MDedge Rheumatology

Key clinical point: Guselkumab treatment every 4 or 8 weeks (Q4W/Q8W) showed minimal clinically important improvements (MCII) in Clinical Disease Activity Index for Psoriatic Arthritis (cDAPSA) after the first dose and sustained disease control for up to 1 year in patients with psoriatic arthritis (PsA).

Major finding: Both guselkumab doses (Q4W and Q8W) vs placebo led to early achievement of MCII in cDAPSA (hazard ratio 1.6-1.7; all P < .0001), with higher response rates at week 4 (P < .01). Achieving early MCII in cDAPSA was associated with sustained disease control at 24 and 52 weeks (odds ratio 1.4-3.5; all P < .05).

Study details: This post hoc analysis of phase 3 trials, DISCOVER-1 and DISCOVER-2, included 1120 patients with active PsA who received guselkumab (Q4W or Q8W) or placebo with a crossover to guselkumab Q4W at week 24.

Disclosures: This study was supported by Janssen Research & Development (JRD), LLC. Four authors declared being employees or shareholders of JRD or other sources. Several authors declared having ties with various sources, including JRD.

Source: Curtis JR, Deodhar A, Soriano ER, et al. Early Improvements with guselkumab associate with sustained control of psoriatic arthritis: Post hoc analyses of two phase 3 trials. Rheumatol Ther. 2024 (Sept 11). doi: 10.1007/s40744-024-00702-0 Source

Key clinical point: Guselkumab treatment every 4 or 8 weeks (Q4W/Q8W) showed minimal clinically important improvements (MCII) in Clinical Disease Activity Index for Psoriatic Arthritis (cDAPSA) after the first dose and sustained disease control for up to 1 year in patients with psoriatic arthritis (PsA).

Major finding: Both guselkumab doses (Q4W and Q8W) vs placebo led to early achievement of MCII in cDAPSA (hazard ratio 1.6-1.7; all P < .0001), with higher response rates at week 4 (P < .01). Achieving early MCII in cDAPSA was associated with sustained disease control at 24 and 52 weeks (odds ratio 1.4-3.5; all P < .05).

Study details: This post hoc analysis of phase 3 trials, DISCOVER-1 and DISCOVER-2, included 1120 patients with active PsA who received guselkumab (Q4W or Q8W) or placebo with a crossover to guselkumab Q4W at week 24.

Disclosures: This study was supported by Janssen Research & Development (JRD), LLC. Four authors declared being employees or shareholders of JRD or other sources. Several authors declared having ties with various sources, including JRD.

Source: Curtis JR, Deodhar A, Soriano ER, et al. Early Improvements with guselkumab associate with sustained control of psoriatic arthritis: Post hoc analyses of two phase 3 trials. Rheumatol Ther. 2024 (Sept 11). doi: 10.1007/s40744-024-00702-0 Source

Key clinical point: Guselkumab treatment every 4 or 8 weeks (Q4W/Q8W) showed minimal clinically important improvements (MCII) in Clinical Disease Activity Index for Psoriatic Arthritis (cDAPSA) after the first dose and sustained disease control for up to 1 year in patients with psoriatic arthritis (PsA).

Major finding: Both guselkumab doses (Q4W and Q8W) vs placebo led to early achievement of MCII in cDAPSA (hazard ratio 1.6-1.7; all P < .0001), with higher response rates at week 4 (P < .01). Achieving early MCII in cDAPSA was associated with sustained disease control at 24 and 52 weeks (odds ratio 1.4-3.5; all P < .05).

Study details: This post hoc analysis of phase 3 trials, DISCOVER-1 and DISCOVER-2, included 1120 patients with active PsA who received guselkumab (Q4W or Q8W) or placebo with a crossover to guselkumab Q4W at week 24.

Disclosures: This study was supported by Janssen Research & Development (JRD), LLC. Four authors declared being employees or shareholders of JRD or other sources. Several authors declared having ties with various sources, including JRD.

Source: Curtis JR, Deodhar A, Soriano ER, et al. Early Improvements with guselkumab associate with sustained control of psoriatic arthritis: Post hoc analyses of two phase 3 trials. Rheumatol Ther. 2024 (Sept 11). doi: 10.1007/s40744-024-00702-0 Source

Key clinical point: Treatment with biologics, such as tumor necrosis factor inhibitors (TNFi) and interleukin-17 inhibitors (IL-17i), altered serum levels of matrix metalloproteinase-3 (MMP3), S100 calcium-binding protein A8 (S100A8), acid phosphatase 5, tartrate resistant (ACP5), and CXC motif chemokine 10 (CXCL10), with initial levels of these biomarkers effectively predicting treatment response to biologics in patients with psoriatic arthritis (PsA).

Major finding: The serum levels of MMP3, S100A8, ACP5, CCL2, and CXCL10 were significantly reduced with TNFi (all P < .05), whereas ACP5 and CCL2 levels increased with IL-17i (both P < .05). The baseline levels of MMP3, S100A8, ACP5, and CXCL10 effectively predicted response to biologic treatment (area under the receiver operating characteristic curve > 0.8).

Study details: This study retrospectively analyzed data from 205 patients with PsA who did (n = 130) or did not (n = 75) receive biologics or conventional synthetic disease-modifying antirheumatic drugs and 56 patients with psoriasis without arthritis, of whom 28 patients received biologics.

Disclosures: This study was partially funded by the Canadian Institute of Health Research, with additional funding provided by the Krembil Foundation. The authors declared no conflicts of interest.

Source: Offenheim R, Cruz-Correa OF, Ganatra D, Gladman DD. Candidate biomarkers for response to treatment in psoriatic disease. J Rheumatol. 2024 (Sept 1). doi: 10.3899/jrheum.2024-0396 Source

Key clinical point: Treatment with biologics, such as tumor necrosis factor inhibitors (TNFi) and interleukin-17 inhibitors (IL-17i), altered serum levels of matrix metalloproteinase-3 (MMP3), S100 calcium-binding protein A8 (S100A8), acid phosphatase 5, tartrate resistant (ACP5), and CXC motif chemokine 10 (CXCL10), with initial levels of these biomarkers effectively predicting treatment response to biologics in patients with psoriatic arthritis (PsA).

Major finding: The serum levels of MMP3, S100A8, ACP5, CCL2, and CXCL10 were significantly reduced with TNFi (all P < .05), whereas ACP5 and CCL2 levels increased with IL-17i (both P < .05). The baseline levels of MMP3, S100A8, ACP5, and CXCL10 effectively predicted response to biologic treatment (area under the receiver operating characteristic curve > 0.8).

Study details: This study retrospectively analyzed data from 205 patients with PsA who did (n = 130) or did not (n = 75) receive biologics or conventional synthetic disease-modifying antirheumatic drugs and 56 patients with psoriasis without arthritis, of whom 28 patients received biologics.

Disclosures: This study was partially funded by the Canadian Institute of Health Research, with additional funding provided by the Krembil Foundation. The authors declared no conflicts of interest.

Source: Offenheim R, Cruz-Correa OF, Ganatra D, Gladman DD. Candidate biomarkers for response to treatment in psoriatic disease. J Rheumatol. 2024 (Sept 1). doi: 10.3899/jrheum.2024-0396 Source

Key clinical point: Treatment with biologics, such as tumor necrosis factor inhibitors (TNFi) and interleukin-17 inhibitors (IL-17i), altered serum levels of matrix metalloproteinase-3 (MMP3), S100 calcium-binding protein A8 (S100A8), acid phosphatase 5, tartrate resistant (ACP5), and CXC motif chemokine 10 (CXCL10), with initial levels of these biomarkers effectively predicting treatment response to biologics in patients with psoriatic arthritis (PsA).

