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FDA Expands Indication for Amivantamab in Lung Cancer
Amivantamab with carboplatin and pemetrexed is now indicated for adults with locally advanced or metastatic NSCLC with EGFR exon 19 deletions or exon 21 L858R substitution mutations whose disease has progressed on or after treatment with an EGFR tyrosine kinase inhibitor (TKI).
The FDA has already approved first-line use of amivantamab in combination with carboplatin and pemetrexed in patients with locally advanced or metastatic NSCLC with EGFR exon 20 insertion mutations, as reported by Medscape Medical News.
The second-line approval for amivantamab plus chemotherapy “may address the most common mechanisms of treatment resistance to third-generation EGFR TKIs, such as osimertinib, in the first line,” Martin Dietrich, MD, PhD, oncologist, Cancer Care Centers of Brevard in Florida, said in a company news release.
“This multitargeted combination extended progression-free survival (PFS) and improved overall response compared to chemotherapy alone, offering an important and effective new second-line option for patients,” Dr. Dietrich added.
The second-line indication is supported by the phase 3 MARIPOSA-2 study, which included 657 patients with locally advanced or metastatic NSCLC with EGFR exon 19 deletions or exon 21 L858R substitution mutations and disease progression on or after receiving osimertinib.
The study demonstrated a 52% reduced risk of disease progression or death when amivantamab was added to carboplatin and pemetrexed (hazard ratio, 0.48).
Median PFS was 6.3 months with amivantamab vs 4.2 months with chemotherapy alone. The confirmed objective response rate was 53% in the amivantamab plus chemotherapy group vs 29% in the chemotherapy only group.
The most common adverse reactions, occurring in at least 20% of patients, were rash, infusion-related reactions, fatigue, nail toxicity, nausea, constipation, edema, stomatitis, decreased appetite, musculoskeletal pain, vomiting, and COVID-19 infection.
The company noted that amivantamab in combination with chemotherapy is the only category 1 treatment option in National Comprehensive Cancer Network clinical practice guidelines for patients with EGFR-mutated NSCLC who have progressed on osimertinib and who are symptomatic with multiple lesions.
A version of this article appeared on Medscape.com.
Amivantamab with carboplatin and pemetrexed is now indicated for adults with locally advanced or metastatic NSCLC with EGFR exon 19 deletions or exon 21 L858R substitution mutations whose disease has progressed on or after treatment with an EGFR tyrosine kinase inhibitor (TKI).
The FDA has already approved first-line use of amivantamab in combination with carboplatin and pemetrexed in patients with locally advanced or metastatic NSCLC with EGFR exon 20 insertion mutations, as reported by Medscape Medical News.
The second-line approval for amivantamab plus chemotherapy “may address the most common mechanisms of treatment resistance to third-generation EGFR TKIs, such as osimertinib, in the first line,” Martin Dietrich, MD, PhD, oncologist, Cancer Care Centers of Brevard in Florida, said in a company news release.
“This multitargeted combination extended progression-free survival (PFS) and improved overall response compared to chemotherapy alone, offering an important and effective new second-line option for patients,” Dr. Dietrich added.
The second-line indication is supported by the phase 3 MARIPOSA-2 study, which included 657 patients with locally advanced or metastatic NSCLC with EGFR exon 19 deletions or exon 21 L858R substitution mutations and disease progression on or after receiving osimertinib.
The study demonstrated a 52% reduced risk of disease progression or death when amivantamab was added to carboplatin and pemetrexed (hazard ratio, 0.48).
Median PFS was 6.3 months with amivantamab vs 4.2 months with chemotherapy alone. The confirmed objective response rate was 53% in the amivantamab plus chemotherapy group vs 29% in the chemotherapy only group.
The most common adverse reactions, occurring in at least 20% of patients, were rash, infusion-related reactions, fatigue, nail toxicity, nausea, constipation, edema, stomatitis, decreased appetite, musculoskeletal pain, vomiting, and COVID-19 infection.
The company noted that amivantamab in combination with chemotherapy is the only category 1 treatment option in National Comprehensive Cancer Network clinical practice guidelines for patients with EGFR-mutated NSCLC who have progressed on osimertinib and who are symptomatic with multiple lesions.
A version of this article appeared on Medscape.com.
Amivantamab with carboplatin and pemetrexed is now indicated for adults with locally advanced or metastatic NSCLC with EGFR exon 19 deletions or exon 21 L858R substitution mutations whose disease has progressed on or after treatment with an EGFR tyrosine kinase inhibitor (TKI).
The FDA has already approved first-line use of amivantamab in combination with carboplatin and pemetrexed in patients with locally advanced or metastatic NSCLC with EGFR exon 20 insertion mutations, as reported by Medscape Medical News.
The second-line approval for amivantamab plus chemotherapy “may address the most common mechanisms of treatment resistance to third-generation EGFR TKIs, such as osimertinib, in the first line,” Martin Dietrich, MD, PhD, oncologist, Cancer Care Centers of Brevard in Florida, said in a company news release.
“This multitargeted combination extended progression-free survival (PFS) and improved overall response compared to chemotherapy alone, offering an important and effective new second-line option for patients,” Dr. Dietrich added.
The second-line indication is supported by the phase 3 MARIPOSA-2 study, which included 657 patients with locally advanced or metastatic NSCLC with EGFR exon 19 deletions or exon 21 L858R substitution mutations and disease progression on or after receiving osimertinib.
The study demonstrated a 52% reduced risk of disease progression or death when amivantamab was added to carboplatin and pemetrexed (hazard ratio, 0.48).
Median PFS was 6.3 months with amivantamab vs 4.2 months with chemotherapy alone. The confirmed objective response rate was 53% in the amivantamab plus chemotherapy group vs 29% in the chemotherapy only group.
The most common adverse reactions, occurring in at least 20% of patients, were rash, infusion-related reactions, fatigue, nail toxicity, nausea, constipation, edema, stomatitis, decreased appetite, musculoskeletal pain, vomiting, and COVID-19 infection.
The company noted that amivantamab in combination with chemotherapy is the only category 1 treatment option in National Comprehensive Cancer Network clinical practice guidelines for patients with EGFR-mutated NSCLC who have progressed on osimertinib and who are symptomatic with multiple lesions.
A version of this article appeared on Medscape.com.
Epilepsy Drug May Reduce Symptoms of OSA
An epilepsy drug sold in Europe as Ospolot and also known as sulthiame showed promise in reducing sleep disordered breathing and other symptoms of obstructive sleep apnea (OSA), based on data from nearly 300 individuals presented in a late-breaking study at the annual congress of the European Respiratory Society.
“Current therapies are mechanical and based on the notion of an airway splint,” presenting author Jan Hedner, MD, professor of respiratory medicine at Sahlgrenska University Hospital and the University of Gothenburg, both in Sweden, said in an interview. “In other words, applying an airflow at elevated pressure [continuous positive airway pressure] or advancing the jaw with a dental device. Adherence to this type of therapy is limited. In the case of continuous positive airway pressure [CPAP], it is < 50% after 3-4 years of therapy.” Therefore, there is a need for a better-tolerated therapy, such as a drug, and possibly a combination of mechanical and pharmaceutical therapies.
The use of medication has emerged as a viable option for OSA, with a high rate of compliance and acceptable safety profile, Dr. Hedner said in his presentation.
“Modified carbonic anhydrase activity may be a pathophysiological mechanism in OSA,” said Dr. Hedner. Sulthiame, a carbonic anhydrase inhibitor, showed safety and effectiveness for improving OSA in a previous phase 2b trial.
In the current study, the researchers sought to determine the most effective dose of sulthiame for patients with OSA. They randomized 298 adults with OSA who could not accept or tolerate oral splints or CPAP to 100 mg, 200 mg, or 300 mg of sulthiame daily (74, 74, and 75 patients, respectively) or placebo (75 patients).
The mean age of the patients was 56 years, 26.2% were women, and the average apnea-hypopnea index (AHI3a) at baseline was 29 n/h. Patients were treated at centers in Spain, France, Belgium, Germany, and the Czech Republic. Baseline demographics and clinical characteristics were similar among the treatment groups.
The primary endpoint was the change in AHI3a from baseline to 15 weeks, and significant changes occurred in patients who received the 100-mg, 200-mg, and 300-mg doses, with decreases of 17.8%, 34.8%, and 39.9%, respectively.
Dr. Hedner said in his presentation.
Notably, in a post hoc analysis, apnea improved by 47.1% at a 300-mg dose when the AHI4 measure (apnea/hypopnea with ≥ 4% O2 desaturation) was used in a placebo-adjusted dose-dependent reduction, the researchers wrote. The changes in AHI4 from baseline in this analysis also were significant for 200 mg and 100 mg doses (36.8% and 26.2%, respectively).
Patients underwent polysomnography at baseline and at weeks 4 and 12.
Mean overnight oxygen saturation also improved significantly from baseline with doses of 200 mg and 300 mg, compared with placebo (P < .0001 for both).
In addition, scores on the Epworth Sleepiness Scale (ESS) improved from baseline to week 15 in all dosage groups, and the subgroup of patients with ESS scores of ≥ 11 at baseline showed even greater improvement in ESS, Dr. Hedner said in his presentation.
Total arousal index and sleep quality also improved from baseline compared with placebo, and no clinically relevant reduction in REM sleep was noted, Dr. Hedner added.
Treatment-emergent adverse events were in line with the known safety profile of sulthiame and included paresthesia, headache, fatigue, and nausea; these were mainly moderate and dose-dependent, with no evidence of cardiovascular safety issues, he said.
Although the study results were not surprising given previous research, the investigators were pleased with the potency of the therapy. “We are also happy about potential added values such as a blood pressure lowering effect, which is beneficial in this group of patients; however, we need to further study these mechanisms in detail,” Dr. Hedner noted.
The study findings were limited by the relatively small scale, and larger studies on long-term efficacy and tolerability are also needed, he said.
“The current study was a dose-finding study, and we now have useful information on most suitable dose,” he said.
However, the results support sulthiame as an effective, well-tolerated, and promising novel candidate for drug therapy in patients with OSA, worthy of phase 3 studies, Dr. Hedner said.
Oral Option Could Be Game-Changer, But Not Yet
The gold standard of treatment for OSA is a CPAP machine, but the effectiveness is limited by patient tolerance, Q. Afifa Shamim-Uzzaman, MD, an associate professor and a sleep medicine specialist at the University of Michigan, Ann Arbor, said in an interview.
“Presently, there are no effective pharmacological treatments for OSA — having a pill that treats OSA would be a total game changer and huge advance for the treatment of OSA and the field of sleep medicine,” said Dr. Shamim-Uzzaman, who was not involved in the study. “More patients may be able to obtain treatment for OSA and thereby reduce the potential complications of untreated OSA.
“Carbonic anhydrase inhibitors such as acetazolamide and sulthiame have been studied with limited success for the treatment of other forms of sleep disordered breathing such as central sleep apnea [CSA] but have shown less efficacy for OSA and are presently not recommended in the treatment of OSA by the American Academy of Sleep Medicine,” Dr. Shamim-Uzzaman said.
Recently, emerging evidence about different phenotypes of OSA suggests that nonanatomic features (such as high loop gain) may play a role in patients with OSA, not only in those with CSA, she said. Whether carbonic anhydrase inhibitors could play a greater role in treating sleep apnea in patients with predominantly nonanatomic pathophysiologic traits remains to be seen.
The sulthiame data are promising, but more research is needed, Dr. Shamim-Uzzaman said. Although patients in the highest dose group showed a reduction in AHI of nearly 40%, they still would have moderate OSA, and the OSA did not appear to decrease to a normal range in any of the treatment groups.
“More research is needed to identify which types of patients would be responders to this form of therapy, to understand if these effects are maintained long term (beyond 15 weeks), to evaluate patient-centered outcomes, especially in different sleep apnea subgroups (such as phenotypes with high loop gain vs those without), and to assess interactions with other therapies,” she said.
The study was supported by manufacturer Desitin. Dr. Hedner disclosed serving as a consultant to AstraZeneca, Bayer, CereusScience, Jazz Pharmaceuticals, MSD, Weinmann, Desitin, SomnoMed, and Itamar Medical; serving on the speakers’ bureau for Almirall, AstraZeneca, Jazz Pharmaceuticals, ResMed, Philips Respironics, and Weinmann; and receiving grants or research support from Bayer, ResMed, Philips Respironics, and SomnoMed. He also disclosed shared ownership of intellectual property related to sleep apnea therapy. Dr. Shamim-Uzzaman had no financial conflicts to disclose.
A version of this article appeared on Medscape.com.
An epilepsy drug sold in Europe as Ospolot and also known as sulthiame showed promise in reducing sleep disordered breathing and other symptoms of obstructive sleep apnea (OSA), based on data from nearly 300 individuals presented in a late-breaking study at the annual congress of the European Respiratory Society.
“Current therapies are mechanical and based on the notion of an airway splint,” presenting author Jan Hedner, MD, professor of respiratory medicine at Sahlgrenska University Hospital and the University of Gothenburg, both in Sweden, said in an interview. “In other words, applying an airflow at elevated pressure [continuous positive airway pressure] or advancing the jaw with a dental device. Adherence to this type of therapy is limited. In the case of continuous positive airway pressure [CPAP], it is < 50% after 3-4 years of therapy.” Therefore, there is a need for a better-tolerated therapy, such as a drug, and possibly a combination of mechanical and pharmaceutical therapies.
The use of medication has emerged as a viable option for OSA, with a high rate of compliance and acceptable safety profile, Dr. Hedner said in his presentation.
“Modified carbonic anhydrase activity may be a pathophysiological mechanism in OSA,” said Dr. Hedner. Sulthiame, a carbonic anhydrase inhibitor, showed safety and effectiveness for improving OSA in a previous phase 2b trial.
