. The adverse effects of synthetic cannabinoid toxicity reported in the literature include tachycardia, cardiac ischemia, acute kidney injury, agitation, first episode of psychosis, seizures, and death. Adolescents are the largest age group presenting to the emergency department with acute synthetic cannabinoid toxicity, and this population requires more intensive care than adults with the same presentation.
 

A multicenter registry analysis

To describe the neuropsychiatric presentation of adolescents to the emergency department after synthetic cannabinoid exposure, compared with that of cannabis exposure, Sarah Ann R. Anderson, MD, PhD, an adolescent medicine fellow at Columbia University Irving Medical Center in New York, and colleagues performed a multicenter registry analysis. They examined data collected from January 2010 through September 2018 from adolescent patients who presented to sites that participate in the Toxicology Investigators Consortium. For each patient, clinicians requested a consultation by a medical toxicologist to aid care. The exposures recorded in the case registry are reported by the patients or witnesses.

Eligible patients were between ages 13 and 19 years and presented to an emergency department with synthetic cannabinoid or cannabis exposure. Dr. Anderson and colleagues collected variables such as age, sex, reported exposures, death in hospital, location of toxicology encounter, and neuropsychiatric signs or symptoms. Patients whose exposure report came from a service outside of an emergency department and those with concomitant use of cannabis and synthetic cannabinoids were excluded. For the purpose of analysis, the investigators classified patients into the following four categories: exposure to synthetic cannabinoids alone, exposure to synthetic cannabinoids and other drugs, exposure to cannabis alone, and exposure to cannabis and other drugs.

Dr. Anderson and colleagues included 348 patients in their study. The sample included 107 patients in the synthetic cannabinoid–only group, 38 in the synthetic cannabinoid/polydrug group, 86 in the cannabis-only group, and 117 in the cannabis/polydrug group. Males predominated in all groups. The one death in the study occurred in the synthetic cannabinoid–only group.
 

Synthetic cannabinoid exposure increased risk for seizures

Compared with the cannabis-only group, the synthetic cannabinoid–only group had an increased risk of coma or CNS depression (odds ratio, 3.42) and seizures (OR, 3.89). The risk of agitation was significantly lower in the synthetic cannabinoid–only group, compared with the cannabis-only group (OR, 0.18). The two single-drug exposure groups did not differ in their associated risks of delirium or toxic psychosis, extrapyramidal signs, dystonia or rigidity, or hallucinations.

Exposure to synthetic cannabinoids plus other drugs was associated with increased risk of agitation (OR, 3.11) and seizures (OR, 4.8), compared with exposure to cannabis plus other drugs. Among patients exposed to synthetic cannabinoids plus other drugs, the most common class of other drug was sympathomimetics (such as synthetic cathinones, cocaine, and amphetamines). Sympathomimetics and ethanol were the two most common classes of drugs among patients exposed to cannabis plus other drugs.
 

Synthetic cannabinoids may have distinctive neuropsychiatric outcomes

“Findings from our study further confirm the previously described association between synthetic cannabinoid–specific overdose and severe neuropsychiatric outcomes,” wrote Dr. Anderson and colleagues. They underscore “the need for targeted public health messaging to adolescents about the dangers of using synthetic cannabinoids alone or combined with other substances.”

The investigators’ finding that patients exposed to synthetic cannabinoids alone had a lower risk of agitation than those exposed to cannabis alone is not consistent with contemporary literature on synthetic cannabinoid–associated agitation. This discordance may reflect differences in the populations studied, “with more severe toxicity prompting the emergency department presentations reported in this study,” wrote Dr. Anderson and colleagues. The current study also may be affected by selection bias, they added.

The researchers acknowledged several limitations of their study. For example, the registry lacked data for variables such as race or ethnicity, concurrent illness, previous drug use, and comorbid conditions. Another limitation was that substance exposure was patient- or witness-reported, and no testing to confirm exposure to synthetic cannabinoids was performed. Finally, the study had a relatively small sample size and lacked information about patients’ long-term outcomes.

Dr. Anderson and colleagues described future research that could address open questions. Analyzing urine to identify the synthetic cannabinoid used and correlating it with the presentation in the emergency department could illuminate specific toxidromes associated with particular compounds, they wrote. Longitudinal data on the long-term effects of adolescent exposure to synthetic cannabinoids would be valuable for understanding potential long-term neurocognitive impairments. “Lastly, additional investigations into the management of adolescent synthetic cannabinoid toxicity in the emergency department is warranted, given the health care cost burden of synthetic cannabinoid–related emergency department visits,” they concluded.

The study was not supported by external funding, and the authors had no relevant disclosures.

[email protected]

SOURCE: Anderson SAR et al. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-2690.

Among adolescents examined in the emergency department, exposure to synthetic cannabinoids is strongly associated with neuropsychiatric morbidity, according to data published online July 8 ahead of print in Pediatrics. The results support a distinct neuropsychiatric profile of acute synthetic cannabinoid toxicity in adolescents, wrote the investigators.

Synthetic cannabinoids have become popular and accessible and primarily are used for recreation. The adverse effects of synthetic cannabinoid toxicity reported in the literature include tachycardia, cardiac ischemia, acute kidney injury, agitation, first episode of psychosis, seizures, and death. Adolescents are the largest age group presenting to the emergency department with acute synthetic cannabinoid toxicity, and this population requires more intensive care than adults with the same presentation.
 

A multicenter registry analysis

To describe the neuropsychiatric presentation of adolescents to the emergency department after synthetic cannabinoid exposure, compared with that of cannabis exposure, Sarah Ann R. Anderson, MD, PhD, an adolescent medicine fellow at Columbia University Irving Medical Center in New York, and colleagues performed a multicenter registry analysis. They examined data collected from January 2010 through September 2018 from adolescent patients who presented to sites that participate in the Toxicology Investigators Consortium. For each patient, clinicians requested a consultation by a medical toxicologist to aid care. The exposures recorded in the case registry are reported by the patients or witnesses.

Eligible patients were between ages 13 and 19 years and presented to an emergency department with synthetic cannabinoid or cannabis exposure. Dr. Anderson and colleagues collected variables such as age, sex, reported exposures, death in hospital, location of toxicology encounter, and neuropsychiatric signs or symptoms. Patients whose exposure report came from a service outside of an emergency department and those with concomitant use of cannabis and synthetic cannabinoids were excluded. For the purpose of analysis, the investigators classified patients into the following four categories: exposure to synthetic cannabinoids alone, exposure to synthetic cannabinoids and other drugs, exposure to cannabis alone, and exposure to cannabis and other drugs.

Dr. Anderson and colleagues included 348 patients in their study. The sample included 107 patients in the synthetic cannabinoid–only group, 38 in the synthetic cannabinoid/polydrug group, 86 in the cannabis-only group, and 117 in the cannabis/polydrug group. Males predominated in all groups. The one death in the study occurred in the synthetic cannabinoid–only group.
 

Synthetic cannabinoid exposure increased risk for seizures

Compared with the cannabis-only group, the synthetic cannabinoid–only group had an increased risk of coma or CNS depression (odds ratio, 3.42) and seizures (OR, 3.89). The risk of agitation was significantly lower in the synthetic cannabinoid–only group, compared with the cannabis-only group (OR, 0.18). The two single-drug exposure groups did not differ in their associated risks of delirium or toxic psychosis, extrapyramidal signs, dystonia or rigidity, or hallucinations.

Exposure to synthetic cannabinoids plus other drugs was associated with increased risk of agitation (OR, 3.11) and seizures (OR, 4.8), compared with exposure to cannabis plus other drugs. Among patients exposed to synthetic cannabinoids plus other drugs, the most common class of other drug was sympathomimetics (such as synthetic cathinones, cocaine, and amphetamines). Sympathomimetics and ethanol were the two most common classes of drugs among patients exposed to cannabis plus other drugs.
 

Synthetic cannabinoids may have distinctive neuropsychiatric outcomes

“Findings from our study further confirm the previously described association between synthetic cannabinoid–specific overdose and severe neuropsychiatric outcomes,” wrote Dr. Anderson and colleagues. They underscore “the need for targeted public health messaging to adolescents about the dangers of using synthetic cannabinoids alone or combined with other substances.”

The investigators’ finding that patients exposed to synthetic cannabinoids alone had a lower risk of agitation than those exposed to cannabis alone is not consistent with contemporary literature on synthetic cannabinoid–associated agitation. This discordance may reflect differences in the populations studied, “with more severe toxicity prompting the emergency department presentations reported in this study,” wrote Dr. Anderson and colleagues. The current study also may be affected by selection bias, they added.

The researchers acknowledged several limitations of their study. For example, the registry lacked data for variables such as race or ethnicity, concurrent illness, previous drug use, and comorbid conditions. Another limitation was that substance exposure was patient- or witness-reported, and no testing to confirm exposure to synthetic cannabinoids was performed. Finally, the study had a relatively small sample size and lacked information about patients’ long-term outcomes.

Dr. Anderson and colleagues described future research that could address open questions. Analyzing urine to identify the synthetic cannabinoid used and correlating it with the presentation in the emergency department could illuminate specific toxidromes associated with particular compounds, they wrote. Longitudinal data on the long-term effects of adolescent exposure to synthetic cannabinoids would be valuable for understanding potential long-term neurocognitive impairments. “Lastly, additional investigations into the management of adolescent synthetic cannabinoid toxicity in the emergency department is warranted, given the health care cost burden of synthetic cannabinoid–related emergency department visits,” they concluded.

The study was not supported by external funding, and the authors had no relevant disclosures.

[email protected]

SOURCE: Anderson SAR et al. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-2690.

Among adolescents examined in the emergency department, exposure to synthetic cannabinoids is strongly associated with neuropsychiatric morbidity, according to data published online July 8 ahead of print in Pediatrics. The results support a distinct neuropsychiatric profile of acute synthetic cannabinoid toxicity in adolescents, wrote the investigators.

Synthetic cannabinoids have become popular and accessible and primarily are used for recreation. The adverse effects of synthetic cannabinoid toxicity reported in the literature include tachycardia, cardiac ischemia, acute kidney injury, agitation, first episode of psychosis, seizures, and death. Adolescents are the largest age group presenting to the emergency department with acute synthetic cannabinoid toxicity, and this population requires more intensive care than adults with the same presentation.
 

A multicenter registry analysis

To describe the neuropsychiatric presentation of adolescents to the emergency department after synthetic cannabinoid exposure, compared with that of cannabis exposure, Sarah Ann R. Anderson, MD, PhD, an adolescent medicine fellow at Columbia University Irving Medical Center in New York, and colleagues performed a multicenter registry analysis. They examined data collected from January 2010 through September 2018 from adolescent patients who presented to sites that participate in the Toxicology Investigators Consortium. For each patient, clinicians requested a consultation by a medical toxicologist to aid care. The exposures recorded in the case registry are reported by the patients or witnesses.

Eligible patients were between ages 13 and 19 years and presented to an emergency department with synthetic cannabinoid or cannabis exposure. Dr. Anderson and colleagues collected variables such as age, sex, reported exposures, death in hospital, location of toxicology encounter, and neuropsychiatric signs or symptoms. Patients whose exposure report came from a service outside of an emergency department and those with concomitant use of cannabis and synthetic cannabinoids were excluded. For the purpose of analysis, the investigators classified patients into the following four categories: exposure to synthetic cannabinoids alone, exposure to synthetic cannabinoids and other drugs, exposure to cannabis alone, and exposure to cannabis and other drugs.

Dr. Anderson and colleagues included 348 patients in their study. The sample included 107 patients in the synthetic cannabinoid–only group, 38 in the synthetic cannabinoid/polydrug group, 86 in the cannabis-only group, and 117 in the cannabis/polydrug group. Males predominated in all groups. The one death in the study occurred in the synthetic cannabinoid–only group.
 

Synthetic cannabinoid exposure increased risk for seizures

Compared with the cannabis-only group, the synthetic cannabinoid–only group had an increased risk of coma or CNS depression (odds ratio, 3.42) and seizures (OR, 3.89). The risk of agitation was significantly lower in the synthetic cannabinoid–only group, compared with the cannabis-only group (OR, 0.18). The two single-drug exposure groups did not differ in their associated risks of delirium or toxic psychosis, extrapyramidal signs, dystonia or rigidity, or hallucinations.

Exposure to synthetic cannabinoids plus other drugs was associated with increased risk of agitation (OR, 3.11) and seizures (OR, 4.8), compared with exposure to cannabis plus other drugs. Among patients exposed to synthetic cannabinoids plus other drugs, the most common class of other drug was sympathomimetics (such as synthetic cathinones, cocaine, and amphetamines). Sympathomimetics and ethanol were the two most common classes of drugs among patients exposed to cannabis plus other drugs.
 