Major finding: The serum levels of MMP3, S100A8, ACP5, CCL2, and CXCL10 were significantly reduced with TNFi (all P < .05), whereas ACP5 and CCL2 levels increased with IL-17i (both P < .05). The baseline levels of MMP3, S100A8, ACP5, and CXCL10 effectively predicted response to biologic treatment (area under the receiver operating characteristic curve > 0.8).

Study details: This study retrospectively analyzed data from 205 patients with PsA who did (n = 130) or did not (n = 75) receive biologics or conventional synthetic disease-modifying antirheumatic drugs and 56 patients with psoriasis without arthritis, of whom 28 patients received biologics.

Disclosures: This study was partially funded by the Canadian Institute of Health Research, with additional funding provided by the Krembil Foundation. The authors declared no conflicts of interest.

Source: Offenheim R, Cruz-Correa OF, Ganatra D, Gladman DD. Candidate biomarkers for response to treatment in psoriatic disease. J Rheumatol. 2024 (Sept 1). doi: 10.3899/jrheum.2024-0396 Source

Key clinical point: Patients with psoriatic arthritis (PsA) initiating biologic disease-modifying antirheumatic drugs (bDMARD) had a significantly higher risk for interstitial lung disease (ILD) than control individuals in the general population; with methotrexate co-medication not being a risk factor for ILD.

Major finding: The 5-year risk for ILD was significantly higher in patients with PsA vs individuals in the general population (adjusted hazard ratio [aHR] 4.4; 95% CI 2.8-7.0). The risk for ILD did not increase among patients with PsA who did vs did not use methotrexate as co-medication (aHR 1.0; 95% CI 0.4-2.2).

Study details: This observational cohort study included 10,919 patients with PsA and 29,478 patients with rheumatoid arthritis from five Nordic rheumatology registers (all age ≥ 18 years) who initiated bDMARD treatment, along with 362,087 control individuals from the general population.

Disclosures: This study was supported by NordForsk, Foreum, and other sources. Several authors declared receiving grants, honoraria, or consulting fees from or having other ties with various sources.

Source: Provan SA, Ljung L, Kristianslund EK, et al. Interstitial lung disease in rheumatoid or psoriatic arthritis patients initiating biologics, and controls - Data from five Nordic registries. J Rheumatol.  2024 (Sept 1). doi: 0.3899/jrheum.2024-0252 Source

Key clinical point: Patients with psoriatic arthritis (PsA) initiating biologic disease-modifying antirheumatic drugs (bDMARD) had a significantly higher risk for interstitial lung disease (ILD) than control individuals in the general population; with methotrexate co-medication not being a risk factor for ILD.

Major finding: The 5-year risk for ILD was significantly higher in patients with PsA vs individuals in the general population (adjusted hazard ratio [aHR] 4.4; 95% CI 2.8-7.0). The risk for ILD did not increase among patients with PsA who did vs did not use methotrexate as co-medication (aHR 1.0; 95% CI 0.4-2.2).

Study details: This observational cohort study included 10,919 patients with PsA and 29,478 patients with rheumatoid arthritis from five Nordic rheumatology registers (all age ≥ 18 years) who initiated bDMARD treatment, along with 362,087 control individuals from the general population.

Disclosures: This study was supported by NordForsk, Foreum, and other sources. Several authors declared receiving grants, honoraria, or consulting fees from or having other ties with various sources.

Source: Provan SA, Ljung L, Kristianslund EK, et al. Interstitial lung disease in rheumatoid or psoriatic arthritis patients initiating biologics, and controls - Data from five Nordic registries. J Rheumatol.  2024 (Sept 1). doi: 0.3899/jrheum.2024-0252 Source

Key clinical point: Patients with psoriatic arthritis (PsA) initiating biologic disease-modifying antirheumatic drugs (bDMARD) had a significantly higher risk for interstitial lung disease (ILD) than control individuals in the general population; with methotrexate co-medication not being a risk factor for ILD.

Major finding: The 5-year risk for ILD was significantly higher in patients with PsA vs individuals in the general population (adjusted hazard ratio [aHR] 4.4; 95% CI 2.8-7.0). The risk for ILD did not increase among patients with PsA who did vs did not use methotrexate as co-medication (aHR 1.0; 95% CI 0.4-2.2).

Study details: This observational cohort study included 10,919 patients with PsA and 29,478 patients with rheumatoid arthritis from five Nordic rheumatology registers (all age ≥ 18 years) who initiated bDMARD treatment, along with 362,087 control individuals from the general population.

Disclosures: This study was supported by NordForsk, Foreum, and other sources. Several authors declared receiving grants, honoraria, or consulting fees from or having other ties with various sources.

Source: Provan SA, Ljung L, Kristianslund EK, et al. Interstitial lung disease in rheumatoid or psoriatic arthritis patients initiating biologics, and controls - Data from five Nordic registries. J Rheumatol.  2024 (Sept 1). doi: 0.3899/jrheum.2024-0252 Source

Key clinical point: Bimekizumab showed better clinical efficacy outcomes than risankizumab in patients with psoriatic arthritis (PsA) who were biologic-naive or showed inadequate response to tumor necrosis factor inhibitors (TNFi-IR).

Major finding: At week 52, bimekizumab vs risankizumab led to a higher likelihood of achieving ≥70% improvement in the American College of Rheumatology response in biologic-naive (adjusted odds ratio [aOR] 1.80; P < .001) and TNFi-IR (aOR 3.69; P < .001) patients. It was also linked to greater odds of minimal disease activity response in TNFi-IR patients (aOR 2.43; P = .003).

Study details: This matching-adjusted indirect comparison of data from four phase 3 trials (BE OPTIMAL, BE COMPLETE, KEEPsAKE-1, and KEEPsAKE-2) that involved biologic-naive or TNFi-IR patients with PsA who received bimekizumab (n = 698) or risankizumab (n = 589).

Disclosures: This study was supported by UCB Pharma and the National Institute of Health and Care Research Manchester Biomedical Research Centre, UK. Four authors declared being employees and shareholders of UCB Pharma. Other authors declared having ties with various sources, including UCB Pharma.

Source: Mease PJ, Warren RB, Nash P, et al. Comparative effectiveness of bimekizumab and risankizumab in patients with psoriatic arthritis at 52 weeks assessed using a matching-adjusted indirect comparison. Rheumatol Ther. 2024 (Aug 9). doi: 10.1007/s40744-024-00706-w Source

Key clinical point: Bimekizumab showed better clinical efficacy outcomes than risankizumab in patients with psoriatic arthritis (PsA) who were biologic-naive or showed inadequate response to tumor necrosis factor inhibitors (TNFi-IR).

Major finding: At week 52, bimekizumab vs risankizumab led to a higher likelihood of achieving ≥70% improvement in the American College of Rheumatology response in biologic-naive (adjusted odds ratio [aOR] 1.80; P < .001) and TNFi-IR (aOR 3.69; P < .001) patients. It was also linked to greater odds of minimal disease activity response in TNFi-IR patients (aOR 2.43; P = .003).

Study details: This matching-adjusted indirect comparison of data from four phase 3 trials (BE OPTIMAL, BE COMPLETE, KEEPsAKE-1, and KEEPsAKE-2) that involved biologic-naive or TNFi-IR patients with PsA who received bimekizumab (n = 698) or risankizumab (n = 589).