In the current study, the researchers sought to determine the most effective dose of sulthiame for patients with OSA. They randomized 298 adults with OSA who could not accept or tolerate oral splints or CPAP to 100 mg, 200 mg, or 300 mg of sulthiame daily (74, 74, and 75 patients, respectively) or placebo (75 patients).
The mean age of the patients was 56 years, 26.2% were women, and the average apnea-hypopnea index (AHI3a) at baseline was 29 n/h. Patients were treated at centers in Spain, France, Belgium, Germany, and the Czech Republic. Baseline demographics and clinical characteristics were similar among the treatment groups.
The primary endpoint was the change in AHI3a from baseline to 15 weeks, and significant changes occurred in patients who received the 100-mg, 200-mg, and 300-mg doses, with decreases of 17.8%, 34.8%, and 39.9%, respectively.
Dr. Hedner said in his presentation.
Notably, in a post hoc analysis, apnea improved by 47.1% at a 300-mg dose when the AHI4 measure (apnea/hypopnea with ≥ 4% O2 desaturation) was used in a placebo-adjusted dose-dependent reduction, the researchers wrote. The changes in AHI4 from baseline in this analysis also were significant for 200 mg and 100 mg doses (36.8% and 26.2%, respectively).
Patients underwent polysomnography at baseline and at weeks 4 and 12.
Mean overnight oxygen saturation also improved significantly from baseline with doses of 200 mg and 300 mg, compared with placebo (P < .0001 for both).
In addition, scores on the Epworth Sleepiness Scale (ESS) improved from baseline to week 15 in all dosage groups, and the subgroup of patients with ESS scores of ≥ 11 at baseline showed even greater improvement in ESS, Dr. Hedner said in his presentation.
Total arousal index and sleep quality also improved from baseline compared with placebo, and no clinically relevant reduction in REM sleep was noted, Dr. Hedner added.
Treatment-emergent adverse events were in line with the known safety profile of sulthiame and included paresthesia, headache, fatigue, and nausea; these were mainly moderate and dose-dependent, with no evidence of cardiovascular safety issues, he said.
Although the study results were not surprising given previous research, the investigators were pleased with the potency of the therapy. “We are also happy about potential added values such as a blood pressure lowering effect, which is beneficial in this group of patients; however, we need to further study these mechanisms in detail,” Dr. Hedner noted.
The study findings were limited by the relatively small scale, and larger studies on long-term efficacy and tolerability are also needed, he said.
“The current study was a dose-finding study, and we now have useful information on most suitable dose,” he said.
However, the results support sulthiame as an effective, well-tolerated, and promising novel candidate for drug therapy in patients with OSA, worthy of phase 3 studies, Dr. Hedner said.
Oral Option Could Be Game-Changer, But Not Yet
The gold standard of treatment for OSA is a CPAP machine, but the effectiveness is limited by patient tolerance, Q. Afifa Shamim-Uzzaman, MD, an associate professor and a sleep medicine specialist at the University of Michigan, Ann Arbor, said in an interview.
“Presently, there are no effective pharmacological treatments for OSA — having a pill that treats OSA would be a total game changer and huge advance for the treatment of OSA and the field of sleep medicine,” said Dr. Shamim-Uzzaman, who was not involved in the study. “More patients may be able to obtain treatment for OSA and thereby reduce the potential complications of untreated OSA.
“Carbonic anhydrase inhibitors such as acetazolamide and sulthiame have been studied with limited success for the treatment of other forms of sleep disordered breathing such as central sleep apnea [CSA] but have shown less efficacy for OSA and are presently not recommended in the treatment of OSA by the American Academy of Sleep Medicine,” Dr. Shamim-Uzzaman said.
Recently, emerging evidence about different phenotypes of OSA suggests that nonanatomic features (such as high loop gain) may play a role in patients with OSA, not only in those with CSA, she said. Whether carbonic anhydrase inhibitors could play a greater role in treating sleep apnea in patients with predominantly nonanatomic pathophysiologic traits remains to be seen.
The sulthiame data are promising, but more research is needed, Dr. Shamim-Uzzaman said. Although patients in the highest dose group showed a reduction in AHI of nearly 40%, they still would have moderate OSA, and the OSA did not appear to decrease to a normal range in any of the treatment groups.
“More research is needed to identify which types of patients would be responders to this form of therapy, to understand if these effects are maintained long term (beyond 15 weeks), to evaluate patient-centered outcomes, especially in different sleep apnea subgroups (such as phenotypes with high loop gain vs those without), and to assess interactions with other therapies,” she said.
The study was supported by manufacturer Desitin. Dr. Hedner disclosed serving as a consultant to AstraZeneca, Bayer, CereusScience, Jazz Pharmaceuticals, MSD, Weinmann, Desitin, SomnoMed, and Itamar Medical; serving on the speakers’ bureau for Almirall, AstraZeneca, Jazz Pharmaceuticals, ResMed, Philips Respironics, and Weinmann; and receiving grants or research support from Bayer, ResMed, Philips Respironics, and SomnoMed. He also disclosed shared ownership of intellectual property related to sleep apnea therapy. Dr. Shamim-Uzzaman had no financial conflicts to disclose.
A version of this article appeared on Medscape.com.
An epilepsy drug sold in Europe as Ospolot and also known as sulthiame showed promise in reducing sleep disordered breathing and other symptoms of obstructive sleep apnea (OSA), based on data from nearly 300 individuals presented in a late-breaking study at the annual congress of the European Respiratory Society.
“Current therapies are mechanical and based on the notion of an airway splint,” presenting author Jan Hedner, MD, professor of respiratory medicine at Sahlgrenska University Hospital and the University of Gothenburg, both in Sweden, said in an interview. “In other words, applying an airflow at elevated pressure [continuous positive airway pressure] or advancing the jaw with a dental device. Adherence to this type of therapy is limited. In the case of continuous positive airway pressure [CPAP], it is < 50% after 3-4 years of therapy.” Therefore, there is a need for a better-tolerated therapy, such as a drug, and possibly a combination of mechanical and pharmaceutical therapies.
The use of medication has emerged as a viable option for OSA, with a high rate of compliance and acceptable safety profile, Dr. Hedner said in his presentation.
“Modified carbonic anhydrase activity may be a pathophysiological mechanism in OSA,” said Dr. Hedner. Sulthiame, a carbonic anhydrase inhibitor, showed safety and effectiveness for improving OSA in a previous phase 2b trial.
In the current study, the researchers sought to determine the most effective dose of sulthiame for patients with OSA. They randomized 298 adults with OSA who could not accept or tolerate oral splints or CPAP to 100 mg, 200 mg, or 300 mg of sulthiame daily (74, 74, and 75 patients, respectively) or placebo (75 patients).
The mean age of the patients was 56 years, 26.2% were women, and the average apnea-hypopnea index (AHI3a) at baseline was 29 n/h. Patients were treated at centers in Spain, France, Belgium, Germany, and the Czech Republic. Baseline demographics and clinical characteristics were similar among the treatment groups.
The primary endpoint was the change in AHI3a from baseline to 15 weeks, and significant changes occurred in patients who received the 100-mg, 200-mg, and 300-mg doses, with decreases of 17.8%, 34.8%, and 39.9%, respectively.
Dr. Hedner said in his presentation.
Notably, in a post hoc analysis, apnea improved by 47.1% at a 300-mg dose when the AHI4 measure (apnea/hypopnea with ≥ 4% O2 desaturation) was used in a placebo-adjusted dose-dependent reduction, the researchers wrote. The changes in AHI4 from baseline in this analysis also were significant for 200 mg and 100 mg doses (36.8% and 26.2%, respectively).
Patients underwent polysomnography at baseline and at weeks 4 and 12.
Mean overnight oxygen saturation also improved significantly from baseline with doses of 200 mg and 300 mg, compared with placebo (P < .0001 for both).
In addition, scores on the Epworth Sleepiness Scale (ESS) improved from baseline to week 15 in all dosage groups, and the subgroup of patients with ESS scores of ≥ 11 at baseline showed even greater improvement in ESS, Dr. Hedner said in his presentation.
Total arousal index and sleep quality also improved from baseline compared with placebo, and no clinically relevant reduction in REM sleep was noted, Dr. Hedner added.
Treatment-emergent adverse events were in line with the known safety profile of sulthiame and included paresthesia, headache, fatigue, and nausea; these were mainly moderate and dose-dependent, with no evidence of cardiovascular safety issues, he said.
Although the study results were not surprising given previous research, the investigators were pleased with the potency of the therapy. “We are also happy about potential added values such as a blood pressure lowering effect, which is beneficial in this group of patients; however, we need to further study these mechanisms in detail,” Dr. Hedner noted.
The study findings were limited by the relatively small scale, and larger studies on long-term efficacy and tolerability are also needed, he said.
“The current study was a dose-finding study, and we now have useful information on most suitable dose,” he said.
However, the results support sulthiame as an effective, well-tolerated, and promising novel candidate for drug therapy in patients with OSA, worthy of phase 3 studies, Dr. Hedner said.
Oral Option Could Be Game-Changer, But Not Yet
The gold standard of treatment for OSA is a CPAP machine, but the effectiveness is limited by patient tolerance, Q. Afifa Shamim-Uzzaman, MD, an associate professor and a sleep medicine specialist at the University of Michigan, Ann Arbor, said in an interview.
“Presently, there are no effective pharmacological treatments for OSA — having a pill that treats OSA would be a total game changer and huge advance for the treatment of OSA and the field of sleep medicine,” said Dr. Shamim-Uzzaman, who was not involved in the study. “More patients may be able to obtain treatment for OSA and thereby reduce the potential complications of untreated OSA.
“Carbonic anhydrase inhibitors such as acetazolamide and sulthiame have been studied with limited success for the treatment of other forms of sleep disordered breathing such as central sleep apnea [CSA] but have shown less efficacy for OSA and are presently not recommended in the treatment of OSA by the American Academy of Sleep Medicine,” Dr. Shamim-Uzzaman said.
Recently, emerging evidence about different phenotypes of OSA suggests that nonanatomic features (such as high loop gain) may play a role in patients with OSA, not only in those with CSA, she said. Whether carbonic anhydrase inhibitors could play a greater role in treating sleep apnea in patients with predominantly nonanatomic pathophysiologic traits remains to be seen.
The sulthiame data are promising, but more research is needed, Dr. Shamim-Uzzaman said. Although patients in the highest dose group showed a reduction in AHI of nearly 40%, they still would have moderate OSA, and the OSA did not appear to decrease to a normal range in any of the treatment groups.
“More research is needed to identify which types of patients would be responders to this form of therapy, to understand if these effects are maintained long term (beyond 15 weeks), to evaluate patient-centered outcomes, especially in different sleep apnea subgroups (such as phenotypes with high loop gain vs those without), and to assess interactions with other therapies,” she said.
The study was supported by manufacturer Desitin. Dr. Hedner disclosed serving as a consultant to AstraZeneca, Bayer, CereusScience, Jazz Pharmaceuticals, MSD, Weinmann, Desitin, SomnoMed, and Itamar Medical; serving on the speakers’ bureau for Almirall, AstraZeneca, Jazz Pharmaceuticals, ResMed, Philips Respironics, and Weinmann; and receiving grants or research support from Bayer, ResMed, Philips Respironics, and SomnoMed. He also disclosed shared ownership of intellectual property related to sleep apnea therapy. Dr. Shamim-Uzzaman had no financial conflicts to disclose.
A version of this article appeared on Medscape.com.
FROM ERS CONGRESS 2024
Whooping Cough Rising Fast, Especially Among Teens
Whooping cough is surging in the United States, with four times as many cases reported so far this year, compared to all of 2023.
The CDC said 14,569 cases had been reported as of Sept. 14, compared to 3475 in all of 2023.
Whooping cough, also called pertussis, is a respiratory illness spread through coughing, sneezing, or breathing very close to another person. Babies are given the DTaP vaccine to protect against whooping cough, diphtheria, and tetanus. Because the vaccine effectiveness wanes faster for whooping cough than the two other illnesses, boosters are recommended every decade or so.
Why the Whooping Cough Vaccine Is Important
Whooping cough is a very contagious bacteria, so vaccination is an important step to avoid it.
But many children in their tweens aren’t getting boosters, and that age group is driving the whooping cough outbreak.
“With the increase in vaccine hesitancy that has been going on since the COVID-19 pandemic, we’re seeing outbreaks occurring in kids who are not vaccinated,” Tina Tan, MD, president-elect of the Infectious Diseases Society of America, told NBC News.
Also, people are not social distancing the way they did during the height of the COVID pandemic, when whooping cough numbers went down.
“Levels of pertussis dropped dramatically when we were all masking, and now this huge increase is getting us back to pre-pandemic levels, and probably a little above that,” Thomas Murray, MD, a Yale Medicine pediatric infectious diseases specialist, said in a news release from the school. “It’s a contagious respiratory virus that can spread fairly quickly through the population.”
FDA advisers were scheduled to meet Sept. 20 to discuss developing more effective boosters for whooping cough.
A version of this article appeared on WebMD.com.
Whooping cough is surging in the United States, with four times as many cases reported so far this year, compared to all of 2023.
The CDC said 14,569 cases had been reported as of Sept. 14, compared to 3475 in all of 2023.
Whooping cough, also called pertussis, is a respiratory illness spread through coughing, sneezing, or breathing very close to another person. Babies are given the DTaP vaccine to protect against whooping cough, diphtheria, and tetanus. Because the vaccine effectiveness wanes faster for whooping cough than the two other illnesses, boosters are recommended every decade or so.
Why the Whooping Cough Vaccine Is Important
Whooping cough is a very contagious bacteria, so vaccination is an important step to avoid it.
But many children in their tweens aren’t getting boosters, and that age group is driving the whooping cough outbreak.
“With the increase in vaccine hesitancy that has been going on since the COVID-19 pandemic, we’re seeing outbreaks occurring in kids who are not vaccinated,” Tina Tan, MD, president-elect of the Infectious Diseases Society of America, told NBC News.
