Various dermatological conditions have been reported during tumor necrosis factor (TNF)-alpha-blocking therapy, but until now no prospective studies have been focused on this aspect. The present study was set up to investigate the number and nature of clinically important dermatological conditions during TNF-alpha-blocking therapy in patients with rheumatoid arthritis (RA). RA patients starting on TNF-alpha-blocking therapy were prospectively followed up. The numbers and natures of dermatological events giving rise to a dermatological consultation were recorded. The patients with a dermatological event were compared with a group of prospectively followed up RA control patients, naive to TNF-alpha-blocking therapy and matched for follow-up period. 289 RA patients started TNF-alpha-blocking therapy. 128 dermatological events were recorded in 72 patients (25%) during 911 patient-years of follow-up. TNF-alpha-blocking therapy was stopped in 19 (26%) of these 72 patients because of the dermatological event. More of the RA patients given TNF-alpha-blocking therapy (25%) than of the anti-TNF-alpha-naive patients (13%) visited a dermatologist during follow-up (P < 0.0005). Events were recorded more often during active treatment (0.16 events per patient-year) than during the period of withdrawal of TNF-alpha-blocking therapy (0.09 events per patient-year, P < 0.0005). The events recorded most frequently were skin infections (n = 33), eczema (n = 20), and drug-related eruptions (n = 15). Other events with a possible relation to TNF-alpha-blocking therapy included vasculitis, psoriasis, drug-induced systemic lupus erythematosus, dermatomyositis, and a lymphomatoid-papulosis-like eruption. This study is the first large prospective study focusing on dermatological conditions during TNF-alpha-blocking therapy. It shows that dermatological conditions are a significant and clinically important problem in RA patients receiving TNF-alpha-blocking therapy.
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http://dx.doi.org/10.1186/ar1724 | DOI Listing |
Cartilage
July 2024
Section of Orthopedic Surgery, Pingtung Christian Hospital, Pingtung, Taiwan.
Objective: Mounting evidence suggests that histone deacetylases (HDAC) inhibitors reduce cartilage destruction in animal models of osteoarthritis (OA). Tumor necrosis factor (TNF)-α-blocking treatment for OA may provide effective joint protection by slowing joint damage. To investigate the effects of intraperitoneal administration of etanercept (a TNF-α inhibitor) on OA development in rats and changes in the nociceptive behavior of rats and expression of HDACs, RUNX2, and MMP13 in cartilage.
View Article and Find Full Text PDFNed Tijdschr Geneeskd
May 2024
Amsterdam UMC, locatie VUmc, MS Centrum Amsterdam, afd. Neurologie, Amsterdam.
Multiple sclerosis is a chronic inflammatory disease of the central nervous system, caused by an autoimmune reaction. Treatment options have largely increased over the years. In this article, we present two clinical cases.
View Article and Find Full Text PDFEur Arch Otorhinolaryngol
May 2024
Dermatology Department, Hospital Universitari de Bellvitge, Universitat de Barcelona (UB), IDIBELL, Feixa Llarga, s/n, 08907, L'Hospitalet de Llobregat, Spain.
Purpose: To investigate the clinical manifestations, management and outcomes of Leishmania lesions in the ear-nose-throat (ENT) region, and its relationship with tumor necrosis factor (TNF)-α blocking drugs.
Methods: Single-center retrospective observational study. Patients diagnosed with cutaneous and mucosal leishmaniasis in the otorhinolaryngologic area at a tertiary referral center over a period of 8 years.
Cells
December 2023
Department of Medicine, Surgery and Neuroscience, University of Siena, Viale Bracci 2, 53100 Siena, Italy.
This review analyzes the role of TNF-α and its increase in biological fluids in mild cognitive impairment, and Alzheimer's disease (AD). The potential inhibition of TNF-α with pharmacological strategies paves the way for preventing AD and improving cognitive function in people at risk for dementia. We conducted a narrative review to characterize the evidence in relation to the involvement of TNF-α in AD and its possible therapeutic inhibition.
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