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Clin Rheumatol (2012) 31:2934
DOI 10.1007/s10067-011-1767-5
ORIGINAL ARTICLE
Tryptophan degradation and neopterin levels in treated rheumatoid arthritis patients
Yesim Ozkan & Guray Mete & Aylin Sepici-Dincel &
Vesile Sepici & Bolkan Simsek
Received: 20 August 2010 /Revised: 20 April 2011 /Accepted: 22 April 2011 /Published online: 10 May 2011 # Clinical Rheumatology 2011
Abstract Increased kynurenine/tryptophanreflects trytophan degradationand neopterin levels have been regarded as a biochemical marker of cell-mediated immune response and inflammation. This study was designed to evaluate the usefulness of tryptophan degradation and neopterin levels in active rheumatoid arthritis patients under therapy. In this case control study, kynurenine and tryptophan levels were determined by HPLC; neopterin and tumor necrosis factor- levels were measured with ELISA in 32 active rheumatoid arthritis patients and 20 healthy controls. Although mean values of tryptophan, kynurenine, ratio of kynurenine to tryptophan, neopterin, and tumor necrosis factor- levels did not show statistically significant differences between patient and control groups, neopterin levels correlated positively with kynurenine (r=0.582, p<0.02), kynurenine/tryptophan (r=0.486, p<0.05), erythrocyte sedimentation rate (r=0.472, p<0.05) and RF (r=0.478, p<0.05) in the rheumatoid arthritis group. CRP levels of the patient group correlated with kynurenine levels (r=0.524, p<0.03). Determination of tryptophan degradation and neopterin levels in chronic inflammatory
disease may provide a better understanding of progression of the disease.
Keywords Indoleamine 2,3-dioxygenase . Kynurenine . Neopterin . Rheumatoid arthritis . Tryptophan
Introduction
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent and uncontrolled inflammation of the joints. Depending on duration of the disease, significant functional losses due to persistent inflammatory activity cause destructions in the joints and bone. Despite current research, the main cause of RA is unclear. Articular inflammation causes activation and proliferation of the synovial lining, expression of inflammatory cytokines, and B cell activation with autoantibody production. Altered cytokine and signal transduction pathways and inhibition of programmed cell death contribute to synoviocyte- and osteoclast-mediated cartilage and bone destruction [1]. Tryptophan (Trp), the least abundant essential amino acid for mammals, is critical in a number of metabolic functions. Apart from protein and serotonin synthesis, kynurenine (Kyn) pathway is a major route of Trp metabolism and accounts for approximately 90% of its catabolism. Regulation of tryptophan levels depends on tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO) activities. Both enzymes...