Disclosures: This study was supported by UCB Pharma and the National Institute of Health and Care Research Manchester Biomedical Research Centre, UK. Four authors declared being employees and shareholders of UCB Pharma. Other authors declared having ties with various sources, including UCB Pharma.

Source: Mease PJ, Warren RB, Nash P, et al. Comparative effectiveness of bimekizumab and risankizumab in patients with psoriatic arthritis at 52 weeks assessed using a matching-adjusted indirect comparison. Rheumatol Ther. 2024 (Aug 9). doi: 10.1007/s40744-024-00706-w Source

Key clinical point: Bimekizumab showed better clinical efficacy outcomes than risankizumab in patients with psoriatic arthritis (PsA) who were biologic-naive or showed inadequate response to tumor necrosis factor inhibitors (TNFi-IR).

Major finding: At week 52, bimekizumab vs risankizumab led to a higher likelihood of achieving ≥70% improvement in the American College of Rheumatology response in biologic-naive (adjusted odds ratio [aOR] 1.80; P < .001) and TNFi-IR (aOR 3.69; P < .001) patients. It was also linked to greater odds of minimal disease activity response in TNFi-IR patients (aOR 2.43; P = .003).

Study details: This matching-adjusted indirect comparison of data from four phase 3 trials (BE OPTIMAL, BE COMPLETE, KEEPsAKE-1, and KEEPsAKE-2) that involved biologic-naive or TNFi-IR patients with PsA who received bimekizumab (n = 698) or risankizumab (n = 589).

Disclosures: This study was supported by UCB Pharma and the National Institute of Health and Care Research Manchester Biomedical Research Centre, UK. Four authors declared being employees and shareholders of UCB Pharma. Other authors declared having ties with various sources, including UCB Pharma.

Source: Mease PJ, Warren RB, Nash P, et al. Comparative effectiveness of bimekizumab and risankizumab in patients with psoriatic arthritis at 52 weeks assessed using a matching-adjusted indirect comparison. Rheumatol Ther. 2024 (Aug 9). doi: 10.1007/s40744-024-00706-w Source

Key clinical point: Patients with psoriatic arthritis (PsA) who were disease-modifying antirheumatic drug (DMARD)-naive or non-responders to previous conventional synthetic DMARD treatment (DMARD-failure) showed similar inflammation and structural damage on imaging.

Major finding: After adjusting for patient characteristics, structural imaging parameters including Achilles tendon structural damage and Joint Space Narrowing scores (both P > .6) were similar in DMARD-naive and DMARD-failure patients. Additionally, inflammatory imaging parameters (P > .2) showed no significant differences between the two groups, indicating that failing a DMARD was not associated with worsened imaging outcomes.

Study details: This cross-sectional study evaluated 80 patients with PsA from TOFA-PREDICT trial who were either DMARD-naive (n = 40) or DMARD non-responders (n = 40).

Disclosures: This study was supported by Pfizer. The collaboration project was co-funded by the public-private partnerships allowance by Health~Holland, Top Sector Life Sciences & Health. Six authors declared receiving research grants, consulting fees, and support from various sources, including Pfizer. Other authors declared no conflicts of interest.

Source: Renkli NÖ, Kleinrensink NJ, Spierings J, et al, and the TOFA-PREDICT author group. Multimodal imaging of structural damage and inflammation in psoriatic arthritis: A comparison of DMARD-naive and DMARD-failure patients. Rheumatology (Oxford). 2024 (Aug 17). doi: 10.1093/rheumatology/keae450 Source

Key clinical point: Patients with psoriatic arthritis (PsA) who were disease-modifying antirheumatic drug (DMARD)-naive or non-responders to previous conventional synthetic DMARD treatment (DMARD-failure) showed similar inflammation and structural damage on imaging.

Major finding: After adjusting for patient characteristics, structural imaging parameters including Achilles tendon structural damage and Joint Space Narrowing scores (both P > .6) were similar in DMARD-naive and DMARD-failure patients. Additionally, inflammatory imaging parameters (P > .2) showed no significant differences between the two groups, indicating that failing a DMARD was not associated with worsened imaging outcomes.

Study details: This cross-sectional study evaluated 80 patients with PsA from TOFA-PREDICT trial who were either DMARD-naive (n = 40) or DMARD non-responders (n = 40).

Disclosures: This study was supported by Pfizer. The collaboration project was co-funded by the public-private partnerships allowance by Health~Holland, Top Sector Life Sciences & Health. Six authors declared receiving research grants, consulting fees, and support from various sources, including Pfizer. Other authors declared no conflicts of interest.

Source: Renkli NÖ, Kleinrensink NJ, Spierings J, et al, and the TOFA-PREDICT author group. Multimodal imaging of structural damage and inflammation in psoriatic arthritis: A comparison of DMARD-naive and DMARD-failure patients. Rheumatology (Oxford). 2024 (Aug 17). doi: 10.1093/rheumatology/keae450 Source

Key clinical point: Patients with psoriatic arthritis (PsA) who were disease-modifying antirheumatic drug (DMARD)-naive or non-responders to previous conventional synthetic DMARD treatment (DMARD-failure) showed similar inflammation and structural damage on imaging.

Major finding: After adjusting for patient characteristics, structural imaging parameters including Achilles tendon structural damage and Joint Space Narrowing scores (both P > .6) were similar in DMARD-naive and DMARD-failure patients. Additionally, inflammatory imaging parameters (P > .2) showed no significant differences between the two groups, indicating that failing a DMARD was not associated with worsened imaging outcomes.

Study details: This cross-sectional study evaluated 80 patients with PsA from TOFA-PREDICT trial who were either DMARD-naive (n = 40) or DMARD non-responders (n = 40).

Disclosures: This study was supported by Pfizer. The collaboration project was co-funded by the public-private partnerships allowance by Health~Holland, Top Sector Life Sciences & Health. Six authors declared receiving research grants, consulting fees, and support from various sources, including Pfizer. Other authors declared no conflicts of interest.

Source: Renkli NÖ, Kleinrensink NJ, Spierings J, et al, and the TOFA-PREDICT author group. Multimodal imaging of structural damage and inflammation in psoriatic arthritis: A comparison of DMARD-naive and DMARD-failure patients. Rheumatology (Oxford). 2024 (Aug 17). doi: 10.1093/rheumatology/keae450 Source

Key clinical point: This largest and longest safety analysis on risankizumab demonstrated its long-term safety in patients with psoriatic arthritis (PsA), consistent with previously published reports.

Major finding: The rate of treatment-emergent adverse events (AE) was 142.6 events per 100 patient-years (E/100 PY), serious AE was 8.6 E/100 PY, and AE leading to discontinuation was 1.8 E/100 PY. The rates of serious infections, cancer, major cardiovascular events, and hepatic events remained consistent or decreased in frequency through 6 months or 1 year. No additional safety concerns were reported.

Study details: This integrated safety analysis used data from four phase 2-3 trials involving 1542 patients with PsA and 20 phase 1-4 trials involving 3658 patients with plaque psoriasis, all of whom received ≥1 dose of risankizumab.

Disclosures: This study was funded by AbbVie. Risankizumab was jointly developed by AbbVie and Boehringer Ingelheim. Five authors declared being full-time employees of and may own stock or stock options of AbbVie. Other authors declared having ties with various sources, including AbbVie.

Source: Gordon KB, Blauvelt A, Bachelez H, et al. Long-term safety of risankizumab in patients with psoriatic disease: A comprehensive analysis from clinical trials. Dermatol Ther (Heidelb). 2024;14:2523-2538 (Aug 17). doi: 10.1007/s13555-024-01238-5 Source

Key clinical point: This largest and longest safety analysis on risankizumab demonstrated its long-term safety in patients with psoriatic arthritis (PsA), consistent with previously published reports.