Synthetic cannabinoids may have distinctive neuropsychiatric outcomes

“Findings from our study further confirm the previously described association between synthetic cannabinoid–specific overdose and severe neuropsychiatric outcomes,” wrote Dr. Anderson and colleagues. They underscore “the need for targeted public health messaging to adolescents about the dangers of using synthetic cannabinoids alone or combined with other substances.”

The investigators’ finding that patients exposed to synthetic cannabinoids alone had a lower risk of agitation than those exposed to cannabis alone is not consistent with contemporary literature on synthetic cannabinoid–associated agitation. This discordance may reflect differences in the populations studied, “with more severe toxicity prompting the emergency department presentations reported in this study,” wrote Dr. Anderson and colleagues. The current study also may be affected by selection bias, they added.

The researchers acknowledged several limitations of their study. For example, the registry lacked data for variables such as race or ethnicity, concurrent illness, previous drug use, and comorbid conditions. Another limitation was that substance exposure was patient- or witness-reported, and no testing to confirm exposure to synthetic cannabinoids was performed. Finally, the study had a relatively small sample size and lacked information about patients’ long-term outcomes.

Dr. Anderson and colleagues described future research that could address open questions. Analyzing urine to identify the synthetic cannabinoid used and correlating it with the presentation in the emergency department could illuminate specific toxidromes associated with particular compounds, they wrote. Longitudinal data on the long-term effects of adolescent exposure to synthetic cannabinoids would be valuable for understanding potential long-term neurocognitive impairments. “Lastly, additional investigations into the management of adolescent synthetic cannabinoid toxicity in the emergency department is warranted, given the health care cost burden of synthetic cannabinoid–related emergency department visits,” they concluded.

The study was not supported by external funding, and the authors had no relevant disclosures.

[email protected]

SOURCE: Anderson SAR et al. Pediatrics. 2019 Jul 8. doi: 10.1542/peds.2018-2690.

MADRID – When biologic treatment is indicated after initial tumor necrosis factor (TNF) inhibitor therapy for juvenile idiopathic arthritis (JIA) has failed, the mechanism of action of the second biologic does not appear to matter, according to data presented at the European Congress of Rheumatology.

Sara Freeman/MDedge News

“There appears to be no difference in effectiveness outcomes or drug survival in patients starting a second TNF inhibitor versus an alternative class of biologic,” said Lianne Kearsley-Fleet, an epidemiologist at the Centre for Epidemiology Versus Arthritis at the University of Manchester (England).

Indeed, at 6 months, there were no significant differences among patients who had switched from a TNF inhibitor to another TNF inhibitor or to a biologic with an alternative mechanism of action in terms of:

• The change in Juvenile Arthritis Disease Activity Score (JADAS)-71 from baseline (mean score change, 7.3 with second TNF inhibitor vs. 8.5 with an alternative biologic class).
• The percentage of patients achieving an American College of Rheumatology Pediatric 90% response (22% vs. 15%).
• The proportion of patients achieving minimal disease activity (30% vs. 23%).
• The percentage reaching a minimal clinically important difference (MCID; 44% vs. 43%).

There was also no difference between switching to a TNF inhibitor or alternative biologic in terms of the duration of time patients remained treated with the second-line agent.

“After 1 year, 62% of patients remained on their biologic therapy, and when we looked at drug survival over the course of that year, there was no difference between the two cohorts,” Mrs. Kearsley-Fleet reported. There was no difference also in the reasons for stopping the second biologic.

“We now have a wide range of biologic therapies available; however, there is no evidence regarding which biologic should be prescribed [in JIA], and if patients switch, which order this should be,” Mrs. Kearsley-Fleet stated. Current NHS England guidelines recommend that most patients with JIA should start a TNF inhibitor (unless they are rheumatoid factor positive, in which case they should be treated with rituximab [Rituxan]), and if the first fails, to switch to a second TNF inhibitor rather than to change class. The evidence for this is limited, she noted, adding that adult guidelines for rheumatoid arthritis now recommended a change of class if not contraindicated.

Using data from two pediatric biologics registers – the British Society for Paediatric and Adolescent Rheumatology Etanercept Cohort Study (BSPAR-ETN) and Biologics for Children with Rheumatic Diseases (BCRD) – Mrs. Kearsley-Fleet and her associates looked at data on 241 children and adolescents with polyarticular JIA (or oligoarticular-extended JIA) starting a second biologic. The aim was to compare the effectiveness of starting a second TNF inhibitor versus switching to an alternative class of agent, such as a B-cell depleting agent such as rituximab, in routine clinical practice.

A majority (n = 188; 78%) of patients had etanercept (Enbrel) as their starting TNF inhibitor and those switching to a second TNF inhibitor (n = 196) were most likely to be given adalimumab (Humira; 58%). Patients starting a biologic with another mode of action (n = 45) were most likely to be given the interleukin-6 inhibitor tocilizumab (73%), followed by rituximab in 13%, and abatacept (Orencia) in 11%. The main reasons for switching to another biologic – TNF inhibitor or otherwise – were ineffectiveness (60% with a second TNF inhibitor vs. 62% with another biologic drug class) or adverse events or intolerance (19% vs. 13%, respectively).

The strength of these data are that they come from a very large cohort of children and adolescents starting biologics for JIA, with systematic follow-up and robust statistical methods, Mrs. Kearsley-Fleet said. However, she noted that JIA was rare and that only one-fifth of patients would start a biologic, and just 30% of those patients would then switch to a second biologic.

“We don’t see any reason that the guidelines should be changed,” Mrs. Kearsley-Fleet observed. “However, repeat analysis with a larger sample size is required to reinforce whether there is any advantage of switching or not.”

Versus Arthritis (formerly Arthritis Research UK) and The British Society for Rheumatology provided funding support. Mrs. Kearsley-Fleet had no financial conflicts of interest to disclose.
 

SOURCE: Kearsley-Fleet L et al. Ann Rheum Dis, Jun 2019;8(Suppl 2):74-5. Abstract OP0016. doi: 10.1136/annrheumdis-2019-eular.415.

MADRID – When biologic treatment is indicated after initial tumor necrosis factor (TNF) inhibitor therapy for juvenile idiopathic arthritis (JIA) has failed, the mechanism of action of the second biologic does not appear to matter, according to data presented at the European Congress of Rheumatology.

Sara Freeman/MDedge News

“There appears to be no difference in effectiveness outcomes or drug survival in patients starting a second TNF inhibitor versus an alternative class of biologic,” said Lianne Kearsley-Fleet, an epidemiologist at the Centre for Epidemiology Versus Arthritis at the University of Manchester (England).

Indeed, at 6 months, there were no significant differences among patients who had switched from a TNF inhibitor to another TNF inhibitor or to a biologic with an alternative mechanism of action in terms of:

• The change in Juvenile Arthritis Disease Activity Score (JADAS)-71 from baseline (mean score change, 7.3 with second TNF inhibitor vs. 8.5 with an alternative biologic class).
• The percentage of patients achieving an American College of Rheumatology Pediatric 90% response (22% vs. 15%).
• The proportion of patients achieving minimal disease activity (30% vs. 23%).
• The percentage reaching a minimal clinically important difference (MCID; 44% vs. 43%).

There was also no difference between switching to a TNF inhibitor or alternative biologic in terms of the duration of time patients remained treated with the second-line agent.

“After 1 year, 62% of patients remained on their biologic therapy, and when we looked at drug survival over the course of that year, there was no difference between the two cohorts,” Mrs. Kearsley-Fleet reported. There was no difference also in the reasons for stopping the second biologic.

“We now have a wide range of biologic therapies available; however, there is no evidence regarding which biologic should be prescribed [in JIA], and if patients switch, which order this should be,” Mrs. Kearsley-Fleet stated. Current NHS England guidelines recommend that most patients with JIA should start a TNF inhibitor (unless they are rheumatoid factor positive, in which case they should be treated with rituximab [Rituxan]), and if the first fails, to switch to a second TNF inhibitor rather than to change class. The evidence for this is limited, she noted, adding that adult guidelines for rheumatoid arthritis now recommended a change of class if not contraindicated.

Using data from two pediatric biologics registers – the British Society for Paediatric and Adolescent Rheumatology Etanercept Cohort Study (BSPAR-ETN) and Biologics for Children with Rheumatic Diseases (BCRD) – Mrs. Kearsley-Fleet and her associates looked at data on 241 children and adolescents with polyarticular JIA (or oligoarticular-extended JIA) starting a second biologic. The aim was to compare the effectiveness of starting a second TNF inhibitor versus switching to an alternative class of agent, such as a B-cell depleting agent such as rituximab, in routine clinical practice.

A majority (n = 188; 78%) of patients had etanercept (Enbrel) as their starting TNF inhibitor and those switching to a second TNF inhibitor (n = 196) were most likely to be given adalimumab (Humira; 58%). Patients starting a biologic with another mode of action (n = 45) were most likely to be given the interleukin-6 inhibitor tocilizumab (73%), followed by rituximab in 13%, and abatacept (Orencia) in 11%. The main reasons for switching to another biologic – TNF inhibitor or otherwise – were ineffectiveness (60% with a second TNF inhibitor vs. 62% with another biologic drug class) or adverse events or intolerance (19% vs. 13%, respectively).

The strength of these data are that they come from a very large cohort of children and adolescents starting biologics for JIA, with systematic follow-up and robust statistical methods, Mrs. Kearsley-Fleet said. However, she noted that JIA was rare and that only one-fifth of patients would start a biologic, and just 30% of those patients would then switch to a second biologic.

“We don’t see any reason that the guidelines should be changed,” Mrs. Kearsley-Fleet observed. “However, repeat analysis with a larger sample size is required to reinforce whether there is any advantage of switching or not.”

Versus Arthritis (formerly Arthritis Research UK) and The British Society for Rheumatology provided funding support. Mrs. Kearsley-Fleet had no financial conflicts of interest to disclose.
 

SOURCE: Kearsley-Fleet L et al. Ann Rheum Dis, Jun 2019;8(Suppl 2):74-5. Abstract OP0016. doi: 10.1136/annrheumdis-2019-eular.415.

MADRID – When biologic treatment is indicated after initial tumor necrosis factor (TNF) inhibitor therapy for juvenile idiopathic arthritis (JIA) has failed, the mechanism of action of the second biologic does not appear to matter, according to data presented at the European Congress of Rheumatology.

Sara Freeman/MDedge News

“There appears to be no difference in effectiveness outcomes or drug survival in patients starting a second TNF inhibitor versus an alternative class of biologic,” said Lianne Kearsley-Fleet, an epidemiologist at the Centre for Epidemiology Versus Arthritis at the University of Manchester (England).

Indeed, at 6 months, there were no significant differences among patients who had switched from a TNF inhibitor to another TNF inhibitor or to a biologic with an alternative mechanism of action in terms of:

• The change in Juvenile Arthritis Disease Activity Score (JADAS)-71 from baseline (mean score change, 7.3 with second TNF inhibitor vs. 8.5 with an alternative biologic class).
• The percentage of patients achieving an American College of Rheumatology Pediatric 90% response (22% vs. 15%).
• The proportion of patients achieving minimal disease activity (30% vs. 23%).
• The percentage reaching a minimal clinically important difference (MCID; 44% vs. 43%).

There was also no difference between switching to a TNF inhibitor or alternative biologic in terms of the duration of time patients remained treated with the second-line agent.

“After 1 year, 62% of patients remained on their biologic therapy, and when we looked at drug survival over the course of that year, there was no difference between the two cohorts,” Mrs. Kearsley-Fleet reported. There was no difference also in the reasons for stopping the second biologic.

“We now have a wide range of biologic therapies available; however, there is no evidence regarding which biologic should be prescribed [in JIA], and if patients switch, which order this should be,” Mrs. Kearsley-Fleet stated. Current NHS England guidelines recommend that most patients with JIA should start a TNF inhibitor (unless they are rheumatoid factor positive, in which case they should be treated with rituximab [Rituxan]), and if the first fails, to switch to a second TNF inhibitor rather than to change class. The evidence for this is limited, she noted, adding that adult guidelines for rheumatoid arthritis now recommended a change of class if not contraindicated.

Using data from two pediatric biologics registers – the British Society for Paediatric and Adolescent Rheumatology Etanercept Cohort Study (BSPAR-ETN) and Biologics for Children with Rheumatic Diseases (BCRD) – Mrs. Kearsley-Fleet and her associates looked at data on 241 children and adolescents with polyarticular JIA (or oligoarticular-extended JIA) starting a second biologic. The aim was to compare the effectiveness of starting a second TNF inhibitor versus switching to an alternative class of agent, such as a B-cell depleting agent such as rituximab, in routine clinical practice.