Also, people are not social distancing the way they did during the height of the COVID pandemic, when whooping cough numbers went down.
“Levels of pertussis dropped dramatically when we were all masking, and now this huge increase is getting us back to pre-pandemic levels, and probably a little above that,” Thomas Murray, MD, a Yale Medicine pediatric infectious diseases specialist, said in a news release from the school. “It’s a contagious respiratory virus that can spread fairly quickly through the population.”
FDA advisers were scheduled to meet Sept. 20 to discuss developing more effective boosters for whooping cough.
A version of this article appeared on WebMD.com.
Whooping cough is surging in the United States, with four times as many cases reported so far this year, compared to all of 2023.
The CDC said 14,569 cases had been reported as of Sept. 14, compared to 3475 in all of 2023.
Whooping cough, also called pertussis, is a respiratory illness spread through coughing, sneezing, or breathing very close to another person. Babies are given the DTaP vaccine to protect against whooping cough, diphtheria, and tetanus. Because the vaccine effectiveness wanes faster for whooping cough than the two other illnesses, boosters are recommended every decade or so.
Why the Whooping Cough Vaccine Is Important
Whooping cough is a very contagious bacteria, so vaccination is an important step to avoid it.
But many children in their tweens aren’t getting boosters, and that age group is driving the whooping cough outbreak.
“With the increase in vaccine hesitancy that has been going on since the COVID-19 pandemic, we’re seeing outbreaks occurring in kids who are not vaccinated,” Tina Tan, MD, president-elect of the Infectious Diseases Society of America, told NBC News.
Also, people are not social distancing the way they did during the height of the COVID pandemic, when whooping cough numbers went down.
“Levels of pertussis dropped dramatically when we were all masking, and now this huge increase is getting us back to pre-pandemic levels, and probably a little above that,” Thomas Murray, MD, a Yale Medicine pediatric infectious diseases specialist, said in a news release from the school. “It’s a contagious respiratory virus that can spread fairly quickly through the population.”
FDA advisers were scheduled to meet Sept. 20 to discuss developing more effective boosters for whooping cough.
A version of this article appeared on WebMD.com.
Treating Family: Ethicist Discusses Whether It’s Appropriate
This transcript has been edited for clarity.
There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.
He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.
This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.
The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.
By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.
If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.
I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.
It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.
All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.
You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.
What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.
It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”
Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.
Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.
At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.
At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”
Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.
Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.
He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.
This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.
The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.
By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.
If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.
I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.
It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.
All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.
You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.
What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.
It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”
Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.
Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.
At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.
At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”
Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.
Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
There’s a very interesting story in the medical press. A few years ago, a plastic surgeon named Edmond Cabbabe was preparing to do a follow-up cosmetic procedure on his wife at Mercy Hospital South, which is a big hospital in the St. Louis, Missouri, area.
He put her on the operating schedule, and he had done that when he had performed the original operation on her. On the day of the surgery, he got a call from the hospital saying the procedure was canceled. They said that the hospital’s policy, maybe a new one, would not allow doctors to operate on family members.
This physician was a past president of the Missouri State Medical Association. I think he was also on the board or president of the American Medical Association (AMA) Foundation. This was a physician not only in a skilled area where he felt confident he could take care of his wife, but also someone who was prominent in medical politics and medical policy.
The AMA forever has had a policy that says don’t treat relatives. This physician basically said, I think that policy is too restrictive, too cautious, and it doesn’t make much sense to continue to say that you can’t treat family and friends.
By implication, he was saying, I know exactly what I’m doing in my field and I know exactly what I’m doing with her procedure. I should have a right to perform it. I think I do a great job and I’d be best for her.
If you look at medical boards, every once in a while in some state, someone is brought up on a charge of doing different things with family members and saying that they’re going to get censured. They don’t usually lose their license, but they get a reprimand or get told that is just not ethical to do.
I think, in the long run, the policy about not treating your family and friends makes sense. The problem is, as is well known from the social sciences and psychology, people get biased when they deal with those they care about, love, and hold close to them.
It’s hard for the doctor to be objective when dealing with people that they really like or love. It’s also difficult for patients because they may not want to bring up something or they are uncomfortable talking with a doctor who’s a family member or close friend. They may not want to complain. They may be a little bit embarrassed about things. It just adds an emotional edge, I think, that’s difficult.
All that said, do I know doctors who regularly prescribe, say, an ointment for something that’s itchy or some kind of a pill when allergy season breaks out? I do. Do I think they’re acting in a horribly unethical manner? I don’t.
You need some judgment here. There are absolutely minor things where objectivity, fear, and anxiety are not in play. You’re going to be able to prescribe the routine thing for the routine itch without worrying too much about whether it’s a stranger, a friend, or your daughter.
What sorts of things am I really talking about when I say that minor variability ought to be allowed? It’s one thing when someone has poison ivy and they’re going to need some kind of standard medicine to treat it. A very different area that’s much more dangerous, and one I would avoid, is in the mental health field, and for that matter, the pain field.
It’s tempting to say: “Oh, my relative is just having a bad time. I’ll give her a little bit of antidepressant medicine,” or “They seem to be having pain after an operation or something, and I’m going to give them a little bit of pain meds just to get them through.”
Those areas are flying red flags. It’s easy to abuse and easy for someone to become a user and manipulate a friend or a doctor who’s a relative into getting things that another doctor wouldn’t be giving. I think that’s the space where you’ve got to exercise extreme caution.
Time and again, when those people get called up in front of the boards for treating relatives, it’s in those spaces of mental health, anxiety, and pain control. Again, when you know that there’s a likelihood of abuse, I think that’s the place where the line has to hold. Don’t treat the relative. Don’t treat the friend.
At the end of the day, I wouldn’t change the AMA policy. I think we should keep it in place and morally try to discourage doctors from caring for those they’re close to or they have emotional ties to.
At the same time, as with all ethical situations, there has to be a little bit of wiggle room for those super-minor cases where it just makes sense to say: “You don’t have to go find somebody else to do this. I can prescribe this ointment or this minor thing for you. No one’s objectivity is going to be soured, and you’re not going to feel in any way at risk because I’m going to prescribe this for you.”
Common sense ought to prevail. The default position is don’t do it; however, maybe with a tiny bit of space for what’s minor, what’s routine, and what really does just save people some inconvenience, there I might just give a little.
Dr. Caplan, Director, Division of Medical Ethics, New York University Langone Medical Center, New York City, has disclosed relationships with Johnson & Johnson’s Panel for Compassionate Drug Use and Medscape.
A version of this article first appeared on Medscape.com.
Are You Using the Correct Medication or a Look-Alike?
Five years have passed since the member states of the World Health Organization (WHO) gathered at the 72nd World Health Assembly and decided that September 17 should be recognized as World Patient Safety Day, acknowledging it as a global health priority.
WHO data indicate the following findings related to medical safety:
- One in 10 patients is harmed while receiving healthcare, and 3 million die as a result.
- More than half of these incidents could be prevented.
- Indirect costs could amount to several billion US dollars annually.
Given the magnitude of preventable harm related to medication use, in 2017, the WHO launched the third Global Patient Safety Challenge: Medication Without Harm with the goal of reducing serious and preventable harm related to medication by 50%. In addition, considering the volume of medication packages prescribed in 2023 by physicians in Spain’s National Health System, it is necessary to understand the most common types of medication errors to provide an effective and efficient response.
According to Spain’s Institute for Safe Medication Practices (ISMP), the 10 types of medication errors detected in 2020 with the most serious consequences were the following:
- Errors due to omission or delay in medication.
- Administration of medication to the wrong patient.
- Errors related to allergies or known adverse effects of medications.
- Dosing errors in pediatric patients.
- Errors due to similarities in the labeling or packaging of marketed medications.
- Errors associated with the lack of use of smart infusion pumps.
- Errors due to accidental administration of neuromuscular blocking agents.
- Incorrect intravenous administration of oral liquid medications.
- Errors in medication reconciliation upon hospital admission and discharge.
- Errors due to patient misunderstandings regarding medication use.
I would like to focus on the fifth item, errors due to similarities in the labeling or packaging of marketed medications.
Medications with similar names or with similar labeling or packaging are known as “look alike–sound alike” medications. They are estimated to account for between 6.2% and 14.7% of all medication errors. Confusion can arise due to spelling and phonetic similarities.
As shown in bulletin no. 50 of the ISMP, difficulties in distinguishing different medications or different presentations of the same medication due to similar packaging and labeling have frequently been associated with reported incidents.
Most cases involve either medications marketed by the same laboratory with a design based on brand image or different medications marketed by different laboratories in screen-printed ampoules used in the same settings.
In 2020, the ISMP published 11 new cases of labeling or packaging that may promote errors on its website. It reported 49 incidents to the Spanish Agency for Medicines and Medical Devices.
Shortages caused by the COVID-19 pandemic have further contributed to these incidents, as healthcare facilities sometimes had to change the medications they usually acquired and purchase whatever was available, without being able to select products that would not be confused with existing medications in the facility.
The ISMP recommends the following general practices for healthcare institutions, professionals, and patients to prevent these errors:
- Develop short lists of easily confused medication names and distribute them among all healthcare professionals.
- Prioritize medication names by active ingredient instead of brand name.
- For similar names, highlight the differences in capital letters, eg, DOBUTamine, DOPamine.
- For similar active ingredients, use brand names.
- Avoid placing similar medications near each other.
- Prescribe all medications electronically to minimize the risk of selecting the wrong medication.
- Make manual prescriptions legible, with clearly written dosages and pharmaceutical forms.
- Encourage patients to actively participate in their treatment and consult a clinician if they have any questions about the medications they are receiving.
- Raise awareness among patients, family members, and caregivers about the issues caused by medication name confusion and inform them about how to avoid these errors.
- Instruct patients to focus on and always use the active ingredient name as an identifying element for the medications they are taking.
- Review treatments with patients to ensure they know the medications they are taking.
Julia María Ruiz Redondo is the regional nursing advisor inspector of Spanish Society of General and Family Physicians of Castilla-La Mancha (SEMG-CLM), coordinator of the National Working Group on Public Health in the SEMG, and director of the international public health master’s degree at TECH Technological University. This article is the result of an editorial collaboration between the SEMG and Univadis, which you can access here.
This story was translated from Univadis Spain, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Five years have passed since the member states of the World Health Organization (WHO) gathered at the 72nd World Health Assembly and decided that September 17 should be recognized as World Patient Safety Day, acknowledging it as a global health priority.
WHO data indicate the following findings related to medical safety:
- One in 10 patients is harmed while receiving healthcare, and 3 million die as a result.
- More than half of these incidents could be prevented.
- Indirect costs could amount to several billion US dollars annually.
Given the magnitude of preventable harm related to medication use, in 2017, the WHO launched the third Global Patient Safety Challenge: Medication Without Harm with the goal of reducing serious and preventable harm related to medication by 50%. In addition, considering the volume of medication packages prescribed in 2023 by physicians in Spain’s National Health System, it is necessary to understand the most common types of medication errors to provide an effective and efficient response.
According to Spain’s Institute for Safe Medication Practices (ISMP), the 10 types of medication errors detected in 2020 with the most serious consequences were the following:
- Errors due to omission or delay in medication.
- Administration of medication to the wrong patient.
- Errors related to allergies or known adverse effects of medications.
- Dosing errors in pediatric patients.
- Errors due to similarities in the labeling or packaging of marketed medications.
- Errors associated with the lack of use of smart infusion pumps.
- Errors due to accidental administration of neuromuscular blocking agents.
- Incorrect intravenous administration of oral liquid medications.
- Errors in medication reconciliation upon hospital admission and discharge.
- Errors due to patient misunderstandings regarding medication use.
I would like to focus on the fifth item, errors due to similarities in the labeling or packaging of marketed medications.
Medications with similar names or with similar labeling or packaging are known as “look alike–sound alike” medications. They are estimated to account for between 6.2% and 14.7% of all medication errors. Confusion can arise due to spelling and phonetic similarities.
As shown in bulletin no. 50 of the ISMP, difficulties in distinguishing different medications or different presentations of the same medication due to similar packaging and labeling have frequently been associated with reported incidents.
Most cases involve either medications marketed by the same laboratory with a design based on brand image or different medications marketed by different laboratories in screen-printed ampoules used in the same settings.
In 2020, the ISMP published 11 new cases of labeling or packaging that may promote errors on its website. It reported 49 incidents to the Spanish Agency for Medicines and Medical Devices.
Shortages caused by the COVID-19 pandemic have further contributed to these incidents, as healthcare facilities sometimes had to change the medications they usually acquired and purchase whatever was available, without being able to select products that would not be confused with existing medications in the facility.
The ISMP recommends the following general practices for healthcare institutions, professionals, and patients to prevent these errors:
- Develop short lists of easily confused medication names and distribute them among all healthcare professionals.
- Prioritize medication names by active ingredient instead of brand name.
- For similar names, highlight the differences in capital letters, eg, DOBUTamine, DOPamine.
- For similar active ingredients, use brand names.
- Avoid placing similar medications near each other.
- Prescribe all medications electronically to minimize the risk of selecting the wrong medication.
- Make manual prescriptions legible, with clearly written dosages and pharmaceutical forms.
- Encourage patients to actively participate in their treatment and consult a clinician if they have any questions about the medications they are receiving.
- Raise awareness among patients, family members, and caregivers about the issues caused by medication name confusion and inform them about how to avoid these errors.
- Instruct patients to focus on and always use the active ingredient name as an identifying element for the medications they are taking.
- Review treatments with patients to ensure they know the medications they are taking.
Julia María Ruiz Redondo is the regional nursing advisor inspector of Spanish Society of General and Family Physicians of Castilla-La Mancha (SEMG-CLM), coordinator of the National Working Group on Public Health in the SEMG, and director of the international public health master’s degree at TECH Technological University. This article is the result of an editorial collaboration between the SEMG and Univadis, which you can access here.