Major finding: The rate of treatment-emergent adverse events (AE) was 142.6 events per 100 patient-years (E/100 PY), serious AE was 8.6 E/100 PY, and AE leading to discontinuation was 1.8 E/100 PY. The rates of serious infections, cancer, major cardiovascular events, and hepatic events remained consistent or decreased in frequency through 6 months or 1 year. No additional safety concerns were reported.

Study details: This integrated safety analysis used data from four phase 2-3 trials involving 1542 patients with PsA and 20 phase 1-4 trials involving 3658 patients with plaque psoriasis, all of whom received ≥1 dose of risankizumab.

Disclosures: This study was funded by AbbVie. Risankizumab was jointly developed by AbbVie and Boehringer Ingelheim. Five authors declared being full-time employees of and may own stock or stock options of AbbVie. Other authors declared having ties with various sources, including AbbVie.

Source: Gordon KB, Blauvelt A, Bachelez H, et al. Long-term safety of risankizumab in patients with psoriatic disease: A comprehensive analysis from clinical trials. Dermatol Ther (Heidelb). 2024;14:2523-2538 (Aug 17). doi: 10.1007/s13555-024-01238-5 Source

Key clinical point: This largest and longest safety analysis on risankizumab demonstrated its long-term safety in patients with psoriatic arthritis (PsA), consistent with previously published reports.

Major finding: The rate of treatment-emergent adverse events (AE) was 142.6 events per 100 patient-years (E/100 PY), serious AE was 8.6 E/100 PY, and AE leading to discontinuation was 1.8 E/100 PY. The rates of serious infections, cancer, major cardiovascular events, and hepatic events remained consistent or decreased in frequency through 6 months or 1 year. No additional safety concerns were reported.

Study details: This integrated safety analysis used data from four phase 2-3 trials involving 1542 patients with PsA and 20 phase 1-4 trials involving 3658 patients with plaque psoriasis, all of whom received ≥1 dose of risankizumab.

Disclosures: This study was funded by AbbVie. Risankizumab was jointly developed by AbbVie and Boehringer Ingelheim. Five authors declared being full-time employees of and may own stock or stock options of AbbVie. Other authors declared having ties with various sources, including AbbVie.

Source: Gordon KB, Blauvelt A, Bachelez H, et al. Long-term safety of risankizumab in patients with psoriatic disease: A comprehensive analysis from clinical trials. Dermatol Ther (Heidelb). 2024;14:2523-2538 (Aug 17). doi: 10.1007/s13555-024-01238-5 Source

You’ve been sued for medical malpractice. If you are a physician in the United States, that is not an unlikely scenario.

An analysis by the American Medical Association shows that almost half of all physicians are sued by the time they reach 54. In some specialties, such as ob.gyn., one is almost guaranteed to be sued at some point.

But that’s what medical malpractice insurance is for, right? Your medical malpractice insurer will assign an attorney to take care of you and help you through this situation. Won’t they?

Maybe so, but the attorney and the claims representative your insurer assigns to your case may have a different idea about how to proceed than you do. Though the defense attorney assigned to you represents you, he or she gets paid by the insurance carrier.

This can create a conflict when your defense counsel and your insurance claims representative aim to take your case in a direction you don’t like.

Issues dividing defendant physicians, their insurers, and insurance company lawyers who represent them often arise from conflicting perspectives on risk, financial considerations, and reputation damage. Disagreements might include:

• Choice of expert witnesses
• Tactical decisions related to trial strategy
• Public relations considerations
• Admissions of liability
• Allocation of resources

To Settle or Not?

One of the most challenging — and common — disagreements is whether to settle the case.

Sometimes a malpractice insurer wants to settle the case against the defendant doctor’s wishes. Or the doctor wants to settle but is pushed into going to trial. In the following case, one doctor had to face the consequences of a decision he didn’t even make.
 

The Underlying Medical Malpractice Case

Dr. D was sued by a patient who had allegedly called Dr. D’s office six times in 2 days complaining of intermittent chest pain.

Dr. D had been swamped with patients and couldn’t squeeze this patient in for an office visit, but he did call back. The patient later claimed that during the call he told the doctor he was suffering from chest pain. The doctor recalled that the patient had complained of abdominal discomfort that began after he had exercised.

The physician wrote a prescription for an ECG at the local hospital and called to ensure that the patient could just walk in. The ECG was allegedly abnormal but was not read as representing an impending or current heart attack. Later that evening, however, the patient went to the emergency department of another hospital where it was confirmed that he had suffered a heart attack. The patient underwent cardiac catheterization and stent placement to address a blockage in his left anterior descending artery.

The patient subsequently sued Dr. D and the hospital where he had the original ECG. Dr. D contacted his medical malpractice insurance company. The insurance company assigned an attorney to represent Dr. D. Discovery in the case began.

The plaintiff’s own medical expert testified in a deposition that there was no way for the heart attack to have been prevented and that the treatment would have been the same either way. But Dr. D could not find a record of the phone calls with the patient, and he had not noted his conversation the patient in their medical records.

Dr. D held a policy for $1 million, and his state had a fund that would kick in an additional $1 million. But the plaintiffs demanded $4 million to settle.

A month before trial, the plaintiff’s attorney sent a threatening letter to Dr. D’s attorney warning him that Dr. D was underinsured and suggesting that it would be in the physician’s best interests to settle.

“I want to stress to you that it is not my desire to harm your client’s reputation or to destroy his business,” wrote the plaintiff’s attorney. “However, now is the time to avoid consequences such as these by making a good faith effort to get this case resolved.”

The letter went on to note that the defense attorney should give Dr. D a copy of the letter so that everyone would be aware of the potential consequences of an award against Dr. D in excess of his limits of insurance coverage. The plaintiff’s attorney even suggested that Dr. D should retain personal counsel.

Dr. D’s defense attorney downplayed the letter and assured him that there was no reason to worry.

Meanwhile the case inched closer to trial.

The codefendant hospital settled with the plaintiff on the night before jury selection, leaving Dr. D in the uncomfortable position of being the only defendant in the case. At this point, Dr. D decided he would like to settle, and he sent his attorney an email telling him so. But the attorney instead referred him to an insurance company claims.

Just days before the trial was to start, Dr. D repeatedly told the claims representative assigned to his claim that he did not want to go to trial but rather wanted to settle. The representative told Dr. D that he had no choice in whether the action settled.

A committee at the insurance company had decided to proceed with the trial rather than settle.

The trial proved a painful debacle for Dr. D. His attorney’s idea of showing a “gotcha” video of the allegedly permanently injured plaintiff carrying a large, heavy box backfired when the jury was shown by the plaintiff that the box actually contained ice cream cones and weighed very little.

Prior to trial, the plaintiff offered to settle for $1 million. On the first day of trial, they lowered that amount to $750,000, yet the defense attorney did not settle the case, and it proceeded to a jury verdict. The jury awarded the plaintiff over $4 million — well in excess of Dr. D’s policy limits.
 

The Follow-up

Dr. D was horrified, but the insurance company claims representative said the insurer would promptly offer $2 million in available insurance coverage to settle the case post verdict. This did not happen. Instead, the insurer chose to appeal the verdict against Dr. D’s wishes.

Ultimately, Dr. D was forced to hire his own lawyer. He ultimately sued the insurance company for breach of contract and bad faith.

