MDedge Rheumatology

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

This article was created 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.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

This article was created 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.

TOPLINE:

The cumulative effect of frequent corticosteroid injections (CSIs), a common treatment for musculoskeletal pain, does not appear to increase the risk for fractures.

METHODOLOGY:

• Researchers utilized an institutional electronic health record database to identify adults in Olmsted County, Minnesota, receiving corticosteroid injections from May 1, 2018, to July 1, 2022.
• Corticosteroid equivalents were calculated for medications injected, including methylprednisolone, triamcinolone, betamethasone, and dexamethasone.
• Patients were excluded if they had a prescription for oral prednisone equivalents greater than 2.5 mg/day for more than 30 days.
• Fracture events were identified using ICD-9 and ICD-10 codes and were included only if they occurred after the first corticosteroid injection.

TAKEAWAY:

• A total of 7197 patients were analyzed, with a mean age of 64.4 years, and of these patients, 346 (4.8%) had a new fracture in a mean time of 329 days from the first corticosteroid injection, including 149 (43.1%) in classic osteoporotic locations.
• The study reported no increased fracture risk associated with corticosteroid injections and no significant difference in fracture rates across cumulative corticosteroid injection dose quartiles, regardless of osteoporosis status.
• Factors such as previous fractures, age, and Charlson Comorbidity Index were associated with a higher risk for fractures, not corticosteroid injections.

IN PRACTICE:

“Clinicians should be reassured that frequent CSI is not associated with higher fracture risk and should not withhold these important pain treatments owing to concern for fracture,” wrote the authors of the study.

SOURCE:

The study was led by Terin T. Sytsma, MD, Division of Community Internal Medicine, Geriatrics, and Palliative Care, Mayo Clinic, Rochester, Minnesota. It was published online in JAMA Network Open.

LIMITATIONS:

The study’s retrospective cohort design and its focus on a predominantly White population in a single community may limit the generalizability of the findings. Confounding variables such as smoking status, alcohol intake, and physical activity were acknowledged as potential contributors to fracture risk. Only clinically apparent fractures were considered, excluding silent vertebral fractures, and differences in corticosteroid formulation were not delineated.

DISCLOSURES:

The study was supported by a Mayo Clinic Catalyst Award to Dr. Sytsma. The authors had no conflicts of interest to report.

This article was created 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.

BASEL, SWITZERLAND — The anti-inflammatory agent colchicine failed to show significant benefit in the treatment of patients with non-cardioembolic ischemic stroke in the primary analysis of the CONVINCE trial. However, the results did reveal a significant reduction in recurrent stroke and cardiovascular events in the per-protocol analysis and in the subgroup of patients with coronary artery disease.

“Although the primary endpoint was neutral, the CONVINCE results support the hypothesis that long-term anti-inflammatory therapy with colchicine may reduce recurrent stroke and cardiovascular events, specifically in stroke patients with atherosclerosis,” lead investigator Peter Kelly, MD, University College Dublin School of Medicine, Dublin, Ireland, concluded.

The results were presented at the European Stroke Organization Conference (ESOC) 2024.

Inflammation, Dr. Kelly said, plays an important role in the pathophysiology of atherosclerotic plaque, a major cause of cardiovascular events and ischemic strokes.

Colchicine, an established, widely available, low-cost drug that reduces inflammatory response, has been shown to reduce recurrent vascular events in patients with coronary artery disease.

The CONVINCE trial was conducted to see whether colchicine could show similar benefits in patients with non-severe, non-cardioembolic stroke or transient ischemic attack.

Conducted in 16 European countries and Canada, the CONVINCE trial included 3154 patients with a recent non-cardioembolic nondisabling ischemic stroke or high-risk transient ischemic attack. They were randomly assigned to receive colchicine (0.5 mg/d) or placebo.

Key exclusion criteria included evidence of atrial fibrillation or other source of cardioembolism, a defined cause of stroke other than atherosclerosis or small vessel disease, a glomerular filtration rate below 50 mL/min, and the use of drugs that interact with colchicine.

The primary endpoint was a composite of first recurrent ischemic stroke, myocardial infarction, cardiac arrest, or hospitalization for unstable angina. Study participants were followed-up over 36 months.

Results of the primary intention-to-treat analysis showed that the primary endpoint occurred in 153 patients randomized to low-dose colchicine (9.8%) versus 185 in the placebo group (11.8%). This translated into a hazard ratio (HR) of 0.84 (95% CI, 0.68-1.05; P = .12) — a nonsignificant result.

Reduced levels of C-reactive protein in the colchicine group showed the anti-inflammatory effect of treatment with colchicine, Dr. Kelly reported.

In a prespecified on-treatment analysis (excluding patients with major protocol violations), colchicine did show a significant benefit in the primary endpoint (HR, 0.80; 95% CI, 0.63-0.99).
 

A Novel Target for Stroke Treatment

In addition, significantly reduced rates of recurrent stroke or cardiovascular events were observed in the subgroup of patients with a history of coronary artery disease.

In an updated meta-analysis of existing colchicine studies including CONVINCE, there was a significant reduction in the risk for ischemic stroke (risk ratio, 0.73; 95% CI, 0.58-0.90).

“The signals of benefit of colchicine in secondary analyses are in line with findings from previous trials and indicate the potential of colchicine in prevention after stroke,” Dr. Kelly said.

He pointed out that the COVID pandemic reduced the planned follow-up time in the CONVINCE trial, which led to the study being underpowered for the primary analysis.

“Further trials are needed in all stroke subtypes, but with particular focus on patients with objective evidence of atherosclerosis,” he said.

Commenting on the findings, Mira Katan, MD, University Hospital of Basel, Switzerland, noted that inflammation represents a novel target for stroke treatment.

“We have never before looked at treating inflammation in stroke. Although the primary endpoint was not reached in the CONVINCE study, the on-treatment analysis and meta-analysis showed a risk reduction, and we know colchicine works in cardiology. I think this is a fantastic trial, giving us a new target for stroke therapy,” Dr. Katan said.

“I think we have a new tool, but of course we need further trials to confirm that,” she added.

The CONVINCE trial was supported by Health Research Board Ireland, Deutsche Forschungsgesellschaft, Fonds Wetenschappelijk Onderzoek (FWO), and the Irish Heart Foundation. Dr. Kelly received funding from the Irish Heart Foundation. Dr. Katan reported no relevant disclosures.
 

A version of this article appeared on Medscape.com.

BASEL, SWITZERLAND — The anti-inflammatory agent colchicine failed to show significant benefit in the treatment of patients with non-cardioembolic ischemic stroke in the primary analysis of the CONVINCE trial. However, the results did reveal a significant reduction in recurrent stroke and cardiovascular events in the per-protocol analysis and in the subgroup of patients with coronary artery disease.

“Although the primary endpoint was neutral, the CONVINCE results support the hypothesis that long-term anti-inflammatory therapy with colchicine may reduce recurrent stroke and cardiovascular events, specifically in stroke patients with atherosclerosis,” lead investigator Peter Kelly, MD, University College Dublin School of Medicine, Dublin, Ireland, concluded.

The results were presented at the European Stroke Organization Conference (ESOC) 2024.

Inflammation, Dr. Kelly said, plays an important role in the pathophysiology of atherosclerotic plaque, a major cause of cardiovascular events and ischemic strokes.

Colchicine, an established, widely available, low-cost drug that reduces inflammatory response, has been shown to reduce recurrent vascular events in patients with coronary artery disease.

The CONVINCE trial was conducted to see whether colchicine could show similar benefits in patients with non-severe, non-cardioembolic stroke or transient ischemic attack.

Conducted in 16 European countries and Canada, the CONVINCE trial included 3154 patients with a recent non-cardioembolic nondisabling ischemic stroke or high-risk transient ischemic attack. They were randomly assigned to receive colchicine (0.5 mg/d) or placebo.

Key exclusion criteria included evidence of atrial fibrillation or other source of cardioembolism, a defined cause of stroke other than atherosclerosis or small vessel disease, a glomerular filtration rate below 50 mL/min, and the use of drugs that interact with colchicine.

The primary endpoint was a composite of first recurrent ischemic stroke, myocardial infarction, cardiac arrest, or hospitalization for unstable angina. Study participants were followed-up over 36 months.

Results of the primary intention-to-treat analysis showed that the primary endpoint occurred in 153 patients randomized to low-dose colchicine (9.8%) versus 185 in the placebo group (11.8%). This translated into a hazard ratio (HR) of 0.84 (95% CI, 0.68-1.05; P = .12) — a nonsignificant result.

Reduced levels of C-reactive protein in the colchicine group showed the anti-inflammatory effect of treatment with colchicine, Dr. Kelly reported.

In a prespecified on-treatment analysis (excluding patients with major protocol violations), colchicine did show a significant benefit in the primary endpoint (HR, 0.80; 95% CI, 0.63-0.99).
 

A Novel Target for Stroke Treatment

In addition, significantly reduced rates of recurrent stroke or cardiovascular events were observed in the subgroup of patients with a history of coronary artery disease.

In an updated meta-analysis of existing colchicine studies including CONVINCE, there was a significant reduction in the risk for ischemic stroke (risk ratio, 0.73; 95% CI, 0.58-0.90).

“The signals of benefit of colchicine in secondary analyses are in line with findings from previous trials and indicate the potential of colchicine in prevention after stroke,” Dr. Kelly said.

He pointed out that the COVID pandemic reduced the planned follow-up time in the CONVINCE trial, which led to the study being underpowered for the primary analysis.

“Further trials are needed in all stroke subtypes, but with particular focus on patients with objective evidence of atherosclerosis,” he said.

Commenting on the findings, Mira Katan, MD, University Hospital of Basel, Switzerland, noted that inflammation represents a novel target for stroke treatment.

“We have never before looked at treating inflammation in stroke. Although the primary endpoint was not reached in the CONVINCE study, the on-treatment analysis and meta-analysis showed a risk reduction, and we know colchicine works in cardiology. I think this is a fantastic trial, giving us a new target for stroke therapy,” Dr. Katan said.

“I think we have a new tool, but of course we need further trials to confirm that,” she added.

The CONVINCE trial was supported by Health Research Board Ireland, Deutsche Forschungsgesellschaft, Fonds Wetenschappelijk Onderzoek (FWO), and the Irish Heart Foundation. Dr. Kelly received funding from the Irish Heart Foundation. Dr. Katan reported no relevant disclosures.
 

A version of this article appeared on Medscape.com.

BASEL, SWITZERLAND — The anti-inflammatory agent colchicine failed to show significant benefit in the treatment of patients with non-cardioembolic ischemic stroke in the primary analysis of the CONVINCE trial. However, the results did reveal a significant reduction in recurrent stroke and cardiovascular events in the per-protocol analysis and in the subgroup of patients with coronary artery disease.

“Although the primary endpoint was neutral, the CONVINCE results support the hypothesis that long-term anti-inflammatory therapy with colchicine may reduce recurrent stroke and cardiovascular events, specifically in stroke patients with atherosclerosis,” lead investigator Peter Kelly, MD, University College Dublin School of Medicine, Dublin, Ireland, concluded.

The results were presented at the European Stroke Organization Conference (ESOC) 2024.

Inflammation, Dr. Kelly said, plays an important role in the pathophysiology of atherosclerotic plaque, a major cause of cardiovascular events and ischemic strokes.

Colchicine, an established, widely available, low-cost drug that reduces inflammatory response, has been shown to reduce recurrent vascular events in patients with coronary artery disease.

The CONVINCE trial was conducted to see whether colchicine could show similar benefits in patients with non-severe, non-cardioembolic stroke or transient ischemic attack.

Conducted in 16 European countries and Canada, the CONVINCE trial included 3154 patients with a recent non-cardioembolic nondisabling ischemic stroke or high-risk transient ischemic attack. They were randomly assigned to receive colchicine (0.5 mg/d) or placebo.

Key exclusion criteria included evidence of atrial fibrillation or other source of cardioembolism, a defined cause of stroke other than atherosclerosis or small vessel disease, a glomerular filtration rate below 50 mL/min, and the use of drugs that interact with colchicine.

The primary endpoint was a composite of first recurrent ischemic stroke, myocardial infarction, cardiac arrest, or hospitalization for unstable angina. Study participants were followed-up over 36 months.

Results of the primary intention-to-treat analysis showed that the primary endpoint occurred in 153 patients randomized to low-dose colchicine (9.8%) versus 185 in the placebo group (11.8%). This translated into a hazard ratio (HR) of 0.84 (95% CI, 0.68-1.05; P = .12) — a nonsignificant result.