A majority (n = 188; 78%) of patients had etanercept (Enbrel) as their starting TNF inhibitor and those switching to a second TNF inhibitor (n = 196) were most likely to be given adalimumab (Humira; 58%). Patients starting a biologic with another mode of action (n = 45) were most likely to be given the interleukin-6 inhibitor tocilizumab (73%), followed by rituximab in 13%, and abatacept (Orencia) in 11%. The main reasons for switching to another biologic – TNF inhibitor or otherwise – were ineffectiveness (60% with a second TNF inhibitor vs. 62% with another biologic drug class) or adverse events or intolerance (19% vs. 13%, respectively).

The strength of these data are that they come from a very large cohort of children and adolescents starting biologics for JIA, with systematic follow-up and robust statistical methods, Mrs. Kearsley-Fleet said. However, she noted that JIA was rare and that only one-fifth of patients would start a biologic, and just 30% of those patients would then switch to a second biologic.

“We don’t see any reason that the guidelines should be changed,” Mrs. Kearsley-Fleet observed. “However, repeat analysis with a larger sample size is required to reinforce whether there is any advantage of switching or not.”

Versus Arthritis (formerly Arthritis Research UK) and The British Society for Rheumatology provided funding support. Mrs. Kearsley-Fleet had no financial conflicts of interest to disclose.
 

SOURCE: Kearsley-Fleet L et al. Ann Rheum Dis, Jun 2019;8(Suppl 2):74-5. Abstract OP0016. doi: 10.1136/annrheumdis-2019-eular.415.

Individuals who spontaneously cleared their primary hepatitis C virus (HCV) infection or reinfection had significantly more antibodies that recognized multiple HCV genotypes beyond the initial infection, compared with chronically infected individuals, according to a small molecular study of immortalized cultured B cells from patient.

Svisio/Thinkstock

In a study published in the Journal of Hepatology, Sabrina J. Merat of AIMM Therapeutics and colleagues classified patients into two groups based on the outcome of their HCV infection: individuals who became chronically infected (CHRs; n = 5) either after primary infection or after HCV reinfection and individuals who cleared one or more HCV infections and were HCV RNA negative at the end of follow-up (CLs; n = 8). The researchers considered that all CLs who cleared the infection were presumably re-exposed to HCV as they continued injecting drugs for a median of 5.9 years after primary infection. The median follow-up time of individuals after primary HCV infection was 17.5 years.

Although the frequency of total antibodies did not differ between the two groups, the antibodies from CHRs were mainly genotype specific and directed against the genotype of the ongoing infection. Antibodies from CLs showed a much broader reactivity than CHR-derived antibodies, with the absolute number of antibodies recognizing at least three or more genotypes was significantly higher in CLs than in CHRs (13 vs. 0, respectively; P = .03).

In addition, in order to determine which epitopes were being targeted in the CL patients, the researchers tested the antibodies secreted in the B-cell supernatant for binding to E2 alanine mutants in the four epitopes known to be recognized by broadly neutralizing HCV antibodies. They found that the majority of the cross-genotype antibodies (82/113; 73%) were specific for AR3 because they bound to the AR3-specific mutants.

“In chronically infected individuals, AR3-specific antibody responses may be too weak and/or may develop too late to prevent chronic infection. If confirmed, this means that a strong and broadly neutralizing antibody response should be established very early after infection in order to confer protection,” the researchers concluded.

This study was supported by the Virgo consortium, funded by the Dutch government. Sabrina Merat and several coauthors are employees of AIMM Therapeutics, as well as shareholders.

[email protected]

SOURCE: Merat SJ et al. J Hepatol 2019;71:14-24.

Individuals who spontaneously cleared their primary hepatitis C virus (HCV) infection or reinfection had significantly more antibodies that recognized multiple HCV genotypes beyond the initial infection, compared with chronically infected individuals, according to a small molecular study of immortalized cultured B cells from patient.

Svisio/Thinkstock

In a study published in the Journal of Hepatology, Sabrina J. Merat of AIMM Therapeutics and colleagues classified patients into two groups based on the outcome of their HCV infection: individuals who became chronically infected (CHRs; n = 5) either after primary infection or after HCV reinfection and individuals who cleared one or more HCV infections and were HCV RNA negative at the end of follow-up (CLs; n = 8). The researchers considered that all CLs who cleared the infection were presumably re-exposed to HCV as they continued injecting drugs for a median of 5.9 years after primary infection. The median follow-up time of individuals after primary HCV infection was 17.5 years.

Although the frequency of total antibodies did not differ between the two groups, the antibodies from CHRs were mainly genotype specific and directed against the genotype of the ongoing infection. Antibodies from CLs showed a much broader reactivity than CHR-derived antibodies, with the absolute number of antibodies recognizing at least three or more genotypes was significantly higher in CLs than in CHRs (13 vs. 0, respectively; P = .03).

In addition, in order to determine which epitopes were being targeted in the CL patients, the researchers tested the antibodies secreted in the B-cell supernatant for binding to E2 alanine mutants in the four epitopes known to be recognized by broadly neutralizing HCV antibodies. They found that the majority of the cross-genotype antibodies (82/113; 73%) were specific for AR3 because they bound to the AR3-specific mutants.

“In chronically infected individuals, AR3-specific antibody responses may be too weak and/or may develop too late to prevent chronic infection. If confirmed, this means that a strong and broadly neutralizing antibody response should be established very early after infection in order to confer protection,” the researchers concluded.

This study was supported by the Virgo consortium, funded by the Dutch government. Sabrina Merat and several coauthors are employees of AIMM Therapeutics, as well as shareholders.

[email protected]

SOURCE: Merat SJ et al. J Hepatol 2019;71:14-24.

Individuals who spontaneously cleared their primary hepatitis C virus (HCV) infection or reinfection had significantly more antibodies that recognized multiple HCV genotypes beyond the initial infection, compared with chronically infected individuals, according to a small molecular study of immortalized cultured B cells from patient.

Svisio/Thinkstock

In a study published in the Journal of Hepatology, Sabrina J. Merat of AIMM Therapeutics and colleagues classified patients into two groups based on the outcome of their HCV infection: individuals who became chronically infected (CHRs; n = 5) either after primary infection or after HCV reinfection and individuals who cleared one or more HCV infections and were HCV RNA negative at the end of follow-up (CLs; n = 8). The researchers considered that all CLs who cleared the infection were presumably re-exposed to HCV as they continued injecting drugs for a median of 5.9 years after primary infection. The median follow-up time of individuals after primary HCV infection was 17.5 years.

Although the frequency of total antibodies did not differ between the two groups, the antibodies from CHRs were mainly genotype specific and directed against the genotype of the ongoing infection. Antibodies from CLs showed a much broader reactivity than CHR-derived antibodies, with the absolute number of antibodies recognizing at least three or more genotypes was significantly higher in CLs than in CHRs (13 vs. 0, respectively; P = .03).

In addition, in order to determine which epitopes were being targeted in the CL patients, the researchers tested the antibodies secreted in the B-cell supernatant for binding to E2 alanine mutants in the four epitopes known to be recognized by broadly neutralizing HCV antibodies. They found that the majority of the cross-genotype antibodies (82/113; 73%) were specific for AR3 because they bound to the AR3-specific mutants.

“In chronically infected individuals, AR3-specific antibody responses may be too weak and/or may develop too late to prevent chronic infection. If confirmed, this means that a strong and broadly neutralizing antibody response should be established very early after infection in order to confer protection,” the researchers concluded.

This study was supported by the Virgo consortium, funded by the Dutch government. Sabrina Merat and several coauthors are employees of AIMM Therapeutics, as well as shareholders.

[email protected]

SOURCE: Merat SJ et al. J Hepatol 2019;71:14-24.

Body art as a form of human expression is prevalent. The most common types are skin tattoos and piercings, but also include scarification, branding, subdermal implants, and body painting. Body painting has made headlines for its artistic creativity and artistic significance at annual week long temporary communities such as the annual Burning Man art festival.

Culture and history

Medioimages/Photodisc

Culturally, however, body painting has significant historical significance, with Henna painting described in the earliest Hindu Vedic ritual books dating back 5,000 years. Henna painting, most commonly of the hands and feet, known as Mehndi in the Indian subcontinent, signifies painting of symbolic representations of the outer and the inner sun, with the idea of “awakening the inner light.” It is also a common tradition of Hindu weddings and applied in Muslim tradition in India during Eid festivals. Body painting has also been used in other cultures for ceremonial, religious reasons, as well as forms of camouflage during hunting or war. Branding and scarification were used as methods of punishment during the Middle Ages in England and commonly during slavery in the Americas. Traditionally, though, branding and scarification have been seen in darker-skinned individuals as a form of self-expression where tattoos are not as effective visually. African tribes in Ethiopia and Sudan, as well as the Maasai people in Kenya, have used scarification and branding as an ancient art that can signify everything from beauty to transition to adulthood. Some black fraternities also use it as a mark of collegiality.

While tattoos are the most recognized form of body art, body and facial piercing are far more common in the general population among cultures throughout the world. While ear piercings are the most common, historically, nostril piercing has been documented in the Middle East as far back as 4,000 years ago, and both ear and nostril piercing and jewelry are mentioned historically in the Bible (Genesis 24:22, Isaiah 3:21). Ritual tongue piercing was reportedly performed by Aztec and Mayan Indians during ceremonies to honor their deities.



Current Practice

In practice, we see different types of piercings, including but not limited to ear, nose (alar, septum, bridge), eyebrow, lip, tongue, face, nipple, umbilical, and genital piercings. Ear piercings alone may come in many forms. Not only do location, cartilage versus no cartilage involvement, and age of piercing have different implications for care and potential risks/complications, so do the size, type, and shape of jewelry used for the piercing.

Having a better understanding of piercing art is important for dermatologists and dermatologic surgeons because we sometimes treat the sequelae, including infection, allergic reactions from the jewelry, and keloid scars. Patients may intentionally create large size piercings, known as gauge piercings, and decide later they no longer want them. Or earlobe piercings can unintentionally stretch and enlarge over time from prolonged wearing of heavy earrings or trauma, sometimes resulting in a partial or complete earlobe split, requiring surgical treatment for gauge or split earlobe repair. If repiercing earlobe repair is desired, most physicians wait at least 6-8 weeks. While different earlobe surgical repair techniques (most commonly Z-plasty) and even recommendations for subdermal implant removal are described in the literature, there are no real guidelines on when to repierce in the evidenced-based literature. Healing time in general for piercings also varies by site. For example, initial earlobe piercings typically take 1-2 months to heal, whereas ear cartilage and navel piercings may take 4-12 months.

Some medical practitioners may not be aware of tips known to top piercing professionals that can help guide patients on piercing care. Cartilage piercings can sometimes present with inflammation and nodule formation, even prior to true keloid formation. In my experience, a simple solution of washing daily with a highly alkaline but gentle natural soap, such as Dr. Bronner’s mild baby soap, or compresses or soaks with warm salt water, can sometimes reduce the inflammation and resolve nodule formation before topical, intralesional corticosteroids, or surgery is needed (a situation in which surgery may lead to further cartilage inflammation and hypertrophic scar formation). Additionally, certain pressure earrings may be used to help prevent keloid formation, in addition to wearing jewelry of a metal that is nonallergenic to the user, to prevent further inflammation.

Piercing is a common form of body art and self-expression. Understanding piercing art can not only help us understand how to better treat the sequelae of piercing, but also develop a better understanding of and relationship with our patients by virtue of their means of artistic self-expression.
 

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
 

Body art as a form of human expression is prevalent. The most common types are skin tattoos and piercings, but also include scarification, branding, subdermal implants, and body painting. Body painting has made headlines for its artistic creativity and artistic significance at annual week long temporary communities such as the annual Burning Man art festival.

Culture and history

Medioimages/Photodisc

Culturally, however, body painting has significant historical significance, with Henna painting described in the earliest Hindu Vedic ritual books dating back 5,000 years. Henna painting, most commonly of the hands and feet, known as Mehndi in the Indian subcontinent, signifies painting of symbolic representations of the outer and the inner sun, with the idea of “awakening the inner light.” It is also a common tradition of Hindu weddings and applied in Muslim tradition in India during Eid festivals. Body painting has also been used in other cultures for ceremonial, religious reasons, as well as forms of camouflage during hunting or war. Branding and scarification were used as methods of punishment during the Middle Ages in England and commonly during slavery in the Americas. Traditionally, though, branding and scarification have been seen in darker-skinned individuals as a form of self-expression where tattoos are not as effective visually. African tribes in Ethiopia and Sudan, as well as the Maasai people in Kenya, have used scarification and branding as an ancient art that can signify everything from beauty to transition to adulthood. Some black fraternities also use it as a mark of collegiality.

While tattoos are the most recognized form of body art, body and facial piercing are far more common in the general population among cultures throughout the world. While ear piercings are the most common, historically, nostril piercing has been documented in the Middle East as far back as 4,000 years ago, and both ear and nostril piercing and jewelry are mentioned historically in the Bible (Genesis 24:22, Isaiah 3:21). Ritual tongue piercing was reportedly performed by Aztec and Mayan Indians during ceremonies to honor their deities.