The insurance company eventually attempted to settle with the plaintiffs’ counsel, but the plaintiff refused to accept the available insurance coverage. The insurance carrier still has not posted the entire appeal bond. The case is still pending.
 

Protecting Yourself

The lesson from Dr. D’s experience: Understand that the insurance company is not your friend. It’s a business looking out for its own interests.

The plaintiff’s attorney was absolutely correct in suggesting that Dr. D retain his own attorney to represent his own interests. You should hire your own lawyer when:

• You disagree with your insurer on how to proceed in a case.
• You receive a demand that exceeds your available insurance coverage or for damages that may not be covered by your policy, such as punitive damages.
• Your insurance carrier attempts to deny insurance coverage for your claim or sends you a letter stating that it is “reserving its rights” not to cover or to limit coverage for your claim.

Retaining independent counsel protects your interests, not those of your insurance company.

Independent counsel can give you a second opinion on the strengths and weaknesses of your claim, help you prepare for your deposition, and attend court dates with you to ensure that you are completely protected.

Independent counsel can challenge your insurance company’s decision to deny or limit your insurance coverage and ensure that you receive all of the benefits to which you are entitled under your insurance policy. Some policies may include an independent lawyer to be paid for by your insurance carrier in case of a conflicts.

The most important takeaway? Your medical malpractice insurance carrier is not your friend, so act accordingly in times of conflict.

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

You’ve been sued for medical malpractice. If you are a physician in the United States, that is not an unlikely scenario.

An analysis by the American Medical Association shows that almost half of all physicians are sued by the time they reach 54. In some specialties, such as ob.gyn., one is almost guaranteed to be sued at some point.

But that’s what medical malpractice insurance is for, right? Your medical malpractice insurer will assign an attorney to take care of you and help you through this situation. Won’t they?

Maybe so, but the attorney and the claims representative your insurer assigns to your case may have a different idea about how to proceed than you do. Though the defense attorney assigned to you represents you, he or she gets paid by the insurance carrier.

This can create a conflict when your defense counsel and your insurance claims representative aim to take your case in a direction you don’t like.

Issues dividing defendant physicians, their insurers, and insurance company lawyers who represent them often arise from conflicting perspectives on risk, financial considerations, and reputation damage. Disagreements might include:

• Choice of expert witnesses
• Tactical decisions related to trial strategy
• Public relations considerations
• Admissions of liability
• Allocation of resources

To Settle or Not?

One of the most challenging — and common — disagreements is whether to settle the case.

Sometimes a malpractice insurer wants to settle the case against the defendant doctor’s wishes. Or the doctor wants to settle but is pushed into going to trial. In the following case, one doctor had to face the consequences of a decision he didn’t even make.
 

The Underlying Medical Malpractice Case

Dr. D was sued by a patient who had allegedly called Dr. D’s office six times in 2 days complaining of intermittent chest pain.

Dr. D had been swamped with patients and couldn’t squeeze this patient in for an office visit, but he did call back. The patient later claimed that during the call he told the doctor he was suffering from chest pain. The doctor recalled that the patient had complained of abdominal discomfort that began after he had exercised.

The physician wrote a prescription for an ECG at the local hospital and called to ensure that the patient could just walk in. The ECG was allegedly abnormal but was not read as representing an impending or current heart attack. Later that evening, however, the patient went to the emergency department of another hospital where it was confirmed that he had suffered a heart attack. The patient underwent cardiac catheterization and stent placement to address a blockage in his left anterior descending artery.

The patient subsequently sued Dr. D and the hospital where he had the original ECG. Dr. D contacted his medical malpractice insurance company. The insurance company assigned an attorney to represent Dr. D. Discovery in the case began.

The plaintiff’s own medical expert testified in a deposition that there was no way for the heart attack to have been prevented and that the treatment would have been the same either way. But Dr. D could not find a record of the phone calls with the patient, and he had not noted his conversation the patient in their medical records.

Dr. D held a policy for $1 million, and his state had a fund that would kick in an additional $1 million. But the plaintiffs demanded $4 million to settle.

A month before trial, the plaintiff’s attorney sent a threatening letter to Dr. D’s attorney warning him that Dr. D was underinsured and suggesting that it would be in the physician’s best interests to settle.

“I want to stress to you that it is not my desire to harm your client’s reputation or to destroy his business,” wrote the plaintiff’s attorney. “However, now is the time to avoid consequences such as these by making a good faith effort to get this case resolved.”

The letter went on to note that the defense attorney should give Dr. D a copy of the letter so that everyone would be aware of the potential consequences of an award against Dr. D in excess of his limits of insurance coverage. The plaintiff’s attorney even suggested that Dr. D should retain personal counsel.

Dr. D’s defense attorney downplayed the letter and assured him that there was no reason to worry.

Meanwhile the case inched closer to trial.

The codefendant hospital settled with the plaintiff on the night before jury selection, leaving Dr. D in the uncomfortable position of being the only defendant in the case. At this point, Dr. D decided he would like to settle, and he sent his attorney an email telling him so. But the attorney instead referred him to an insurance company claims.

Just days before the trial was to start, Dr. D repeatedly told the claims representative assigned to his claim that he did not want to go to trial but rather wanted to settle. The representative told Dr. D that he had no choice in whether the action settled.

A committee at the insurance company had decided to proceed with the trial rather than settle.

The trial proved a painful debacle for Dr. D. His attorney’s idea of showing a “gotcha” video of the allegedly permanently injured plaintiff carrying a large, heavy box backfired when the jury was shown by the plaintiff that the box actually contained ice cream cones and weighed very little.

Prior to trial, the plaintiff offered to settle for $1 million. On the first day of trial, they lowered that amount to $750,000, yet the defense attorney did not settle the case, and it proceeded to a jury verdict. The jury awarded the plaintiff over $4 million — well in excess of Dr. D’s policy limits.
 

The Follow-up

Dr. D was horrified, but the insurance company claims representative said the insurer would promptly offer $2 million in available insurance coverage to settle the case post verdict. This did not happen. Instead, the insurer chose to appeal the verdict against Dr. D’s wishes.

Ultimately, Dr. D was forced to hire his own lawyer. He ultimately sued the insurance company for breach of contract and bad faith.

The insurance company eventually attempted to settle with the plaintiffs’ counsel, but the plaintiff refused to accept the available insurance coverage. The insurance carrier still has not posted the entire appeal bond. The case is still pending.
 

Protecting Yourself

The lesson from Dr. D’s experience: Understand that the insurance company is not your friend. It’s a business looking out for its own interests.

The plaintiff’s attorney was absolutely correct in suggesting that Dr. D retain his own attorney to represent his own interests. You should hire your own lawyer when:

• You disagree with your insurer on how to proceed in a case.
• You receive a demand that exceeds your available insurance coverage or for damages that may not be covered by your policy, such as punitive damages.
• Your insurance carrier attempts to deny insurance coverage for your claim or sends you a letter stating that it is “reserving its rights” not to cover or to limit coverage for your claim.

Retaining independent counsel protects your interests, not those of your insurance company.

Independent counsel can give you a second opinion on the strengths and weaknesses of your claim, help you prepare for your deposition, and attend court dates with you to ensure that you are completely protected.

Independent counsel can challenge your insurance company’s decision to deny or limit your insurance coverage and ensure that you receive all of the benefits to which you are entitled under your insurance policy. Some policies may include an independent lawyer to be paid for by your insurance carrier in case of a conflicts.

The most important takeaway? Your medical malpractice insurance carrier is not your friend, so act accordingly in times of conflict.

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

You’ve been sued for medical malpractice. If you are a physician in the United States, that is not an unlikely scenario.

