title: Plasma homocysteine status in patients with ankylosing spondylitis.
abstract: Homocysteine (Hcy), a sulfur-containing amino acid, is eliminated through B vitamins-dependent pathways. Hyperhomocysteinemia has been found to be an independent risk factor for atherosclerotic cardiovascular, cerebrovascular, and peripheral vascular diseases. Recently, psoriasis, lupus, and rheumatoid arthritis were reported to be associated with hyperhomocysteinemia. This study was aimed to evaluate the changes of plasma Hcy level before and after sulfasalazine and MTX therapy in patients with ankylosing spondylitis (AS). One hundred and two patients with AS and ten normal controls were enrolled in the cross-sectional case-control study. Fasting plasma Hcy levels were determined by ELISA kits (IMX, Abbott). Hcy levels were compared to their Bath AS disease activity index (BASDAI) and the usage of sulfasalazine and/or MTX. Active disease was defined by BASDAI as more than 3 in a 10-cm scale with ESR >20 mm/h. For those patients with plasma Hcy >or=15 micromol/l, a perspective trial of daily supplement of vitamin B-12 0.5 mg, B-6 50 mg, and folic acid 5 mg for 2 weeks were also tested for the efficacy. Plasma Hcy level increased significantly in AS patients under sulfasalazine (10.4+/-3.8 micromol/l, p<0.05), MTX (11.9+/-4.7, p<0.05) and sulfasalazine/MTX combination treatment (11.2+/-2.6, p<0.05) compared with normal controls (8.6+/-1.2 micromol/l) and AS patients without DMARD(9.4+/- 2.6 micromol/l). No correlation between disease activity and plasma Hcy level was found. Daily supplement of vitamin B-12 0.5 mg, B-6 50 mg, and folic acid 5 mg can lower Hcy level in 2 weeks (32.3+/-24.0 vs 15.6+/-11.1 micromol/l, p=0.007). Plasma homocysteine level did significantly increase in AS patients under sulfasalazine or MTX treatment. B-vitamins should be considered as a routine supplementation for patients who underwent sulfasalazine and/or MTX treatment. Further longitudinal studies are required to confirm the conclusions.
authors.affiliation: Division of Allergy, Immunology and Rheumatology, Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: James Cheng-Chung
authors.initials: JC
authors.lastname: Wei
authors.forename: Ming-Shiou
authors.initials: MS
authors.lastname: Jan
authors.forename: Chen-Tung
authors.initials: CT
authors.lastname: Yu
authors.forename: Yi-Chia
authors.initials: YC
authors.lastname: Huang
authors.forename: Chi-Chiang
authors.initials: CC
authors.lastname: Yang
authors.forename: Hsi-Kai
authors.initials: HK
authors.lastname: Tsou
authors.forename: Hong-Shan
authors.initials: HS
authors.lastname: Lee
authors.forename: Chang-Tei
authors.initials: CT
authors.lastname: Chou
authors.forename: Gregory
authors.initials: G
authors.lastname: Tsay
authors.forename: Ming-Chih
authors.initials: MC
authors.lastname: Chou
mesh_terms: D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004359:Drug Therapy, Combination; D006710:Homocysteine / Q000097:blood* / Q000187:drug effects; D006801:Humans; D008727:Methotrexate / Q000494:pharmacology / Q000627:therapeutic use*; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy*; D012460:Sulfasalazine / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D018501:Antirheumatic Agents; D006710:Homocysteine; D012460:Sulfasalazine; D008727:Methotrexate