This story was translated from Univadis Spain, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Five years have passed since the member states of the World Health Organization (WHO) gathered at the 72nd World Health Assembly and decided that September 17 should be recognized as World Patient Safety Day, acknowledging it as a global health priority.
WHO data indicate the following findings related to medical safety:
- One in 10 patients is harmed while receiving healthcare, and 3 million die as a result.
- More than half of these incidents could be prevented.
- Indirect costs could amount to several billion US dollars annually.
Given the magnitude of preventable harm related to medication use, in 2017, the WHO launched the third Global Patient Safety Challenge: Medication Without Harm with the goal of reducing serious and preventable harm related to medication by 50%. In addition, considering the volume of medication packages prescribed in 2023 by physicians in Spain’s National Health System, it is necessary to understand the most common types of medication errors to provide an effective and efficient response.
According to Spain’s Institute for Safe Medication Practices (ISMP), the 10 types of medication errors detected in 2020 with the most serious consequences were the following:
- Errors due to omission or delay in medication.
- Administration of medication to the wrong patient.
- Errors related to allergies or known adverse effects of medications.
- Dosing errors in pediatric patients.
- Errors due to similarities in the labeling or packaging of marketed medications.
- Errors associated with the lack of use of smart infusion pumps.
- Errors due to accidental administration of neuromuscular blocking agents.
- Incorrect intravenous administration of oral liquid medications.
- Errors in medication reconciliation upon hospital admission and discharge.
- Errors due to patient misunderstandings regarding medication use.
I would like to focus on the fifth item, errors due to similarities in the labeling or packaging of marketed medications.
Medications with similar names or with similar labeling or packaging are known as “look alike–sound alike” medications. They are estimated to account for between 6.2% and 14.7% of all medication errors. Confusion can arise due to spelling and phonetic similarities.
As shown in bulletin no. 50 of the ISMP, difficulties in distinguishing different medications or different presentations of the same medication due to similar packaging and labeling have frequently been associated with reported incidents.
Most cases involve either medications marketed by the same laboratory with a design based on brand image or different medications marketed by different laboratories in screen-printed ampoules used in the same settings.
In 2020, the ISMP published 11 new cases of labeling or packaging that may promote errors on its website. It reported 49 incidents to the Spanish Agency for Medicines and Medical Devices.
Shortages caused by the COVID-19 pandemic have further contributed to these incidents, as healthcare facilities sometimes had to change the medications they usually acquired and purchase whatever was available, without being able to select products that would not be confused with existing medications in the facility.
The ISMP recommends the following general practices for healthcare institutions, professionals, and patients to prevent these errors:
- Develop short lists of easily confused medication names and distribute them among all healthcare professionals.
- Prioritize medication names by active ingredient instead of brand name.
- For similar names, highlight the differences in capital letters, eg, DOBUTamine, DOPamine.
- For similar active ingredients, use brand names.
- Avoid placing similar medications near each other.
- Prescribe all medications electronically to minimize the risk of selecting the wrong medication.
- Make manual prescriptions legible, with clearly written dosages and pharmaceutical forms.
- Encourage patients to actively participate in their treatment and consult a clinician if they have any questions about the medications they are receiving.
- Raise awareness among patients, family members, and caregivers about the issues caused by medication name confusion and inform them about how to avoid these errors.
- Instruct patients to focus on and always use the active ingredient name as an identifying element for the medications they are taking.
- Review treatments with patients to ensure they know the medications they are taking.
Julia María Ruiz Redondo is the regional nursing advisor inspector of Spanish Society of General and Family Physicians of Castilla-La Mancha (SEMG-CLM), coordinator of the National Working Group on Public Health in the SEMG, and director of the international public health master’s degree at TECH Technological University. This article is the result of an editorial collaboration between the SEMG and Univadis, which you can access here.
This story was translated from Univadis Spain, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Cancer Risk: Are Pesticides the New Smoking?
Pesticides have transformed modern agriculture by boosting production yields and helping alleviate food insecurity amid rapid global population growth. However, from a public health perspective, exposure to pesticides has been linked to numerous harmful effects, including neurologic disorders like Parkinson’s disease, weakened immune function, and an increased risk for cancer.
A comprehensive assessment of how pesticide use affects cancer risk across a broader population has yet to be conducted.
A recent population-level study aimed to address this gap by evaluating cancer risks in the US population using a model that accounts for pesticide use and adjusts for various factors. The goal was to identify regional disparities in exposure and contribute to the development of public health policies that protect populations from potential harm.
Calculating Cancer Risk
Researchers developed a model using several data sources to estimate the additional cancer risk from agricultural pesticide use. Key data included:
- Pesticide use data from the US Geological Survey in 2019, which covered 69 agricultural pesticides across 3143 counties
- Cancer incidence rates per 100,000 people, which were collected between 2015 and 2019 by the National Institutes of Health and the Centers for Disease Control and Prevention; these data covered various cancers, including bladder, colorectal, leukemia, lung, non-Hodgkin lymphoma, and pancreatic cancers
- Covariates, including smoking prevalence, the Social Vulnerability Index, agricultural land use, and total US population in 2019
Pesticide use profile patterns were developed using latent class analysis, a statistical method used to identify homogeneous subgroups within a heterogeneous population. A generalized linear model then estimated how these pesticide use patterns and the covariates affected cancer incidence.
The model highlighted regions with the highest and lowest “additional” cancer risks linked to pesticide exposure, calculating the estimated increase in cancer cases per year that resulted from variations in agricultural pesticide use.
Midwest Most Affected
While this model doesn’t establish causality or assess individual risk, it reveals regional trends in the association between pesticide use patterns and cancer incidence from a population-based perspective.
The Midwest, known for its high corn production, emerged as the region most affected by pesticide use. Compared with regions with the lowest risk, the Midwest faced an additional 154,541 cancer cases annually across all types. For colorectal and pancreatic cancers, the yearly increases were 20,927 and 3835 cases, respectively. Similar trends were observed for leukemia and non-Hodgkin lymphoma.
Pesticides vs Smoking
The researchers also estimated the additional cancer risk related to smoking, using the same model. They found that pesticides contributed to a higher risk for cancer than smoking in several cases.
The most significant difference was observed with non-Hodgkin lymphoma, where pesticides were linked to 154.1% more cases than smoking. For all cancers combined, as well as bladder cancer and leukemia, the increases were moderate: 18.7%, 19.3%, and 21.0%, respectively.
This result highlights the importance of considering pesticide exposure alongside smoking when studying cancer risks.
Expanding Scope of Research
Some limitations of this study should be noted. Certain counties lacked complete data, and there was heterogeneity in the size and population of the counties studied. The research also did not account for seasonal and migrant workers, who are likely to be heavily exposed. In addition, the data used in the study were not independently validated, and they could not be used to assess individual risk.
The effect of pesticides on human health is a vast and critical field of research, often focusing on a limited range of pesticides or specific cancers. This study stands out by taking a broader, more holistic approach, aiming to highlight regional inequalities and identify less-studied pesticides that could be future research priorities.
Given the significant public health impact, the authors encouraged the authorities to share these findings with the most vulnerable communities to raise awareness.
This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Pesticides have transformed modern agriculture by boosting production yields and helping alleviate food insecurity amid rapid global population growth. However, from a public health perspective, exposure to pesticides has been linked to numerous harmful effects, including neurologic disorders like Parkinson’s disease, weakened immune function, and an increased risk for cancer.
A comprehensive assessment of how pesticide use affects cancer risk across a broader population has yet to be conducted.
A recent population-level study aimed to address this gap by evaluating cancer risks in the US population using a model that accounts for pesticide use and adjusts for various factors. The goal was to identify regional disparities in exposure and contribute to the development of public health policies that protect populations from potential harm.
Calculating Cancer Risk
Researchers developed a model using several data sources to estimate the additional cancer risk from agricultural pesticide use. Key data included:
- Pesticide use data from the US Geological Survey in 2019, which covered 69 agricultural pesticides across 3143 counties
- Cancer incidence rates per 100,000 people, which were collected between 2015 and 2019 by the National Institutes of Health and the Centers for Disease Control and Prevention; these data covered various cancers, including bladder, colorectal, leukemia, lung, non-Hodgkin lymphoma, and pancreatic cancers
- Covariates, including smoking prevalence, the Social Vulnerability Index, agricultural land use, and total US population in 2019
Pesticide use profile patterns were developed using latent class analysis, a statistical method used to identify homogeneous subgroups within a heterogeneous population. A generalized linear model then estimated how these pesticide use patterns and the covariates affected cancer incidence.
The model highlighted regions with the highest and lowest “additional” cancer risks linked to pesticide exposure, calculating the estimated increase in cancer cases per year that resulted from variations in agricultural pesticide use.
Midwest Most Affected
While this model doesn’t establish causality or assess individual risk, it reveals regional trends in the association between pesticide use patterns and cancer incidence from a population-based perspective.
The Midwest, known for its high corn production, emerged as the region most affected by pesticide use. Compared with regions with the lowest risk, the Midwest faced an additional 154,541 cancer cases annually across all types. For colorectal and pancreatic cancers, the yearly increases were 20,927 and 3835 cases, respectively. Similar trends were observed for leukemia and non-Hodgkin lymphoma.
Pesticides vs Smoking
The researchers also estimated the additional cancer risk related to smoking, using the same model. They found that pesticides contributed to a higher risk for cancer than smoking in several cases.
The most significant difference was observed with non-Hodgkin lymphoma, where pesticides were linked to 154.1% more cases than smoking. For all cancers combined, as well as bladder cancer and leukemia, the increases were moderate: 18.7%, 19.3%, and 21.0%, respectively.
This result highlights the importance of considering pesticide exposure alongside smoking when studying cancer risks.
Expanding Scope of Research
Some limitations of this study should be noted. Certain counties lacked complete data, and there was heterogeneity in the size and population of the counties studied. The research also did not account for seasonal and migrant workers, who are likely to be heavily exposed. In addition, the data used in the study were not independently validated, and they could not be used to assess individual risk.
The effect of pesticides on human health is a vast and critical field of research, often focusing on a limited range of pesticides or specific cancers. This study stands out by taking a broader, more holistic approach, aiming to highlight regional inequalities and identify less-studied pesticides that could be future research priorities.
Given the significant public health impact, the authors encouraged the authorities to share these findings with the most vulnerable communities to raise awareness.
This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Pesticides have transformed modern agriculture by boosting production yields and helping alleviate food insecurity amid rapid global population growth. However, from a public health perspective, exposure to pesticides has been linked to numerous harmful effects, including neurologic disorders like Parkinson’s disease, weakened immune function, and an increased risk for cancer.
A comprehensive assessment of how pesticide use affects cancer risk across a broader population has yet to be conducted.
A recent population-level study aimed to address this gap by evaluating cancer risks in the US population using a model that accounts for pesticide use and adjusts for various factors. The goal was to identify regional disparities in exposure and contribute to the development of public health policies that protect populations from potential harm.
Calculating Cancer Risk
Researchers developed a model using several data sources to estimate the additional cancer risk from agricultural pesticide use. Key data included:
- Pesticide use data from the US Geological Survey in 2019, which covered 69 agricultural pesticides across 3143 counties
- Cancer incidence rates per 100,000 people, which were collected between 2015 and 2019 by the National Institutes of Health and the Centers for Disease Control and Prevention; these data covered various cancers, including bladder, colorectal, leukemia, lung, non-Hodgkin lymphoma, and pancreatic cancers
- Covariates, including smoking prevalence, the Social Vulnerability Index, agricultural land use, and total US population in 2019
Pesticide use profile patterns were developed using latent class analysis, a statistical method used to identify homogeneous subgroups within a heterogeneous population. A generalized linear model then estimated how these pesticide use patterns and the covariates affected cancer incidence.
The model highlighted regions with the highest and lowest “additional” cancer risks linked to pesticide exposure, calculating the estimated increase in cancer cases per year that resulted from variations in agricultural pesticide use.
Midwest Most Affected
While this model doesn’t establish causality or assess individual risk, it reveals regional trends in the association between pesticide use patterns and cancer incidence from a population-based perspective.
The Midwest, known for its high corn production, emerged as the region most affected by pesticide use. Compared with regions with the lowest risk, the Midwest faced an additional 154,541 cancer cases annually across all types. For colorectal and pancreatic cancers, the yearly increases were 20,927 and 3835 cases, respectively. Similar trends were observed for leukemia and non-Hodgkin lymphoma.
Pesticides vs Smoking
The researchers also estimated the additional cancer risk related to smoking, using the same model. They found that pesticides contributed to a higher risk for cancer than smoking in several cases.
The most significant difference was observed with non-Hodgkin lymphoma, where pesticides were linked to 154.1% more cases than smoking. For all cancers combined, as well as bladder cancer and leukemia, the increases were moderate: 18.7%, 19.3%, and 21.0%, respectively.
This result highlights the importance of considering pesticide exposure alongside smoking when studying cancer risks.
Expanding Scope of Research
Some limitations of this study should be noted. Certain counties lacked complete data, and there was heterogeneity in the size and population of the counties studied. The research also did not account for seasonal and migrant workers, who are likely to be heavily exposed. In addition, the data used in the study were not independently validated, and they could not be used to assess individual risk.
The effect of pesticides on human health is a vast and critical field of research, often focusing on a limited range of pesticides or specific cancers. This study stands out by taking a broader, more holistic approach, aiming to highlight regional inequalities and identify less-studied pesticides that could be future research priorities.
Given the significant public health impact, the authors encouraged the authorities to share these findings with the most vulnerable communities to raise awareness.
This story was translated from JIM using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Should There Be a Mandatory Retirement Age for Physicians?
This transcript has been edited for clarity.