Current Practice

In practice, we see different types of piercings, including but not limited to ear, nose (alar, septum, bridge), eyebrow, lip, tongue, face, nipple, umbilical, and genital piercings. Ear piercings alone may come in many forms. Not only do location, cartilage versus no cartilage involvement, and age of piercing have different implications for care and potential risks/complications, so do the size, type, and shape of jewelry used for the piercing.

Having a better understanding of piercing art is important for dermatologists and dermatologic surgeons because we sometimes treat the sequelae, including infection, allergic reactions from the jewelry, and keloid scars. Patients may intentionally create large size piercings, known as gauge piercings, and decide later they no longer want them. Or earlobe piercings can unintentionally stretch and enlarge over time from prolonged wearing of heavy earrings or trauma, sometimes resulting in a partial or complete earlobe split, requiring surgical treatment for gauge or split earlobe repair. If repiercing earlobe repair is desired, most physicians wait at least 6-8 weeks. While different earlobe surgical repair techniques (most commonly Z-plasty) and even recommendations for subdermal implant removal are described in the literature, there are no real guidelines on when to repierce in the evidenced-based literature. Healing time in general for piercings also varies by site. For example, initial earlobe piercings typically take 1-2 months to heal, whereas ear cartilage and navel piercings may take 4-12 months.

Some medical practitioners may not be aware of tips known to top piercing professionals that can help guide patients on piercing care. Cartilage piercings can sometimes present with inflammation and nodule formation, even prior to true keloid formation. In my experience, a simple solution of washing daily with a highly alkaline but gentle natural soap, such as Dr. Bronner’s mild baby soap, or compresses or soaks with warm salt water, can sometimes reduce the inflammation and resolve nodule formation before topical, intralesional corticosteroids, or surgery is needed (a situation in which surgery may lead to further cartilage inflammation and hypertrophic scar formation). Additionally, certain pressure earrings may be used to help prevent keloid formation, in addition to wearing jewelry of a metal that is nonallergenic to the user, to prevent further inflammation.

Piercing is a common form of body art and self-expression. Understanding piercing art can not only help us understand how to better treat the sequelae of piercing, but also develop a better understanding of and relationship with our patients by virtue of their means of artistic self-expression.
 

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
 

Body art as a form of human expression is prevalent. The most common types are skin tattoos and piercings, but also include scarification, branding, subdermal implants, and body painting. Body painting has made headlines for its artistic creativity and artistic significance at annual week long temporary communities such as the annual Burning Man art festival.

Culture and history

Medioimages/Photodisc

Culturally, however, body painting has significant historical significance, with Henna painting described in the earliest Hindu Vedic ritual books dating back 5,000 years. Henna painting, most commonly of the hands and feet, known as Mehndi in the Indian subcontinent, signifies painting of symbolic representations of the outer and the inner sun, with the idea of “awakening the inner light.” It is also a common tradition of Hindu weddings and applied in Muslim tradition in India during Eid festivals. Body painting has also been used in other cultures for ceremonial, religious reasons, as well as forms of camouflage during hunting or war. Branding and scarification were used as methods of punishment during the Middle Ages in England and commonly during slavery in the Americas. Traditionally, though, branding and scarification have been seen in darker-skinned individuals as a form of self-expression where tattoos are not as effective visually. African tribes in Ethiopia and Sudan, as well as the Maasai people in Kenya, have used scarification and branding as an ancient art that can signify everything from beauty to transition to adulthood. Some black fraternities also use it as a mark of collegiality.

While tattoos are the most recognized form of body art, body and facial piercing are far more common in the general population among cultures throughout the world. While ear piercings are the most common, historically, nostril piercing has been documented in the Middle East as far back as 4,000 years ago, and both ear and nostril piercing and jewelry are mentioned historically in the Bible (Genesis 24:22, Isaiah 3:21). Ritual tongue piercing was reportedly performed by Aztec and Mayan Indians during ceremonies to honor their deities.



Current Practice

In practice, we see different types of piercings, including but not limited to ear, nose (alar, septum, bridge), eyebrow, lip, tongue, face, nipple, umbilical, and genital piercings. Ear piercings alone may come in many forms. Not only do location, cartilage versus no cartilage involvement, and age of piercing have different implications for care and potential risks/complications, so do the size, type, and shape of jewelry used for the piercing.

Having a better understanding of piercing art is important for dermatologists and dermatologic surgeons because we sometimes treat the sequelae, including infection, allergic reactions from the jewelry, and keloid scars. Patients may intentionally create large size piercings, known as gauge piercings, and decide later they no longer want them. Or earlobe piercings can unintentionally stretch and enlarge over time from prolonged wearing of heavy earrings or trauma, sometimes resulting in a partial or complete earlobe split, requiring surgical treatment for gauge or split earlobe repair. If repiercing earlobe repair is desired, most physicians wait at least 6-8 weeks. While different earlobe surgical repair techniques (most commonly Z-plasty) and even recommendations for subdermal implant removal are described in the literature, there are no real guidelines on when to repierce in the evidenced-based literature. Healing time in general for piercings also varies by site. For example, initial earlobe piercings typically take 1-2 months to heal, whereas ear cartilage and navel piercings may take 4-12 months.

Some medical practitioners may not be aware of tips known to top piercing professionals that can help guide patients on piercing care. Cartilage piercings can sometimes present with inflammation and nodule formation, even prior to true keloid formation. In my experience, a simple solution of washing daily with a highly alkaline but gentle natural soap, such as Dr. Bronner’s mild baby soap, or compresses or soaks with warm salt water, can sometimes reduce the inflammation and resolve nodule formation before topical, intralesional corticosteroids, or surgery is needed (a situation in which surgery may lead to further cartilage inflammation and hypertrophic scar formation). Additionally, certain pressure earrings may be used to help prevent keloid formation, in addition to wearing jewelry of a metal that is nonallergenic to the user, to prevent further inflammation.

Piercing is a common form of body art and self-expression. Understanding piercing art can not only help us understand how to better treat the sequelae of piercing, but also develop a better understanding of and relationship with our patients by virtue of their means of artistic self-expression.
 

Dr. Wesley and Dr. Talakoub are cocontributors to this column. Dr. Wesley practices dermatology in Beverly Hills, Calif. Dr. Talakoub is in private practice in McLean, Va. This month’s column is by Dr. Wesley. Write to them at [email protected]. They had no relevant disclosures.
 

BANGKOK – Statin therapy, even when initiated only upon hospitalization for acute ischemic stroke, was associated with a striking reduction in the risk of early poststroke symptomatic seizure in a large observational study.

Bruce Jancin/MDedge News

Using propensity-score matching to control for potential confounders, use of a statin during acute stroke management was associated with a “robust” 77% reduction in the risk of developing a symptomatic seizure within 7 days after hospital admission, Soichiro Matsubara, MD, reported at the International Epilepsy Congress.

This is an important finding because early symptomatic seizure (ESS) occurs in 2%-7% of patients following an acute ischemic stroke. Moreover, an Italian meta-analysis concluded that ESS was associated with a 4.4-fold increased risk of developing poststroke epilepsy (Epilepsia. 2016 Aug;57[8]:1205-14), noted Dr. Matsubara, a neurologist at the National Cerebral and Cardiovascular Center in Suita, Japan, as well as at Kumamoto (Japan) University.

He presented a study of 2,969 consecutive acute ischemic stroke patients with no history of epilepsy who were admitted to the Japanese comprehensive stroke center, of whom 2.2% experienced ESS. At physician discretion, 19% of the ESS cohort were on a statin during their acute stroke management, as were 55% of the no-ESS group. Four-fifths of patients on a statin initiated the drug only upon hospital admission.

Strokes tended to be more severe in the ESS group, with a median initial National Institutes of Health Stroke Scale score of 12.5, compared with 4 in the seizure-free patients. A cortical stroke lesion was evident upon imaging in 89% of the ESS group and 55% of no-ESS patients. Among ESS patients, 46% had a cardiometabolic stroke, compared with 34% of the no-ESS cohort. Mean C-reactive protein levels and white blood cell counts were significantly higher in the ESS cohort as well. Their median hospital length of stay was 25.5 days, versus 18 days in the no-ESS group, Dr. Matsubara said at the congress sponsored by the International League Against Epilepsy.

Of the 76 ESSs that occurred in 66 patients, 37% were focal awareness seizures, 35% were focal to bilateral tonic-clonic seizures, and 28% were focal impaired awareness seizures.

In a multivariate analysis adjusted for age, sex, body mass index, stroke subtype, and other potential confounders, statin therapy during acute management of stroke was independently associated with a 56% reduction in the relative risk of ESS. In contrast, a cortical stroke lesion was associated with a 2.83-fold increased risk.

Since this wasn’t a randomized trial of statin therapy, Dr. Matsubara and his coinvestigators felt the need to go further in analyzing the data. After extensive propensity score matching for atrial fibrillation, current smoking, systolic blood pressure, the presence or absence of a cortical stroke lesion, large vessel stenosis, and other possible confounders, they were left with two closely comparable groups: 886 statin-treated stroke patients and an equal number who were not on statin therapy during their acute stroke management. The key finding: The risk of ESS was reduced by a whopping 77% in the patients on statin therapy.

The neurologist observed that these new findings in acute ischemic stroke patients are consistent with an earlier study in a U.S. Veterans Affairs population, which demonstrated that statin therapy was associated with a significantly lower risk of new-onset geriatric epilepsy (J Am Geriatr Soc. 2009 Feb;57[2]:237-42).

As to the possible mechanism by which statins may protect against ESS, Dr. Matsubara noted that acute ischemic stroke causes toxic neuronal excitation because of blood-brain barrier disruption, ion channel dysfunction, altered gene expression, and increased release of neurotransmitters. In animal models, statins provide a neuroprotective effect by reducing glutamate levels, activating endothelial nitric oxide synthase, and inhibiting production of interleukin-6, tumor necrosis factor-alpha, and other inflammatory cytokines.

Asked about the intensity of the statin therapy, Dr. Matsubara replied that the target was typically an LDL cholesterol below 100 mg/dL.

He reported having no financial conflicts regarding the study, conducted free of commercial support.

[email protected]

SOURCE: Matsubara S et al. IEC 219, Abstract P002.

BANGKOK – Statin therapy, even when initiated only upon hospitalization for acute ischemic stroke, was associated with a striking reduction in the risk of early poststroke symptomatic seizure in a large observational study.

Bruce Jancin/MDedge News

Using propensity-score matching to control for potential confounders, use of a statin during acute stroke management was associated with a “robust” 77% reduction in the risk of developing a symptomatic seizure within 7 days after hospital admission, Soichiro Matsubara, MD, reported at the International Epilepsy Congress.

This is an important finding because early symptomatic seizure (ESS) occurs in 2%-7% of patients following an acute ischemic stroke. Moreover, an Italian meta-analysis concluded that ESS was associated with a 4.4-fold increased risk of developing poststroke epilepsy (Epilepsia. 2016 Aug;57[8]:1205-14), noted Dr. Matsubara, a neurologist at the National Cerebral and Cardiovascular Center in Suita, Japan, as well as at Kumamoto (Japan) University.

He presented a study of 2,969 consecutive acute ischemic stroke patients with no history of epilepsy who were admitted to the Japanese comprehensive stroke center, of whom 2.2% experienced ESS. At physician discretion, 19% of the ESS cohort were on a statin during their acute stroke management, as were 55% of the no-ESS group. Four-fifths of patients on a statin initiated the drug only upon hospital admission.

Strokes tended to be more severe in the ESS group, with a median initial National Institutes of Health Stroke Scale score of 12.5, compared with 4 in the seizure-free patients. A cortical stroke lesion was evident upon imaging in 89% of the ESS group and 55% of no-ESS patients. Among ESS patients, 46% had a cardiometabolic stroke, compared with 34% of the no-ESS cohort. Mean C-reactive protein levels and white blood cell counts were significantly higher in the ESS cohort as well. Their median hospital length of stay was 25.5 days, versus 18 days in the no-ESS group, Dr. Matsubara said at the congress sponsored by the International League Against Epilepsy.

Of the 76 ESSs that occurred in 66 patients, 37% were focal awareness seizures, 35% were focal to bilateral tonic-clonic seizures, and 28% were focal impaired awareness seizures.

In a multivariate analysis adjusted for age, sex, body mass index, stroke subtype, and other potential confounders, statin therapy during acute management of stroke was independently associated with a 56% reduction in the relative risk of ESS. In contrast, a cortical stroke lesion was associated with a 2.83-fold increased risk.