An analysis by the American Medical Association shows that almost half of all physicians are sued by the time they reach 54. In some specialties, such as ob.gyn., one is almost guaranteed to be sued at some point.

But that’s what medical malpractice insurance is for, right? Your medical malpractice insurer will assign an attorney to take care of you and help you through this situation. Won’t they?

Maybe so, but the attorney and the claims representative your insurer assigns to your case may have a different idea about how to proceed than you do. Though the defense attorney assigned to you represents you, he or she gets paid by the insurance carrier.

This can create a conflict when your defense counsel and your insurance claims representative aim to take your case in a direction you don’t like.

Issues dividing defendant physicians, their insurers, and insurance company lawyers who represent them often arise from conflicting perspectives on risk, financial considerations, and reputation damage. Disagreements might include:

• Choice of expert witnesses
• Tactical decisions related to trial strategy
• Public relations considerations
• Admissions of liability
• Allocation of resources

To Settle or Not?

One of the most challenging — and common — disagreements is whether to settle the case.

Sometimes a malpractice insurer wants to settle the case against the defendant doctor’s wishes. Or the doctor wants to settle but is pushed into going to trial. In the following case, one doctor had to face the consequences of a decision he didn’t even make.
 

The Underlying Medical Malpractice Case

Dr. D was sued by a patient who had allegedly called Dr. D’s office six times in 2 days complaining of intermittent chest pain.

Dr. D had been swamped with patients and couldn’t squeeze this patient in for an office visit, but he did call back. The patient later claimed that during the call he told the doctor he was suffering from chest pain. The doctor recalled that the patient had complained of abdominal discomfort that began after he had exercised.

The physician wrote a prescription for an ECG at the local hospital and called to ensure that the patient could just walk in. The ECG was allegedly abnormal but was not read as representing an impending or current heart attack. Later that evening, however, the patient went to the emergency department of another hospital where it was confirmed that he had suffered a heart attack. The patient underwent cardiac catheterization and stent placement to address a blockage in his left anterior descending artery.

The patient subsequently sued Dr. D and the hospital where he had the original ECG. Dr. D contacted his medical malpractice insurance company. The insurance company assigned an attorney to represent Dr. D. Discovery in the case began.

The plaintiff’s own medical expert testified in a deposition that there was no way for the heart attack to have been prevented and that the treatment would have been the same either way. But Dr. D could not find a record of the phone calls with the patient, and he had not noted his conversation the patient in their medical records.

Dr. D held a policy for $1 million, and his state had a fund that would kick in an additional $1 million. But the plaintiffs demanded $4 million to settle.

A month before trial, the plaintiff’s attorney sent a threatening letter to Dr. D’s attorney warning him that Dr. D was underinsured and suggesting that it would be in the physician’s best interests to settle.

“I want to stress to you that it is not my desire to harm your client’s reputation or to destroy his business,” wrote the plaintiff’s attorney. “However, now is the time to avoid consequences such as these by making a good faith effort to get this case resolved.”

The letter went on to note that the defense attorney should give Dr. D a copy of the letter so that everyone would be aware of the potential consequences of an award against Dr. D in excess of his limits of insurance coverage. The plaintiff’s attorney even suggested that Dr. D should retain personal counsel.

Dr. D’s defense attorney downplayed the letter and assured him that there was no reason to worry.

Meanwhile the case inched closer to trial.

The codefendant hospital settled with the plaintiff on the night before jury selection, leaving Dr. D in the uncomfortable position of being the only defendant in the case. At this point, Dr. D decided he would like to settle, and he sent his attorney an email telling him so. But the attorney instead referred him to an insurance company claims.

Just days before the trial was to start, Dr. D repeatedly told the claims representative assigned to his claim that he did not want to go to trial but rather wanted to settle. The representative told Dr. D that he had no choice in whether the action settled.

A committee at the insurance company had decided to proceed with the trial rather than settle.

The trial proved a painful debacle for Dr. D. His attorney’s idea of showing a “gotcha” video of the allegedly permanently injured plaintiff carrying a large, heavy box backfired when the jury was shown by the plaintiff that the box actually contained ice cream cones and weighed very little.

Prior to trial, the plaintiff offered to settle for $1 million. On the first day of trial, they lowered that amount to $750,000, yet the defense attorney did not settle the case, and it proceeded to a jury verdict. The jury awarded the plaintiff over $4 million — well in excess of Dr. D’s policy limits.
 

The Follow-up

Dr. D was horrified, but the insurance company claims representative said the insurer would promptly offer $2 million in available insurance coverage to settle the case post verdict. This did not happen. Instead, the insurer chose to appeal the verdict against Dr. D’s wishes.

Ultimately, Dr. D was forced to hire his own lawyer. He ultimately sued the insurance company for breach of contract and bad faith.

The insurance company eventually attempted to settle with the plaintiffs’ counsel, but the plaintiff refused to accept the available insurance coverage. The insurance carrier still has not posted the entire appeal bond. The case is still pending.
 

Protecting Yourself

The lesson from Dr. D’s experience: Understand that the insurance company is not your friend. It’s a business looking out for its own interests.

The plaintiff’s attorney was absolutely correct in suggesting that Dr. D retain his own attorney to represent his own interests. You should hire your own lawyer when:

• You disagree with your insurer on how to proceed in a case.
• You receive a demand that exceeds your available insurance coverage or for damages that may not be covered by your policy, such as punitive damages.
• Your insurance carrier attempts to deny insurance coverage for your claim or sends you a letter stating that it is “reserving its rights” not to cover or to limit coverage for your claim.

Retaining independent counsel protects your interests, not those of your insurance company.

Independent counsel can give you a second opinion on the strengths and weaknesses of your claim, help you prepare for your deposition, and attend court dates with you to ensure that you are completely protected.

Independent counsel can challenge your insurance company’s decision to deny or limit your insurance coverage and ensure that you receive all of the benefits to which you are entitled under your insurance policy. Some policies may include an independent lawyer to be paid for by your insurance carrier in case of a conflicts.

The most important takeaway? Your medical malpractice insurance carrier is not your friend, so act accordingly in times of conflict.

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

Key clinical point: Switching between biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARD) was common due to treatment inefficacy in patients with psoriatic arthritis (PsA), with concomitant therapies and multiple prior treatments being significant risk factors.

Major finding: Overall, 40% of patients switched between b/tsDMARD, with 85.1% switches due to treatment inefficacy. The risk for switching was not affected by b/tsDMARD type (P > .05) but increased with multiple b/tsDMARD courses (adjusted hazard ratio [aHR] 1.22; P = .010), concomitant glucocorticoids (aHR 2.05; P = .001), and sulfalazine use (aHR 2.25; P = .006). Women and those with inflammatory back pain also faced an increased risk for switching.

Study details: This longitudinal retrospective study included 141 patients with PsA (age ≥ 16 years) who were treated with b/tsDMARD.

Disclosures: This study was supported by the Instituto de Salud Carlos III, Ministry of Health, Spain, and Red de Enfermedades Inflamatorias, with co-funding from el Fondo Europeo de Desarrollo Regional. The authors declared no conflicts of interest.

Source: Freites-Nuñez D, Leon L, Toledano E, et al. Switching related to inefficacy in biologics and targeted synthetic therapies for psoriatic arthritis: A comparative real-life study. Ther Adv Musculoskelet Dis. 2024 (Aug 31). doi:10.1177/1759720X241273083 Source

Key clinical point: Switching between biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARD) was common due to treatment inefficacy in patients with psoriatic arthritis (PsA), with concomitant therapies and multiple prior treatments being significant risk factors.