I’d like to pose a question: When should doctors retire? When, as practicing physicians or surgeons, do we become too old to deliver competent service?
You will be amazed to hear, those of you who have listened to my videos before — and although it is a matter of public knowledge — that I’m 68. I know it’s impossible to imagine, due to this youthful appearance, visage, and so on, but I am. I’ve been a cancer doctor for 40 years; therefore, I need to think a little about retirement.
There are two elements of this for me. I’m a university professor, and in Oxford we did vote, as a democracy of scholars, to have a mandatory retirement age around 68. This is so that we can bring new blood forward so that we can create the space to promote new professors, to bring youngsters in to make new ideas, and to get rid of us fusty old lot.
The other argument would be, of course, that we are wise, we’re experienced, we are world-weary, and we’re successful — otherwise, we wouldn’t have lasted as academics as long. Nevertheless, we voted to do that.
It’s possible to have a discussion with the university to extend this, and for those of us who are clinical academics, I have an honorary appointment as a consultant cancer physician in the hospital and my university professorial appointment, too.
I can extend it probably until I’m about 70. It feels like a nice, round number at which to retire — somewhat arbitrarily, one would admit. But does that feel right?
In the United States, more than 25% of the physician workforce is over the age of 65. There are many studies showing that there is a 20% cognitive decline for most individuals between the ages of 45 and 65.
Are we as capable as an elderly workforce as once we were? Clearly, it’s hardly individualistic. It depends on each of our own health status, where we started from, and so on, but are there any general rules that we can apply? I think these are starting to creep in around the sense of revalidation.
In the United Kingdom, we have a General Medical Council (GMC). I need to have a license to practice from the GMC and a sense of fitness to practice. I have annual appraisals within the hospital system, in which I explore delivery of care, how I’m doing as a mentor, am I reaching the milestones I’ve set in terms of academic achievements, and so on.
This is a peer-to-peer process. We have senior physicians — people like myself — who act as appraisers to support our colleagues and to maintain that sense of fitness to practice. Every 5 years, I’m revalidated by the GMC. They take account of the annual appraisals and a report made by the senior physician within my hospital network who’s a so-called designated person.
These two elements come together with patient feedback, with 360-degree feedback from colleagues, and so on. This is quite a firmly regulated system that I think works. Our mandatory retirement age of 65 has gone. That was phased out by the government. In fact, our NHS is making an effort to retain older elders in the workforce.
They see the benefits of mentorship, experience, leadership, and networks. At a time when the majority of NHS are actively seeking to retire when 65, the NHS is trying to retain and pull back those of us who have been around for that wee bit longer and who still feel committed to doing it.
I’d be really interested to see what you think. There’s variation from country to country. I know that, in Australia, they’re talking about annual appraisals of doctors over the age of 70. I’d be very interested to hear what you think is likely to happen in the United States.
I think our system works pretty well, as long as you’re within the NHS and hospital system. If you wanted to still practice, but practice privately, you would still have to find somebody who’d be prepared to conduct appraisals and so on outside of the NHS. It’s an interesting area.
For myself, I still feel competent. Patients seem to like me. That’s an objective assessment by this 360-degree thing in which patients reflected very positively, indeed, in my approach to the delivery of the care and so on, as did colleagues. I’m still publishing, I go to meetings, I cheer things, bits and bobs. I’d say I’m a wee bit unusual in terms of still having a strong academic profile in doing stuff.
It’s an interesting question. Richard Doll, one of the world’s great epidemiologists who, of course, was the dominant discoverer of the link between smoking and lung cancer, was attending seminars, sitting in the front row, and coming into university 3 days a week at age 90, continuing to be contributory with his extraordinarily sharp intellect and vast, vast experience.
When I think of experience, all young cancer doctors are now immunologists. When I was a young doctor, I was a clinical pharmacologist. There are many lessons and tricks that I learned which I do need to pass on to the younger generation of today. What do you think? Should there be a mandatory retirement age? How do we best measure, assess, and revalidate elderly physicians and surgeons? How can we continue to contribute to those who choose to do so? For the time being, as always, thanks for listening.
Dr. Kerr is professor, Nuffield Department of Clinical Laboratory Science, University of Oxford, and professor of cancer medicine, Oxford Cancer Centre, Oxford, United Kingdom. He has disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers (Board of Directors); Afrox (charity; Trustee); GlaxoSmithKline and Bayer HealthCare Pharmaceuticals (Consultant), Genomic Health; Merck Serono, and Roche.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I’d like to pose a question: When should doctors retire? When, as practicing physicians or surgeons, do we become too old to deliver competent service?
You will be amazed to hear, those of you who have listened to my videos before — and although it is a matter of public knowledge — that I’m 68. I know it’s impossible to imagine, due to this youthful appearance, visage, and so on, but I am. I’ve been a cancer doctor for 40 years; therefore, I need to think a little about retirement.
There are two elements of this for me. I’m a university professor, and in Oxford we did vote, as a democracy of scholars, to have a mandatory retirement age around 68. This is so that we can bring new blood forward so that we can create the space to promote new professors, to bring youngsters in to make new ideas, and to get rid of us fusty old lot.
The other argument would be, of course, that we are wise, we’re experienced, we are world-weary, and we’re successful — otherwise, we wouldn’t have lasted as academics as long. Nevertheless, we voted to do that.
It’s possible to have a discussion with the university to extend this, and for those of us who are clinical academics, I have an honorary appointment as a consultant cancer physician in the hospital and my university professorial appointment, too.
I can extend it probably until I’m about 70. It feels like a nice, round number at which to retire — somewhat arbitrarily, one would admit. But does that feel right?
In the United States, more than 25% of the physician workforce is over the age of 65. There are many studies showing that there is a 20% cognitive decline for most individuals between the ages of 45 and 65.
Are we as capable as an elderly workforce as once we were? Clearly, it’s hardly individualistic. It depends on each of our own health status, where we started from, and so on, but are there any general rules that we can apply? I think these are starting to creep in around the sense of revalidation.
In the United Kingdom, we have a General Medical Council (GMC). I need to have a license to practice from the GMC and a sense of fitness to practice. I have annual appraisals within the hospital system, in which I explore delivery of care, how I’m doing as a mentor, am I reaching the milestones I’ve set in terms of academic achievements, and so on.
This is a peer-to-peer process. We have senior physicians — people like myself — who act as appraisers to support our colleagues and to maintain that sense of fitness to practice. Every 5 years, I’m revalidated by the GMC. They take account of the annual appraisals and a report made by the senior physician within my hospital network who’s a so-called designated person.
These two elements come together with patient feedback, with 360-degree feedback from colleagues, and so on. This is quite a firmly regulated system that I think works. Our mandatory retirement age of 65 has gone. That was phased out by the government. In fact, our NHS is making an effort to retain older elders in the workforce.
They see the benefits of mentorship, experience, leadership, and networks. At a time when the majority of NHS are actively seeking to retire when 65, the NHS is trying to retain and pull back those of us who have been around for that wee bit longer and who still feel committed to doing it.
I’d be really interested to see what you think. There’s variation from country to country. I know that, in Australia, they’re talking about annual appraisals of doctors over the age of 70. I’d be very interested to hear what you think is likely to happen in the United States.
I think our system works pretty well, as long as you’re within the NHS and hospital system. If you wanted to still practice, but practice privately, you would still have to find somebody who’d be prepared to conduct appraisals and so on outside of the NHS. It’s an interesting area.
For myself, I still feel competent. Patients seem to like me. That’s an objective assessment by this 360-degree thing in which patients reflected very positively, indeed, in my approach to the delivery of the care and so on, as did colleagues. I’m still publishing, I go to meetings, I cheer things, bits and bobs. I’d say I’m a wee bit unusual in terms of still having a strong academic profile in doing stuff.
It’s an interesting question. Richard Doll, one of the world’s great epidemiologists who, of course, was the dominant discoverer of the link between smoking and lung cancer, was attending seminars, sitting in the front row, and coming into university 3 days a week at age 90, continuing to be contributory with his extraordinarily sharp intellect and vast, vast experience.
When I think of experience, all young cancer doctors are now immunologists. When I was a young doctor, I was a clinical pharmacologist. There are many lessons and tricks that I learned which I do need to pass on to the younger generation of today. What do you think? Should there be a mandatory retirement age? How do we best measure, assess, and revalidate elderly physicians and surgeons? How can we continue to contribute to those who choose to do so? For the time being, as always, thanks for listening.
Dr. Kerr is professor, Nuffield Department of Clinical Laboratory Science, University of Oxford, and professor of cancer medicine, Oxford Cancer Centre, Oxford, United Kingdom. He has disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers (Board of Directors); Afrox (charity; Trustee); GlaxoSmithKline and Bayer HealthCare Pharmaceuticals (Consultant), Genomic Health; Merck Serono, and Roche.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I’d like to pose a question: When should doctors retire? When, as practicing physicians or surgeons, do we become too old to deliver competent service?
You will be amazed to hear, those of you who have listened to my videos before — and although it is a matter of public knowledge — that I’m 68. I know it’s impossible to imagine, due to this youthful appearance, visage, and so on, but I am. I’ve been a cancer doctor for 40 years; therefore, I need to think a little about retirement.
There are two elements of this for me. I’m a university professor, and in Oxford we did vote, as a democracy of scholars, to have a mandatory retirement age around 68. This is so that we can bring new blood forward so that we can create the space to promote new professors, to bring youngsters in to make new ideas, and to get rid of us fusty old lot.
The other argument would be, of course, that we are wise, we’re experienced, we are world-weary, and we’re successful — otherwise, we wouldn’t have lasted as academics as long. Nevertheless, we voted to do that.
It’s possible to have a discussion with the university to extend this, and for those of us who are clinical academics, I have an honorary appointment as a consultant cancer physician in the hospital and my university professorial appointment, too.
I can extend it probably until I’m about 70. It feels like a nice, round number at which to retire — somewhat arbitrarily, one would admit. But does that feel right?
In the United States, more than 25% of the physician workforce is over the age of 65. There are many studies showing that there is a 20% cognitive decline for most individuals between the ages of 45 and 65.
Are we as capable as an elderly workforce as once we were? Clearly, it’s hardly individualistic. It depends on each of our own health status, where we started from, and so on, but are there any general rules that we can apply? I think these are starting to creep in around the sense of revalidation.
In the United Kingdom, we have a General Medical Council (GMC). I need to have a license to practice from the GMC and a sense of fitness to practice. I have annual appraisals within the hospital system, in which I explore delivery of care, how I’m doing as a mentor, am I reaching the milestones I’ve set in terms of academic achievements, and so on.
This is a peer-to-peer process. We have senior physicians — people like myself — who act as appraisers to support our colleagues and to maintain that sense of fitness to practice. Every 5 years, I’m revalidated by the GMC. They take account of the annual appraisals and a report made by the senior physician within my hospital network who’s a so-called designated person.
These two elements come together with patient feedback, with 360-degree feedback from colleagues, and so on. This is quite a firmly regulated system that I think works. Our mandatory retirement age of 65 has gone. That was phased out by the government. In fact, our NHS is making an effort to retain older elders in the workforce.
They see the benefits of mentorship, experience, leadership, and networks. At a time when the majority of NHS are actively seeking to retire when 65, the NHS is trying to retain and pull back those of us who have been around for that wee bit longer and who still feel committed to doing it.
I’d be really interested to see what you think. There’s variation from country to country. I know that, in Australia, they’re talking about annual appraisals of doctors over the age of 70. I’d be very interested to hear what you think is likely to happen in the United States.
I think our system works pretty well, as long as you’re within the NHS and hospital system. If you wanted to still practice, but practice privately, you would still have to find somebody who’d be prepared to conduct appraisals and so on outside of the NHS. It’s an interesting area.
For myself, I still feel competent. Patients seem to like me. That’s an objective assessment by this 360-degree thing in which patients reflected very positively, indeed, in my approach to the delivery of the care and so on, as did colleagues. I’m still publishing, I go to meetings, I cheer things, bits and bobs. I’d say I’m a wee bit unusual in terms of still having a strong academic profile in doing stuff.
It’s an interesting question. Richard Doll, one of the world’s great epidemiologists who, of course, was the dominant discoverer of the link between smoking and lung cancer, was attending seminars, sitting in the front row, and coming into university 3 days a week at age 90, continuing to be contributory with his extraordinarily sharp intellect and vast, vast experience.
When I think of experience, all young cancer doctors are now immunologists. When I was a young doctor, I was a clinical pharmacologist. There are many lessons and tricks that I learned which I do need to pass on to the younger generation of today. What do you think? Should there be a mandatory retirement age? How do we best measure, assess, and revalidate elderly physicians and surgeons? How can we continue to contribute to those who choose to do so? For the time being, as always, thanks for listening.
Dr. Kerr is professor, Nuffield Department of Clinical Laboratory Science, University of Oxford, and professor of cancer medicine, Oxford Cancer Centre, Oxford, United Kingdom. He has disclosed ties with Celleron Therapeutics, Oxford Cancer Biomarkers (Board of Directors); Afrox (charity; Trustee); GlaxoSmithKline and Bayer HealthCare Pharmaceuticals (Consultant), Genomic Health; Merck Serono, and Roche.
A version of this article appeared on Medscape.com.
Benralizumab Now FDA Approved to Treat EGPA Vasculitis
The Food and Drug Administration (FDA) has approved benralizumab (Fasenra) for the treatment of adults with eosinophilic granulomatosis with polyangiitis (EGPA), formerly known as Churg-Strauss syndrome.
The drug is the second approved biologic for the treatment of EGPA. The first, mepolizumab (Nucala), was approved in 2017.
“This disease has a devastating impact on patients and the quality of their life, and they need more treatment options. The approval of another treatment in EGPA is welcome news to the approximately 15,000 patients living in the US with this difficult-to-treat rare disease,” said Joyce Kullman, executive director of the Vasculitis Foundation, in a press release on September 18.
