title: Plasma leptin and neuropeptide Y concentrations in patients with rheumatoid arthritis treated with infliximab, a TNF-α antagonist.
abstract: TNF-α is one of the key proinflammatory cytokines in pathogenesis of rheumatoid arthritis (RA). TNF-α was also found to enhance synthesis of leptin. Leptin is mainly adipocyte-derived hormone controlling appetite and energy expenditure. It acts through inhibition of neuropeptide Y secretion. It is possible that TNF-α-induced leptin secretion contributes to body mass reduction in patients with RA. The study was designed to determine the influence of inactivation of the TNF-α with infliximab on plasma leptin and neuropeptide Y concentrations in patients with RA. Sixteen female patients with RA treated with infliximab and 16 healthy women were investigated. Plasma leptin and neuropeptide Y concentrations were determined before, during and after 1 year management of the patients with infliximab and were compared with body mass index and body fatty and lean mass. There was no difference in plasma leptin concentration between the rheumatoid patients before therapy and the controls (15.6 ± 1.85 and 14.5 ± 2.15 ng/ml, respectively). Neuropeptide Y concentration was higher in the patients than in the controls (54.5 ± 3.96 and 24.8 ± 2.80 pmol/l, respectively). Treatment with infliximab resulted in enhancement in leptin concentration (18.5 ± 2.34 ng/ml) and a slight increase in neuropeptide Y concentration (58.7 ± 4.66 pmol/l). Physiological relationship between leptin and body mass was shown in the patients and was not altered during the treatment. There was no significant correlation between the disease activity and plasma leptin or neuropeptide Y concentrations.
authors: Medical University of Silesia, Katowice, Poland. magda.kopec@gazeta.pl
authors: Magdalena
authors: M
authors: Kopec-Medrek
authors: Anna
authors: A
authors: Kotulska
authors: Malgorzata
authors: M
authors: Widuchowska
authors: Marcin
authors: M
authors: Adamczak
authors: Andrzej
authors: A
authors: Więcek
authors: Eugene J
authors: EJ
authors: Kucharz
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy; D015992:Body Mass Index; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D000069285:Infliximab; D020738:Leptin / Q000097:blood*; D008727:Methotrexate / Q000627:therapeutic use; D009478:Neuropeptide Y / Q000097:blood*; D011241:Prednisone / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D020738:Leptin; D009478:Neuropeptide Y; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D011241:Prednisone; D008727:Methotrexate