Major finding: Overall, 40% of patients switched between b/tsDMARD, with 85.1% switches due to treatment inefficacy. The risk for switching was not affected by b/tsDMARD type (P > .05) but increased with multiple b/tsDMARD courses (adjusted hazard ratio [aHR] 1.22; P = .010), concomitant glucocorticoids (aHR 2.05; P = .001), and sulfalazine use (aHR 2.25; P = .006). Women and those with inflammatory back pain also faced an increased risk for switching.

Study details: This longitudinal retrospective study included 141 patients with PsA (age ≥ 16 years) who were treated with b/tsDMARD.

Disclosures: This study was supported by the Instituto de Salud Carlos III, Ministry of Health, Spain, and Red de Enfermedades Inflamatorias, with co-funding from el Fondo Europeo de Desarrollo Regional. The authors declared no conflicts of interest.

Source: Freites-Nuñez D, Leon L, Toledano E, et al. Switching related to inefficacy in biologics and targeted synthetic therapies for psoriatic arthritis: A comparative real-life study. Ther Adv Musculoskelet Dis. 2024 (Aug 31). doi:10.1177/1759720X241273083 Source

Key clinical point: Switching between biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARD) was common due to treatment inefficacy in patients with psoriatic arthritis (PsA), with concomitant therapies and multiple prior treatments being significant risk factors.

Major finding: Overall, 40% of patients switched between b/tsDMARD, with 85.1% switches due to treatment inefficacy. The risk for switching was not affected by b/tsDMARD type (P > .05) but increased with multiple b/tsDMARD courses (adjusted hazard ratio [aHR] 1.22; P = .010), concomitant glucocorticoids (aHR 2.05; P = .001), and sulfalazine use (aHR 2.25; P = .006). Women and those with inflammatory back pain also faced an increased risk for switching.

Study details: This longitudinal retrospective study included 141 patients with PsA (age ≥ 16 years) who were treated with b/tsDMARD.

Disclosures: This study was supported by the Instituto de Salud Carlos III, Ministry of Health, Spain, and Red de Enfermedades Inflamatorias, with co-funding from el Fondo Europeo de Desarrollo Regional. The authors declared no conflicts of interest.

Source: Freites-Nuñez D, Leon L, Toledano E, et al. Switching related to inefficacy in biologics and targeted synthetic therapies for psoriatic arthritis: A comparative real-life study. Ther Adv Musculoskelet Dis. 2024 (Aug 31). doi:10.1177/1759720X241273083 Source

Key clinical point: Patients with early oligoarticular psoriatic arthritis (PsA) treated with apremilast vs placebo showed greater disease control and minimal disease activity response with a maximum of one swollen joint and one tender joint count (MDA-Joints).

Major finding: At week 16, a higher proportion of patients receiving apremilast vs placebo achieved MDA-Joints response based on sentinel joints (33.9% vs 16.0%; P = .0008) and total joints (21.3% vs 7.9%; nominal P = .0028). No new safety signals were reported.

Study details: This phase 4 FOREMOST trial included 308 patients with early oligoarticular PsA previously treated with non-steroidal anti-inflammatory drugs or ≥2 conventional synthetic disease-modifying antirheumatic drugs and were randomly assigned to receive apremilast (n = 203) or placebo (n = 105).

Disclosures: This study was funded by Amgen. Five authors declared being employees and owning stocks of Amgen. Several authors have declared other ties with Amgen and other sources.

Source: Gossec L, Coates LC, Gladman DD, et al. Treatment of early oligoarticular psoriatic arthritis with apremilast: Primary outcomes at week 16 from the FOREMOST randomised controlled trial. Ann Rheum Dis. 2024 (Aug 20). doi: 10.1136/ard-2024-225833 Source

Key clinical point: Patients with early oligoarticular psoriatic arthritis (PsA) treated with apremilast vs placebo showed greater disease control and minimal disease activity response with a maximum of one swollen joint and one tender joint count (MDA-Joints).

Major finding: At week 16, a higher proportion of patients receiving apremilast vs placebo achieved MDA-Joints response based on sentinel joints (33.9% vs 16.0%; P = .0008) and total joints (21.3% vs 7.9%; nominal P = .0028). No new safety signals were reported.

Study details: This phase 4 FOREMOST trial included 308 patients with early oligoarticular PsA previously treated with non-steroidal anti-inflammatory drugs or ≥2 conventional synthetic disease-modifying antirheumatic drugs and were randomly assigned to receive apremilast (n = 203) or placebo (n = 105).

Disclosures: This study was funded by Amgen. Five authors declared being employees and owning stocks of Amgen. Several authors have declared other ties with Amgen and other sources.

Source: Gossec L, Coates LC, Gladman DD, et al. Treatment of early oligoarticular psoriatic arthritis with apremilast: Primary outcomes at week 16 from the FOREMOST randomised controlled trial. Ann Rheum Dis. 2024 (Aug 20). doi: 10.1136/ard-2024-225833 Source

Key clinical point: Patients with early oligoarticular psoriatic arthritis (PsA) treated with apremilast vs placebo showed greater disease control and minimal disease activity response with a maximum of one swollen joint and one tender joint count (MDA-Joints).

Major finding: At week 16, a higher proportion of patients receiving apremilast vs placebo achieved MDA-Joints response based on sentinel joints (33.9% vs 16.0%; P = .0008) and total joints (21.3% vs 7.9%; nominal P = .0028). No new safety signals were reported.

Study details: This phase 4 FOREMOST trial included 308 patients with early oligoarticular PsA previously treated with non-steroidal anti-inflammatory drugs or ≥2 conventional synthetic disease-modifying antirheumatic drugs and were randomly assigned to receive apremilast (n = 203) or placebo (n = 105).

Disclosures: This study was funded by Amgen. Five authors declared being employees and owning stocks of Amgen. Several authors have declared other ties with Amgen and other sources.

Source: Gossec L, Coates LC, Gladman DD, et al. Treatment of early oligoarticular psoriatic arthritis with apremilast: Primary outcomes at week 16 from the FOREMOST randomised controlled trial. Ann Rheum Dis. 2024 (Aug 20). doi: 10.1136/ard-2024-225833 Source

TOPLINE:

A data-driven subclassification of antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis has identified five distinct clusters with varying degrees of kidney involvement and systemic inflammation, offering insights into improved patient stratification and treatment approaches.

METHODOLOGY:

• ANCA-associated vasculitis is a rare and complex autoimmune disease that is traditionally classified into granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA).
• Researchers employed advanced artificial intelligence and big data techniques to identify phenotypically distinct subgroups of ANCA-associated vasculitis and developed a classification system using real-world patient data from the Federated Vasculitis Registry consortium.
• They included 3868 patients diagnosed with ANCA-associated vasculitis between November 1, 1966, and March 1, 2023 (mean age at diagnosis, 57.2 years; 51.9% men), across six European vasculitis registries; while a majority of patients (62.9%) were diagnosed with GPA, the remaining 37.1% were diagnosed with MPA.
• Overall, 17 clinical and demographic variables such as the age at diagnosis, gender, serum creatinine and C-reactive protein levels, the type of ANCA, and the involvement of various organ systems were used to create a model for categorizing patients into different clusters.
• The median follow-up duration was 4.2 years.