Benralizumab, developed by AstraZeneca, is a monoclonal antibody against the interleukin-5 alpha receptor expressed on eosinophils. The drug was first approved in 2017 as an add-on treatment for patients 12 years and older with severe eosinophilic asthma, and is now approved for use in children aged 6 years and older.
The new indication was based on positive results from a noninferiority trial comparing benralizumab and mepolizumab. For the trial, published in the New England Journal of Medicine earlier in 2024, 140 adults with relapsing or refractory EGPA were randomized to a 30-mg subcutaneous injection of benralizumab or three separate 100-mg mepolizumab injections every 4 weeks for 1 year. At weeks 36 and 48, 59% of patients in the benralizumab group and 56% of patients in the mepolizumab group achieved remission (95% CI, –13 to 18; P = .73 for superiority). From week 42 to 52, 41% of patients who received benralizumab completely stopped taking oral glucocorticoids, compared with 26% of those who received mepolizumab.
“Patients often rely on long-term oral corticosteroids, which can cause serious and lasting side effects. Benralizumab is a much-needed treatment option, with data showing that not only is remission an achievable goal for EGPA patients, but benralizumab can also help patients taper off steroid therapy,” Michael Wechsler, MD, director of The Asthma Institute at National Jewish Health in Denver, Colorado, and the international coordinating investigator for the clinical trial, said in the press release.
Benralizumab is administered via subcutaneous injection. In adults with EGPA, the recommended dosage is 30 mg every 4 weeks for the first three doses, then once every 8 weeks.
The most common adverse reactions include headache and pharyngitis, according to the prescribing information.
Benralizumab is also in development for the treatment of chronic obstructive pulmonary disease, chronic rhinosinusitis with nasal polyps, and hypereosinophilic syndrome.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration (FDA) has approved benralizumab (Fasenra) for the treatment of adults with eosinophilic granulomatosis with polyangiitis (EGPA), formerly known as Churg-Strauss syndrome.
The drug is the second approved biologic for the treatment of EGPA. The first, mepolizumab (Nucala), was approved in 2017.
“This disease has a devastating impact on patients and the quality of their life, and they need more treatment options. The approval of another treatment in EGPA is welcome news to the approximately 15,000 patients living in the US with this difficult-to-treat rare disease,” said Joyce Kullman, executive director of the Vasculitis Foundation, in a press release on September 18.
Benralizumab, developed by AstraZeneca, is a monoclonal antibody against the interleukin-5 alpha receptor expressed on eosinophils. The drug was first approved in 2017 as an add-on treatment for patients 12 years and older with severe eosinophilic asthma, and is now approved for use in children aged 6 years and older.
The new indication was based on positive results from a noninferiority trial comparing benralizumab and mepolizumab. For the trial, published in the New England Journal of Medicine earlier in 2024, 140 adults with relapsing or refractory EGPA were randomized to a 30-mg subcutaneous injection of benralizumab or three separate 100-mg mepolizumab injections every 4 weeks for 1 year. At weeks 36 and 48, 59% of patients in the benralizumab group and 56% of patients in the mepolizumab group achieved remission (95% CI, –13 to 18; P = .73 for superiority). From week 42 to 52, 41% of patients who received benralizumab completely stopped taking oral glucocorticoids, compared with 26% of those who received mepolizumab.
“Patients often rely on long-term oral corticosteroids, which can cause serious and lasting side effects. Benralizumab is a much-needed treatment option, with data showing that not only is remission an achievable goal for EGPA patients, but benralizumab can also help patients taper off steroid therapy,” Michael Wechsler, MD, director of The Asthma Institute at National Jewish Health in Denver, Colorado, and the international coordinating investigator for the clinical trial, said in the press release.
Benralizumab is administered via subcutaneous injection. In adults with EGPA, the recommended dosage is 30 mg every 4 weeks for the first three doses, then once every 8 weeks.
The most common adverse reactions include headache and pharyngitis, according to the prescribing information.
Benralizumab is also in development for the treatment of chronic obstructive pulmonary disease, chronic rhinosinusitis with nasal polyps, and hypereosinophilic syndrome.
A version of this article first appeared on Medscape.com.
The Food and Drug Administration (FDA) has approved benralizumab (Fasenra) for the treatment of adults with eosinophilic granulomatosis with polyangiitis (EGPA), formerly known as Churg-Strauss syndrome.
The drug is the second approved biologic for the treatment of EGPA. The first, mepolizumab (Nucala), was approved in 2017.
“This disease has a devastating impact on patients and the quality of their life, and they need more treatment options. The approval of another treatment in EGPA is welcome news to the approximately 15,000 patients living in the US with this difficult-to-treat rare disease,” said Joyce Kullman, executive director of the Vasculitis Foundation, in a press release on September 18.
Benralizumab, developed by AstraZeneca, is a monoclonal antibody against the interleukin-5 alpha receptor expressed on eosinophils. The drug was first approved in 2017 as an add-on treatment for patients 12 years and older with severe eosinophilic asthma, and is now approved for use in children aged 6 years and older.
The new indication was based on positive results from a noninferiority trial comparing benralizumab and mepolizumab. For the trial, published in the New England Journal of Medicine earlier in 2024, 140 adults with relapsing or refractory EGPA were randomized to a 30-mg subcutaneous injection of benralizumab or three separate 100-mg mepolizumab injections every 4 weeks for 1 year. At weeks 36 and 48, 59% of patients in the benralizumab group and 56% of patients in the mepolizumab group achieved remission (95% CI, –13 to 18; P = .73 for superiority). From week 42 to 52, 41% of patients who received benralizumab completely stopped taking oral glucocorticoids, compared with 26% of those who received mepolizumab.
“Patients often rely on long-term oral corticosteroids, which can cause serious and lasting side effects. Benralizumab is a much-needed treatment option, with data showing that not only is remission an achievable goal for EGPA patients, but benralizumab can also help patients taper off steroid therapy,” Michael Wechsler, MD, director of The Asthma Institute at National Jewish Health in Denver, Colorado, and the international coordinating investigator for the clinical trial, said in the press release.
Benralizumab is administered via subcutaneous injection. In adults with EGPA, the recommended dosage is 30 mg every 4 weeks for the first three doses, then once every 8 weeks.
The most common adverse reactions include headache and pharyngitis, according to the prescribing information.
Benralizumab is also in development for the treatment of chronic obstructive pulmonary disease, chronic rhinosinusitis with nasal polyps, and hypereosinophilic syndrome.
A version of this article first appeared on Medscape.com.
When You and Your Malpractice Insurer Disagree on Your Case
You’ve been sued for medical malpractice. If you are a physician in the United States, that is not an unlikely scenario.
An analysis by the American Medical Association shows that almost half of all physicians are sued by the time they reach 54. In some specialties, such as ob.gyn., one is almost guaranteed to be sued at some point.
But that’s what medical malpractice insurance is for, right? Your medical malpractice insurer will assign an attorney to take care of you and help you through this situation. Won’t they?
Maybe so, but the attorney and the claims representative your insurer assigns to your case may have a different idea about how to proceed than you do. Though the defense attorney assigned to you represents you, he or she gets paid by the insurance carrier.
This can create a conflict when your defense counsel and your insurance claims representative aim to take your case in a direction you don’t like.
Disagreements might include:
- Choice of expert witnesses
- Tactical decisions related to trial strategy
- Public relations considerations
- Admissions of liability
- Allocation of resources
To Settle or Not?
One of the most challenging — and common — disagreements is whether to settle the case.
Sometimes a malpractice insurer wants to settle the case against the defendant doctor’s wishes. Or the doctor wants to settle but is pushed into going to trial. In the following case, one doctor had to face the consequences of a decision he didn’t even make.
The Underlying Medical Malpractice Case
Dr. D was sued by a patient who had allegedly called Dr. D’s office six times in 2 days complaining of intermittent chest pain.
Dr. D had been swamped with patients and couldn’t squeeze this patient in for an office visit, but he did call back. The patient later claimed that during the call he told the doctor he was suffering from chest pain. The doctor recalled that the patient had complained of abdominal discomfort that began after he had exercised.
The physician wrote a prescription for an ECG at the local hospital and called to ensure that the patient could just walk in. The ECG was allegedly abnormal but was not read as representing an impending or current heart attack. Later that evening, however, the patient went to the emergency department of another hospital where it was confirmed that he had suffered a heart attack. The patient underwent cardiac catheterization and stent placement to address a blockage in his left anterior descending artery.
The patient subsequently sued Dr. D and the hospital where he had the original ECG. Dr. D contacted his medical malpractice insurance company. The insurance company assigned an attorney to represent Dr. D. Discovery in the case began.
The plaintiff’s own medical expert testified in a deposition that there was no way for the heart attack to have been prevented and that the treatment would have been the same either way. But Dr. D could not find a record of the phone calls with the patient, and he had not noted his conversation the patient in their medical records.
Dr. D held a policy for $1 million, and his state had a fund that would kick in an additional $1 million. But the plaintiffs demanded $4 million to settle.
A month before trial, the plaintiff’s attorney sent a threatening letter to Dr. D’s attorney warning him that Dr. D was underinsured and suggesting that it would be in the physician’s best interests to settle.
“I want to stress to you that it is not my desire to harm your client’s reputation or to destroy his business,” wrote the plaintiff’s attorney. “However, now is the time to avoid consequences such as these by making a good faith effort to get this case resolved.”
The letter went on to note that the defense attorney should give Dr. D a copy of the letter so that everyone would be aware of the potential consequences of an award against Dr. D in excess of his limits of insurance coverage. The plaintiff’s attorney even suggested that Dr. D should retain personal counsel.
Dr. D’s defense attorney downplayed the letter and assured him that there was no reason to worry.
Meanwhile the case inched closer to trial.
The codefendant hospital settled with the plaintiff on the night before jury selection, leaving Dr. D in the uncomfortable position of being the only defendant in the case. At this point, Dr. D decided he would like to settle, and he sent his attorney an email telling him so. But the attorney instead referred him to an insurance company claims.
Just days before the trial was to start, Dr. D repeatedly told the claims representative assigned to his claim that he did not want to go to trial but rather wanted to settle. The representative told Dr. D that he had no choice in whether the action settled.
A committee at the insurance company had decided to proceed with the trial rather than settle.
The trial proved a painful debacle for Dr. D. His attorney’s idea of showing a “gotcha” video of the allegedly permanently injured plaintiff carrying a large, heavy box backfired when the jury was shown by the plaintiff that the box actually contained ice cream cones and weighed very little.
Prior to trial, the plaintiff offered to settle for $1 million. On the first day of trial, they lowered that amount to $750,000, yet the defense attorney did not settle the case, and it proceeded to a jury verdict. The jury awarded the plaintiff over $4 million — well in excess of Dr. D’s policy limits.
The Follow-up
Dr. D was horrified, but the insurance company claims representative said the insurer would promptly offer $2 million in available insurance coverage to settle the case post verdict. This did not happen. Instead, the insurer chose to appeal the verdict against Dr. D’s wishes.
Ultimately, Dr. D was forced to hire his own lawyer. He ultimately sued the insurance company for breach of contract and bad faith.
The insurance company eventually attempted to settle with the plaintiffs’ counsel, but the plaintiff refused to accept the available insurance coverage. The insurance carrier still has not posted the entire appeal bond. The case is still pending.
Protecting Yourself
The lesson from Dr. D’s experience: Understand that the insurance company is not your friend. It’s a business looking out for its own interests.
The plaintiff’s attorney was absolutely correct in suggesting that Dr. D retain his own attorney to represent his own interests. You should hire your own lawyer when:
- You disagree with your insurer on how to proceed in a case.
- You receive a demand that exceeds your available insurance coverage or for damages that may not be covered by your policy, such as punitive damages.
- Your insurance carrier attempts to deny insurance coverage for your claim or sends you a letter stating that it is “reserving its rights” not to cover or to limit coverage for your claim.
Retaining independent counsel protects your interests, not those of your insurance company.
Independent counsel can give you a second opinion on the strengths and weaknesses of your claim, help you prepare for your deposition, and attend court dates with you to ensure that you are completely protected.
Independent counsel can challenge your insurance company’s decision to deny or limit your insurance coverage and ensure that you receive all of the benefits to which you are entitled under your insurance policy. Some policies may include an independent lawyer to be paid for by your insurance carrier in case of a conflicts.
The most important takeaway? Your medical malpractice insurance carrier is not your friend, so act accordingly in times of conflict.
A version of this article first appeared on Medscape.com.
You’ve been sued for medical malpractice. If you are a physician in the United States, that is not an unlikely scenario.
An analysis by the American Medical Association shows that almost half of all physicians are sued by the time they reach 54. In some specialties, such as ob.gyn., one is almost guaranteed to be sued at some point.
But that’s what medical malpractice insurance is for, right? Your medical malpractice insurer will assign an attorney to take care of you and help you through this situation. Won’t they?
Maybe so, but the attorney and the claims representative your insurer assigns to your case may have a different idea about how to proceed than you do. Though the defense attorney assigned to you represents you, he or she gets paid by the insurance carrier.
This can create a conflict when your defense counsel and your insurance claims representative aim to take your case in a direction you don’t like.
Disagreements might include:
- Choice of expert witnesses
- Tactical decisions related to trial strategy
- Public relations considerations
- Admissions of liability
- Allocation of resources
To Settle or Not?
One of the most challenging — and common — disagreements is whether to settle the case.
Sometimes a malpractice insurer wants to settle the case against the defendant doctor’s wishes. Or the doctor wants to settle but is pushed into going to trial. In the following case, one doctor had to face the consequences of a decision he didn’t even make.
The Underlying Medical Malpractice Case
Dr. D was sued by a patient who had allegedly called Dr. D’s office six times in 2 days complaining of intermittent chest pain.
