Sachithanandan S, Fielding J F
Mater Private Hospital, Dublin, Ireland.
J Clin Gastroenterol. 1997 Oct;25(3):522-4. doi: 10.1097/00004836-199710000-00008.
To determine the prevalence of autoimmune disease, autoantibody positivity, or both in Irish persons with hepatitis C, we surveyed 98 such patients (55 recipients of anti-D, 25 intravenous drug abusers, and 18 blood transfusion recipients). We studied them clinically and tested for anti-nuclear, anti-smooth muscle, and anti-mitochondrial, liver-kidney microsomal, thyroid microsomal, thyroid globulin, and gastric parietal antibodies; and also for rheumatoid factor. In the anti-D antibody group (all female), two patients reported generalized musculoskeletal symptoms but had no demonstrable physical signs. We did not find cryoglobulins in any patient. We detected thyroid microsomal antibodies in only 6 of 55 (10.9%) patients. (In two of these, thyroid globulin antibodies were also positive). These patients were all clinically euthyroid, but two had borderline low-normal thyroid function tests. Titers for anti-nuclear antibodies were weakly positive in 5 of 55 (9.1%) patients, and gastric parietal antibodies were positive in 5 of 55 (9.1%) patients. In particular, we noted no antibodies to liver-kidney microsome. Rheumatoid factor was detected in eight patients. Forty-seven of 55 patients were genotype 1b, and 8 of 55 were genotype 3. In the intravenous drug abusers (8 women, 17 men), we detected no autoantibodies. Seven of the 25 genotypes were tested; three were genotype 3 and four were genotype 1b. In the transfusion group (10 women, 8 men), we detected no autoantibodies apart from weak anti-nuclear antibody Titers (1:10), which we found three patients. Five of 10 genotypes tested were of genotype 3 and the other five were of genotype 1b. These findings suggest that in Irish patients with hepatitis C, neither genotype nor source (and dose) of inoculum contributes to the development of autoimmune disease. How hepatitis C virus is associated with autoimmune disease in other studies remains unknown. The answer may, at least in part, be found in genetic; HLA typing studies should provide useful information.
为了确定爱尔兰丙型肝炎患者自身免疫性疾病、自身抗体阳性或两者兼有的患病率,我们调查了98例此类患者(55例抗-D接受者、25例静脉吸毒者和18例输血接受者)。我们对他们进行了临床研究,并检测了抗核抗体、抗平滑肌抗体、抗线粒体抗体、肝肾微粒体抗体、甲状腺微粒体抗体、甲状腺球蛋白抗体和胃壁细胞抗体;还检测了类风湿因子。在抗-D抗体组(均为女性)中,两名患者报告有全身性肌肉骨骼症状,但无明显体征。我们在任何患者中均未发现冷球蛋白。在55例患者中,仅6例(10.9%)检测到甲状腺微粒体抗体。(其中2例甲状腺球蛋白抗体也呈阳性)。这些患者临床甲状腺功能均正常,但有2例甲状腺功能测试结果处于临界低正常范围。55例患者中有5例(9.1%)抗核抗体滴度弱阳性,55例患者中有5例(9.1%)胃壁细胞抗体呈阳性。特别要指出的是,我们未发现肝肾微粒体抗体。8例患者检测到类风湿因子。55例患者中有47例为1b基因型,8例为3基因型。在静脉吸毒者(8名女性,17名男性)中,我们未检测到自身抗体。对25例基因型中的7例进行了检测;3例为3基因型,4例为1b基因型。在输血组(10名女性,8名男性)中,除3例患者抗核抗体滴度弱阳性(1:10)外,我们未检测到其他自身抗体。检测的10例基因型中有5例为3基因型,另外5例为1b基因型。这些发现表明,在爱尔兰丙型肝炎患者中,基因型和接种物的来源(及剂量)均与自身免疫性疾病的发生无关。在其他研究中,丙型肝炎病毒与自身免疫性疾病如何关联尚不清楚。答案可能至少部分存在于基因方面;HLA分型研究应能提供有用信息。