Nishiyama S, Matsukura M, Fujimoto S, Matsuda I
Eur J Pediatr. 1983 Apr;140(2):116-7. doi: 10.1007/BF00441656.
Two cases, one a 15-year-old girl and the other a 12-year-old girl, with goitrous hypothyroidism associated with elevated anti-DNA and antithyroid antibodies are reported. Abnormalities were noticed 1 year and 3 months and 5 years after the start of anticonvulsant therapy in case 1 and case 2, respectively. Alternation of drug (Valproate from ethosuximide) in case 1 resulted in disappearance of the goitre, and the thyroid function tests became normal. The titers of the antithyroglobulin and the antimicrosomal antibodies were reduced (below 1:100) from 1:400 and 1:1600, respectively. Discontinuance of anticonvulsant therapy and replacement therapy with desiccated thyroid in case 2 resulted in clinical improvement, reduction of antithyroglobulin antibody from 1:6400 to 1:400 and of antimicrosomal antibody from 1:409,600 to 1:25,600, and the thyroid function tests becoming normal. The present observations suggest that the anticonvulsants may induce or exacerbate autoimmune mechanisms in certain thyroid diseases.
报告了两例患有甲状腺肿性甲状腺功能减退症且抗DNA和抗甲状腺抗体升高的病例,一例为15岁女孩,另一例为12岁女孩。病例1和病例2分别在抗惊厥治疗开始后1年3个月和5年出现异常。病例1中药物更换(从乙琥胺换成丙戊酸盐)导致甲状腺肿消失,甲状腺功能测试恢复正常。抗甲状腺球蛋白和抗微粒体抗体滴度分别从1:400和1:1600降至(低于1:100)。病例2中停用抗惊厥治疗并用干燥甲状腺进行替代治疗后,临床症状改善,抗甲状腺球蛋白抗体从1:6400降至1:400,抗微粒体抗体从1:409,600降至1:25,600,甲状腺功能测试恢复正常。目前的观察结果表明,抗惊厥药物可能在某些甲状腺疾病中诱发或加剧自身免疫机制。