Dr. D had been swamped with patients and couldn’t squeeze this patient in for an office visit, but he did call back. The patient later claimed that during the call he told the doctor he was suffering from chest pain. The doctor recalled that the patient had complained of abdominal discomfort that began after he had exercised.
The physician wrote a prescription for an ECG at the local hospital and called to ensure that the patient could just walk in. The ECG was allegedly abnormal but was not read as representing an impending or current heart attack. Later that evening, however, the patient went to the emergency department of another hospital where it was confirmed that he had suffered a heart attack. The patient underwent cardiac catheterization and stent placement to address a blockage in his left anterior descending artery.
The patient subsequently sued Dr. D and the hospital where he had the original ECG. Dr. D contacted his medical malpractice insurance company. The insurance company assigned an attorney to represent Dr. D. Discovery in the case began.
The plaintiff’s own medical expert testified in a deposition that there was no way for the heart attack to have been prevented and that the treatment would have been the same either way. But Dr. D could not find a record of the phone calls with the patient, and he had not noted his conversation the patient in their medical records.
Dr. D held a policy for $1 million, and his state had a fund that would kick in an additional $1 million. But the plaintiffs demanded $4 million to settle.
A month before trial, the plaintiff’s attorney sent a threatening letter to Dr. D’s attorney warning him that Dr. D was underinsured and suggesting that it would be in the physician’s best interests to settle.
“I want to stress to you that it is not my desire to harm your client’s reputation or to destroy his business,” wrote the plaintiff’s attorney. “However, now is the time to avoid consequences such as these by making a good faith effort to get this case resolved.”
The letter went on to note that the defense attorney should give Dr. D a copy of the letter so that everyone would be aware of the potential consequences of an award against Dr. D in excess of his limits of insurance coverage. The plaintiff’s attorney even suggested that Dr. D should retain personal counsel.
Dr. D’s defense attorney downplayed the letter and assured him that there was no reason to worry.
Meanwhile the case inched closer to trial.
The codefendant hospital settled with the plaintiff on the night before jury selection, leaving Dr. D in the uncomfortable position of being the only defendant in the case. At this point, Dr. D decided he would like to settle, and he sent his attorney an email telling him so. But the attorney instead referred him to an insurance company claims.
Just days before the trial was to start, Dr. D repeatedly told the claims representative assigned to his claim that he did not want to go to trial but rather wanted to settle. The representative told Dr. D that he had no choice in whether the action settled.
A committee at the insurance company had decided to proceed with the trial rather than settle.
The trial proved a painful debacle for Dr. D. His attorney’s idea of showing a “gotcha” video of the allegedly permanently injured plaintiff carrying a large, heavy box backfired when the jury was shown by the plaintiff that the box actually contained ice cream cones and weighed very little.
Prior to trial, the plaintiff offered to settle for $1 million. On the first day of trial, they lowered that amount to $750,000, yet the defense attorney did not settle the case, and it proceeded to a jury verdict. The jury awarded the plaintiff over $4 million — well in excess of Dr. D’s policy limits.
The Follow-up
Dr. D was horrified, but the insurance company claims representative said the insurer would promptly offer $2 million in available insurance coverage to settle the case post verdict. This did not happen. Instead, the insurer chose to appeal the verdict against Dr. D’s wishes.
Ultimately, Dr. D was forced to hire his own lawyer. He ultimately sued the insurance company for breach of contract and bad faith.
The insurance company eventually attempted to settle with the plaintiffs’ counsel, but the plaintiff refused to accept the available insurance coverage. The insurance carrier still has not posted the entire appeal bond. The case is still pending.
Protecting Yourself
The lesson from Dr. D’s experience: Understand that the insurance company is not your friend. It’s a business looking out for its own interests.
The plaintiff’s attorney was absolutely correct in suggesting that Dr. D retain his own attorney to represent his own interests. You should hire your own lawyer when:
- You disagree with your insurer on how to proceed in a case.
- You receive a demand that exceeds your available insurance coverage or for damages that may not be covered by your policy, such as punitive damages.
- Your insurance carrier attempts to deny insurance coverage for your claim or sends you a letter stating that it is “reserving its rights” not to cover or to limit coverage for your claim.
Retaining independent counsel protects your interests, not those of your insurance company.
Independent counsel can give you a second opinion on the strengths and weaknesses of your claim, help you prepare for your deposition, and attend court dates with you to ensure that you are completely protected.
Independent counsel can challenge your insurance company’s decision to deny or limit your insurance coverage and ensure that you receive all of the benefits to which you are entitled under your insurance policy. Some policies may include an independent lawyer to be paid for by your insurance carrier in case of a conflicts.
The most important takeaway? Your medical malpractice insurance carrier is not your friend, so act accordingly in times of conflict.
A version of this article first appeared on Medscape.com.
You’ve been sued for medical malpractice. If you are a physician in the United States, that is not an unlikely scenario.
An analysis by the American Medical Association shows that almost half of all physicians are sued by the time they reach 54. In some specialties, such as ob.gyn., one is almost guaranteed to be sued at some point.
But that’s what medical malpractice insurance is for, right? Your medical malpractice insurer will assign an attorney to take care of you and help you through this situation. Won’t they?
Maybe so, but the attorney and the claims representative your insurer assigns to your case may have a different idea about how to proceed than you do. Though the defense attorney assigned to you represents you, he or she gets paid by the insurance carrier.
This can create a conflict when your defense counsel and your insurance claims representative aim to take your case in a direction you don’t like.
Disagreements might include:
- Choice of expert witnesses
- Tactical decisions related to trial strategy
- Public relations considerations
- Admissions of liability
- Allocation of resources
To Settle or Not?
One of the most challenging — and common — disagreements is whether to settle the case.
Sometimes a malpractice insurer wants to settle the case against the defendant doctor’s wishes. Or the doctor wants to settle but is pushed into going to trial. In the following case, one doctor had to face the consequences of a decision he didn’t even make.
The Underlying Medical Malpractice Case
Dr. D was sued by a patient who had allegedly called Dr. D’s office six times in 2 days complaining of intermittent chest pain.
Dr. D had been swamped with patients and couldn’t squeeze this patient in for an office visit, but he did call back. The patient later claimed that during the call he told the doctor he was suffering from chest pain. The doctor recalled that the patient had complained of abdominal discomfort that began after he had exercised.
The physician wrote a prescription for an ECG at the local hospital and called to ensure that the patient could just walk in. The ECG was allegedly abnormal but was not read as representing an impending or current heart attack. Later that evening, however, the patient went to the emergency department of another hospital where it was confirmed that he had suffered a heart attack. The patient underwent cardiac catheterization and stent placement to address a blockage in his left anterior descending artery.
The patient subsequently sued Dr. D and the hospital where he had the original ECG. Dr. D contacted his medical malpractice insurance company. The insurance company assigned an attorney to represent Dr. D. Discovery in the case began.
The plaintiff’s own medical expert testified in a deposition that there was no way for the heart attack to have been prevented and that the treatment would have been the same either way. But Dr. D could not find a record of the phone calls with the patient, and he had not noted his conversation the patient in their medical records.
Dr. D held a policy for $1 million, and his state had a fund that would kick in an additional $1 million. But the plaintiffs demanded $4 million to settle.
A month before trial, the plaintiff’s attorney sent a threatening letter to Dr. D’s attorney warning him that Dr. D was underinsured and suggesting that it would be in the physician’s best interests to settle.
“I want to stress to you that it is not my desire to harm your client’s reputation or to destroy his business,” wrote the plaintiff’s attorney. “However, now is the time to avoid consequences such as these by making a good faith effort to get this case resolved.”
The letter went on to note that the defense attorney should give Dr. D a copy of the letter so that everyone would be aware of the potential consequences of an award against Dr. D in excess of his limits of insurance coverage. The plaintiff’s attorney even suggested that Dr. D should retain personal counsel.
Dr. D’s defense attorney downplayed the letter and assured him that there was no reason to worry.
Meanwhile the case inched closer to trial.
The codefendant hospital settled with the plaintiff on the night before jury selection, leaving Dr. D in the uncomfortable position of being the only defendant in the case. At this point, Dr. D decided he would like to settle, and he sent his attorney an email telling him so. But the attorney instead referred him to an insurance company claims.
Just days before the trial was to start, Dr. D repeatedly told the claims representative assigned to his claim that he did not want to go to trial but rather wanted to settle. The representative told Dr. D that he had no choice in whether the action settled.
A committee at the insurance company had decided to proceed with the trial rather than settle.
The trial proved a painful debacle for Dr. D. His attorney’s idea of showing a “gotcha” video of the allegedly permanently injured plaintiff carrying a large, heavy box backfired when the jury was shown by the plaintiff that the box actually contained ice cream cones and weighed very little.
Prior to trial, the plaintiff offered to settle for $1 million. On the first day of trial, they lowered that amount to $750,000, yet the defense attorney did not settle the case, and it proceeded to a jury verdict. The jury awarded the plaintiff over $4 million — well in excess of Dr. D’s policy limits.
The Follow-up
Dr. D was horrified, but the insurance company claims representative said the insurer would promptly offer $2 million in available insurance coverage to settle the case post verdict. This did not happen. Instead, the insurer chose to appeal the verdict against Dr. D’s wishes.
Ultimately, Dr. D was forced to hire his own lawyer. He ultimately sued the insurance company for breach of contract and bad faith.
The insurance company eventually attempted to settle with the plaintiffs’ counsel, but the plaintiff refused to accept the available insurance coverage. The insurance carrier still has not posted the entire appeal bond. The case is still pending.
Protecting Yourself
The lesson from Dr. D’s experience: Understand that the insurance company is not your friend. It’s a business looking out for its own interests.
The plaintiff’s attorney was absolutely correct in suggesting that Dr. D retain his own attorney to represent his own interests. You should hire your own lawyer when:
- You disagree with your insurer on how to proceed in a case.
- You receive a demand that exceeds your available insurance coverage or for damages that may not be covered by your policy, such as punitive damages.
- Your insurance carrier attempts to deny insurance coverage for your claim or sends you a letter stating that it is “reserving its rights” not to cover or to limit coverage for your claim.
Retaining independent counsel protects your interests, not those of your insurance company.
Independent counsel can give you a second opinion on the strengths and weaknesses of your claim, help you prepare for your deposition, and attend court dates with you to ensure that you are completely protected.
Independent counsel can challenge your insurance company’s decision to deny or limit your insurance coverage and ensure that you receive all of the benefits to which you are entitled under your insurance policy. Some policies may include an independent lawyer to be paid for by your insurance carrier in case of a conflicts.
The most important takeaway? Your medical malpractice insurance carrier is not your friend, so act accordingly in times of conflict.
A version of this article first appeared on Medscape.com.
Coffee’s ‘Sweet Spot’: Daily Consumption and Cardiometabolic Risk
Each and every day, 1 billion people on this planet ingest a particular psychoactive substance. This chemical has fairly profound physiologic effects. It increases levels of nitric oxide in the blood, leads to vasodilation, and, of course, makes you feel more awake. The substance comes in many forms but almost always in a liquid medium. Do you have it yet? That’s right. The substance is caffeine, quite possibly the healthiest recreational drug that has ever been discovered.
This might be my New England upbringing speaking, but when it comes to lifestyle and health, one of the rules I’ve internalized is that things that are pleasurable are generally bad for you. I know, I know — some of you love to exercise. Some of you love doing crosswords. But you know what I mean. I’m talking French fries, smoked meats, drugs, smoking, alcohol, binge-watching Firefly. You’d be suspicious if a study came out suggesting that eating ice cream in bed reduces your risk for heart attack, and so would I. So I’m always on the lookout for those unicorns of lifestyle factors, those rare things that you want to do and are also good for you.
So far, the data are strong for three things: sleeping, (safe) sexual activity, and coffee. You’ll have to stay tuned for articles about the first two. Today, we’re brewing up some deeper insights about the power of java.
I was inspired to write this article because of a paper, “Habitual Coffee, Tea, and Caffeine Consumption, Circulating Metabolites, and the Risk of Cardiometabolic Multimorbidity,” appearing September 17 in The Journal of Clinical Endocrinology and Metabolism (JCEM).
This is not the first study to suggest that coffee intake may be beneficial. A 2013 meta-analysis summarized the results of 36 studies with more than a million participants and found a U-shaped relationship between coffee intake and cardiovascular risk. The sweet spot was at three to five cups a day; people drinking that much coffee had about a 15% reduced risk for cardiovascular disease compared with nondrinkers.
But here’s the thing. Coffee contains caffeine, but it is much more than that. It is a heady brew of various chemicals and compounds, phenols, and chlorogenic acids. And, of course, you can get caffeine from stuff that isn’t coffee — natural things like tea — and decidedly unnatural things like energy drinks. How do you figure out where the benefit really lies?
The JCEM study leveraged the impressive UK Biobank dataset to figure this out. The Biobank recruited more than half a million people from the UK between 2006 and 2010 and collected a wealth of data from each of them: surveys, blood samples, biometrics, medical imaging — the works. And then they followed what would happen to those people medically over time. It’s a pretty amazing resource.
But for the purposes of this study, what you need to know is that just under 200,000 of those participants met the key criteria for this study: being free from cardiovascular disease at baseline; having completed a detailed survey about their coffee, tea, and other caffeinated beverage intake; and having adequate follow-up. A subset of that number, just under 100,000, had metabolomic data — which is where this study really gets interesting.
We’ll dive into the metabolome in a moment, but first let’s just talk about the main finding, the relationship between coffee, tea, or caffeine and cardiovascular disease. But to do that, we need to acknowledge that people who drink a lot of coffee are different from people who don’t, and it might be those differences, not the coffee itself, that are beneficial.
What were those differences? People who drank more coffee tended to be a bit older, were less likely to be female, and were slightly more likely to engage in physical activity. They ate less processed meat but also fewer vegetables. Some of those factors, like being female, are generally protective against cardiovascular disease; but some, like age, are definitely not. The authors adjusted for these and multiple other factors, including alcohol intake, BMI, kidney function, and many others to try to disentangle the effect of being the type of person who drinks a lot of coffee from the drinking a lot of coffee itself.