TAKEAWAY:

• Five distinct clusters were identified in ANCA-associated vasculitis; three had significant kidney involvement (the severe kidney cluster, myeloperoxidase-ANCA-positive kidney cluster, and proteinase 3-ANCA-positive kidney cluster) and two had minimal kidney involvement (young respiratory cluster and inflammatory multisystem cluster).
• The clusters with significant kidney involvement were associated with poorer outcomes, including a higher risk for kidney failure and death. The severe kidney cluster had the poorest prognosis, with mortality and the rate of end-stage kidney failure being 30.5% and 41.6%, respectively.
• The young respiratory cluster, characterized by predominant ear-nose-throat involvement and low systemic inflammation, showed the best prognostic outcomes.
• This cluster membership model showed a greater predictive accuracy for patient and kidney survival than traditional methods based on clinical diagnosis or ANCA specificity.

IN PRACTICE:

“These findings highlight the necessity of recognizing severe kidney disease at the time of diagnosis as an indicator of poor outcome, thereby necessitating intensified treatment approaches,” experts from the Department of Internal Medicine IV (Nephrology and Hypertension), Medical University of Innsbruck, Austria, wrote in an accompanying editorial published online on August 22, 2024, in The Lancet Rheumatology.

SOURCE:

This study was led by Karl Gisslander, Department of Clinical Sciences, Lund University, Lund, Sweden, and was published online on August 22, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Data on estimated glomerular filtration rate recovery in clusters with kidney disease were lacking. Populations from East Asia, where myeloperoxidase-ANCA positivity is more prevalent, were not included.

DISCLOSURES:

This study received funding from the European Union’s Horizon 2020 research and innovation program under the European Joint Programme on Rare Diseases. Some authors declared serving on advisory boards or receiving grants, contracts, travel support, consulting fees, payments, or honoraria from various pharmaceutical companies and other institutions.

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:

A data-driven subclassification of antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis has identified five distinct clusters with varying degrees of kidney involvement and systemic inflammation, offering insights into improved patient stratification and treatment approaches.

METHODOLOGY:

• ANCA-associated vasculitis is a rare and complex autoimmune disease that is traditionally classified into granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA).
• Researchers employed advanced artificial intelligence and big data techniques to identify phenotypically distinct subgroups of ANCA-associated vasculitis and developed a classification system using real-world patient data from the Federated Vasculitis Registry consortium.
• They included 3868 patients diagnosed with ANCA-associated vasculitis between November 1, 1966, and March 1, 2023 (mean age at diagnosis, 57.2 years; 51.9% men), across six European vasculitis registries; while a majority of patients (62.9%) were diagnosed with GPA, the remaining 37.1% were diagnosed with MPA.
• Overall, 17 clinical and demographic variables such as the age at diagnosis, gender, serum creatinine and C-reactive protein levels, the type of ANCA, and the involvement of various organ systems were used to create a model for categorizing patients into different clusters.
• The median follow-up duration was 4.2 years.

TAKEAWAY:

• Five distinct clusters were identified in ANCA-associated vasculitis; three had significant kidney involvement (the severe kidney cluster, myeloperoxidase-ANCA-positive kidney cluster, and proteinase 3-ANCA-positive kidney cluster) and two had minimal kidney involvement (young respiratory cluster and inflammatory multisystem cluster).
• The clusters with significant kidney involvement were associated with poorer outcomes, including a higher risk for kidney failure and death. The severe kidney cluster had the poorest prognosis, with mortality and the rate of end-stage kidney failure being 30.5% and 41.6%, respectively.
• The young respiratory cluster, characterized by predominant ear-nose-throat involvement and low systemic inflammation, showed the best prognostic outcomes.
• This cluster membership model showed a greater predictive accuracy for patient and kidney survival than traditional methods based on clinical diagnosis or ANCA specificity.

IN PRACTICE:

“These findings highlight the necessity of recognizing severe kidney disease at the time of diagnosis as an indicator of poor outcome, thereby necessitating intensified treatment approaches,” experts from the Department of Internal Medicine IV (Nephrology and Hypertension), Medical University of Innsbruck, Austria, wrote in an accompanying editorial published online on August 22, 2024, in The Lancet Rheumatology.

SOURCE:

This study was led by Karl Gisslander, Department of Clinical Sciences, Lund University, Lund, Sweden, and was published online on August 22, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Data on estimated glomerular filtration rate recovery in clusters with kidney disease were lacking. Populations from East Asia, where myeloperoxidase-ANCA positivity is more prevalent, were not included.

DISCLOSURES:

This study received funding from the European Union’s Horizon 2020 research and innovation program under the European Joint Programme on Rare Diseases. Some authors declared serving on advisory boards or receiving grants, contracts, travel support, consulting fees, payments, or honoraria from various pharmaceutical companies and other institutions.

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:

A data-driven subclassification of antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis has identified five distinct clusters with varying degrees of kidney involvement and systemic inflammation, offering insights into improved patient stratification and treatment approaches.

METHODOLOGY:

• ANCA-associated vasculitis is a rare and complex autoimmune disease that is traditionally classified into granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA).
• Researchers employed advanced artificial intelligence and big data techniques to identify phenotypically distinct subgroups of ANCA-associated vasculitis and developed a classification system using real-world patient data from the Federated Vasculitis Registry consortium.
• They included 3868 patients diagnosed with ANCA-associated vasculitis between November 1, 1966, and March 1, 2023 (mean age at diagnosis, 57.2 years; 51.9% men), across six European vasculitis registries; while a majority of patients (62.9%) were diagnosed with GPA, the remaining 37.1% were diagnosed with MPA.
• Overall, 17 clinical and demographic variables such as the age at diagnosis, gender, serum creatinine and C-reactive protein levels, the type of ANCA, and the involvement of various organ systems were used to create a model for categorizing patients into different clusters.
• The median follow-up duration was 4.2 years.

TAKEAWAY:

• Five distinct clusters were identified in ANCA-associated vasculitis; three had significant kidney involvement (the severe kidney cluster, myeloperoxidase-ANCA-positive kidney cluster, and proteinase 3-ANCA-positive kidney cluster) and two had minimal kidney involvement (young respiratory cluster and inflammatory multisystem cluster).
• The clusters with significant kidney involvement were associated with poorer outcomes, including a higher risk for kidney failure and death. The severe kidney cluster had the poorest prognosis, with mortality and the rate of end-stage kidney failure being 30.5% and 41.6%, respectively.
• The young respiratory cluster, characterized by predominant ear-nose-throat involvement and low systemic inflammation, showed the best prognostic outcomes.
• This cluster membership model showed a greater predictive accuracy for patient and kidney survival than traditional methods based on clinical diagnosis or ANCA specificity.

IN PRACTICE:

“These findings highlight the necessity of recognizing severe kidney disease at the time of diagnosis as an indicator of poor outcome, thereby necessitating intensified treatment approaches,” experts from the Department of Internal Medicine IV (Nephrology and Hypertension), Medical University of Innsbruck, Austria, wrote in an accompanying editorial published online on August 22, 2024, in The Lancet Rheumatology.

SOURCE:

This study was led by Karl Gisslander, Department of Clinical Sciences, Lund University, Lund, Sweden, and was published online on August 22, 2024, in The Lancet Rheumatology.

LIMITATIONS:

Data on estimated glomerular filtration rate recovery in clusters with kidney disease were lacking. Populations from East Asia, where myeloperoxidase-ANCA positivity is more prevalent, were not included.

DISCLOSURES:

This study received funding from the European Union’s Horizon 2020 research and innovation program under the European Joint Programme on Rare Diseases. Some authors declared serving on advisory boards or receiving grants, contracts, travel support, consulting fees, payments, or honoraria from various pharmaceutical companies and other institutions.

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.