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Published in: Clinical Rheumatology 5/2007

01-05-2007 | Original Article

Plasma homocysteine status in patients with ankylosing spondylitis

Authors: James Cheng-Chung Wei, Ming-Shiou Jan, Chen-Tung Yu, Yi-Chia Huang, Chi-Chiang Yang, Hsi-Kai Tsou, Hong-Shan Lee, Chang-Tei Chou, Gregory Tsay, Ming-Chih Chou

Published in: Clinical Rheumatology | Issue 5/2007

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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 ≥15 μmol/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 μmol/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 μmol/l) and AS patients without DMARD(9.4± 2.6μmol/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 μmol/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.
Literature
1.
go back to reference Montalescot G, Ankri A, Chadefaux-Vekemans B et al (1997) Plasma homocysteine and the extent of atherosclerosis in patients with coronary artery disease. Int J Cardiol 60:295–300PubMedCrossRef Montalescot G, Ankri A, Chadefaux-Vekemans B et al (1997) Plasma homocysteine and the extent of atherosclerosis in patients with coronary artery disease. Int J Cardiol 60:295–300PubMedCrossRef
2.
go back to reference Boers GH, Smals AG, Trijbels FJ et al (1985) Heterozygosity for homocystinuria in premature peripheral and cerebral occlusive arterial disease. N Engl J Med 313:709–815PubMedCrossRef Boers GH, Smals AG, Trijbels FJ et al (1985) Heterozygosity for homocystinuria in premature peripheral and cerebral occlusive arterial disease. N Engl J Med 313:709–815PubMedCrossRef
3.
go back to reference Taylor LM Jr, DeFrang RD, Harris EJ Jr, Porter JM (1991) The association of elevated plasma homocyst(e)ine with progression of symptomatic peripheral arterial disease. J Vasc Surg 13:128–136PubMedCrossRef Taylor LM Jr, DeFrang RD, Harris EJ Jr, Porter JM (1991) The association of elevated plasma homocyst(e)ine with progression of symptomatic peripheral arterial disease. J Vasc Surg 13:128–136PubMedCrossRef
4.
go back to reference Brattstrom LE, Hardebp E, Hultberg BL (1984) Moderate homocysteinemia—a possible risk factor for arteriosclerotic cerebrovascular disease. Stroke 15:1012–1016PubMed Brattstrom LE, Hardebp E, Hultberg BL (1984) Moderate homocysteinemia—a possible risk factor for arteriosclerotic cerebrovascular disease. Stroke 15:1012–1016PubMed
5.
go back to reference Hornung N, Ellingsen T, Stengaard-Pedersen K, Poulsen JH (2004) Folate, homocysteine, and cobalamin status in patients with rheumatoid arthritis treated with methotrexate, and the effect of low dose folic acid supplement. J Rheumatol 31(12):2374–2381PubMed Hornung N, Ellingsen T, Stengaard-Pedersen K, Poulsen JH (2004) Folate, homocysteine, and cobalamin status in patients with rheumatoid arthritis treated with methotrexate, and the effect of low dose folic acid supplement. J Rheumatol 31(12):2374–2381PubMed
6.
go back to reference Krogh Jensen M, Ekelund S, Svendsen L (1996) Folate and homocysteine status and haemolysis in patients treated with sulphasalazine for arthritis. Scand J Clin Lab Invest 56(5):421–429PubMed Krogh Jensen M, Ekelund S, Svendsen L (1996) Folate and homocysteine status and haemolysis in patients treated with sulphasalazine for arthritis. Scand J Clin Lab Invest 56(5):421–429PubMed
7.
go back to reference Chilvers MM, Wordsworth P, Stubbs A, Gao XM (1998) TCR usage by homocysteine-specific human CTL. J Immunol 160(8):3737–3742PubMed Chilvers MM, Wordsworth P, Stubbs A, Gao XM (1998) TCR usage by homocysteine-specific human CTL. J Immunol 160(8):3737–3742PubMed
8.
go back to reference Divecha H, Sattar N, Rumley A, Cherry L, Lowe GD, Sturrock R (2005) Cardiovascular risk parameters in men with ankylosing spondylitis in comparison with non-inflammatory control subjects: relevance of systemic inflammation. Clin Sci (Lond) 109(2):171–176CrossRef Divecha H, Sattar N, Rumley A, Cherry L, Lowe GD, Sturrock R (2005) Cardiovascular risk parameters in men with ankylosing spondylitis in comparison with non-inflammatory control subjects: relevance of systemic inflammation. Clin Sci (Lond) 109(2):171–176CrossRef
9.
go back to reference Gao XM, Wordsworth P, McMichael AJ, Kyaw MM, Seifert M, Rees D et al (1996) Homocysteine modification of HLA antigens and its immunological consequences. Eur J Immunol 26(7):1443–1450PubMedCrossRef Gao XM, Wordsworth P, McMichael AJ, Kyaw MM, Seifert M, Rees D et al (1996) Homocysteine modification of HLA antigens and its immunological consequences. Eur J Immunol 26(7):1443–1450PubMedCrossRef
10.
go back to reference D’Angelo A, Selhub J (1997) Homocysteine and thrombotic disease. Blood 90:1–11PubMed D’Angelo A, Selhub J (1997) Homocysteine and thrombotic disease. Blood 90:1–11PubMed
11.
go back to reference Clarke R, Daly L, Robinson K et al (1991) Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med 324:1149–1155PubMedCrossRef Clarke R, Daly L, Robinson K et al (1991) Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med 324:1149–1155PubMedCrossRef
Metadata
Title
Plasma homocysteine status in patients with ankylosing spondylitis
Authors
James Cheng-Chung Wei
Ming-Shiou Jan
Chen-Tung Yu
Yi-Chia Huang
Chi-Chiang Yang
Hsi-Kai Tsou
Hong-Shan Lee
Chang-Tei Chou
Gregory Tsay
Ming-Chih Chou
Publication date
01-05-2007
Publisher
Springer-Verlag
Published in
Clinical Rheumatology / Issue 5/2007
Print ISSN: 0770-3198
Electronic ISSN: 1434-9949
DOI
https://doi.org/10.1007/s10067-006-0396-x

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