Gordon C, Bradley H, Waring R H, Emery P
Department of Rheumatology, University of Birmingham, UK.
Lancet. 1992 Jan 4;339(8784):25-6. doi: 10.1016/0140-6736(92)90144-r.
S-carboxy-L-methylcysteine was used to assess the activity of the S-oxidation pathway of sulphur metabolism in 35 patients with systemic lupus erythematosus (SLE); 25 (71%) showed impaired sulphoxidation and 21 (60%) produced virtually no sulphoxides, compared with 17 (36%) and 2 (4%), respectively, of 47 healthy controls. The substrate/product ratio of cysteine oxygenase (plasma cysteine/sulphate) was significantly higher in SLE patients than in controls (median [interquartile range] 362 [224-588] vs 65 [44-111]; p less than 0.00001). The alternative pathway of sulphur metabolism, S-methylation, catalysed by thiolmethyltransferase, was not impaired in the SLE patients. There is a biochemical difference in sulphur metabolism between SLE and rheumatoid arthritis, since both pathways are impaired in the latter disorder.
使用S-羧基-L-甲基半胱氨酸评估35例系统性红斑狼疮（SLE）患者硫代谢的S-氧化途径活性；与47名健康对照者中分别为17例（36%）和2例（4%）相比，25例（71%）患者硫氧化受损，21例（60%）几乎不产生亚砜。SLE患者中半胱氨酸加氧酶的底物/产物比（血浆半胱氨酸/硫酸盐）显著高于对照组（中位数[四分位间距]362[224 - 588] vs 65[44 - 111]；p<0.00001）。硫代谢的另一条途径，即由硫醇甲基转移酶催化的S-甲基化，在SLE患者中未受损。SLE与类风湿性关节炎在硫代谢方面存在生化差异，因为在后者疾病中两条途径均受损。