Reduced levels of C-reactive protein in the colchicine group showed the anti-inflammatory effect of treatment with colchicine, Dr. Kelly reported.

In a prespecified on-treatment analysis (excluding patients with major protocol violations), colchicine did show a significant benefit in the primary endpoint (HR, 0.80; 95% CI, 0.63-0.99).
 

A Novel Target for Stroke Treatment

In addition, significantly reduced rates of recurrent stroke or cardiovascular events were observed in the subgroup of patients with a history of coronary artery disease.

In an updated meta-analysis of existing colchicine studies including CONVINCE, there was a significant reduction in the risk for ischemic stroke (risk ratio, 0.73; 95% CI, 0.58-0.90).

“The signals of benefit of colchicine in secondary analyses are in line with findings from previous trials and indicate the potential of colchicine in prevention after stroke,” Dr. Kelly said.

He pointed out that the COVID pandemic reduced the planned follow-up time in the CONVINCE trial, which led to the study being underpowered for the primary analysis.

“Further trials are needed in all stroke subtypes, but with particular focus on patients with objective evidence of atherosclerosis,” he said.

Commenting on the findings, Mira Katan, MD, University Hospital of Basel, Switzerland, noted that inflammation represents a novel target for stroke treatment.

“We have never before looked at treating inflammation in stroke. Although the primary endpoint was not reached in the CONVINCE study, the on-treatment analysis and meta-analysis showed a risk reduction, and we know colchicine works in cardiology. I think this is a fantastic trial, giving us a new target for stroke therapy,” Dr. Katan said.

“I think we have a new tool, but of course we need further trials to confirm that,” she added.

The CONVINCE trial was supported by Health Research Board Ireland, Deutsche Forschungsgesellschaft, Fonds Wetenschappelijk Onderzoek (FWO), and the Irish Heart Foundation. Dr. Kelly received funding from the Irish Heart Foundation. Dr. Katan reported no relevant disclosures.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Metformin use lowers the risk for gout by 32% in individuals with prediabetes; however, the treatment doesn’t change serum urate or C-reactive protein levels.

METHODOLOGY:

• Individuals with prediabetes not only are at an elevated risk for diabetes but also face an increased risk for incident gout. Many previous reports have demonstrated the efficacy of antidiabetic medications in reducing the risk for gout in adults with diabetes.
• This study assessed the gout-lowering properties of metformin in 25,064 individuals with prediabetes (age ≥ 18 years; A1c levels, 5.7%-6.4%) who had never reported A1c levels > 6.4%.
• Patients who were initiated on metformin within 18 months after the diagnosis of prediabetes (n = 1154) were propensity score–matched with those who did not initiate metformin or other antidiabetic medications in this period (n = 13,877) and were followed for a median of 3.9 years for the primary outcome of incident gout.

TAKEAWAY:

• Initiation vs no initiation of metformin resulted in 2.4 fewer cases of gout per 1000 person-years and a 32% reduced relative risk for incident gout (hazard ratio, 0.68; 95% CI, 0.48-0.96).
• The results were consistent across different subgroups stratified on the basis of sex, age (≤ 60 vs > 60 years), estimated glomerular filtration rate (≥ 90 vs < 90 mL/min/1.73 m²), and baseline diuretic use.
• Metformin initiation was not associated with significant changes in serum urate or C-reactive protein levels.
• Metformin use was associated with a reduction in A1c levels and body mass index.

IN PRACTICE:

The authors suggested that “metformin may be important in lowering gout risk in individuals with prediabetes.”

SOURCE:

Javier Marrugo, MD, Department of Medicine, Brigham and Women’s Hospital, Boston, led this study, which was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

Although gout is more commonly observed in men, around 60% of the study population consisted of women. Owing to the observational nature of this study, exposure misclassifications might have occurred. Misclassification of the outcome is also possible due to the presence of two or more diagnostic codes for gout and/or the combination of urate-lowering therapies or colchicine with at least one diagnostic code.

DISCLOSURES:

This work was supported by the National Institutes of Health. Some authors declared serving as consultants or receiving salary support or consulting fees from various sources.

A version of this article first appeared on Medscape.com.

TOPLINE:

Metformin use lowers the risk for gout by 32% in individuals with prediabetes; however, the treatment doesn’t change serum urate or C-reactive protein levels.

METHODOLOGY:

• Individuals with prediabetes not only are at an elevated risk for diabetes but also face an increased risk for incident gout. Many previous reports have demonstrated the efficacy of antidiabetic medications in reducing the risk for gout in adults with diabetes.
• This study assessed the gout-lowering properties of metformin in 25,064 individuals with prediabetes (age ≥ 18 years; A1c levels, 5.7%-6.4%) who had never reported A1c levels > 6.4%.
• Patients who were initiated on metformin within 18 months after the diagnosis of prediabetes (n = 1154) were propensity score–matched with those who did not initiate metformin or other antidiabetic medications in this period (n = 13,877) and were followed for a median of 3.9 years for the primary outcome of incident gout.

TAKEAWAY:

• Initiation vs no initiation of metformin resulted in 2.4 fewer cases of gout per 1000 person-years and a 32% reduced relative risk for incident gout (hazard ratio, 0.68; 95% CI, 0.48-0.96).
• The results were consistent across different subgroups stratified on the basis of sex, age (≤ 60 vs > 60 years), estimated glomerular filtration rate (≥ 90 vs < 90 mL/min/1.73 m²), and baseline diuretic use.
• Metformin initiation was not associated with significant changes in serum urate or C-reactive protein levels.
• Metformin use was associated with a reduction in A1c levels and body mass index.

IN PRACTICE:

The authors suggested that “metformin may be important in lowering gout risk in individuals with prediabetes.”

SOURCE:

Javier Marrugo, MD, Department of Medicine, Brigham and Women’s Hospital, Boston, led this study, which was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

Although gout is more commonly observed in men, around 60% of the study population consisted of women. Owing to the observational nature of this study, exposure misclassifications might have occurred. Misclassification of the outcome is also possible due to the presence of two or more diagnostic codes for gout and/or the combination of urate-lowering therapies or colchicine with at least one diagnostic code.

DISCLOSURES:

This work was supported by the National Institutes of Health. Some authors declared serving as consultants or receiving salary support or consulting fees from various sources.

A version of this article first appeared on Medscape.com.

TOPLINE:

Metformin use lowers the risk for gout by 32% in individuals with prediabetes; however, the treatment doesn’t change serum urate or C-reactive protein levels.

METHODOLOGY:

• Individuals with prediabetes not only are at an elevated risk for diabetes but also face an increased risk for incident gout. Many previous reports have demonstrated the efficacy of antidiabetic medications in reducing the risk for gout in adults with diabetes.
• This study assessed the gout-lowering properties of metformin in 25,064 individuals with prediabetes (age ≥ 18 years; A1c levels, 5.7%-6.4%) who had never reported A1c levels > 6.4%.
• Patients who were initiated on metformin within 18 months after the diagnosis of prediabetes (n = 1154) were propensity score–matched with those who did not initiate metformin or other antidiabetic medications in this period (n = 13,877) and were followed for a median of 3.9 years for the primary outcome of incident gout.

TAKEAWAY:

• Initiation vs no initiation of metformin resulted in 2.4 fewer cases of gout per 1000 person-years and a 32% reduced relative risk for incident gout (hazard ratio, 0.68; 95% CI, 0.48-0.96).
• The results were consistent across different subgroups stratified on the basis of sex, age (≤ 60 vs > 60 years), estimated glomerular filtration rate (≥ 90 vs < 90 mL/min/1.73 m²), and baseline diuretic use.
• Metformin initiation was not associated with significant changes in serum urate or C-reactive protein levels.
• Metformin use was associated with a reduction in A1c levels and body mass index.

IN PRACTICE:

The authors suggested that “metformin may be important in lowering gout risk in individuals with prediabetes.”

SOURCE:

Javier Marrugo, MD, Department of Medicine, Brigham and Women’s Hospital, Boston, led this study, which was published online in Annals of the Rheumatic Diseases.

LIMITATIONS:

Although gout is more commonly observed in men, around 60% of the study population consisted of women. Owing to the observational nature of this study, exposure misclassifications might have occurred. Misclassification of the outcome is also possible due to the presence of two or more diagnostic codes for gout and/or the combination of urate-lowering therapies or colchicine with at least one diagnostic code.

DISCLOSURES:

This work was supported by the National Institutes of Health. Some authors declared serving as consultants or receiving salary support or consulting fees from various sources.

A version of this article first appeared on Medscape.com.

TOPLINE:

Patients with axial spondyloarthritis (axSpA) who reported high nonsteroidal anti-inflammatory drug (NSAID) use did not have a higher risk for hypertension than those who reported low NSAID use.

METHODOLOGY:

• NSAIDs are first-line therapy for axSpA and are associated with a high risk for hypertension in the general population, but it’s unknown whether NSAID use increases the risk for hypertension in patients with axSpA, who are already at higher risk for cardiovascular disease and hypertension than the general population
• This study used the DESIR cohort, a multicenter cohort of patients with recent-onset axSpA in France, including 631 individuals aged 18-50 years who did not have hypertension at baseline and had 6 years of follow-up.
• NSAID use was evaluated at each follow-up visit, using the Assessment of Spondyloarthritis International Society NSAID index.
• A score ≥ 50 was categorized as high use, and a score < 50 was considered low use.
• The primary outcome was hypertension, defined by the use of antihypertensive medication, self-reported hypertension, and/or systolic blood pressure (BP) ≥ 140 mm Hg or diastolic BP ≥ 90 mm Hg on at least two visits.

TAKEAWAY:

• A total of 39% of patients were categorized as high NSAID users.
• Over 6 years of follow-up, 70 patients (11%) developed hypertension.
• There was no significant association between high NSAID use and the risk for hypertension.

IN PRACTICE:

The study is too preliminary to have practice application.

SOURCE:

The research was led and presented by Jose Meade-Aguilar, MD, of Boston University School of Medicine, at the Spondyloarthritis Research and Treatment Network (SPARTAN) 2024 annual meeting in Cleveland.

LIMITATIONS:

The study had a low number of hypertension events, which could be due to the younger age of participants and earlier disease stage. The study was observational, so residual or unmeasured confounding is possible.

DISCLOSURES:

The DESIR cohort study is financially supported by unrestricted grants from both the French Society for Rheumatology and Pfizer France. One coauthor reported receiving research grants and/or consultancy fees from AbbVie, Eli Lilly, Galapagos, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, UCB, and Sanofi. Another coauthor reported receiving research grants from UCB and consulting fees from Eli Lilly, Novartis, Pfizer, and UCB. The remaining authors had no financial, relational, or commercial conflicts to disclose.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with axial spondyloarthritis (axSpA) who reported high nonsteroidal anti-inflammatory drug (NSAID) use did not have a higher risk for hypertension than those who reported low NSAID use.

METHODOLOGY:

• NSAIDs are first-line therapy for axSpA and are associated with a high risk for hypertension in the general population, but it’s unknown whether NSAID use increases the risk for hypertension in patients with axSpA, who are already at higher risk for cardiovascular disease and hypertension than the general population
• This study used the DESIR cohort, a multicenter cohort of patients with recent-onset axSpA in France, including 631 individuals aged 18-50 years who did not have hypertension at baseline and had 6 years of follow-up.
• NSAID use was evaluated at each follow-up visit, using the Assessment of Spondyloarthritis International Society NSAID index.
• A score ≥ 50 was categorized as high use, and a score < 50 was considered low use.
• The primary outcome was hypertension, defined by the use of antihypertensive medication, self-reported hypertension, and/or systolic blood pressure (BP) ≥ 140 mm Hg or diastolic BP ≥ 90 mm Hg on at least two visits.

TAKEAWAY:

• A total of 39% of patients were categorized as high NSAID users.
• Over 6 years of follow-up, 70 patients (11%) developed hypertension.
• There was no significant association between high NSAID use and the risk for hypertension.

IN PRACTICE:

The study is too preliminary to have practice application.

SOURCE:

The research was led and presented by Jose Meade-Aguilar, MD, of Boston University School of Medicine, at the Spondyloarthritis Research and Treatment Network (SPARTAN) 2024 annual meeting in Cleveland.

LIMITATIONS:

The study had a low number of hypertension events, which could be due to the younger age of participants and earlier disease stage. The study was observational, so residual or unmeasured confounding is possible.

