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May 2024

Correlations of IL-6 as a humoral disease activity parameter with ESR CRP and serum cortisol in active rheumatoid-arthritis

Journal/Book: Z Rheumatol 1999; 58: 312-314. 1999;

Abstract: B. Boss G. Neeck; Kerckhoff Klinik Rheumatologie Stiftung W. G. Kerckhoff Herz- und Rheumazentrum Bad Nauheim Introduction RA is a systemic rheumatic disease of unknown etiology [1] defined by the revised classification criteria of the American College of Rheumatology (ACR) of 1987 [2]. Different proinflammatory cytokines are released in its pathogenesis like IL-6 as one of the most important mediators of the acute phase response (APR) [3] or IL-1 and to a lesser extent TNFa as mediators mostly of local joint inflammation less of systemic effects [2]. In chronic inflammatory conditions like RA disease activity is usually monitored by the erythrocyte sedimentation rate (ESR) and C reactive protein (CRP). These parameters reflect changes of disease activity after several hours (CRP) or days (ESR) [3]. Use of proinflammatory cytokines as possible parameters of disease activity in RA is discussed controversial [3]. We examined correlations of the proinflammatory cytokines IL-6 IL-1a and the sIL-2R with the classical humoral inflammatory parameters ESR and CRP. These parameters were also correlated with the clinical disease activity parameters MST and pain intensity which are known to reflect the disease activity of RA very close [7 8] and with serum cortisol. An activation of the hypothalamic-pituary-adrenal (HPA) axis with elevated cortisol secretion and a disturbed circadian cortisol rhythm in RA depending on disease activity is known and seems to play an important role during the inflammatory processes in RA [4]. Although a pathological resistance of the HPA-axis to circulating IL-6 and other proinflammatory cytokines in active RA is suggested [5]. Patients and methods We studied 64 patients who fulfilled the ACR classification criteria [2] with active RA 10 male 54 female and were previously never treated with CS. ... le


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