Background We investigated the effect of Infliximab, a mouse-human chimaeric monoclonal antibody that binds and inhibits the activity of TNF a, on Lipid Metabolism in patients with Rheumatoid arthritis (RA) and Psoriatic arthritis (Psa).
Methods Fifteen persons hospitalised in our division of rheumatology were studied. Over a period of eight months 5 male and 10 female patients with a mean age of 56,7 years (age range: 30–81) were included in this study. The subjects included 7 patients with rheumatoid arthritis (RA) according to the ARA criteria (12) and 8 patients with Psoriatic arthritis (PsA). Eight patients had been treated with methotrexat (MTX), 4 with other DMARDs than MTX, 2 patients only received NSAIDs and 5 corticosteroids. Treatment resistant patients with active disease (fulfilling inclusions criteria) received infusions of 3 mg/kg infliximab (at week 0, 2, 6 14, 22 and 30). Two of the patients received 4 mg/kg infliximab after 14 weeks. Lipoprotein (a), Cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol were measured by commercially available kits from Boehringer Mannheim (Mannheim, Germany).
Results Infliximab was well tolerated; no toxic effects were observed, no major abnormalities in hematologic findings were noted during or after the study. There was no significant difference either in total cholesterol before and after treatment (209 ± 25 vs. 25 ± 36 mg/dl) or in LDL-cholesterol (1311 ± 24 vs. 1188 ± 4 mg/dl). Lp (a) levels also did not show a change during treatment (median: 1,1 vs. 1,4 mg/dl). However there was a significant rise in triglyceride (TG) levels during treatment with Remicade (1122 ± 48 vs. 1333 ± 5 mg/dl, p < 0.01). HDL levels on the other hand were significantly lowered (566 ± 12 vs. 50 ± 1 mg (dl, p < 0.006) by the treatment. The changes of the main parameters are summarised in Table 1.
Conclusion This study shows that elevated TG and decreased HDL levels occur in patients with RA and PsA after Infliximab therapy. We suggest that these changes in lipid metabolism may be a factor responsible for an increased development of vascular pathology.
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