DISCLOSURES:

The DESIR cohort study is financially supported by unrestricted grants from both the French Society for Rheumatology and Pfizer France. One coauthor reported receiving research grants and/or consultancy fees from AbbVie, Eli Lilly, Galapagos, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, UCB, and Sanofi. Another coauthor reported receiving research grants from UCB and consulting fees from Eli Lilly, Novartis, Pfizer, and UCB. The remaining authors had no financial, relational, or commercial conflicts to disclose.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with axial spondyloarthritis (axSpA) who reported high nonsteroidal anti-inflammatory drug (NSAID) use did not have a higher risk for hypertension than those who reported low NSAID use.

METHODOLOGY:

• NSAIDs are first-line therapy for axSpA and are associated with a high risk for hypertension in the general population, but it’s unknown whether NSAID use increases the risk for hypertension in patients with axSpA, who are already at higher risk for cardiovascular disease and hypertension than the general population
• This study used the DESIR cohort, a multicenter cohort of patients with recent-onset axSpA in France, including 631 individuals aged 18-50 years who did not have hypertension at baseline and had 6 years of follow-up.
• NSAID use was evaluated at each follow-up visit, using the Assessment of Spondyloarthritis International Society NSAID index.
• A score ≥ 50 was categorized as high use, and a score < 50 was considered low use.
• The primary outcome was hypertension, defined by the use of antihypertensive medication, self-reported hypertension, and/or systolic blood pressure (BP) ≥ 140 mm Hg or diastolic BP ≥ 90 mm Hg on at least two visits.

TAKEAWAY:

• A total of 39% of patients were categorized as high NSAID users.
• Over 6 years of follow-up, 70 patients (11%) developed hypertension.
• There was no significant association between high NSAID use and the risk for hypertension.

IN PRACTICE:

The study is too preliminary to have practice application.

SOURCE:

The research was led and presented by Jose Meade-Aguilar, MD, of Boston University School of Medicine, at the Spondyloarthritis Research and Treatment Network (SPARTAN) 2024 annual meeting in Cleveland.

LIMITATIONS:

The study had a low number of hypertension events, which could be due to the younger age of participants and earlier disease stage. The study was observational, so residual or unmeasured confounding is possible.

DISCLOSURES:

The DESIR cohort study is financially supported by unrestricted grants from both the French Society for Rheumatology and Pfizer France. One coauthor reported receiving research grants and/or consultancy fees from AbbVie, Eli Lilly, Galapagos, Janssen, Merck Sharp & Dohme, Novartis, Pfizer, UCB, and Sanofi. Another coauthor reported receiving research grants from UCB and consulting fees from Eli Lilly, Novartis, Pfizer, and UCB. The remaining authors had no financial, relational, or commercial conflicts to disclose.
 

A version of this article appeared on Medscape.com.

In regard to treatment, bimekizumab is a new monoclonal antibody that dually targets interleukin (IL)-17A and IL-17F and is highly efficacious for the treatment of psoriasis. In a meta-analysis of four placebo-controlled randomized clinical trials that included 1323 patients with PsA (age 18 years or older), of whom 853 received bimekizumab, Su and colleagues demonstrated that bimekizumab led to a significantly higher response rate for minimal disease activity (risk ratio [RR] 4.188; P < .001) and a 70% or greater improvement in the American College of Rheumatology (ACR) criteria (RR 7.932; P < .0001) when compared with placebo. Bimekizumab was superior to placebo in achieving ACR20/50/70 response at a dose of 160 mg. The risk for treatment-emergent adverse events was modestly higher with bimekizumab vs placebo (RR 1.423; P = .023), whereas the risk for serious cancers, upper respiratory tract infection, injection site reactions, and pharyngitis was similar for both. Thus, bimekizumab is an efficacious agent for the treatment of PsA. Future head-to-head studies will help clinicians determine the role of this drug in the management of PsA.

Not all patients respond equally well to targeted therapies, and the so-called challenging-to-treat patients are being increasingly described. Kivitz and colleagues recently described the efficacy of secukinumab, a monoclonal antibody targeting IL-17A, in these challenging-to-treat patients from the United States. In a post hoc subgroup analysis of four phase 3 studies that included 279 patients, they demonstrated that patients receiving 300 mg secukinumab and 150 mg  with a loading dose had a higher rate of achieving the ACR20 response (59.7% and 43.4%, respectively) vs 15.6% for placebo (both P < .0001). The Psoriasis Area and Severity Index 90 response was 47.1% and 22.2%, respectively, vs 5.3% (both P < .05). Thus, secukinumab is efficacious in more challenging-to-treat patients. However, such patients need to be better characterized so that effective treatment strategies to achieve a state of low disease activity may be implemented.

In regard to treatment, bimekizumab is a new monoclonal antibody that dually targets interleukin (IL)-17A and IL-17F and is highly efficacious for the treatment of psoriasis. In a meta-analysis of four placebo-controlled randomized clinical trials that included 1323 patients with PsA (age 18 years or older), of whom 853 received bimekizumab, Su and colleagues demonstrated that bimekizumab led to a significantly higher response rate for minimal disease activity (risk ratio [RR] 4.188; P < .001) and a 70% or greater improvement in the American College of Rheumatology (ACR) criteria (RR 7.932; P < .0001) when compared with placebo. Bimekizumab was superior to placebo in achieving ACR20/50/70 response at a dose of 160 mg. The risk for treatment-emergent adverse events was modestly higher with bimekizumab vs placebo (RR 1.423; P = .023), whereas the risk for serious cancers, upper respiratory tract infection, injection site reactions, and pharyngitis was similar for both. Thus, bimekizumab is an efficacious agent for the treatment of PsA. Future head-to-head studies will help clinicians determine the role of this drug in the management of PsA.

Not all patients respond equally well to targeted therapies, and the so-called challenging-to-treat patients are being increasingly described. Kivitz and colleagues recently described the efficacy of secukinumab, a monoclonal antibody targeting IL-17A, in these challenging-to-treat patients from the United States. In a post hoc subgroup analysis of four phase 3 studies that included 279 patients, they demonstrated that patients receiving 300 mg secukinumab and 150 mg  with a loading dose had a higher rate of achieving the ACR20 response (59.7% and 43.4%, respectively) vs 15.6% for placebo (both P < .0001). The Psoriasis Area and Severity Index 90 response was 47.1% and 22.2%, respectively, vs 5.3% (both P < .05). Thus, secukinumab is efficacious in more challenging-to-treat patients. However, such patients need to be better characterized so that effective treatment strategies to achieve a state of low disease activity may be implemented.

In regard to treatment, bimekizumab is a new monoclonal antibody that dually targets interleukin (IL)-17A and IL-17F and is highly efficacious for the treatment of psoriasis. In a meta-analysis of four placebo-controlled randomized clinical trials that included 1323 patients with PsA (age 18 years or older), of whom 853 received bimekizumab, Su and colleagues demonstrated that bimekizumab led to a significantly higher response rate for minimal disease activity (risk ratio [RR] 4.188; P < .001) and a 70% or greater improvement in the American College of Rheumatology (ACR) criteria (RR 7.932; P < .0001) when compared with placebo. Bimekizumab was superior to placebo in achieving ACR20/50/70 response at a dose of 160 mg. The risk for treatment-emergent adverse events was modestly higher with bimekizumab vs placebo (RR 1.423; P = .023), whereas the risk for serious cancers, upper respiratory tract infection, injection site reactions, and pharyngitis was similar for both. Thus, bimekizumab is an efficacious agent for the treatment of PsA. Future head-to-head studies will help clinicians determine the role of this drug in the management of PsA.

Not all patients respond equally well to targeted therapies, and the so-called challenging-to-treat patients are being increasingly described. Kivitz and colleagues recently described the efficacy of secukinumab, a monoclonal antibody targeting IL-17A, in these challenging-to-treat patients from the United States. In a post hoc subgroup analysis of four phase 3 studies that included 279 patients, they demonstrated that patients receiving 300 mg secukinumab and 150 mg  with a loading dose had a higher rate of achieving the ACR20 response (59.7% and 43.4%, respectively) vs 15.6% for placebo (both P < .0001). The Psoriasis Area and Severity Index 90 response was 47.1% and 22.2%, respectively, vs 5.3% (both P < .05). Thus, secukinumab is efficacious in more challenging-to-treat patients. However, such patients need to be better characterized so that effective treatment strategies to achieve a state of low disease activity may be implemented.

TOPLINE:

An early serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) has been validated as a safe and useful screening test with 100% specificity for predicting recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients on tapering regimes from long‐term chronic glucocorticoid therapy (CGT).

METHODOLOGY:

• A retrospective review of 250-µg Synacthen test (SST) results performed in patients on tapering CGT doses from a single-center rheumatology department over 12 months.
• A total of 60 SSTs were performed in 58 patients, all in the morning (7-12 AM) after withholding CGT for 48 hours.
• Peripheral blood was sampled for cortisol at baseline, 30 minutes, and 60 minutes.
• Adrenal insufficiency (AI) was defined as a peak serum cortisol concentration.

TAKEAWAY:

• The mean duration of CGT (all prednisolone) was 63 months, prescribed primarily for giant cell arteritis/polymyalgia rheumatica (48%) and inflammatory arthritis (18%), with a mean daily dose of 3.4 mg at the time of SST.
• With the investigators’ previously reported basal serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) used to confirm an intact HPA axis, no patient with AI would have been missed, but 37 of 51 (73%) unnecessary SSTs in euadrenal patients would have been avoided.
• A basal serum cortisol concentration of > 227 nmol/L had a specificity of 100% for predicting passing the SST, while a basal serum cortisol concentration of ≤ 55 nmol/L had a 100% sensitivity for predicting failure.
• A mean daily prednisolone dosing at the time of SST in patients with AI was significantly higher than that with normal SSTs (5.7 vs 2.9 mg, respectively; P = .01).

IN PRACTICE:

“This offers a more rapid, convenient, and cost‐effective screening method for patients requiring biochemical assessment of the HPA axis with the potential for significant resource savings without any adverse impact on patient safety,” the authors wrote.

SOURCE:

The study was conducted by Ella Sharma, of the Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and colleagues and published online on May 19, 2024, as a letter in Clinical Endocrinology.

LIMITATIONS:

Not provided.

DISCLOSURES: 

Not provided.
 

A version of this article appeared on Medscape.com.

TOPLINE:

An early serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) has been validated as a safe and useful screening test with 100% specificity for predicting recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients on tapering regimes from long‐term chronic glucocorticoid therapy (CGT).

METHODOLOGY:

• A retrospective review of 250-µg Synacthen test (SST) results performed in patients on tapering CGT doses from a single-center rheumatology department over 12 months.
• A total of 60 SSTs were performed in 58 patients, all in the morning (7-12 AM) after withholding CGT for 48 hours.
• Peripheral blood was sampled for cortisol at baseline, 30 minutes, and 60 minutes.
• Adrenal insufficiency (AI) was defined as a peak serum cortisol concentration.

TAKEAWAY:

• The mean duration of CGT (all prednisolone) was 63 months, prescribed primarily for giant cell arteritis/polymyalgia rheumatica (48%) and inflammatory arthritis (18%), with a mean daily dose of 3.4 mg at the time of SST.
• With the investigators’ previously reported basal serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) used to confirm an intact HPA axis, no patient with AI would have been missed, but 37 of 51 (73%) unnecessary SSTs in euadrenal patients would have been avoided.
• A basal serum cortisol concentration of > 227 nmol/L had a specificity of 100% for predicting passing the SST, while a basal serum cortisol concentration of ≤ 55 nmol/L had a 100% sensitivity for predicting failure.
• A mean daily prednisolone dosing at the time of SST in patients with AI was significantly higher than that with normal SSTs (5.7 vs 2.9 mg, respectively; P = .01).

IN PRACTICE:

“This offers a more rapid, convenient, and cost‐effective screening method for patients requiring biochemical assessment of the HPA axis with the potential for significant resource savings without any adverse impact on patient safety,” the authors wrote.

SOURCE:

The study was conducted by Ella Sharma, of the Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and colleagues and published online on May 19, 2024, as a letter in Clinical Endocrinology.

LIMITATIONS:

Not provided.

DISCLOSURES: 

Not provided.
 

A version of this article appeared on Medscape.com.

TOPLINE:

An early serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) has been validated as a safe and useful screening test with 100% specificity for predicting recovery of the hypothalamic-pituitary-adrenal (HPA) axis in patients on tapering regimes from long‐term chronic glucocorticoid therapy (CGT).