Since this wasn’t a randomized trial of statin therapy, Dr. Matsubara and his coinvestigators felt the need to go further in analyzing the data. After extensive propensity score matching for atrial fibrillation, current smoking, systolic blood pressure, the presence or absence of a cortical stroke lesion, large vessel stenosis, and other possible confounders, they were left with two closely comparable groups: 886 statin-treated stroke patients and an equal number who were not on statin therapy during their acute stroke management. The key finding: The risk of ESS was reduced by a whopping 77% in the patients on statin therapy.

The neurologist observed that these new findings in acute ischemic stroke patients are consistent with an earlier study in a U.S. Veterans Affairs population, which demonstrated that statin therapy was associated with a significantly lower risk of new-onset geriatric epilepsy (J Am Geriatr Soc. 2009 Feb;57[2]:237-42).

As to the possible mechanism by which statins may protect against ESS, Dr. Matsubara noted that acute ischemic stroke causes toxic neuronal excitation because of blood-brain barrier disruption, ion channel dysfunction, altered gene expression, and increased release of neurotransmitters. In animal models, statins provide a neuroprotective effect by reducing glutamate levels, activating endothelial nitric oxide synthase, and inhibiting production of interleukin-6, tumor necrosis factor-alpha, and other inflammatory cytokines.

Asked about the intensity of the statin therapy, Dr. Matsubara replied that the target was typically an LDL cholesterol below 100 mg/dL.

He reported having no financial conflicts regarding the study, conducted free of commercial support.

[email protected]

SOURCE: Matsubara S et al. IEC 219, Abstract P002.

BANGKOK – Statin therapy, even when initiated only upon hospitalization for acute ischemic stroke, was associated with a striking reduction in the risk of early poststroke symptomatic seizure in a large observational study.

Bruce Jancin/MDedge News

Using propensity-score matching to control for potential confounders, use of a statin during acute stroke management was associated with a “robust” 77% reduction in the risk of developing a symptomatic seizure within 7 days after hospital admission, Soichiro Matsubara, MD, reported at the International Epilepsy Congress.

This is an important finding because early symptomatic seizure (ESS) occurs in 2%-7% of patients following an acute ischemic stroke. Moreover, an Italian meta-analysis concluded that ESS was associated with a 4.4-fold increased risk of developing poststroke epilepsy (Epilepsia. 2016 Aug;57[8]:1205-14), noted Dr. Matsubara, a neurologist at the National Cerebral and Cardiovascular Center in Suita, Japan, as well as at Kumamoto (Japan) University.

He presented a study of 2,969 consecutive acute ischemic stroke patients with no history of epilepsy who were admitted to the Japanese comprehensive stroke center, of whom 2.2% experienced ESS. At physician discretion, 19% of the ESS cohort were on a statin during their acute stroke management, as were 55% of the no-ESS group. Four-fifths of patients on a statin initiated the drug only upon hospital admission.

Strokes tended to be more severe in the ESS group, with a median initial National Institutes of Health Stroke Scale score of 12.5, compared with 4 in the seizure-free patients. A cortical stroke lesion was evident upon imaging in 89% of the ESS group and 55% of no-ESS patients. Among ESS patients, 46% had a cardiometabolic stroke, compared with 34% of the no-ESS cohort. Mean C-reactive protein levels and white blood cell counts were significantly higher in the ESS cohort as well. Their median hospital length of stay was 25.5 days, versus 18 days in the no-ESS group, Dr. Matsubara said at the congress sponsored by the International League Against Epilepsy.

Of the 76 ESSs that occurred in 66 patients, 37% were focal awareness seizures, 35% were focal to bilateral tonic-clonic seizures, and 28% were focal impaired awareness seizures.

In a multivariate analysis adjusted for age, sex, body mass index, stroke subtype, and other potential confounders, statin therapy during acute management of stroke was independently associated with a 56% reduction in the relative risk of ESS. In contrast, a cortical stroke lesion was associated with a 2.83-fold increased risk.

Since this wasn’t a randomized trial of statin therapy, Dr. Matsubara and his coinvestigators felt the need to go further in analyzing the data. After extensive propensity score matching for atrial fibrillation, current smoking, systolic blood pressure, the presence or absence of a cortical stroke lesion, large vessel stenosis, and other possible confounders, they were left with two closely comparable groups: 886 statin-treated stroke patients and an equal number who were not on statin therapy during their acute stroke management. The key finding: The risk of ESS was reduced by a whopping 77% in the patients on statin therapy.

The neurologist observed that these new findings in acute ischemic stroke patients are consistent with an earlier study in a U.S. Veterans Affairs population, which demonstrated that statin therapy was associated with a significantly lower risk of new-onset geriatric epilepsy (J Am Geriatr Soc. 2009 Feb;57[2]:237-42).

As to the possible mechanism by which statins may protect against ESS, Dr. Matsubara noted that acute ischemic stroke causes toxic neuronal excitation because of blood-brain barrier disruption, ion channel dysfunction, altered gene expression, and increased release of neurotransmitters. In animal models, statins provide a neuroprotective effect by reducing glutamate levels, activating endothelial nitric oxide synthase, and inhibiting production of interleukin-6, tumor necrosis factor-alpha, and other inflammatory cytokines.

Asked about the intensity of the statin therapy, Dr. Matsubara replied that the target was typically an LDL cholesterol below 100 mg/dL.

He reported having no financial conflicts regarding the study, conducted free of commercial support.

[email protected]

SOURCE: Matsubara S et al. IEC 219, Abstract P002.

I had just received my sign-out for the day. My pager beeped, and I heard it overhead “Code Blue Room X.” Hospitalist physicians lead the code team in our hospital; I quickly headed to the room.

A young man in his forties was found to be unconscious on the floor. One of the nurses had started cardiopulmonary resuscitation (CPR) as the patient was unconscious and had no palpable pulse. It was a long, drawn-out battle: CPR, cracking bones, shouting, lots of needles – an extreme roller-coaster-style situation. The patient had recently had a hip surgery and our suspicion was a massive pulmonary embolism. We ran the exhaustive code for more than an hour and then I started to debrief with my code team; discussed that treatment was getting futile and asked for opinions. Finally, I asked the team to stop and pronounced the patient dead. I felt terrible. Later that day I returned to my house, tossed my bag in the corner, and sympathized with myself – “Hello Dr. B, It was a tough one.”

Stopping resuscitation was one of the toughest decisions I had ever made, and I wondered if I would be able to make such a decision the next day. What if I had carried on? I had led code teams during my residency training and as an attending physician; but there was something different that day. This patient was a young man with no history of medical problems. Every physician knows how to initiate resuscitation for cardiopulmonary arrest (CPA); only a few know when to stop it. Did I miss this learning during my internal medicine training? I checked my red pocket leaflet with advanced cardiac life support (ACLS) algorithms, and it had no mention of it. I searched Google Scholar, PubMed, and UpToDate and surprisingly, I found no predetermined rule but only a few recommendations on when CPR should be stopped. The American Heart Association is clear that the decision to terminate resuscitative efforts rests with the treating physician in the hospital.

In my experience, the length of time to continue a code can vary widely and is mostly dependent on the physician running the code. I have seen it last 15 minutes (which is reasonable) and I have seen it last for 50 minutes when the initial rhythm was ventricular fibrillation. And if perhaps the patient regains a pulse temporarily, only to lose it again, we restart the clock. One needs to take into account various factors including time to CPR, time to defibrillation, comorbid disease, prearrest state, and initial arrest rhythm in making these decisions. It’s well understood that none of these factors alone or in combination is clearly predictive of outcome.¹

Some selected patients potentially have good outcomes with prolonged, aggressive resuscitation. So when should we stop, and when should we continue resuscitation? This is always challenging. Physicians hate to stop CPR even when they know it’s time. We are guided by the Hippocratic Oath to save lives. Sometimes, even if we want to stop, we tend to continue to avoid being criticized for stopping; we are systematically biased against stopping CPR. We routinely run long codes, in part because we are not sure which patients we can bring back.

A 2012 Lancet study highlighted that the median duration of resuscitation was 12 minutes for patients achieving the return of spontaneous circulation and 20 minutes for nonsurvivors.² The ethical guidelines issued by AHA in 2018 highlight that, in the absence of mitigating factors, prolonged resuscitative efforts for adults and children are unlikely to be successful and can be discontinued if there is no return of spontaneous circulation at any time during 30 minutes of cumulative ACLS. If the return of spontaneous circulation of any duration occurs at any time, however, it may be appropriate to consider extending the resuscitative effort.³

I believe a careful balance of the patient’s prognosis for both length of life and quality of life will determine whether continued CPR is appropriate. The responsible clinician should stop the resuscitative effort when he or she determines with a high degree of certainty that the arrest victim will not respond to further efforts. But what will help me guide my decisions next time if I ever come across this situation again?

I discussed my dilemma with one of our intensivist physicians; he expressed that in a similar scenario he would ask for opinions from other members of the code team. The role of good communication among code team members is necessary to exchange relevant knowledge in real time in a collaborative, nonhierarchical environment. The code team can provide the team leader with quick, accurate information about the patient’s clinical history that is critical to good decision making.

Family support is also an essential part of any resuscitation. Health care providers need to offer the opportunity to be present to family members during the resuscitation attempts whenever possible. One team member should be assigned to the family to answer questions, clarify information, and offer comfort, but physicians should not be asking family members to decide to stop the code. It is important to note that the decision should be made by the team leader and not the patient’s family members. Regardless of the age or condition of the patient, the loss of a loved one is difficult to deal with, even if expected. The issue becomes more difficult with changes in legal, cultural, or personal perspectives.

The AHA in 2018 stated that the treating physician is expected to understand the patient and the arrest features, and the system factors that have prognostic importance for resuscitation.³ For clinicians who work in critical care settings, the framework presented by AHA is intuitive. As a code leader, I can always give more epinephrine, try a clot-busting drug or deliver another shock. Situations vary greatly during a code, and the amount of time spent resuscitating a patient before terminating efforts is not set in stone. In many cases, it is a judgment call. The process of CPR is almost as disheartening as its bleak outcomes.

In-hospital CPAs are inevitably gruesome. Each day as an attending physician, we are faced with difficult decisions, but experiencing these incredibly difficult and life-changing events can make for good learning. A CPA situation in action is very difficult for all concerned, particularly when there is almost no chance of success. But an unsuccessful or aborted resuscitation is also a huge loss for both the family and the code team. One of the critical functions of the code team leader is to review the events of a code and exercise judgment while evaluating the length of a code. This can be an intense and emotional experience, but with these principles in mind, we can feel reassured that we are making the best decision possible, for the patient, the family, and our team.

Dr. Basnet is a hospitalist physician in the department of internal medicine at Eastern New Mexico Medical Center, Roswell.

References

1. Part 2: Ethical aspects of CPR and ECC. Circulation. 2000;102(8):I12.

2. Goldberger ZD et al. Duration of resuscitation efforts and survival after in-hospital cardiac arrest: An observational study. The Lancet. 2012;380(9852):1473-81.

3. Sirbaugh PE et al. A prospective, population-based study of the demographics, epidemiology, management, and outcome of out-of-hospital pediatric cardiopulmonary arrest. Ann Emerg Med. 1999;33(2):174-84.

I had just received my sign-out for the day. My pager beeped, and I heard it overhead “Code Blue Room X.” Hospitalist physicians lead the code team in our hospital; I quickly headed to the room.

A young man in his forties was found to be unconscious on the floor. One of the nurses had started cardiopulmonary resuscitation (CPR) as the patient was unconscious and had no palpable pulse. It was a long, drawn-out battle: CPR, cracking bones, shouting, lots of needles – an extreme roller-coaster-style situation. The patient had recently had a hip surgery and our suspicion was a massive pulmonary embolism. We ran the exhaustive code for more than an hour and then I started to debrief with my code team; discussed that treatment was getting futile and asked for opinions. Finally, I asked the team to stop and pronounced the patient dead. I felt terrible. Later that day I returned to my house, tossed my bag in the corner, and sympathized with myself – “Hello Dr. B, It was a tough one.”

Stopping resuscitation was one of the toughest decisions I had ever made, and I wondered if I would be able to make such a decision the next day. What if I had carried on? I had led code teams during my residency training and as an attending physician; but there was something different that day. This patient was a young man with no history of medical problems. Every physician knows how to initiate resuscitation for cardiopulmonary arrest (CPA); only a few know when to stop it. Did I miss this learning during my internal medicine training? I checked my red pocket leaflet with advanced cardiac life support (ACLS) algorithms, and it had no mention of it. I searched Google Scholar, PubMed, and UpToDate and surprisingly, I found no predetermined rule but only a few recommendations on when CPR should be stopped. The American Heart Association is clear that the decision to terminate resuscitative efforts rests with the treating physician in the hospital.

