Anti-TNF-α effects on anemia in rheumatoid and psoriatic arthritis
A key role in the pathogenesis of rheumatoid arthritis (RA) and psoriatic arthritis (PsA) is played by inflammatory cytokines, including tumor necrosis factor-α (TNF-α), which are also involved in inducing inflammatory anemia. We have followed 67 RA patients and 64 PsA patients for 1 year to evaluat...
Gespeichert in:
Veröffentlicht in: | International journal of immunopathology and pharmacology 2017-09, Vol.30 (3), p.302-307 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | A key role in the pathogenesis of rheumatoid arthritis (RA) and psoriatic arthritis (PsA) is played by inflammatory cytokines, including tumor necrosis factor-α (TNF-α), which are also involved in inducing inflammatory anemia. We have followed 67 RA patients and 64 PsA patients for 1 year to evaluate the effects of TNF-α inhibitors on disease activity and on inflammatory anemia. Patients were divided into three different treatment groups, according to a randomized assignment to receive therapy with etanercept, adalimumab, or infliximab. Treatment with anti-TNF-α resulted in a significant reduction in disease activity score-28 (DAS28) values both in RA and PsA patients, already from the third month of treatment (P = 0.01). In both populations, there was an increase in hemoglobin (HB) levels already after 3 months of treatment (P = 0.001), and HB levels were inversely proportional to the disease activity, regardless of the type of medication used. The increased HB values and the reduction of DAS28 values during the observation period suggest the existence of a negative correlation between them both in RA and PsA, regardless of the type of anti-TNF-α used. Our data suggest a pleiotropic action of anti-TNF-α, such as the well-known action on the activity of the disease, and the improvement in inflammatory anemia. |
---|---|
ISSN: | 2058-7384 0394-6320 2058-7384 |
DOI: | 10.1177/0394632017714695 |