METHODOLOGY:

• A retrospective review of 250-µg Synacthen test (SST) results performed in patients on tapering CGT doses from a single-center rheumatology department over 12 months.
• A total of 60 SSTs were performed in 58 patients, all in the morning (7-12 AM) after withholding CGT for 48 hours.
• Peripheral blood was sampled for cortisol at baseline, 30 minutes, and 60 minutes.
• Adrenal insufficiency (AI) was defined as a peak serum cortisol concentration.

TAKEAWAY:

• The mean duration of CGT (all prednisolone) was 63 months, prescribed primarily for giant cell arteritis/polymyalgia rheumatica (48%) and inflammatory arthritis (18%), with a mean daily dose of 3.4 mg at the time of SST.
• With the investigators’ previously reported basal serum cortisol concentration of > 237 nmol/L (> 8.6 μg/dL) used to confirm an intact HPA axis, no patient with AI would have been missed, but 37 of 51 (73%) unnecessary SSTs in euadrenal patients would have been avoided.
• A basal serum cortisol concentration of > 227 nmol/L had a specificity of 100% for predicting passing the SST, while a basal serum cortisol concentration of ≤ 55 nmol/L had a 100% sensitivity for predicting failure.
• A mean daily prednisolone dosing at the time of SST in patients with AI was significantly higher than that with normal SSTs (5.7 vs 2.9 mg, respectively; P = .01).

IN PRACTICE:

“This offers a more rapid, convenient, and cost‐effective screening method for patients requiring biochemical assessment of the HPA axis with the potential for significant resource savings without any adverse impact on patient safety,” the authors wrote.

SOURCE:

The study was conducted by Ella Sharma, of the Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and colleagues and published online on May 19, 2024, as a letter in Clinical Endocrinology.

LIMITATIONS:

Not provided.

DISCLOSURES: 

Not provided.
 

A version of this article appeared on Medscape.com.

Neuropsychiatric symptoms, including nightmares and hallucinatory “daymares,” may be a more important aspect of systemic lupus erythematosus (SLE) than formerly recognized, according to a qualitative mixed methods study published in The Lancet Discovery Science’s eClinicalMedicine. The findings suggested these neuropsychiatric symptoms can sometimes present as prodromal and other times act as an early warning system for a forthcoming flare.

“For clinicians, the key point is to be aware that neurological and psychiatric symptoms are much more common in patients with lupus and other autoimmune systemic rheumatic diseases than previously thought,” lead author Melanie Sloan, PhD, of the Department of Public Health and Primary Care at the University of Cambridge in England, told this news organization.

“If clinicians — and some do already — could all ask about and document these symptoms for each patient, the usual progression of symptoms in a flare can then be monitored, and patients could be supported and treated at an earlier stage,” Dr. Sloan said. “Another key point is to consider systemic autoimmune diseases at an early stage if a patient presents with multiple seemingly unconnected symptoms, which often include both physical and mental health symptoms.”

Alfred Kim, MD, PhD, associate professor of medicine in rheumatology at Washington University School of Medicine in St. Louis, Missouri, noted the difficulty of determining what neuropsychiatric symptoms may be linked to lupus vs those occurring independently or as part of a different condition.

Dr. Kim

Study Details

In planning for the study, the researchers first searched the existing literature for studies involving neuropsychiatric symptoms in patients with systemic autoimmune rheumatic diseases (SARDs). “The literature indicated frequent underreporting and misattributions of neuropsychiatric symptoms in SLE and other SARD patients, and clinician-patient discordance in neuropsychiatric symptom attribution,” the authors reported.

During 2022-2023, the researchers conducted two surveys, one with 676 adult patients with SLE and one with 400 clinicians, recruited through social media, online patient support groups, and professional networks. All patients self-reported an SLE diagnosis that the researchers did not independently confirm. The patients were predominantly White (80%) and female (94%), ranging in age from 18 to over 70, with most falling between ages 40 and 69. Most patients lived in the United Kingdom (76%) or Europe (15%).

The clinicians included 51% rheumatologists, 24% psychiatrists, 13% neurologists, 5% rheumatology nurses, 3% primary care physicians, and 7% other clinicians. Nearly half of the clinicians (45%) were from the United Kingdom, with others from the United States or Canada (16%), Europe (17%), Asia (9%), Latin America (8%), Australia or New Zealand (3%), or elsewhere (3%).

The patient surveys asked whether they had experienced any of the 29 neuropsychiatric symptoms. For the symptoms that patients had experienced at least three times in their lives, the survey asked when they first experienced the symptom in relation to their SLE onset or other SLE symptoms: Over a year before, within a year of (on either side), 1-4 years after, or more than 5 years after onset/other symptoms. “Other quantitative data included timings of disrupted dreaming sleep in relation to hallucinations for those patients reporting experiencing these,” the authors wrote.

The researchers also conducted video conference interviews with 50 clinicians, including 20 rheumatologists, and 69 interviews with patients who had a systemic autoimmune rheumatic disease, including 27 patients with SLE. Other conditions among those interviewed included inflammatory arthritis, vasculitis, Sjögren disease, systemic sclerosis, myositis, undifferentiated and mixed connective tissue diseases, and polymyalgia rheumatica. During interviews, the term “daymare” was used to discuss possible hallucinations.
 

Linking Neuropsychiatric Symptoms and Disease

Four themes emerged from the analysis of the surveys and interviews. First, despite many rheumatologists stating that it was an “established theory” that most neuropsychiatric symptoms related to SLE would initially present around the time of diagnosis or disease onset, the findings from patients and interviews with psychiatrists did not align with this theory. The first presentation of each neuropsychiatric symptom only occurred around the onset of other SLE symptoms, about one fifth to one third of the time. In fact, more than half of the patients with SLE who had experienced hallucinations or delusions/paranoia said they occurred more than a year after they first experienced their other SLE symptoms.

Patient experiences differed in terms of whether they believed their neuropsychiatric symptoms were directly related to their SLE or other rheumatic disease. Some did attribute the symptoms, such as hypomania, to their rheumatic illness, while others, such as a patient with major depression, did not see the two as linked.

A second theme focused on pattern recognition of neuropsychiatric symptoms and the onset of a disease flare. “For example, several patients described how they felt that some types of depressive symptoms were directly attributable to active inflammation due to its time of onset and differences in type and intensity compared to their more ‘reactive’ low mood that could be more attributable to a consequence of psychological distress,” the authors wrote. Another common report from patients was experiencing a sudden, intense fatigue that coincided with a flare and differed from other types of fatigue.

Some patients could recognize that a flare was coming because of familiar neuropsychiatric symptoms that acted like an “early warning system.” Often, however, these symptoms “were absent from current diagnostic guidelines and only rarely identified by clinician interviewees as related to SLE/NPSLE,” the authors found. “These neuropsychiatric prodromal symptoms were reported as sometimes preceding the more widely recognized SLE and other SARD symptoms such as joint pain, rashes, and other organ involvement.” These symptoms included sudden changes in mood (usually a lowering but sometimes mania), increased nightmares, a “feeling of unreality,” or increased sensory symptoms.

Other patients, on the other hand, had not considered a link between neuropsychiatric symptoms and their rheumatic disease until the interview, and many of the clinicians, aside from psychiatrists and nurses, said they had little time in clinic to gather information about symptom progression.
 

Nightmares and Daymares

A third theme centered on disrupted dreaming sleep, nightmares, and “daymares” as a prodromal symptom in particular. Some patients had already drawn a connection between an oncoming flare of their disease and these dreaming-related symptoms, while others had not considered a link until the interviews.

“Several SLE patients recounted flares consistently involving the segueing of increasingly vivid and distressing nightmares into distorted reality and daytime hallucinations,” the authors reported. Flare-related nightmares in particular “often involved being attacked, trapped, crushed, or falling.” Patients tended to be more forthcoming about hallucinatory experiences when the term “daymare” was used to describe them, and they often related to the idea of feeling “in-between asleep and awake.”

Only one of the rheumatologists interviewed had considered nightmares as potentially related to SLE flares, and several appeared skeptical about a link but planned to ask their patients about it. Most of the specialists interviewed, meanwhile, said they often discussed sleep disruption with patients.

“There was agreement that recognizing and eliciting these early flare symptoms may improve care and even reduce clinic times by averting flares at any earlier stage, although some rheumatologists were clear that limited appointment times meant that these symptoms would not be prioritized for discussion,” the authors wrote.

Though Dr. Kim acknowledged the possibility of nightmares as prodromal, he noted other ways in which nightmares may be indirectly linked to lupus. “Trauma is a major risk factor for lupus,” Dr. Kim said, with multiple studies showing childhood traumatic experiences and even posttraumatic stress disorder to be risk factors for lupus. “Whether nightmares represent a traumatic event or prior traumatic events is not clear to me, but one could hypothesize that this may be a manifestation of trauma,” Dr. Kim said.

In addition, nightmares represent a sleep disorder that can substantially reduce sleep quality, Dr. Kim said, and poor sleep is also associated with lupus. “One has to wonder whether disruptive dreaming sleep is one of several specific manifestations of poor sleep quality, which then increases the risk of lupus in those patients,” Dr. Kim said.
 

Misattribution of Neuropsychiatric Symptoms

The final theme to emerge from the findings was patients had been misdiagnosed with psychiatric or psychosomatic conditions shortly before getting their rheumatic disease diagnosis. One patient, for example, reported being diagnosed with borderline personality disorder just 6 months before the lupus diagnosis at age 19 and noticed that the symptoms of one “got under control” when the symptoms of the other did.

“Early misattributions of SARD symptoms to primary psychiatric or psychosomatic conditions were frequently reported to have delayed SARD diagnosis and led to future misattributions,” the authors reported. “Whilst some of these misdiagnoses likely reflect the widespread lack of knowledge and limited definitive tests for SLE, it is plausible that some early SLE neurological and/or psychiatric symptoms may represent a neuropsychiatric prodrome for SLE itself.”

Dr. Kim agreed that misattribution of symptoms to other diagnoses is common with lupus and a common reason for delays in diagnosis, even with symptoms that are not neuropsychiatric. The findings in this study broaden “the type of symptoms we need to put on our radar pre-diagnosis,” Dr. Kim said. “We just also have to be aware that these prodromal symptoms are not diagnostic for lupus, though.”

Dr. Sloan cited earlier work in recommending an “ABC” approach to improving clinician-patient relationships: “Availability is being accessible when patients need them, Belief is demonstrating belief and validating patient self-reports of symptoms, and Continuity is when the same clinician sees the same patient each clinic visit to build up a trusting relationship.” She noted the importance of asking about and normalizing the existence of these symptoms with rheumatic diseases.

The research was funded by The Lupus Trust. Three authors reported consultancy, speaker, or advisory fees from Alumis, Amgen, AstraZeneca, Eli Lilly, GlaxoSmithKline, Janssen, MGP, Novartis, Pfizer, Sanofi, UCB, Vifor, and/or Werfen Group. The other authors, including Dr. Sloan, had no industry-related disclosures. Dr. Kim reported research support from AstraZeneca, GlaxoSmithKline, and Novartis; speaking fees from Exagen Diagnostics and GlaxoSmithKline; and consulting fees from AbbVie, Amgen, ANI Pharmaceuticals, AstraZeneca, Atara Bio, Aurinia Pharmaceuticals, Cargo Therapeutics, Exagen Diagnostics, Hinge Bio, GlaxoSmithKline, Kypha, Miltenyi Biotec, Synthekine, and Tectonic Therapeutic.
 

A version of this article appeared on Medscape.com.

Neuropsychiatric symptoms, including nightmares and hallucinatory “daymares,” may be a more important aspect of systemic lupus erythematosus (SLE) than formerly recognized, according to a qualitative mixed methods study published in The Lancet Discovery Science’s eClinicalMedicine. The findings suggested these neuropsychiatric symptoms can sometimes present as prodromal and other times act as an early warning system for a forthcoming flare.

“For clinicians, the key point is to be aware that neurological and psychiatric symptoms are much more common in patients with lupus and other autoimmune systemic rheumatic diseases than previously thought,” lead author Melanie Sloan, PhD, of the Department of Public Health and Primary Care at the University of Cambridge in England, told this news organization.

“If clinicians — and some do already — could all ask about and document these symptoms for each patient, the usual progression of symptoms in a flare can then be monitored, and patients could be supported and treated at an earlier stage,” Dr. Sloan said. “Another key point is to consider systemic autoimmune diseases at an early stage if a patient presents with multiple seemingly unconnected symptoms, which often include both physical and mental health symptoms.”