In my experience, the length of time to continue a code can vary widely and is mostly dependent on the physician running the code. I have seen it last 15 minutes (which is reasonable) and I have seen it last for 50 minutes when the initial rhythm was ventricular fibrillation. And if perhaps the patient regains a pulse temporarily, only to lose it again, we restart the clock. One needs to take into account various factors including time to CPR, time to defibrillation, comorbid disease, prearrest state, and initial arrest rhythm in making these decisions. It’s well understood that none of these factors alone or in combination is clearly predictive of outcome.¹

Some selected patients potentially have good outcomes with prolonged, aggressive resuscitation. So when should we stop, and when should we continue resuscitation? This is always challenging. Physicians hate to stop CPR even when they know it’s time. We are guided by the Hippocratic Oath to save lives. Sometimes, even if we want to stop, we tend to continue to avoid being criticized for stopping; we are systematically biased against stopping CPR. We routinely run long codes, in part because we are not sure which patients we can bring back.

A 2012 Lancet study highlighted that the median duration of resuscitation was 12 minutes for patients achieving the return of spontaneous circulation and 20 minutes for nonsurvivors.² The ethical guidelines issued by AHA in 2018 highlight that, in the absence of mitigating factors, prolonged resuscitative efforts for adults and children are unlikely to be successful and can be discontinued if there is no return of spontaneous circulation at any time during 30 minutes of cumulative ACLS. If the return of spontaneous circulation of any duration occurs at any time, however, it may be appropriate to consider extending the resuscitative effort.³

I believe a careful balance of the patient’s prognosis for both length of life and quality of life will determine whether continued CPR is appropriate. The responsible clinician should stop the resuscitative effort when he or she determines with a high degree of certainty that the arrest victim will not respond to further efforts. But what will help me guide my decisions next time if I ever come across this situation again?

I discussed my dilemma with one of our intensivist physicians; he expressed that in a similar scenario he would ask for opinions from other members of the code team. The role of good communication among code team members is necessary to exchange relevant knowledge in real time in a collaborative, nonhierarchical environment. The code team can provide the team leader with quick, accurate information about the patient’s clinical history that is critical to good decision making.

Family support is also an essential part of any resuscitation. Health care providers need to offer the opportunity to be present to family members during the resuscitation attempts whenever possible. One team member should be assigned to the family to answer questions, clarify information, and offer comfort, but physicians should not be asking family members to decide to stop the code. It is important to note that the decision should be made by the team leader and not the patient’s family members. Regardless of the age or condition of the patient, the loss of a loved one is difficult to deal with, even if expected. The issue becomes more difficult with changes in legal, cultural, or personal perspectives.

The AHA in 2018 stated that the treating physician is expected to understand the patient and the arrest features, and the system factors that have prognostic importance for resuscitation.³ For clinicians who work in critical care settings, the framework presented by AHA is intuitive. As a code leader, I can always give more epinephrine, try a clot-busting drug or deliver another shock. Situations vary greatly during a code, and the amount of time spent resuscitating a patient before terminating efforts is not set in stone. In many cases, it is a judgment call. The process of CPR is almost as disheartening as its bleak outcomes.

In-hospital CPAs are inevitably gruesome. Each day as an attending physician, we are faced with difficult decisions, but experiencing these incredibly difficult and life-changing events can make for good learning. A CPA situation in action is very difficult for all concerned, particularly when there is almost no chance of success. But an unsuccessful or aborted resuscitation is also a huge loss for both the family and the code team. One of the critical functions of the code team leader is to review the events of a code and exercise judgment while evaluating the length of a code. This can be an intense and emotional experience, but with these principles in mind, we can feel reassured that we are making the best decision possible, for the patient, the family, and our team.

Dr. Basnet is a hospitalist physician in the department of internal medicine at Eastern New Mexico Medical Center, Roswell.

References

1. Part 2: Ethical aspects of CPR and ECC. Circulation. 2000;102(8):I12.

2. Goldberger ZD et al. Duration of resuscitation efforts and survival after in-hospital cardiac arrest: An observational study. The Lancet. 2012;380(9852):1473-81.

3. Sirbaugh PE et al. A prospective, population-based study of the demographics, epidemiology, management, and outcome of out-of-hospital pediatric cardiopulmonary arrest. Ann Emerg Med. 1999;33(2):174-84.

I had just received my sign-out for the day. My pager beeped, and I heard it overhead “Code Blue Room X.” Hospitalist physicians lead the code team in our hospital; I quickly headed to the room.

A young man in his forties was found to be unconscious on the floor. One of the nurses had started cardiopulmonary resuscitation (CPR) as the patient was unconscious and had no palpable pulse. It was a long, drawn-out battle: CPR, cracking bones, shouting, lots of needles – an extreme roller-coaster-style situation. The patient had recently had a hip surgery and our suspicion was a massive pulmonary embolism. We ran the exhaustive code for more than an hour and then I started to debrief with my code team; discussed that treatment was getting futile and asked for opinions. Finally, I asked the team to stop and pronounced the patient dead. I felt terrible. Later that day I returned to my house, tossed my bag in the corner, and sympathized with myself – “Hello Dr. B, It was a tough one.”

Stopping resuscitation was one of the toughest decisions I had ever made, and I wondered if I would be able to make such a decision the next day. What if I had carried on? I had led code teams during my residency training and as an attending physician; but there was something different that day. This patient was a young man with no history of medical problems. Every physician knows how to initiate resuscitation for cardiopulmonary arrest (CPA); only a few know when to stop it. Did I miss this learning during my internal medicine training? I checked my red pocket leaflet with advanced cardiac life support (ACLS) algorithms, and it had no mention of it. I searched Google Scholar, PubMed, and UpToDate and surprisingly, I found no predetermined rule but only a few recommendations on when CPR should be stopped. The American Heart Association is clear that the decision to terminate resuscitative efforts rests with the treating physician in the hospital.

In my experience, the length of time to continue a code can vary widely and is mostly dependent on the physician running the code. I have seen it last 15 minutes (which is reasonable) and I have seen it last for 50 minutes when the initial rhythm was ventricular fibrillation. And if perhaps the patient regains a pulse temporarily, only to lose it again, we restart the clock. One needs to take into account various factors including time to CPR, time to defibrillation, comorbid disease, prearrest state, and initial arrest rhythm in making these decisions. It’s well understood that none of these factors alone or in combination is clearly predictive of outcome.¹

Some selected patients potentially have good outcomes with prolonged, aggressive resuscitation. So when should we stop, and when should we continue resuscitation? This is always challenging. Physicians hate to stop CPR even when they know it’s time. We are guided by the Hippocratic Oath to save lives. Sometimes, even if we want to stop, we tend to continue to avoid being criticized for stopping; we are systematically biased against stopping CPR. We routinely run long codes, in part because we are not sure which patients we can bring back.

A 2012 Lancet study highlighted that the median duration of resuscitation was 12 minutes for patients achieving the return of spontaneous circulation and 20 minutes for nonsurvivors.² The ethical guidelines issued by AHA in 2018 highlight that, in the absence of mitigating factors, prolonged resuscitative efforts for adults and children are unlikely to be successful and can be discontinued if there is no return of spontaneous circulation at any time during 30 minutes of cumulative ACLS. If the return of spontaneous circulation of any duration occurs at any time, however, it may be appropriate to consider extending the resuscitative effort.³

I believe a careful balance of the patient’s prognosis for both length of life and quality of life will determine whether continued CPR is appropriate. The responsible clinician should stop the resuscitative effort when he or she determines with a high degree of certainty that the arrest victim will not respond to further efforts. But what will help me guide my decisions next time if I ever come across this situation again?

I discussed my dilemma with one of our intensivist physicians; he expressed that in a similar scenario he would ask for opinions from other members of the code team. The role of good communication among code team members is necessary to exchange relevant knowledge in real time in a collaborative, nonhierarchical environment. The code team can provide the team leader with quick, accurate information about the patient’s clinical history that is critical to good decision making.

Family support is also an essential part of any resuscitation. Health care providers need to offer the opportunity to be present to family members during the resuscitation attempts whenever possible. One team member should be assigned to the family to answer questions, clarify information, and offer comfort, but physicians should not be asking family members to decide to stop the code. It is important to note that the decision should be made by the team leader and not the patient’s family members. Regardless of the age or condition of the patient, the loss of a loved one is difficult to deal with, even if expected. The issue becomes more difficult with changes in legal, cultural, or personal perspectives.

The AHA in 2018 stated that the treating physician is expected to understand the patient and the arrest features, and the system factors that have prognostic importance for resuscitation.³ For clinicians who work in critical care settings, the framework presented by AHA is intuitive. As a code leader, I can always give more epinephrine, try a clot-busting drug or deliver another shock. Situations vary greatly during a code, and the amount of time spent resuscitating a patient before terminating efforts is not set in stone. In many cases, it is a judgment call. The process of CPR is almost as disheartening as its bleak outcomes.

In-hospital CPAs are inevitably gruesome. Each day as an attending physician, we are faced with difficult decisions, but experiencing these incredibly difficult and life-changing events can make for good learning. A CPA situation in action is very difficult for all concerned, particularly when there is almost no chance of success. But an unsuccessful or aborted resuscitation is also a huge loss for both the family and the code team. One of the critical functions of the code team leader is to review the events of a code and exercise judgment while evaluating the length of a code. This can be an intense and emotional experience, but with these principles in mind, we can feel reassured that we are making the best decision possible, for the patient, the family, and our team.

Dr. Basnet is a hospitalist physician in the department of internal medicine at Eastern New Mexico Medical Center, Roswell.

References

1. Part 2: Ethical aspects of CPR and ECC. Circulation. 2000;102(8):I12.

2. Goldberger ZD et al. Duration of resuscitation efforts and survival after in-hospital cardiac arrest: An observational study. The Lancet. 2012;380(9852):1473-81.

3. Sirbaugh PE et al. A prospective, population-based study of the demographics, epidemiology, management, and outcome of out-of-hospital pediatric cardiopulmonary arrest. Ann Emerg Med. 1999;33(2):174-84.

At a recent Recreation Commission meeting here in Brunswick, the first agenda item under new business was “Coffin Pond Pool Closing.” As I and my fellow commissioners listened, we were told that for the first time in the last 3 decades the town’s only public swimming area would not be opening. While in the past there have been delayed openings and temporary closings due to water conditions, this year the pool would not open, period. The cause of the pool’s closure was the Parks and Recreation Department’s failure to fill even a skeleton crew of lifeguards.

Lokibaho/Getty Images

We learned that the situation here in Brunswick was not unique and most other communities around the state and even around the country were struggling to find lifeguards. The shortage of trained staff has been nationwide for several years, and many beaches and pools particularly in the Northeast and Middle Atlantic states were being forced to close or shorten hours of operation (“During the Pool Season Even Lifeguard Numbers are Taking a Dive,” by Leoneda Inge, July 28, 2015, NPR’s All Thing Considered).

You might think that here on the coast we would have ample places for children to swim, but in Brunswick our shore is rocky and often inaccessible. At the few sandy beaches, the water temperature is too cold for all but the hardy souls until late August. The closure of our lone public swimming venue is going to deprive many of the town’s children a chance to swim. Lower-income families will be particularly affected by the loss of the pool.

When I was growing up, lifeguarding was a plum job that was highly coveted. While it did not pay as well as working construction, the perks of a pleasant atmosphere, the chance to swim every day, and the opportunity to work outside with children prompted me at age 16 to sell my lawn mower and bequeath my lucrative landscaping customers to a couple of preteens. Looking back, my 4 years of lifeguarding were probably a major influence when it came time to choose a specialty.

However, a perfect storm of socioeconomic factors has combined to create a climate in which being a lifeguard has lost its appeal as a summertime job. First, there is record low unemployment nationwide. Young people looking for work have their pick, and while wages still remain low, they can be choosy when it comes to hours and benefits. Lifeguarding does require a skill set and several hoops of certification to be navigated. I don’t recall having to pay much of anything to become certified. But I understand that the process now costs hundreds of dollars of upfront investment with no guarantee of passing the test.

In May, the American Academy of Pediatrics published a policy paper titled “Prevention of Drowning” (Pediatrics. 2019 May 1. doi: 10.1542/peds.2019-0850) in which the authors offer the troubling statistics on the toll that water-related accidents take on the children of this country annually. They go on to provide a broad list of actions that parents, communities, and pediatricians can take to prevent drownings. Under the category of Community Interventions and Advocacy Opportunities, recommendation No. 4 is “Pediatricians should work with community partners to provide access to programs that develop water-competency swim skills for all children.”

Obviously, these programs can’t happen without an adequate supply of lifeguards.

Unfortunately, the AAP’s statement fails to acknowledge or directly address the lifeguard shortage that has been going on for several years. While an adequate supply of lifeguards is probably not as important as increasing parental attentiveness and mandating pool fences in the overall scheme of drowning prevention, it is an issue that demands action both by the academy and those of us practicing in communities both large and small.