These are the results of the fully adjusted model. Compared with nonconsumers, you can see that people in the higher range of coffee, tea, or just caffeine intake have almost a 40% reduction in cardiovascular disease in follow-up.
Looking at the benefit across the spectrum of intake, you again see that U-shaped curve, suggesting that a sweet spot for daily consumption can be found around 3 cups of coffee or tea (or 250 mg of caffeine). A standard energy drink contains about 120 mg of caffeine.
But if this is true, it would be good to know why. To figure that out, the authors turned to the metabolome. The idea here is that your body is constantly breaking stuff down, taking all these proteins and chemicals and compounds that we ingest and turning them into metabolites. Using advanced measurement techniques, researchers can measure hundreds or even thousands of metabolites from a single blood sample. They provide information, obviously, about the food you eat and the drinks you drink, but what is really intriguing is that some metabolites are associated with better health and some with worse
In this study, researchers measured 168 individual metabolites. Eighty of them, nearly half, were significantly altered in people who drank more coffee.
This figure summarizes the findings, and yes, this is way too complicated.
But here’s how to interpret it. The inner ring shows you how certain metabolites are associated with cardiovascular disease. The outer rings show you how those metabolites are associated with coffee, tea, or caffeine. The interesting part is that the sections of the ring (outer rings and inner rings) are very different colors.
Like here.
What you see here is a fairly profound effect that coffee, tea, or caffeine intake has on metabolites of VLDL — bad cholesterol. The beverages lower it, and, of course, higher levels lead to cardiovascular disease. This means that this is a potential causal pathway from coffee intake to heart protection.
And that’s not the only one.
You see a similar relationship for saturated fatty acids. Higher levels lead to cardiovascular disease, and coffee intake lowers levels. The reverse works too: Lower levels of histidine (an amino acid) increase cardiovascular risk, and coffee seems to raise those levels.
Is this all too good to be true? It’s hard to say. The data on coffee’s benefits have been remarkably consistent. Still, I wouldn’t be a good doctor if I didn’t mention that clearly there is a difference between a cup of black coffee and a venti caramel Frappuccino.
Nevertheless, coffee remains firmly in my holy trinity of enjoyable things that are, for whatever reason, still good for you. So, when you’re having that second, or third, or maybe fourth cup of the day, you can take that to heart.
Dr. Wilson, associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator, reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Each and every day, 1 billion people on this planet ingest a particular psychoactive substance. This chemical has fairly profound physiologic effects. It increases levels of nitric oxide in the blood, leads to vasodilation, and, of course, makes you feel more awake. The substance comes in many forms but almost always in a liquid medium. Do you have it yet? That’s right. The substance is caffeine, quite possibly the healthiest recreational drug that has ever been discovered.
This might be my New England upbringing speaking, but when it comes to lifestyle and health, one of the rules I’ve internalized is that things that are pleasurable are generally bad for you. I know, I know — some of you love to exercise. Some of you love doing crosswords. But you know what I mean. I’m talking French fries, smoked meats, drugs, smoking, alcohol, binge-watching Firefly. You’d be suspicious if a study came out suggesting that eating ice cream in bed reduces your risk for heart attack, and so would I. So I’m always on the lookout for those unicorns of lifestyle factors, those rare things that you want to do and are also good for you.
So far, the data are strong for three things: sleeping, (safe) sexual activity, and coffee. You’ll have to stay tuned for articles about the first two. Today, we’re brewing up some deeper insights about the power of java.
I was inspired to write this article because of a paper, “Habitual Coffee, Tea, and Caffeine Consumption, Circulating Metabolites, and the Risk of Cardiometabolic Multimorbidity,” appearing September 17 in The Journal of Clinical Endocrinology and Metabolism (JCEM).
This is not the first study to suggest that coffee intake may be beneficial. A 2013 meta-analysis summarized the results of 36 studies with more than a million participants and found a U-shaped relationship between coffee intake and cardiovascular risk. The sweet spot was at three to five cups a day; people drinking that much coffee had about a 15% reduced risk for cardiovascular disease compared with nondrinkers.
But here’s the thing. Coffee contains caffeine, but it is much more than that. It is a heady brew of various chemicals and compounds, phenols, and chlorogenic acids. And, of course, you can get caffeine from stuff that isn’t coffee — natural things like tea — and decidedly unnatural things like energy drinks. How do you figure out where the benefit really lies?
The JCEM study leveraged the impressive UK Biobank dataset to figure this out. The Biobank recruited more than half a million people from the UK between 2006 and 2010 and collected a wealth of data from each of them: surveys, blood samples, biometrics, medical imaging — the works. And then they followed what would happen to those people medically over time. It’s a pretty amazing resource.
But for the purposes of this study, what you need to know is that just under 200,000 of those participants met the key criteria for this study: being free from cardiovascular disease at baseline; having completed a detailed survey about their coffee, tea, and other caffeinated beverage intake; and having adequate follow-up. A subset of that number, just under 100,000, had metabolomic data — which is where this study really gets interesting.
We’ll dive into the metabolome in a moment, but first let’s just talk about the main finding, the relationship between coffee, tea, or caffeine and cardiovascular disease. But to do that, we need to acknowledge that people who drink a lot of coffee are different from people who don’t, and it might be those differences, not the coffee itself, that are beneficial.
What were those differences? People who drank more coffee tended to be a bit older, were less likely to be female, and were slightly more likely to engage in physical activity. They ate less processed meat but also fewer vegetables. Some of those factors, like being female, are generally protective against cardiovascular disease; but some, like age, are definitely not. The authors adjusted for these and multiple other factors, including alcohol intake, BMI, kidney function, and many others to try to disentangle the effect of being the type of person who drinks a lot of coffee from the drinking a lot of coffee itself.
These are the results of the fully adjusted model. Compared with nonconsumers, you can see that people in the higher range of coffee, tea, or just caffeine intake have almost a 40% reduction in cardiovascular disease in follow-up.
Looking at the benefit across the spectrum of intake, you again see that U-shaped curve, suggesting that a sweet spot for daily consumption can be found around 3 cups of coffee or tea (or 250 mg of caffeine). A standard energy drink contains about 120 mg of caffeine.
But if this is true, it would be good to know why. To figure that out, the authors turned to the metabolome. The idea here is that your body is constantly breaking stuff down, taking all these proteins and chemicals and compounds that we ingest and turning them into metabolites. Using advanced measurement techniques, researchers can measure hundreds or even thousands of metabolites from a single blood sample. They provide information, obviously, about the food you eat and the drinks you drink, but what is really intriguing is that some metabolites are associated with better health and some with worse
In this study, researchers measured 168 individual metabolites. Eighty of them, nearly half, were significantly altered in people who drank more coffee.
This figure summarizes the findings, and yes, this is way too complicated.
But here’s how to interpret it. The inner ring shows you how certain metabolites are associated with cardiovascular disease. The outer rings show you how those metabolites are associated with coffee, tea, or caffeine. The interesting part is that the sections of the ring (outer rings and inner rings) are very different colors.
Like here.
What you see here is a fairly profound effect that coffee, tea, or caffeine intake has on metabolites of VLDL — bad cholesterol. The beverages lower it, and, of course, higher levels lead to cardiovascular disease. This means that this is a potential causal pathway from coffee intake to heart protection.
And that’s not the only one.
You see a similar relationship for saturated fatty acids. Higher levels lead to cardiovascular disease, and coffee intake lowers levels. The reverse works too: Lower levels of histidine (an amino acid) increase cardiovascular risk, and coffee seems to raise those levels.
Is this all too good to be true? It’s hard to say. The data on coffee’s benefits have been remarkably consistent. Still, I wouldn’t be a good doctor if I didn’t mention that clearly there is a difference between a cup of black coffee and a venti caramel Frappuccino.
Nevertheless, coffee remains firmly in my holy trinity of enjoyable things that are, for whatever reason, still good for you. So, when you’re having that second, or third, or maybe fourth cup of the day, you can take that to heart.
Dr. Wilson, associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator, reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Each and every day, 1 billion people on this planet ingest a particular psychoactive substance. This chemical has fairly profound physiologic effects. It increases levels of nitric oxide in the blood, leads to vasodilation, and, of course, makes you feel more awake. The substance comes in many forms but almost always in a liquid medium. Do you have it yet? That’s right. The substance is caffeine, quite possibly the healthiest recreational drug that has ever been discovered.
This might be my New England upbringing speaking, but when it comes to lifestyle and health, one of the rules I’ve internalized is that things that are pleasurable are generally bad for you. I know, I know — some of you love to exercise. Some of you love doing crosswords. But you know what I mean. I’m talking French fries, smoked meats, drugs, smoking, alcohol, binge-watching Firefly. You’d be suspicious if a study came out suggesting that eating ice cream in bed reduces your risk for heart attack, and so would I. So I’m always on the lookout for those unicorns of lifestyle factors, those rare things that you want to do and are also good for you.
So far, the data are strong for three things: sleeping, (safe) sexual activity, and coffee. You’ll have to stay tuned for articles about the first two. Today, we’re brewing up some deeper insights about the power of java.
I was inspired to write this article because of a paper, “Habitual Coffee, Tea, and Caffeine Consumption, Circulating Metabolites, and the Risk of Cardiometabolic Multimorbidity,” appearing September 17 in The Journal of Clinical Endocrinology and Metabolism (JCEM).
This is not the first study to suggest that coffee intake may be beneficial. A 2013 meta-analysis summarized the results of 36 studies with more than a million participants and found a U-shaped relationship between coffee intake and cardiovascular risk. The sweet spot was at three to five cups a day; people drinking that much coffee had about a 15% reduced risk for cardiovascular disease compared with nondrinkers.
But here’s the thing. Coffee contains caffeine, but it is much more than that. It is a heady brew of various chemicals and compounds, phenols, and chlorogenic acids. And, of course, you can get caffeine from stuff that isn’t coffee — natural things like tea — and decidedly unnatural things like energy drinks. How do you figure out where the benefit really lies?
The JCEM study leveraged the impressive UK Biobank dataset to figure this out. The Biobank recruited more than half a million people from the UK between 2006 and 2010 and collected a wealth of data from each of them: surveys, blood samples, biometrics, medical imaging — the works. And then they followed what would happen to those people medically over time. It’s a pretty amazing resource.
But for the purposes of this study, what you need to know is that just under 200,000 of those participants met the key criteria for this study: being free from cardiovascular disease at baseline; having completed a detailed survey about their coffee, tea, and other caffeinated beverage intake; and having adequate follow-up. A subset of that number, just under 100,000, had metabolomic data — which is where this study really gets interesting.
We’ll dive into the metabolome in a moment, but first let’s just talk about the main finding, the relationship between coffee, tea, or caffeine and cardiovascular disease. But to do that, we need to acknowledge that people who drink a lot of coffee are different from people who don’t, and it might be those differences, not the coffee itself, that are beneficial.
What were those differences? People who drank more coffee tended to be a bit older, were less likely to be female, and were slightly more likely to engage in physical activity. They ate less processed meat but also fewer vegetables. Some of those factors, like being female, are generally protective against cardiovascular disease; but some, like age, are definitely not. The authors adjusted for these and multiple other factors, including alcohol intake, BMI, kidney function, and many others to try to disentangle the effect of being the type of person who drinks a lot of coffee from the drinking a lot of coffee itself.
These are the results of the fully adjusted model. Compared with nonconsumers, you can see that people in the higher range of coffee, tea, or just caffeine intake have almost a 40% reduction in cardiovascular disease in follow-up.
Looking at the benefit across the spectrum of intake, you again see that U-shaped curve, suggesting that a sweet spot for daily consumption can be found around 3 cups of coffee or tea (or 250 mg of caffeine). A standard energy drink contains about 120 mg of caffeine.
But if this is true, it would be good to know why. To figure that out, the authors turned to the metabolome. The idea here is that your body is constantly breaking stuff down, taking all these proteins and chemicals and compounds that we ingest and turning them into metabolites. Using advanced measurement techniques, researchers can measure hundreds or even thousands of metabolites from a single blood sample. They provide information, obviously, about the food you eat and the drinks you drink, but what is really intriguing is that some metabolites are associated with better health and some with worse
In this study, researchers measured 168 individual metabolites. Eighty of them, nearly half, were significantly altered in people who drank more coffee.
This figure summarizes the findings, and yes, this is way too complicated.
But here’s how to interpret it. The inner ring shows you how certain metabolites are associated with cardiovascular disease. The outer rings show you how those metabolites are associated with coffee, tea, or caffeine. The interesting part is that the sections of the ring (outer rings and inner rings) are very different colors.
Like here.
What you see here is a fairly profound effect that coffee, tea, or caffeine intake has on metabolites of VLDL — bad cholesterol. The beverages lower it, and, of course, higher levels lead to cardiovascular disease. This means that this is a potential causal pathway from coffee intake to heart protection.
And that’s not the only one.
You see a similar relationship for saturated fatty acids. Higher levels lead to cardiovascular disease, and coffee intake lowers levels. The reverse works too: Lower levels of histidine (an amino acid) increase cardiovascular risk, and coffee seems to raise those levels.
Is this all too good to be true? It’s hard to say. The data on coffee’s benefits have been remarkably consistent. Still, I wouldn’t be a good doctor if I didn’t mention that clearly there is a difference between a cup of black coffee and a venti caramel Frappuccino.
Nevertheless, coffee remains firmly in my holy trinity of enjoyable things that are, for whatever reason, still good for you. So, when you’re having that second, or third, or maybe fourth cup of the day, you can take that to heart.
Dr. Wilson, associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator, reported no conflicts of interest.
A version of this article first appeared on Medscape.com.