Alfred Kim, MD, PhD, associate professor of medicine in rheumatology at Washington University School of Medicine in St. Louis, Missouri, noted the difficulty of determining what neuropsychiatric symptoms may be linked to lupus vs those occurring independently or as part of a different condition.

Dr. Kim

Study Details

In planning for the study, the researchers first searched the existing literature for studies involving neuropsychiatric symptoms in patients with systemic autoimmune rheumatic diseases (SARDs). “The literature indicated frequent underreporting and misattributions of neuropsychiatric symptoms in SLE and other SARD patients, and clinician-patient discordance in neuropsychiatric symptom attribution,” the authors reported.

During 2022-2023, the researchers conducted two surveys, one with 676 adult patients with SLE and one with 400 clinicians, recruited through social media, online patient support groups, and professional networks. All patients self-reported an SLE diagnosis that the researchers did not independently confirm. The patients were predominantly White (80%) and female (94%), ranging in age from 18 to over 70, with most falling between ages 40 and 69. Most patients lived in the United Kingdom (76%) or Europe (15%).

The clinicians included 51% rheumatologists, 24% psychiatrists, 13% neurologists, 5% rheumatology nurses, 3% primary care physicians, and 7% other clinicians. Nearly half of the clinicians (45%) were from the United Kingdom, with others from the United States or Canada (16%), Europe (17%), Asia (9%), Latin America (8%), Australia or New Zealand (3%), or elsewhere (3%).

The patient surveys asked whether they had experienced any of the 29 neuropsychiatric symptoms. For the symptoms that patients had experienced at least three times in their lives, the survey asked when they first experienced the symptom in relation to their SLE onset or other SLE symptoms: Over a year before, within a year of (on either side), 1-4 years after, or more than 5 years after onset/other symptoms. “Other quantitative data included timings of disrupted dreaming sleep in relation to hallucinations for those patients reporting experiencing these,” the authors wrote.

The researchers also conducted video conference interviews with 50 clinicians, including 20 rheumatologists, and 69 interviews with patients who had a systemic autoimmune rheumatic disease, including 27 patients with SLE. Other conditions among those interviewed included inflammatory arthritis, vasculitis, Sjögren disease, systemic sclerosis, myositis, undifferentiated and mixed connective tissue diseases, and polymyalgia rheumatica. During interviews, the term “daymare” was used to discuss possible hallucinations.
 

Linking Neuropsychiatric Symptoms and Disease

Four themes emerged from the analysis of the surveys and interviews. First, despite many rheumatologists stating that it was an “established theory” that most neuropsychiatric symptoms related to SLE would initially present around the time of diagnosis or disease onset, the findings from patients and interviews with psychiatrists did not align with this theory. The first presentation of each neuropsychiatric symptom only occurred around the onset of other SLE symptoms, about one fifth to one third of the time. In fact, more than half of the patients with SLE who had experienced hallucinations or delusions/paranoia said they occurred more than a year after they first experienced their other SLE symptoms.

Patient experiences differed in terms of whether they believed their neuropsychiatric symptoms were directly related to their SLE or other rheumatic disease. Some did attribute the symptoms, such as hypomania, to their rheumatic illness, while others, such as a patient with major depression, did not see the two as linked.

A second theme focused on pattern recognition of neuropsychiatric symptoms and the onset of a disease flare. “For example, several patients described how they felt that some types of depressive symptoms were directly attributable to active inflammation due to its time of onset and differences in type and intensity compared to their more ‘reactive’ low mood that could be more attributable to a consequence of psychological distress,” the authors wrote. Another common report from patients was experiencing a sudden, intense fatigue that coincided with a flare and differed from other types of fatigue.

Some patients could recognize that a flare was coming because of familiar neuropsychiatric symptoms that acted like an “early warning system.” Often, however, these symptoms “were absent from current diagnostic guidelines and only rarely identified by clinician interviewees as related to SLE/NPSLE,” the authors found. “These neuropsychiatric prodromal symptoms were reported as sometimes preceding the more widely recognized SLE and other SARD symptoms such as joint pain, rashes, and other organ involvement.” These symptoms included sudden changes in mood (usually a lowering but sometimes mania), increased nightmares, a “feeling of unreality,” or increased sensory symptoms.

Other patients, on the other hand, had not considered a link between neuropsychiatric symptoms and their rheumatic disease until the interview, and many of the clinicians, aside from psychiatrists and nurses, said they had little time in clinic to gather information about symptom progression.
 

Nightmares and Daymares

A third theme centered on disrupted dreaming sleep, nightmares, and “daymares” as a prodromal symptom in particular. Some patients had already drawn a connection between an oncoming flare of their disease and these dreaming-related symptoms, while others had not considered a link until the interviews.

“Several SLE patients recounted flares consistently involving the segueing of increasingly vivid and distressing nightmares into distorted reality and daytime hallucinations,” the authors reported. Flare-related nightmares in particular “often involved being attacked, trapped, crushed, or falling.” Patients tended to be more forthcoming about hallucinatory experiences when the term “daymare” was used to describe them, and they often related to the idea of feeling “in-between asleep and awake.”

Only one of the rheumatologists interviewed had considered nightmares as potentially related to SLE flares, and several appeared skeptical about a link but planned to ask their patients about it. Most of the specialists interviewed, meanwhile, said they often discussed sleep disruption with patients.

“There was agreement that recognizing and eliciting these early flare symptoms may improve care and even reduce clinic times by averting flares at any earlier stage, although some rheumatologists were clear that limited appointment times meant that these symptoms would not be prioritized for discussion,” the authors wrote.

Though Dr. Kim acknowledged the possibility of nightmares as prodromal, he noted other ways in which nightmares may be indirectly linked to lupus. “Trauma is a major risk factor for lupus,” Dr. Kim said, with multiple studies showing childhood traumatic experiences and even posttraumatic stress disorder to be risk factors for lupus. “Whether nightmares represent a traumatic event or prior traumatic events is not clear to me, but one could hypothesize that this may be a manifestation of trauma,” Dr. Kim said.

In addition, nightmares represent a sleep disorder that can substantially reduce sleep quality, Dr. Kim said, and poor sleep is also associated with lupus. “One has to wonder whether disruptive dreaming sleep is one of several specific manifestations of poor sleep quality, which then increases the risk of lupus in those patients,” Dr. Kim said.
 

Misattribution of Neuropsychiatric Symptoms

The final theme to emerge from the findings was patients had been misdiagnosed with psychiatric or psychosomatic conditions shortly before getting their rheumatic disease diagnosis. One patient, for example, reported being diagnosed with borderline personality disorder just 6 months before the lupus diagnosis at age 19 and noticed that the symptoms of one “got under control” when the symptoms of the other did.

“Early misattributions of SARD symptoms to primary psychiatric or psychosomatic conditions were frequently reported to have delayed SARD diagnosis and led to future misattributions,” the authors reported. “Whilst some of these misdiagnoses likely reflect the widespread lack of knowledge and limited definitive tests for SLE, it is plausible that some early SLE neurological and/or psychiatric symptoms may represent a neuropsychiatric prodrome for SLE itself.”

Dr. Kim agreed that misattribution of symptoms to other diagnoses is common with lupus and a common reason for delays in diagnosis, even with symptoms that are not neuropsychiatric. The findings in this study broaden “the type of symptoms we need to put on our radar pre-diagnosis,” Dr. Kim said. “We just also have to be aware that these prodromal symptoms are not diagnostic for lupus, though.”

Dr. Sloan cited earlier work in recommending an “ABC” approach to improving clinician-patient relationships: “Availability is being accessible when patients need them, Belief is demonstrating belief and validating patient self-reports of symptoms, and Continuity is when the same clinician sees the same patient each clinic visit to build up a trusting relationship.” She noted the importance of asking about and normalizing the existence of these symptoms with rheumatic diseases.

The research was funded by The Lupus Trust. Three authors reported consultancy, speaker, or advisory fees from Alumis, Amgen, AstraZeneca, Eli Lilly, GlaxoSmithKline, Janssen, MGP, Novartis, Pfizer, Sanofi, UCB, Vifor, and/or Werfen Group. The other authors, including Dr. Sloan, had no industry-related disclosures. Dr. Kim reported research support from AstraZeneca, GlaxoSmithKline, and Novartis; speaking fees from Exagen Diagnostics and GlaxoSmithKline; and consulting fees from AbbVie, Amgen, ANI Pharmaceuticals, AstraZeneca, Atara Bio, Aurinia Pharmaceuticals, Cargo Therapeutics, Exagen Diagnostics, Hinge Bio, GlaxoSmithKline, Kypha, Miltenyi Biotec, Synthekine, and Tectonic Therapeutic.
 

A version of this article appeared on Medscape.com.

Neuropsychiatric symptoms, including nightmares and hallucinatory “daymares,” may be a more important aspect of systemic lupus erythematosus (SLE) than formerly recognized, according to a qualitative mixed methods study published in The Lancet Discovery Science’s eClinicalMedicine. The findings suggested these neuropsychiatric symptoms can sometimes present as prodromal and other times act as an early warning system for a forthcoming flare.

“For clinicians, the key point is to be aware that neurological and psychiatric symptoms are much more common in patients with lupus and other autoimmune systemic rheumatic diseases than previously thought,” lead author Melanie Sloan, PhD, of the Department of Public Health and Primary Care at the University of Cambridge in England, told this news organization.

“If clinicians — and some do already — could all ask about and document these symptoms for each patient, the usual progression of symptoms in a flare can then be monitored, and patients could be supported and treated at an earlier stage,” Dr. Sloan said. “Another key point is to consider systemic autoimmune diseases at an early stage if a patient presents with multiple seemingly unconnected symptoms, which often include both physical and mental health symptoms.”

Alfred Kim, MD, PhD, associate professor of medicine in rheumatology at Washington University School of Medicine in St. Louis, Missouri, noted the difficulty of determining what neuropsychiatric symptoms may be linked to lupus vs those occurring independently or as part of a different condition.

Dr. Kim

Study Details

In planning for the study, the researchers first searched the existing literature for studies involving neuropsychiatric symptoms in patients with systemic autoimmune rheumatic diseases (SARDs). “The literature indicated frequent underreporting and misattributions of neuropsychiatric symptoms in SLE and other SARD patients, and clinician-patient discordance in neuropsychiatric symptom attribution,” the authors reported.

During 2022-2023, the researchers conducted two surveys, one with 676 adult patients with SLE and one with 400 clinicians, recruited through social media, online patient support groups, and professional networks. All patients self-reported an SLE diagnosis that the researchers did not independently confirm. The patients were predominantly White (80%) and female (94%), ranging in age from 18 to over 70, with most falling between ages 40 and 69. Most patients lived in the United Kingdom (76%) or Europe (15%).

The clinicians included 51% rheumatologists, 24% psychiatrists, 13% neurologists, 5% rheumatology nurses, 3% primary care physicians, and 7% other clinicians. Nearly half of the clinicians (45%) were from the United Kingdom, with others from the United States or Canada (16%), Europe (17%), Asia (9%), Latin America (8%), Australia or New Zealand (3%), or elsewhere (3%).

The patient surveys asked whether they had experienced any of the 29 neuropsychiatric symptoms. For the symptoms that patients had experienced at least three times in their lives, the survey asked when they first experienced the symptom in relation to their SLE onset or other SLE symptoms: Over a year before, within a year of (on either side), 1-4 years after, or more than 5 years after onset/other symptoms. “Other quantitative data included timings of disrupted dreaming sleep in relation to hallucinations for those patients reporting experiencing these,” the authors wrote.

The researchers also conducted video conference interviews with 50 clinicians, including 20 rheumatologists, and 69 interviews with patients who had a systemic autoimmune rheumatic disease, including 27 patients with SLE. Other conditions among those interviewed included inflammatory arthritis, vasculitis, Sjögren disease, systemic sclerosis, myositis, undifferentiated and mixed connective tissue diseases, and polymyalgia rheumatica. During interviews, the term “daymare” was used to discuss possible hallucinations.
 

Linking Neuropsychiatric Symptoms and Disease

Four themes emerged from the analysis of the surveys and interviews. First, despite many rheumatologists stating that it was an “established theory” that most neuropsychiatric symptoms related to SLE would initially present around the time of diagnosis or disease onset, the findings from patients and interviews with psychiatrists did not align with this theory. The first presentation of each neuropsychiatric symptom only occurred around the onset of other SLE symptoms, about one fifth to one third of the time. In fact, more than half of the patients with SLE who had experienced hallucinations or delusions/paranoia said they occurred more than a year after they first experienced their other SLE symptoms.