For my part, I am going to work here in Brunswick to see that we can offer lifeguards pay that is more than competitive and then develop an in-house training program to ensure a continuing supply for the future. If we are committed to encouraging our patients to be active, swimming is one of the best activities we should promote and support.
 

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].

At a recent Recreation Commission meeting here in Brunswick, the first agenda item under new business was “Coffin Pond Pool Closing.” As I and my fellow commissioners listened, we were told that for the first time in the last 3 decades the town’s only public swimming area would not be opening. While in the past there have been delayed openings and temporary closings due to water conditions, this year the pool would not open, period. The cause of the pool’s closure was the Parks and Recreation Department’s failure to fill even a skeleton crew of lifeguards.

Lokibaho/Getty Images

We learned that the situation here in Brunswick was not unique and most other communities around the state and even around the country were struggling to find lifeguards. The shortage of trained staff has been nationwide for several years, and many beaches and pools particularly in the Northeast and Middle Atlantic states were being forced to close or shorten hours of operation (“During the Pool Season Even Lifeguard Numbers are Taking a Dive,” by Leoneda Inge, July 28, 2015, NPR’s All Thing Considered).

You might think that here on the coast we would have ample places for children to swim, but in Brunswick our shore is rocky and often inaccessible. At the few sandy beaches, the water temperature is too cold for all but the hardy souls until late August. The closure of our lone public swimming venue is going to deprive many of the town’s children a chance to swim. Lower-income families will be particularly affected by the loss of the pool.

When I was growing up, lifeguarding was a plum job that was highly coveted. While it did not pay as well as working construction, the perks of a pleasant atmosphere, the chance to swim every day, and the opportunity to work outside with children prompted me at age 16 to sell my lawn mower and bequeath my lucrative landscaping customers to a couple of preteens. Looking back, my 4 years of lifeguarding were probably a major influence when it came time to choose a specialty.

However, a perfect storm of socioeconomic factors has combined to create a climate in which being a lifeguard has lost its appeal as a summertime job. First, there is record low unemployment nationwide. Young people looking for work have their pick, and while wages still remain low, they can be choosy when it comes to hours and benefits. Lifeguarding does require a skill set and several hoops of certification to be navigated. I don’t recall having to pay much of anything to become certified. But I understand that the process now costs hundreds of dollars of upfront investment with no guarantee of passing the test.

In May, the American Academy of Pediatrics published a policy paper titled “Prevention of Drowning” (Pediatrics. 2019 May 1. doi: 10.1542/peds.2019-0850) in which the authors offer the troubling statistics on the toll that water-related accidents take on the children of this country annually. They go on to provide a broad list of actions that parents, communities, and pediatricians can take to prevent drownings. Under the category of Community Interventions and Advocacy Opportunities, recommendation No. 4 is “Pediatricians should work with community partners to provide access to programs that develop water-competency swim skills for all children.”

Obviously, these programs can’t happen without an adequate supply of lifeguards.

Unfortunately, the AAP’s statement fails to acknowledge or directly address the lifeguard shortage that has been going on for several years. While an adequate supply of lifeguards is probably not as important as increasing parental attentiveness and mandating pool fences in the overall scheme of drowning prevention, it is an issue that demands action both by the academy and those of us practicing in communities both large and small.

For my part, I am going to work here in Brunswick to see that we can offer lifeguards pay that is more than competitive and then develop an in-house training program to ensure a continuing supply for the future. If we are committed to encouraging our patients to be active, swimming is one of the best activities we should promote and support.
 

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].

At a recent Recreation Commission meeting here in Brunswick, the first agenda item under new business was “Coffin Pond Pool Closing.” As I and my fellow commissioners listened, we were told that for the first time in the last 3 decades the town’s only public swimming area would not be opening. While in the past there have been delayed openings and temporary closings due to water conditions, this year the pool would not open, period. The cause of the pool’s closure was the Parks and Recreation Department’s failure to fill even a skeleton crew of lifeguards.

Lokibaho/Getty Images

We learned that the situation here in Brunswick was not unique and most other communities around the state and even around the country were struggling to find lifeguards. The shortage of trained staff has been nationwide for several years, and many beaches and pools particularly in the Northeast and Middle Atlantic states were being forced to close or shorten hours of operation (“During the Pool Season Even Lifeguard Numbers are Taking a Dive,” by Leoneda Inge, July 28, 2015, NPR’s All Thing Considered).

You might think that here on the coast we would have ample places for children to swim, but in Brunswick our shore is rocky and often inaccessible. At the few sandy beaches, the water temperature is too cold for all but the hardy souls until late August. The closure of our lone public swimming venue is going to deprive many of the town’s children a chance to swim. Lower-income families will be particularly affected by the loss of the pool.

When I was growing up, lifeguarding was a plum job that was highly coveted. While it did not pay as well as working construction, the perks of a pleasant atmosphere, the chance to swim every day, and the opportunity to work outside with children prompted me at age 16 to sell my lawn mower and bequeath my lucrative landscaping customers to a couple of preteens. Looking back, my 4 years of lifeguarding were probably a major influence when it came time to choose a specialty.

However, a perfect storm of socioeconomic factors has combined to create a climate in which being a lifeguard has lost its appeal as a summertime job. First, there is record low unemployment nationwide. Young people looking for work have their pick, and while wages still remain low, they can be choosy when it comes to hours and benefits. Lifeguarding does require a skill set and several hoops of certification to be navigated. I don’t recall having to pay much of anything to become certified. But I understand that the process now costs hundreds of dollars of upfront investment with no guarantee of passing the test.

In May, the American Academy of Pediatrics published a policy paper titled “Prevention of Drowning” (Pediatrics. 2019 May 1. doi: 10.1542/peds.2019-0850) in which the authors offer the troubling statistics on the toll that water-related accidents take on the children of this country annually. They go on to provide a broad list of actions that parents, communities, and pediatricians can take to prevent drownings. Under the category of Community Interventions and Advocacy Opportunities, recommendation No. 4 is “Pediatricians should work with community partners to provide access to programs that develop water-competency swim skills for all children.”

Obviously, these programs can’t happen without an adequate supply of lifeguards.

Unfortunately, the AAP’s statement fails to acknowledge or directly address the lifeguard shortage that has been going on for several years. While an adequate supply of lifeguards is probably not as important as increasing parental attentiveness and mandating pool fences in the overall scheme of drowning prevention, it is an issue that demands action both by the academy and those of us practicing in communities both large and small.

For my part, I am going to work here in Brunswick to see that we can offer lifeguards pay that is more than competitive and then develop an in-house training program to ensure a continuing supply for the future. If we are committed to encouraging our patients to be active, swimming is one of the best activities we should promote and support.
 

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].

LOS ANGELES – Estrogen therapy may have scored another goal in its comeback game, as a 7-year prospective study shows that a transdermal formulation preserves some measures of cognitive function and brain architecture in postmenopausal women.

JackF/thinkstockphotos.com

In addition to performing better on subjective tests of memory, women using the estrogen patch experienced less cortical atrophy and were less likely to show amyloid on brain imaging. The observations were moderately associated with the improved sleep these women reported, Burcu Zeydan, MD, said at the Alzheimer’s Association International Conference.

“By 7 years, among the cognitive domains studied ... [less brain and cognitive change] correlated with lower global sleep score, meaning better sleep quality in the estradiol group,” said Dr. Zeydan, assistant professor of radiology at the Mayo Clinic in Rochester, Minn. “We previously found that preservation of dorsolateral prefrontal cortex over 7 years was associated with lower cortical beta-amyloid deposition on PET only in the estradiol group, pointing out the potential role of estrogen receptors in modulating this relationship.”

Dysregulated sleep is more common among women than men, particularly as menopause approaches and estrogen levels fluctuate, then decline, Dr. Zeydan said.

Dr. Zeydan reported the sleep substudy of KEEPS (the Kronos Early Estrogen Prevention Study), a randomized, double-blind, placebo-controlled, multisite trial that compared oral conjugated equine estrogen with transdermal estradiol. A control group received oral placebo and a placebo patch.*

Brain architecture was similar between the placebo and transdermal groups, but it was actually worse in some measures in the oral-estrogen group, compared with the placebo group. Women taking oral estrogen had more white matter hyperintensities, greater ventricle enlargement, and more cortical thinning. Those differences resolved after they stopped taking the oral formulation, bringing them into line with the transdermal and placebo groups.

The investigation also found that the transdermal group showed lower cerebral amyloid binding on PET scans relative to both placebo and oral estrogen.

“The relative preservation of dorsolateral prefrontal cortical volume in the [transdermal estradiol] group over 7 years indicates that hormone therapy may have long-term effects on the brain,” the team concluded. They noted that the original KEEPS study didn’t find any cognitive correlation with these changes.

The subanalysis looked at 69 women of the KEEPS cohort who had been followed for the full 7 years (4 years on treatment and 3 years off treatment). They were randomized to oral placebo and a placebo patch,* oral conjugated equine estrogen (0.45 mg/day), or transdermal estradiol (50 mcg/day). Participants in the active treatment groups received oral micronized progesterone 12 days each month. All had complete data on cognitive testing and brain imaging. Sleep quality was measured by the Pittsburgh Sleep Quality Index. Dr. Zeydan compared cognition and brain architecture findings in relation to the sleep score; lower scores mean better sleep.

The women were aged 42-58 years at baseline, and within 36 months from menopause. They had no history of menopausal hormone therapy or cardiovascular disease.

The investigators were particularly interested in how estrogen might have modulated the disturbed sleep patterns that often accompany perimenopause and early menopause, and whether the observed brain and cognitive changes tracked with sleep quality.

“During this time, 40% to 60% of women report problems sleeping, and estrogen decline seems to play an important role in sleep disturbances during this phase,” Dr. Zeydan said. “Although poor sleep quality is common in recently menopausal women, sleep quality improves with hormone therapy, as was previously demonstrated in KEEPS hormone therapy trial in recently menopausal women.”

By year 7, the cohort’s mean age was 61 years. The majority had at least some college education. The percentage who carried an apolipoprotein E epsilon-4 allele varied by group, with 15% positivity in the oral group, 48% in the transdermal group, and 16% in the placebo group.


Cognitive function was estimated with a global cognitive measure and four cognitive domain scores: verbal learning and memory, auditory attention and working memory, visual attention and executive function, and mental flexibility.

Higher attention and executive function scores were moderately correlated with a lower sleep score in the transdermal group (r = –0.54, a significant difference compared with the oral formulation). Lower sleep scores also showed a moderate correlation with preserved cortical volume of the dorsolateral prefrontal region (r = –0.47, also significantly different from the oral group).

Lower brain amyloid also positively correlated with better sleep. The correlation between sleep and global amyloid burden in the transdermal group was also moderate (r = 0.45), while the correlation in the oral group was significantly weaker (r = 0.18).

“We can say that sleep quality and transdermal estradiol during early postmenopausal years somehow interact to influence beta-amyloid deposition, preservation of dorsolateral prefrontal cortex volume, and attention and executive function,” Dr. Zeydan said.

Dr. Zeydan had no financial disclosures.

[email protected]

*Correction, 8/7/2019: An earlier version of this story did not make clear that participants in the control group received oral placebo and a placebo patch.

LOS ANGELES – Estrogen therapy may have scored another goal in its comeback game, as a 7-year prospective study shows that a transdermal formulation preserves some measures of cognitive function and brain architecture in postmenopausal women.

JackF/thinkstockphotos.com

In addition to performing better on subjective tests of memory, women using the estrogen patch experienced less cortical atrophy and were less likely to show amyloid on brain imaging. The observations were moderately associated with the improved sleep these women reported, Burcu Zeydan, MD, said at the Alzheimer’s Association International Conference.

“By 7 years, among the cognitive domains studied ... [less brain and cognitive change] correlated with lower global sleep score, meaning better sleep quality in the estradiol group,” said Dr. Zeydan, assistant professor of radiology at the Mayo Clinic in Rochester, Minn. “We previously found that preservation of dorsolateral prefrontal cortex over 7 years was associated with lower cortical beta-amyloid deposition on PET only in the estradiol group, pointing out the potential role of estrogen receptors in modulating this relationship.”

Dysregulated sleep is more common among women than men, particularly as menopause approaches and estrogen levels fluctuate, then decline, Dr. Zeydan said.

Dr. Zeydan reported the sleep substudy of KEEPS (the Kronos Early Estrogen Prevention Study), a randomized, double-blind, placebo-controlled, multisite trial that compared oral conjugated equine estrogen with transdermal estradiol. A control group received oral placebo and a placebo patch.*

Brain architecture was similar between the placebo and transdermal groups, but it was actually worse in some measures in the oral-estrogen group, compared with the placebo group. Women taking oral estrogen had more white matter hyperintensities, greater ventricle enlargement, and more cortical thinning. Those differences resolved after they stopped taking the oral formulation, bringing them into line with the transdermal and placebo groups.

