ORIGINAL ARTICLE Tien-Tsai Cheng Æ Han-Ming Lai Æ Hsueh-Wen Chang Shue-Fen Luo Elevated serum homocysteine levels for gouty patients Received: 25 August 2003 / Accepted: 19 April 2004 / Published online: 16 September 2004 Ó Clinical Rheumatology 2004 Abstract Our objective was to analyze serum total homocysteine (tHcy) levels for gouty patients and to study whether there are any level changes following treatment with allopurinol. We enrolled 90 male par- ticipants including patients with primary gout (n=51) and community-based healthy controls (n=39). Fasting tHcy levels were determined for all subjects and repeat measurements performed for 29 patients following treatment with allopurinol. The results revealed that gouty patients exhibited significantly greater serum tHcy levels (12.10±3.19 lmol/l) than healthy controls did (9.96±2.16 lmol/l) (p=0.0003), although there was no obvious difference between the pre-allopurinol treatment group (12.54±3.31 lmol/l) and its post-treatment ana- logue (11.90±4.68 lmol/l) (n=29, p=0.33). Elevated serum levels of tHcy were noted for this cohort of male gouty patients as compared to healthy controls, and these tHcy levels did not appear to change substantially following treatment with allopurinol. Although the pathogenesis of hyperhomocysteinemia for gouty patients still remains somewhat obscure, this study suggests that tHcy levels cannot be effectively modulated by treatment with allopurinol. Keywords Allopurinol Æ Gouty arthritis Æ Homocysteine Introduction Homocysteine (Hcy) is a nonessential, sulfur-containing amino acid, produced as a result of the transmethylation of amino acids during normal metabolism. The rela- tionship between severe hyperhomocysteinemia and arterial disease was first suggested in 1975 by McCully [1]. Hcy is currently well recognized as an independent risk factor for cardiovascular disease [2] and may be associated with cardiovascular events for cases of vari- ous collagen diseases [3, 4]. An increased leves of Hcy is now believed to constitute an important factor for endothelial cell damage processes and potentially medi- ates the subsequent vascular complications [5]. Elevated Hcy levels can be precipitated by genetic and nongenetic factors, relevant nongenetic factors including nutritional deficiency leading to low plasma folate and/or vitamin B 12 levels [6], renal insufficiency [7], certain drug therapy [8], and some chronic inflammatory diseases [3, 9]. Gouty patients exhibit a higher mortality rate than is the case for the general population especially when preceded by cerebrocardiovascular events [10, 11]. Gouty patients typically demonstrate risk factors similar to individuals suffering from cardiovascular diseases, e.g., male gender, smoking, hypertension, hyperlipid- emia, and obesity, all of which may contribute to the observed association between gout and cardiovascular events. Nevertheless, disturbed Hcy metabolism as another independent atherogenic risk factor for patients with gout had not been well studied previously. Materials and methods This investigation was a prospective, case-control study incorporating 51 male patients suffering from primary T.-T. Cheng Æ S.-F. Luo Graduate Institute of Clinical Medical Sciences, Chang Gung University, Kaohsiung, Taiwan, ROC T.-T. Cheng Æ H.-M. Lai Department of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, 123, Ta Pei Road, Niao Sung Hsiang, Kaohsiung, Taiwan, ROC H.-W. Chang Department of Biological Sciences, National Sun Yet-Sen University, Kaohsiung, Taiwan, ROC S.-F. Luo (&) Department of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, No. 5 Fu Shin St., Kuel-Shan, Tao-Yuan, Taiwan, ROC E-mail: lsf00076@adm.cgmh.org.tw Tel.: +886-33281200 Fax: +886-33277970 Clin Rheumatol (2005) 24: 103–106 DOI 10.1007/s10067-004-0978-4