Patient experiences differed in terms of whether they believed their neuropsychiatric symptoms were directly related to their SLE or other rheumatic disease. Some did attribute the symptoms, such as hypomania, to their rheumatic illness, while others, such as a patient with major depression, did not see the two as linked.

A second theme focused on pattern recognition of neuropsychiatric symptoms and the onset of a disease flare. “For example, several patients described how they felt that some types of depressive symptoms were directly attributable to active inflammation due to its time of onset and differences in type and intensity compared to their more ‘reactive’ low mood that could be more attributable to a consequence of psychological distress,” the authors wrote. Another common report from patients was experiencing a sudden, intense fatigue that coincided with a flare and differed from other types of fatigue.

Some patients could recognize that a flare was coming because of familiar neuropsychiatric symptoms that acted like an “early warning system.” Often, however, these symptoms “were absent from current diagnostic guidelines and only rarely identified by clinician interviewees as related to SLE/NPSLE,” the authors found. “These neuropsychiatric prodromal symptoms were reported as sometimes preceding the more widely recognized SLE and other SARD symptoms such as joint pain, rashes, and other organ involvement.” These symptoms included sudden changes in mood (usually a lowering but sometimes mania), increased nightmares, a “feeling of unreality,” or increased sensory symptoms.

Other patients, on the other hand, had not considered a link between neuropsychiatric symptoms and their rheumatic disease until the interview, and many of the clinicians, aside from psychiatrists and nurses, said they had little time in clinic to gather information about symptom progression.
 

Nightmares and Daymares

A third theme centered on disrupted dreaming sleep, nightmares, and “daymares” as a prodromal symptom in particular. Some patients had already drawn a connection between an oncoming flare of their disease and these dreaming-related symptoms, while others had not considered a link until the interviews.

“Several SLE patients recounted flares consistently involving the segueing of increasingly vivid and distressing nightmares into distorted reality and daytime hallucinations,” the authors reported. Flare-related nightmares in particular “often involved being attacked, trapped, crushed, or falling.” Patients tended to be more forthcoming about hallucinatory experiences when the term “daymare” was used to describe them, and they often related to the idea of feeling “in-between asleep and awake.”

Only one of the rheumatologists interviewed had considered nightmares as potentially related to SLE flares, and several appeared skeptical about a link but planned to ask their patients about it. Most of the specialists interviewed, meanwhile, said they often discussed sleep disruption with patients.

“There was agreement that recognizing and eliciting these early flare symptoms may improve care and even reduce clinic times by averting flares at any earlier stage, although some rheumatologists were clear that limited appointment times meant that these symptoms would not be prioritized for discussion,” the authors wrote.

Though Dr. Kim acknowledged the possibility of nightmares as prodromal, he noted other ways in which nightmares may be indirectly linked to lupus. “Trauma is a major risk factor for lupus,” Dr. Kim said, with multiple studies showing childhood traumatic experiences and even posttraumatic stress disorder to be risk factors for lupus. “Whether nightmares represent a traumatic event or prior traumatic events is not clear to me, but one could hypothesize that this may be a manifestation of trauma,” Dr. Kim said.

In addition, nightmares represent a sleep disorder that can substantially reduce sleep quality, Dr. Kim said, and poor sleep is also associated with lupus. “One has to wonder whether disruptive dreaming sleep is one of several specific manifestations of poor sleep quality, which then increases the risk of lupus in those patients,” Dr. Kim said.
 

Misattribution of Neuropsychiatric Symptoms

The final theme to emerge from the findings was patients had been misdiagnosed with psychiatric or psychosomatic conditions shortly before getting their rheumatic disease diagnosis. One patient, for example, reported being diagnosed with borderline personality disorder just 6 months before the lupus diagnosis at age 19 and noticed that the symptoms of one “got under control” when the symptoms of the other did.

“Early misattributions of SARD symptoms to primary psychiatric or psychosomatic conditions were frequently reported to have delayed SARD diagnosis and led to future misattributions,” the authors reported. “Whilst some of these misdiagnoses likely reflect the widespread lack of knowledge and limited definitive tests for SLE, it is plausible that some early SLE neurological and/or psychiatric symptoms may represent a neuropsychiatric prodrome for SLE itself.”

Dr. Kim agreed that misattribution of symptoms to other diagnoses is common with lupus and a common reason for delays in diagnosis, even with symptoms that are not neuropsychiatric. The findings in this study broaden “the type of symptoms we need to put on our radar pre-diagnosis,” Dr. Kim said. “We just also have to be aware that these prodromal symptoms are not diagnostic for lupus, though.”

Dr. Sloan cited earlier work in recommending an “ABC” approach to improving clinician-patient relationships: “Availability is being accessible when patients need them, Belief is demonstrating belief and validating patient self-reports of symptoms, and Continuity is when the same clinician sees the same patient each clinic visit to build up a trusting relationship.” She noted the importance of asking about and normalizing the existence of these symptoms with rheumatic diseases.

The research was funded by The Lupus Trust. Three authors reported consultancy, speaker, or advisory fees from Alumis, Amgen, AstraZeneca, Eli Lilly, GlaxoSmithKline, Janssen, MGP, Novartis, Pfizer, Sanofi, UCB, Vifor, and/or Werfen Group. The other authors, including Dr. Sloan, had no industry-related disclosures. Dr. Kim reported research support from AstraZeneca, GlaxoSmithKline, and Novartis; speaking fees from Exagen Diagnostics and GlaxoSmithKline; and consulting fees from AbbVie, Amgen, ANI Pharmaceuticals, AstraZeneca, Atara Bio, Aurinia Pharmaceuticals, Cargo Therapeutics, Exagen Diagnostics, Hinge Bio, GlaxoSmithKline, Kypha, Miltenyi Biotec, Synthekine, and Tectonic Therapeutic.
 

A version of this article appeared on Medscape.com.

Welcome everyone. I’m Dr. John White. I’m the chief medical officer at WebMD. Does your biologic sex impact your health? Does it have any play in how you’re diagnosed, how you’re treated in terms of what symptoms you have? Of course it does. We all know that. But that’s not something that many people believed 5, 10 years ago, certainly not 20 years ago. And it was only because of leaders like my guest today, Phyllis Greenberger, who really championed the need for research on women’s health. She has a new book out, which I love. It’s called Sex Cells: the Fight to Overcome Bias and Discrimination in Women’s Healthcare. Please welcome my very good friend, Phyllis Greenberger.

Thank you.

Phyllis, It’s great to see you today.

It’s great to see you as well.

Now, you and I have been talking about this for easily 2 decades.

At least.

And some people think, oh, of course it makes sense. Although I saw you disagreeing that not everyone still believes that. But what has been that journey? Why has it been so hard to make people understand, as you point out early on in your book, women are not smaller men?

I think the basic reason was that it was just believed that men and women were the same except for their reproductive organs. So minus the reproductive organs, whether it was a device, a diagnostic, or therapeutic, if it was used and successful on a male, that it would be successful on a female. We’re really very far from understanding the differences, and there’s still a lot of distrust and disbelief and ignorance about it. And so there’s still a long way to go.

But you talk about that in the book, that there’s still a long way to go. Why is that? What’s the biggest obstacle? Is it just misinformation, lack of information? People don’t understand the science? There’s still resistance in some areas. Why is that?

I think it’s misinformation, and I gave a presentation, I don’t know how many years ago, at least 20 years ago, about the curriculum. And at the time, there was no women’s health in the curriculum. It was health. So if it was on cardiovascular issues or on osteoporosis, it was sort of the basic. And at the time, there would maybe be one woman whose job was women’s health, and she’d have an office, and otherwise there was nothing. And maybe they talked about breast cancer, who knows. But I spoke to someone just the other day, in view of all the attention that the book is getting now, whether that’s changed, whether it’s necessary and required. And she said it’s not. So, it’s not necessarily on the curriculum of all research and medical institutions, and even if women’s health, quote unquote, is on the curriculum, it doesn’t mean that they’re really looking at sex differences. And the difference is obvious. I mean, gender is really, it’s a social construct, but biological sex is how disease occurs and develops. And so if you’re not looking, and because there’s so little research now on sex differences that I don’t even know, I mean, how much you could actually teach.

So what needs to change? This book is a manifesto in many ways in how we need to include women; we need to make research more inclusive of everyone. But we’re not there yet. So what needs to change, Phyllis?

During this whole saga of trying to get people to listen to me and to the society, we really started out just looking at clinical trials and that, as you mentioned, I mean, there are issues in rural communities. There’s travel issues for women and child care. There’s a lot of disbelief or fear of clinical trials in some ethnicities. I do think, going to the future, that technology can help that. I mean, if people have broadband, which of course is also an issue in rural areas.

What could women do today? What should women listeners hear and then be doing? Should they be saying something to their doctor? Should they be asking specific questions? When they interact with the health care system, how can they make sure they’re getting the best care that’s appropriate for them when we know that sex cells matter?

Well, that’s a good question. It depends on, frankly, if your doctor is aware of this, if he or she has learned anything about this in school, which, I had already said, we’re not sure about that because research is still ongoing and there’s so much we don’t know. So I mean, you used to think, or I used to think, that you go to, you want a physician who’s older and more experienced. But now I think you should be going to a physician who’s younger and hopefully has learned about this, because the physicians that were educated years ago and have been practicing for 20, 30 years, I don’t know how much they know about this, whether they’re even aware of it.

Phyllis, you are a woman of action. You’ve lived in the DC area. You have championed legislative reforms, executive agendas. What do you want done now? What needs to be changed today? The curriculum is going to take time, but what else needs to change?

That’s a good question. I mean, if curriculum is going to take a while and you can ask your doctor if he prescribes the medication, whether it’s been tested on women, but then if it hasn’t been tested on women, but it’s the only thing that there is for your condition, I mean, so it’s very difficult. The Biden administration, as you know, just allocated a hundred million dollars for women’s health research.

What do you hope to accomplish with this book?

Well, what I’m hoping is that I spoke to someone at AMWA and I’m hoping — and AMWA is an association for women medical students. And I’m hoping that’s the audience. The audience needs to be. I mean, obviously everybody that I know that’s not a doctor that’s read it, found it fascinating and didn’t know a lot of the stuff that was in it. So I think it’s an interesting book anyway, and I think women should be aware of it. But really I think it needs to be for medical students.

And to your credit, you built the Society for Women’s Health Research into a powerful force in Washington under your tenure in really promoting the need for Office of Women’s Health and Research in general. The book is entitled Sex Cells, the Fight to Overcome Bias and Discrimination in Women’s Healthcare. Phyllis Greenberger, thank you so much for all that you’ve done for women’s health, for women’s research. We wouldn’t be where we are today if it wasn’t for you. So thanks.

Thank you very much, John. Thank you. I appreciate the opportunity.

Dr. Whyte, is chief medical officer, WebMD, New York, NY. He has disclosed no relevant financial relationships. Ms. Greenberger is a women’s health advocate and author of “Sex Cells: The Fight to Overcome Bias and Discrimination in Women’s Healthcare”

This interview originally appeared on WebMD on May 23, 2024. A version of this article appeared on Medscape.com .

Welcome everyone. I’m Dr. John White. I’m the chief medical officer at WebMD. Does your biologic sex impact your health? Does it have any play in how you’re diagnosed, how you’re treated in terms of what symptoms you have? Of course it does. We all know that. But that’s not something that many people believed 5, 10 years ago, certainly not 20 years ago. And it was only because of leaders like my guest today, Phyllis Greenberger, who really championed the need for research on women’s health. She has a new book out, which I love. It’s called Sex Cells: the Fight to Overcome Bias and Discrimination in Women’s Healthcare. Please welcome my very good friend, Phyllis Greenberger.

Thank you.

Phyllis, It’s great to see you today.

It’s great to see you as well.

Now, you and I have been talking about this for easily 2 decades.

At least.

And some people think, oh, of course it makes sense. Although I saw you disagreeing that not everyone still believes that. But what has been that journey? Why has it been so hard to make people understand, as you point out early on in your book, women are not smaller men?

I think the basic reason was that it was just believed that men and women were the same except for their reproductive organs. So minus the reproductive organs, whether it was a device, a diagnostic, or therapeutic, if it was used and successful on a male, that it would be successful on a female. We’re really very far from understanding the differences, and there’s still a lot of distrust and disbelief and ignorance about it. And so there’s still a long way to go.

But you talk about that in the book, that there’s still a long way to go. Why is that? What’s the biggest obstacle? Is it just misinformation, lack of information? People don’t understand the science? There’s still resistance in some areas. Why is that?