The investigation also found that the transdermal group showed lower cerebral amyloid binding on PET scans relative to both placebo and oral estrogen.

“The relative preservation of dorsolateral prefrontal cortical volume in the [transdermal estradiol] group over 7 years indicates that hormone therapy may have long-term effects on the brain,” the team concluded. They noted that the original KEEPS study didn’t find any cognitive correlation with these changes.

The subanalysis looked at 69 women of the KEEPS cohort who had been followed for the full 7 years (4 years on treatment and 3 years off treatment). They were randomized to oral placebo and a placebo patch,* oral conjugated equine estrogen (0.45 mg/day), or transdermal estradiol (50 mcg/day). Participants in the active treatment groups received oral micronized progesterone 12 days each month. All had complete data on cognitive testing and brain imaging. Sleep quality was measured by the Pittsburgh Sleep Quality Index. Dr. Zeydan compared cognition and brain architecture findings in relation to the sleep score; lower scores mean better sleep.

The women were aged 42-58 years at baseline, and within 36 months from menopause. They had no history of menopausal hormone therapy or cardiovascular disease.

The investigators were particularly interested in how estrogen might have modulated the disturbed sleep patterns that often accompany perimenopause and early menopause, and whether the observed brain and cognitive changes tracked with sleep quality.

“During this time, 40% to 60% of women report problems sleeping, and estrogen decline seems to play an important role in sleep disturbances during this phase,” Dr. Zeydan said. “Although poor sleep quality is common in recently menopausal women, sleep quality improves with hormone therapy, as was previously demonstrated in KEEPS hormone therapy trial in recently menopausal women.”

By year 7, the cohort’s mean age was 61 years. The majority had at least some college education. The percentage who carried an apolipoprotein E epsilon-4 allele varied by group, with 15% positivity in the oral group, 48% in the transdermal group, and 16% in the placebo group.


Cognitive function was estimated with a global cognitive measure and four cognitive domain scores: verbal learning and memory, auditory attention and working memory, visual attention and executive function, and mental flexibility.

Higher attention and executive function scores were moderately correlated with a lower sleep score in the transdermal group (r = –0.54, a significant difference compared with the oral formulation). Lower sleep scores also showed a moderate correlation with preserved cortical volume of the dorsolateral prefrontal region (r = –0.47, also significantly different from the oral group).

Lower brain amyloid also positively correlated with better sleep. The correlation between sleep and global amyloid burden in the transdermal group was also moderate (r = 0.45), while the correlation in the oral group was significantly weaker (r = 0.18).

“We can say that sleep quality and transdermal estradiol during early postmenopausal years somehow interact to influence beta-amyloid deposition, preservation of dorsolateral prefrontal cortex volume, and attention and executive function,” Dr. Zeydan said.

Dr. Zeydan had no financial disclosures.

[email protected]

*Correction, 8/7/2019: An earlier version of this story did not make clear that participants in the control group received oral placebo and a placebo patch.

LOS ANGELES – Estrogen therapy may have scored another goal in its comeback game, as a 7-year prospective study shows that a transdermal formulation preserves some measures of cognitive function and brain architecture in postmenopausal women.

JackF/thinkstockphotos.com

In addition to performing better on subjective tests of memory, women using the estrogen patch experienced less cortical atrophy and were less likely to show amyloid on brain imaging. The observations were moderately associated with the improved sleep these women reported, Burcu Zeydan, MD, said at the Alzheimer’s Association International Conference.

“By 7 years, among the cognitive domains studied ... [less brain and cognitive change] correlated with lower global sleep score, meaning better sleep quality in the estradiol group,” said Dr. Zeydan, assistant professor of radiology at the Mayo Clinic in Rochester, Minn. “We previously found that preservation of dorsolateral prefrontal cortex over 7 years was associated with lower cortical beta-amyloid deposition on PET only in the estradiol group, pointing out the potential role of estrogen receptors in modulating this relationship.”

Dysregulated sleep is more common among women than men, particularly as menopause approaches and estrogen levels fluctuate, then decline, Dr. Zeydan said.

Dr. Zeydan reported the sleep substudy of KEEPS (the Kronos Early Estrogen Prevention Study), a randomized, double-blind, placebo-controlled, multisite trial that compared oral conjugated equine estrogen with transdermal estradiol. A control group received oral placebo and a placebo patch.*

Brain architecture was similar between the placebo and transdermal groups, but it was actually worse in some measures in the oral-estrogen group, compared with the placebo group. Women taking oral estrogen had more white matter hyperintensities, greater ventricle enlargement, and more cortical thinning. Those differences resolved after they stopped taking the oral formulation, bringing them into line with the transdermal and placebo groups.

The investigation also found that the transdermal group showed lower cerebral amyloid binding on PET scans relative to both placebo and oral estrogen.

“The relative preservation of dorsolateral prefrontal cortical volume in the [transdermal estradiol] group over 7 years indicates that hormone therapy may have long-term effects on the brain,” the team concluded. They noted that the original KEEPS study didn’t find any cognitive correlation with these changes.

The subanalysis looked at 69 women of the KEEPS cohort who had been followed for the full 7 years (4 years on treatment and 3 years off treatment). They were randomized to oral placebo and a placebo patch,* oral conjugated equine estrogen (0.45 mg/day), or transdermal estradiol (50 mcg/day). Participants in the active treatment groups received oral micronized progesterone 12 days each month. All had complete data on cognitive testing and brain imaging. Sleep quality was measured by the Pittsburgh Sleep Quality Index. Dr. Zeydan compared cognition and brain architecture findings in relation to the sleep score; lower scores mean better sleep.

The women were aged 42-58 years at baseline, and within 36 months from menopause. They had no history of menopausal hormone therapy or cardiovascular disease.

The investigators were particularly interested in how estrogen might have modulated the disturbed sleep patterns that often accompany perimenopause and early menopause, and whether the observed brain and cognitive changes tracked with sleep quality.

“During this time, 40% to 60% of women report problems sleeping, and estrogen decline seems to play an important role in sleep disturbances during this phase,” Dr. Zeydan said. “Although poor sleep quality is common in recently menopausal women, sleep quality improves with hormone therapy, as was previously demonstrated in KEEPS hormone therapy trial in recently menopausal women.”

By year 7, the cohort’s mean age was 61 years. The majority had at least some college education. The percentage who carried an apolipoprotein E epsilon-4 allele varied by group, with 15% positivity in the oral group, 48% in the transdermal group, and 16% in the placebo group.


Cognitive function was estimated with a global cognitive measure and four cognitive domain scores: verbal learning and memory, auditory attention and working memory, visual attention and executive function, and mental flexibility.

Higher attention and executive function scores were moderately correlated with a lower sleep score in the transdermal group (r = –0.54, a significant difference compared with the oral formulation). Lower sleep scores also showed a moderate correlation with preserved cortical volume of the dorsolateral prefrontal region (r = –0.47, also significantly different from the oral group).

Lower brain amyloid also positively correlated with better sleep. The correlation between sleep and global amyloid burden in the transdermal group was also moderate (r = 0.45), while the correlation in the oral group was significantly weaker (r = 0.18).

“We can say that sleep quality and transdermal estradiol during early postmenopausal years somehow interact to influence beta-amyloid deposition, preservation of dorsolateral prefrontal cortex volume, and attention and executive function,” Dr. Zeydan said.

Dr. Zeydan had no financial disclosures.

[email protected]

*Correction, 8/7/2019: An earlier version of this story did not make clear that participants in the control group received oral placebo and a placebo patch.

A new bivalent oral polio vaccine was noninferior to a currently licensed vaccine in a phase 3 clinical trial, according to Khalequ Zaman, MBBS, PhD, of the International Center for Diarrheal Disease Research in Dhaka, Bangladesh, and associates.

Courtesy Wikimedia Commons/Shobhit Gosain/Creative Commons License

In the first part of the observer-blind, randomized, controlled study, 40 patients aged 5-6 years received either the new vaccine (BBio bOPV) or the licensed vaccine (SII bOPV). In the second part, 1,080 patients aged 6-8 weeks received either BBio bOPV or SII bOPV at age 6, 10, and 14 weeks. Blood samples were taken to assess neutralizing antibody responses against poliovirus types 1 and 3, and safety also was assessed.

In the first part of the study, 12 adverse events were reported, none of which were serious and none of which were related to the vaccines. All participants demonstrated seroprotective titers against both poliovirus types 1 month after vaccination.

In the second part, more than 96% of infants demonstrated seroprotection and seroconversion against both poliovirus types. Geometric mean titers were equivalent in both groups. A total of 387 participants had at least one adverse event, and 18 serious adverse events were reported. None of these were related to the vaccines.

“The BBio bOPV has been proven safe and immunogenic in the target infant population in Bangladesh. As the use of bOPV is expected to be continued until at least 2022, availability of new bOPV bulk manufacturer will be helpful in securing adequate supplies of bOPV for global demand in the polio endgame strategy,” the investigators concluded.

The study was funded by Bilthoven Biologicals. Four coauthors are employed by Bilthoven, manufacturer of the study vaccine; two others are employed by the Serum Institute of India, which provided the control vaccine.

[email protected]

SOURCE: Zaman K et al. Vaccine. 2019 Jun 22. doi: 10.1016/j.vaccine.2019.06.048.

A new bivalent oral polio vaccine was noninferior to a currently licensed vaccine in a phase 3 clinical trial, according to Khalequ Zaman, MBBS, PhD, of the International Center for Diarrheal Disease Research in Dhaka, Bangladesh, and associates.

Courtesy Wikimedia Commons/Shobhit Gosain/Creative Commons License

In the first part of the observer-blind, randomized, controlled study, 40 patients aged 5-6 years received either the new vaccine (BBio bOPV) or the licensed vaccine (SII bOPV). In the second part, 1,080 patients aged 6-8 weeks received either BBio bOPV or SII bOPV at age 6, 10, and 14 weeks. Blood samples were taken to assess neutralizing antibody responses against poliovirus types 1 and 3, and safety also was assessed.

In the first part of the study, 12 adverse events were reported, none of which were serious and none of which were related to the vaccines. All participants demonstrated seroprotective titers against both poliovirus types 1 month after vaccination.

In the second part, more than 96% of infants demonstrated seroprotection and seroconversion against both poliovirus types. Geometric mean titers were equivalent in both groups. A total of 387 participants had at least one adverse event, and 18 serious adverse events were reported. None of these were related to the vaccines.

“The BBio bOPV has been proven safe and immunogenic in the target infant population in Bangladesh. As the use of bOPV is expected to be continued until at least 2022, availability of new bOPV bulk manufacturer will be helpful in securing adequate supplies of bOPV for global demand in the polio endgame strategy,” the investigators concluded.

The study was funded by Bilthoven Biologicals. Four coauthors are employed by Bilthoven, manufacturer of the study vaccine; two others are employed by the Serum Institute of India, which provided the control vaccine.

[email protected]

SOURCE: Zaman K et al. Vaccine. 2019 Jun 22. doi: 10.1016/j.vaccine.2019.06.048.

A new bivalent oral polio vaccine was noninferior to a currently licensed vaccine in a phase 3 clinical trial, according to Khalequ Zaman, MBBS, PhD, of the International Center for Diarrheal Disease Research in Dhaka, Bangladesh, and associates.

Courtesy Wikimedia Commons/Shobhit Gosain/Creative Commons License

In the first part of the observer-blind, randomized, controlled study, 40 patients aged 5-6 years received either the new vaccine (BBio bOPV) or the licensed vaccine (SII bOPV). In the second part, 1,080 patients aged 6-8 weeks received either BBio bOPV or SII bOPV at age 6, 10, and 14 weeks. Blood samples were taken to assess neutralizing antibody responses against poliovirus types 1 and 3, and safety also was assessed.

In the first part of the study, 12 adverse events were reported, none of which were serious and none of which were related to the vaccines. All participants demonstrated seroprotective titers against both poliovirus types 1 month after vaccination.

In the second part, more than 96% of infants demonstrated seroprotection and seroconversion against both poliovirus types. Geometric mean titers were equivalent in both groups. A total of 387 participants had at least one adverse event, and 18 serious adverse events were reported. None of these were related to the vaccines.

“The BBio bOPV has been proven safe and immunogenic in the target infant population in Bangladesh. As the use of bOPV is expected to be continued until at least 2022, availability of new bOPV bulk manufacturer will be helpful in securing adequate supplies of bOPV for global demand in the polio endgame strategy,” the investigators concluded.

The study was funded by Bilthoven Biologicals. Four coauthors are employed by Bilthoven, manufacturer of the study vaccine; two others are employed by the Serum Institute of India, which provided the control vaccine.

[email protected]

SOURCE: Zaman K et al. Vaccine. 2019 Jun 22. doi: 10.1016/j.vaccine.2019.06.048.