I think it’s misinformation, and I gave a presentation, I don’t know how many years ago, at least 20 years ago, about the curriculum. And at the time, there was no women’s health in the curriculum. It was health. So if it was on cardiovascular issues or on osteoporosis, it was sort of the basic. And at the time, there would maybe be one woman whose job was women’s health, and she’d have an office, and otherwise there was nothing. And maybe they talked about breast cancer, who knows. But I spoke to someone just the other day, in view of all the attention that the book is getting now, whether that’s changed, whether it’s necessary and required. And she said it’s not. So, it’s not necessarily on the curriculum of all research and medical institutions, and even if women’s health, quote unquote, is on the curriculum, it doesn’t mean that they’re really looking at sex differences. And the difference is obvious. I mean, gender is really, it’s a social construct, but biological sex is how disease occurs and develops. And so if you’re not looking, and because there’s so little research now on sex differences that I don’t even know, I mean, how much you could actually teach.

So what needs to change? This book is a manifesto in many ways in how we need to include women; we need to make research more inclusive of everyone. But we’re not there yet. So what needs to change, Phyllis?

During this whole saga of trying to get people to listen to me and to the society, we really started out just looking at clinical trials and that, as you mentioned, I mean, there are issues in rural communities. There’s travel issues for women and child care. There’s a lot of disbelief or fear of clinical trials in some ethnicities. I do think, going to the future, that technology can help that. I mean, if people have broadband, which of course is also an issue in rural areas.

What could women do today? What should women listeners hear and then be doing? Should they be saying something to their doctor? Should they be asking specific questions? When they interact with the health care system, how can they make sure they’re getting the best care that’s appropriate for them when we know that sex cells matter?

Well, that’s a good question. It depends on, frankly, if your doctor is aware of this, if he or she has learned anything about this in school, which, I had already said, we’re not sure about that because research is still ongoing and there’s so much we don’t know. So I mean, you used to think, or I used to think, that you go to, you want a physician who’s older and more experienced. But now I think you should be going to a physician who’s younger and hopefully has learned about this, because the physicians that were educated years ago and have been practicing for 20, 30 years, I don’t know how much they know about this, whether they’re even aware of it.

Phyllis, you are a woman of action. You’ve lived in the DC area. You have championed legislative reforms, executive agendas. What do you want done now? What needs to be changed today? The curriculum is going to take time, but what else needs to change?

That’s a good question. I mean, if curriculum is going to take a while and you can ask your doctor if he prescribes the medication, whether it’s been tested on women, but then if it hasn’t been tested on women, but it’s the only thing that there is for your condition, I mean, so it’s very difficult. The Biden administration, as you know, just allocated a hundred million dollars for women’s health research.

What do you hope to accomplish with this book?

Well, what I’m hoping is that I spoke to someone at AMWA and I’m hoping — and AMWA is an association for women medical students. And I’m hoping that’s the audience. The audience needs to be. I mean, obviously everybody that I know that’s not a doctor that’s read it, found it fascinating and didn’t know a lot of the stuff that was in it. So I think it’s an interesting book anyway, and I think women should be aware of it. But really I think it needs to be for medical students.

And to your credit, you built the Society for Women’s Health Research into a powerful force in Washington under your tenure in really promoting the need for Office of Women’s Health and Research in general. The book is entitled Sex Cells, the Fight to Overcome Bias and Discrimination in Women’s Healthcare. Phyllis Greenberger, thank you so much for all that you’ve done for women’s health, for women’s research. We wouldn’t be where we are today if it wasn’t for you. So thanks.

Thank you very much, John. Thank you. I appreciate the opportunity.

Dr. Whyte, is chief medical officer, WebMD, New York, NY. He has disclosed no relevant financial relationships. Ms. Greenberger is a women’s health advocate and author of “Sex Cells: The Fight to Overcome Bias and Discrimination in Women’s Healthcare”

This interview originally appeared on WebMD on May 23, 2024. A version of this article appeared on Medscape.com .

Welcome everyone. I’m Dr. John White. I’m the chief medical officer at WebMD. Does your biologic sex impact your health? Does it have any play in how you’re diagnosed, how you’re treated in terms of what symptoms you have? Of course it does. We all know that. But that’s not something that many people believed 5, 10 years ago, certainly not 20 years ago. And it was only because of leaders like my guest today, Phyllis Greenberger, who really championed the need for research on women’s health. She has a new book out, which I love. It’s called Sex Cells: the Fight to Overcome Bias and Discrimination in Women’s Healthcare. Please welcome my very good friend, Phyllis Greenberger.

Thank you.

Phyllis, It’s great to see you today.

It’s great to see you as well.

Now, you and I have been talking about this for easily 2 decades.

At least.

And some people think, oh, of course it makes sense. Although I saw you disagreeing that not everyone still believes that. But what has been that journey? Why has it been so hard to make people understand, as you point out early on in your book, women are not smaller men?

I think the basic reason was that it was just believed that men and women were the same except for their reproductive organs. So minus the reproductive organs, whether it was a device, a diagnostic, or therapeutic, if it was used and successful on a male, that it would be successful on a female. We’re really very far from understanding the differences, and there’s still a lot of distrust and disbelief and ignorance about it. And so there’s still a long way to go.

But you talk about that in the book, that there’s still a long way to go. Why is that? What’s the biggest obstacle? Is it just misinformation, lack of information? People don’t understand the science? There’s still resistance in some areas. Why is that?

I think it’s misinformation, and I gave a presentation, I don’t know how many years ago, at least 20 years ago, about the curriculum. And at the time, there was no women’s health in the curriculum. It was health. So if it was on cardiovascular issues or on osteoporosis, it was sort of the basic. And at the time, there would maybe be one woman whose job was women’s health, and she’d have an office, and otherwise there was nothing. And maybe they talked about breast cancer, who knows. But I spoke to someone just the other day, in view of all the attention that the book is getting now, whether that’s changed, whether it’s necessary and required. And she said it’s not. So, it’s not necessarily on the curriculum of all research and medical institutions, and even if women’s health, quote unquote, is on the curriculum, it doesn’t mean that they’re really looking at sex differences. And the difference is obvious. I mean, gender is really, it’s a social construct, but biological sex is how disease occurs and develops. And so if you’re not looking, and because there’s so little research now on sex differences that I don’t even know, I mean, how much you could actually teach.

So what needs to change? This book is a manifesto in many ways in how we need to include women; we need to make research more inclusive of everyone. But we’re not there yet. So what needs to change, Phyllis?

During this whole saga of trying to get people to listen to me and to the society, we really started out just looking at clinical trials and that, as you mentioned, I mean, there are issues in rural communities. There’s travel issues for women and child care. There’s a lot of disbelief or fear of clinical trials in some ethnicities. I do think, going to the future, that technology can help that. I mean, if people have broadband, which of course is also an issue in rural areas.

What could women do today? What should women listeners hear and then be doing? Should they be saying something to their doctor? Should they be asking specific questions? When they interact with the health care system, how can they make sure they’re getting the best care that’s appropriate for them when we know that sex cells matter?

Well, that’s a good question. It depends on, frankly, if your doctor is aware of this, if he or she has learned anything about this in school, which, I had already said, we’re not sure about that because research is still ongoing and there’s so much we don’t know. So I mean, you used to think, or I used to think, that you go to, you want a physician who’s older and more experienced. But now I think you should be going to a physician who’s younger and hopefully has learned about this, because the physicians that were educated years ago and have been practicing for 20, 30 years, I don’t know how much they know about this, whether they’re even aware of it.

Phyllis, you are a woman of action. You’ve lived in the DC area. You have championed legislative reforms, executive agendas. What do you want done now? What needs to be changed today? The curriculum is going to take time, but what else needs to change?

That’s a good question. I mean, if curriculum is going to take a while and you can ask your doctor if he prescribes the medication, whether it’s been tested on women, but then if it hasn’t been tested on women, but it’s the only thing that there is for your condition, I mean, so it’s very difficult. The Biden administration, as you know, just allocated a hundred million dollars for women’s health research.

What do you hope to accomplish with this book?

Well, what I’m hoping is that I spoke to someone at AMWA and I’m hoping — and AMWA is an association for women medical students. And I’m hoping that’s the audience. The audience needs to be. I mean, obviously everybody that I know that’s not a doctor that’s read it, found it fascinating and didn’t know a lot of the stuff that was in it. So I think it’s an interesting book anyway, and I think women should be aware of it. But really I think it needs to be for medical students.

And to your credit, you built the Society for Women’s Health Research into a powerful force in Washington under your tenure in really promoting the need for Office of Women’s Health and Research in general. The book is entitled Sex Cells, the Fight to Overcome Bias and Discrimination in Women’s Healthcare. Phyllis Greenberger, thank you so much for all that you’ve done for women’s health, for women’s research. We wouldn’t be where we are today if it wasn’t for you. So thanks.

Thank you very much, John. Thank you. I appreciate the opportunity.

Dr. Whyte, is chief medical officer, WebMD, New York, NY. He has disclosed no relevant financial relationships. Ms. Greenberger is a women’s health advocate and author of “Sex Cells: The Fight to Overcome Bias and Discrimination in Women’s Healthcare”

This interview originally appeared on WebMD on May 23, 2024. A version of this article appeared on Medscape.com .

Each month I set out on an expedition to find a topic for this column. I came across a new book Rebel Health by Susannah Fox that I thought might be a good one. It’s both a treatise on the shortcomings of healthcare and a Baedeker for patients on how to find their way to being better served. Her argument is that many patients’ needs are unmet and their conditions are often invisible to us in mainstream healthcare. We fail to find solutions to help them. Patients would benefit from more open access to their records and more resources to take control of their own health, she argues. A few chapters in, I thought, “Oh, here we go, another diatribe on doctors and how we care most about how to keep patients in their rightful, subordinate place.” The “Rebel” title is provocative and implies patients need to overthrow the status quo. Well, I am part of the establishment. I stopped reading. This book doesn’t apply to me, I thought.

After all, I’m a healthcare progressive, right? My notes and results have been open for years. I encourage shared decision-making and try to empower patients as much as treat them. The idea that I or my colleagues are unwilling to do whatever is necessary to meet our patients’ needs was maddening. We dedicate our lives to it. My young daughter often greets me in the morning by asking if I’ll be working tonight. Most nights, I am — answering patient messages, collaborating with colleagues to help patients, keeping up with medical knowledge. I was angry at what felt like unjust criticism, especially that we’d neglect patients because their problems are not obvious or worse, there is not enough money to be made helping them. Harrumph.

Kaiser Permanente

That’s when I realized the best thing for me was to read the entire book and digest the arguments. I pride myself on being well-read, but I fall into a common trap: the podcasts I listen to, news I consume, and books I read mostly affirm my beliefs. It is a healthy choice to seek dispositive data and contrasting stories rather than always feeding our personal opinions.

Rebel Health was not written by Robespierre. It was penned by a thoughtful, articulate patient advocate with over 20 years experience. She has far more bona fides than I could achieve in two lifetimes. In the book, she reminds us that scientific advances in the last 100 years have made medicine more effective but also disintermediated caregivers, family, and patients. Patients and caregivers can not only help but also offer innovative and customized solutions to their problems. She describes four patient archetypes: seekers, networkers, solvers, and champions, and offers a four-quadrant model to visualize how some patients are unhelped by our current healthcare system. She advocates for frictionless, open access to health data and tries to inspire patients to connect, innovate, and create to fill the voids that exist in healthcare. We have come a long way from the immured system of a decade ago; much of that is the result of patient advocates. But healthcare is still too costly, too fragmented and too many patients unhelped. “Community is a superpower,” she writes. I agree, we should assemble all the heroes in the universe for this challenge.

Fox also tells stories of patients who solved diagnostic dilemmas through their own research and advocacy. I thought of my own contrasting experiences of patients whose DIY care was based on misinformation and how their false confidence led to poorer outcomes for them. I want to share with her readers how physicians feel hurt when patients question our competence or place the opinion of an adversarial Redditor over ours. Physicians are sometimes wrong and often in doubt. Most of us care deeply about our patients regardless of how visible their diagnosis or how easy they are to appease.

We don’t have time to engage back-and-forth on an insignificantly abnormal test they find in their open chart or why B12 and hormone testing would not be helpful for their disease. It’s also not the patients’ fault. Having unfettered access to their data might add work, but it also adds value. They are trying to learn and be active in their care. Physicians are frustrated mostly because we don’t have time to meet these unmet needs. Everyone is trying their best and we all want the same thing: patients to be satisfied and well.

As for learning the skill of being open-minded, an excellent reference is Adam Grant’s Think Again. It’s inspiring and instructive of how we can all be more open, including how to have productive arguments rather than fruitless fights. We live in divisive times. Perhaps if we all put in effort to be open-minded, push down righteous indignation, and advance more honest humility we’d all be a bit better off.

Patients are the primary audience for the Rebel Health book. Yet, as we care about them and we all want to make healthcare better, it is worth reading in its entirety. I told my daughter I don’t have to work tonight because I’ve written my article this month. When she’s a little older, I’ll tell her all about it. To be successful, she’ll have to be as open-minded as she is smart. She can learn both.

I have no conflict of interest in the book.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Each month I set out on an expedition to find a topic for this column. I came across a new book Rebel Health by Susannah Fox that I thought might be a good one. It’s both a treatise on the shortcomings of healthcare and a Baedeker for patients on how to find their way to being better served. Her argument is that many patients’ needs are unmet and their conditions are often invisible to us in mainstream healthcare. We fail to find solutions to help them. Patients would benefit from more open access to their records and more resources to take control of their own health, she argues. A few chapters in, I thought, “Oh, here we go, another diatribe on doctors and how we care most about how to keep patients in their rightful, subordinate place.” The “Rebel” title is provocative and implies patients need to overthrow the status quo. Well, I am part of the establishment. I stopped reading. This book doesn’t apply to me, I thought.

After all, I’m a healthcare progressive, right? My notes and results have been open for years. I encourage shared decision-making and try to empower patients as much as treat them. The idea that I or my colleagues are unwilling to do whatever is necessary to meet our patients’ needs was maddening. We dedicate our lives to it. My young daughter often greets me in the morning by asking if I’ll be working tonight. Most nights, I am — answering patient messages, collaborating with colleagues to help patients, keeping up with medical knowledge. I was angry at what felt like unjust criticism, especially that we’d neglect patients because their problems are not obvious or worse, there is not enough money to be made helping them. Harrumph.

Kaiser Permanente

That’s when I realized the best thing for me was to read the entire book and digest the arguments. I pride myself on being well-read, but I fall into a common trap: the podcasts I listen to, news I consume, and books I read mostly affirm my beliefs. It is a healthy choice to seek dispositive data and contrasting stories rather than always feeding our personal opinions.

Rebel Health was not written by Robespierre. It was penned by a thoughtful, articulate patient advocate with over 20 years experience. She has far more bona fides than I could achieve in two lifetimes. In the book, she reminds us that scientific advances in the last 100 years have made medicine more effective but also disintermediated caregivers, family, and patients. Patients and caregivers can not only help but also offer innovative and customized solutions to their problems. She describes four patient archetypes: seekers, networkers, solvers, and champions, and offers a four-quadrant model to visualize how some patients are unhelped by our current healthcare system. She advocates for frictionless, open access to health data and tries to inspire patients to connect, innovate, and create to fill the voids that exist in healthcare. We have come a long way from the immured system of a decade ago; much of that is the result of patient advocates. But healthcare is still too costly, too fragmented and too many patients unhelped. “Community is a superpower,” she writes. I agree, we should assemble all the heroes in the universe for this challenge.

Fox also tells stories of patients who solved diagnostic dilemmas through their own research and advocacy. I thought of my own contrasting experiences of patients whose DIY care was based on misinformation and how their false confidence led to poorer outcomes for them. I want to share with her readers how physicians feel hurt when patients question our competence or place the opinion of an adversarial Redditor over ours. Physicians are sometimes wrong and often in doubt. Most of us care deeply about our patients regardless of how visible their diagnosis or how easy they are to appease.

We don’t have time to engage back-and-forth on an insignificantly abnormal test they find in their open chart or why B12 and hormone testing would not be helpful for their disease. It’s also not the patients’ fault. Having unfettered access to their data might add work, but it also adds value. They are trying to learn and be active in their care. Physicians are frustrated mostly because we don’t have time to meet these unmet needs. Everyone is trying their best and we all want the same thing: patients to be satisfied and well.

As for learning the skill of being open-minded, an excellent reference is Adam Grant’s Think Again. It’s inspiring and instructive of how we can all be more open, including how to have productive arguments rather than fruitless fights. We live in divisive times. Perhaps if we all put in effort to be open-minded, push down righteous indignation, and advance more honest humility we’d all be a bit better off.

Patients are the primary audience for the Rebel Health book. Yet, as we care about them and we all want to make healthcare better, it is worth reading in its entirety. I told my daughter I don’t have to work tonight because I’ve written my article this month. When she’s a little older, I’ll tell her all about it. To be successful, she’ll have to be as open-minded as she is smart. She can learn both.

I have no conflict of interest in the book.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

Each month I set out on an expedition to find a topic for this column. I came across a new book Rebel Health by Susannah Fox that I thought might be a good one. It’s both a treatise on the shortcomings of healthcare and a Baedeker for patients on how to find their way to being better served. Her argument is that many patients’ needs are unmet and their conditions are often invisible to us in mainstream healthcare. We fail to find solutions to help them. Patients would benefit from more open access to their records and more resources to take control of their own health, she argues. A few chapters in, I thought, “Oh, here we go, another diatribe on doctors and how we care most about how to keep patients in their rightful, subordinate place.” The “Rebel” title is provocative and implies patients need to overthrow the status quo. Well, I am part of the establishment. I stopped reading. This book doesn’t apply to me, I thought.

After all, I’m a healthcare progressive, right? My notes and results have been open for years. I encourage shared decision-making and try to empower patients as much as treat them. The idea that I or my colleagues are unwilling to do whatever is necessary to meet our patients’ needs was maddening. We dedicate our lives to it. My young daughter often greets me in the morning by asking if I’ll be working tonight. Most nights, I am — answering patient messages, collaborating with colleagues to help patients, keeping up with medical knowledge. I was angry at what felt like unjust criticism, especially that we’d neglect patients because their problems are not obvious or worse, there is not enough money to be made helping them. Harrumph.

Kaiser Permanente

That’s when I realized the best thing for me was to read the entire book and digest the arguments. I pride myself on being well-read, but I fall into a common trap: the podcasts I listen to, news I consume, and books I read mostly affirm my beliefs. It is a healthy choice to seek dispositive data and contrasting stories rather than always feeding our personal opinions.

Rebel Health was not written by Robespierre. It was penned by a thoughtful, articulate patient advocate with over 20 years experience. She has far more bona fides than I could achieve in two lifetimes. In the book, she reminds us that scientific advances in the last 100 years have made medicine more effective but also disintermediated caregivers, family, and patients. Patients and caregivers can not only help but also offer innovative and customized solutions to their problems. She describes four patient archetypes: seekers, networkers, solvers, and champions, and offers a four-quadrant model to visualize how some patients are unhelped by our current healthcare system. She advocates for frictionless, open access to health data and tries to inspire patients to connect, innovate, and create to fill the voids that exist in healthcare. We have come a long way from the immured system of a decade ago; much of that is the result of patient advocates. But healthcare is still too costly, too fragmented and too many patients unhelped. “Community is a superpower,” she writes. I agree, we should assemble all the heroes in the universe for this challenge.

Fox also tells stories of patients who solved diagnostic dilemmas through their own research and advocacy. I thought of my own contrasting experiences of patients whose DIY care was based on misinformation and how their false confidence led to poorer outcomes for them. I want to share with her readers how physicians feel hurt when patients question our competence or place the opinion of an adversarial Redditor over ours. Physicians are sometimes wrong and often in doubt. Most of us care deeply about our patients regardless of how visible their diagnosis or how easy they are to appease.

We don’t have time to engage back-and-forth on an insignificantly abnormal test they find in their open chart or why B12 and hormone testing would not be helpful for their disease. It’s also not the patients’ fault. Having unfettered access to their data might add work, but it also adds value. They are trying to learn and be active in their care. Physicians are frustrated mostly because we don’t have time to meet these unmet needs. Everyone is trying their best and we all want the same thing: patients to be satisfied and well.

As for learning the skill of being open-minded, an excellent reference is Adam Grant’s Think Again. It’s inspiring and instructive of how we can all be more open, including how to have productive arguments rather than fruitless fights. We live in divisive times. Perhaps if we all put in effort to be open-minded, push down righteous indignation, and advance more honest humility we’d all be a bit better off.

Patients are the primary audience for the Rebel Health book. Yet, as we care about them and we all want to make healthcare better, it is worth reading in its entirety. I told my daughter I don’t have to work tonight because I’ve written my article this month. When she’s a little older, I’ll tell her all about it. To be successful, she’ll have to be as open-minded as she is smart. She can learn both.

I have no conflict of interest in the book.

Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected].

In April, the Federal Trade Commission (FTC), by a vote of 3-2, opened a long-anticipated can of worms by approving its final rule that effectively bans employers’ use of all non-compete agreements (with very limited exceptions). The final rule will not go into effect until 120 days after its publication in the Federal Register, which took place on May 7, and numerous legal challenges appear to be on the horizon.

The principal components of the rule are as follows:

• After the effective date, most non-compete agreements (which prevent departing employees from signing with a new employer for a defined period within a specific geographic area) are banned nationwide.
• The rule exempts certain “senior executives,” ie individuals who earn more than $151,164 annually and serve in policy-making positions.
• There is another major exception for non-competes connected with a sale of a business.
• While not explicitly stated, the rule arguably exempts non-profits, tax-exempt hospitals, and other tax-exempt entities.
• Employers must provide verbal and written notice to employees regarding existing agreements, which would be voided under the rule.

The final rule is the latest skirmish in an ongoing, years-long debate. Twelve states have already put non-compete bans in place, according to a recent paper, and they may serve as a harbinger of things to come should the federal ban go into effect. Each state rule varies in its specifics as states respond to local market conditions. While some states ban all non-compete agreements outright, others limit them based on variables, such as income and employment circumstances. Of course, should the federal ban take effect, it will supersede whatever rules the individual states have in place.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

In April, the Federal Trade Commission (FTC), by a vote of 3-2, opened a long-anticipated can of worms by approving its final rule that effectively bans employers’ use of all non-compete agreements (with very limited exceptions). The final rule will not go into effect until 120 days after its publication in the Federal Register, which took place on May 7, and numerous legal challenges appear to be on the horizon.

The principal components of the rule are as follows:

• After the effective date, most non-compete agreements (which prevent departing employees from signing with a new employer for a defined period within a specific geographic area) are banned nationwide.
• The rule exempts certain “senior executives,” ie individuals who earn more than $151,164 annually and serve in policy-making positions.
• There is another major exception for non-competes connected with a sale of a business.
• While not explicitly stated, the rule arguably exempts non-profits, tax-exempt hospitals, and other tax-exempt entities.
• Employers must provide verbal and written notice to employees regarding existing agreements, which would be voided under the rule.

The final rule is the latest skirmish in an ongoing, years-long debate. Twelve states have already put non-compete bans in place, according to a recent paper, and they may serve as a harbinger of things to come should the federal ban go into effect. Each state rule varies in its specifics as states respond to local market conditions. While some states ban all non-compete agreements outright, others limit them based on variables, such as income and employment circumstances. Of course, should the federal ban take effect, it will supersede whatever rules the individual states have in place.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

In April, the Federal Trade Commission (FTC), by a vote of 3-2, opened a long-anticipated can of worms by approving its final rule that effectively bans employers’ use of all non-compete agreements (with very limited exceptions). The final rule will not go into effect until 120 days after its publication in the Federal Register, which took place on May 7, and numerous legal challenges appear to be on the horizon.

The principal components of the rule are as follows:

• After the effective date, most non-compete agreements (which prevent departing employees from signing with a new employer for a defined period within a specific geographic area) are banned nationwide.
• The rule exempts certain “senior executives,” ie individuals who earn more than $151,164 annually and serve in policy-making positions.
• There is another major exception for non-competes connected with a sale of a business.
• While not explicitly stated, the rule arguably exempts non-profits, tax-exempt hospitals, and other tax-exempt entities.
• Employers must provide verbal and written notice to employees regarding existing agreements, which would be voided under the rule.

The final rule is the latest skirmish in an ongoing, years-long debate. Twelve states have already put non-compete bans in place, according to a recent paper, and they may serve as a harbinger of things to come should the federal ban go into effect. Each state rule varies in its specifics as states respond to local market conditions. While some states ban all non-compete agreements outright, others limit them based on variables, such as income and employment circumstances. Of course, should the federal ban take effect, it will supersede whatever rules the individual states have in place.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].