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Graves' Hyperthyroidism Showing Transient Hypothyroidism during Interferon Therapy for Chronic Hepatitis Type C

机译:Graves甲亢表现为C型慢性肝炎的干扰素治疗过程中的短暂性甲状腺功能减退

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We report a patient with Graves' disease in whom thyroid function was changed from initial hyperthyroidism to transient hypothyroidism and back to hyperthyroidism during interferon (IFN) therapy. A 43-year-old man was admitted to our hospital to receive IFN treatment for chronic active hepatitis (type C) in June 1998. His thyroid function was normal and testing for thyroid gland antibodies (TSH binding inhibitor immunoglobulins; TBII, anti-thyroglobulin antibodies; TgAb and anti-thyroid peroxidase antibodies; TPOAb) was negative before IFN therapy. The patient had neither history of thyroid disease nor any particular family history. He developed hyperthyroidism four months after its initiation of IFN therapy. When he was hyperthyroid, TBII, the activity of thyroid-stimulating antibodies (TSAb) and thyroid stimulation-blocking antibodies (TSBAb) were 40.2% (normal range, -15 ~ +15.0%), 1201% (normal range, ≤180%) and 52.0% (normal range, ≤45.6%), respectively. Thyroid ~(99m)Tc(technetium)-uptake ratio (Tc-UTR) was 1.07% (normal range, 0.5-3.0%). He transiently developed hypothyroidism in December 1998 and recurrent hyperthyroidism in February 1999. When he was hypothyroid, TBII, TSAb and TSBAb were 74.3%, 769% and 95.9%, respectively. To investigate the mechanism of his fluctuating thyroid status, we serially assessed the serum levels of cytokines (TNF-α, IFN-γ, IL-1β, IL-2, IL-4) and the soluble form of ICAM-1 (sICAM-1) as well as the activities of two types of TSH receptor antibodies (TRAb), TSAb and TSBAb, before and after IFN therapy. There were no characteristic changes of cytokines or sICAM-1 during the follow-up period. The transient hypothyroid state may be explained by two possible mechanisms: one may be due to the shift in the balance between the stimulating and blocking types of TRAb, and the other may be due to the complication of destructive thyroiditis that developed during IFN therapy.
机译:我们报道了一位患有Graves病的患者,在干扰素(IFN)治疗期间,甲状腺功能从最初的甲状腺功能亢进变为短暂性甲状腺功能减退,然后又转变为甲状腺功能亢进。 1998年6月,一名43岁的男子被送往我院接受IFN治疗,治疗慢性活动性肝炎(C型)。他的甲状腺功能正常,正在检测甲状腺抗体(TSH结合抑制剂免疫球蛋白; TBII,抗甲状腺球蛋白)干扰素治疗前,抗体; TgAb和抗甲状腺过氧化物酶抗体; TPOAb)阴性。该患者既没有甲状腺疾病史,也没有任何特殊的家族史。干扰素治疗开始四个月后,他出现甲亢。甲状腺功能亢进症TBII时,甲状腺刺激抗体(TSAb)和甲状腺刺激阻断抗体(TSBAb)的活性分别为40.2%(正常范围,-15〜+15.0%),1201%(正常范围,≤180%) )和52.0%(正常范围,≤45.6%)。甲状腺〜(99m)Tc(tech)摄取率(Tc-UTR)为1.07%(正常范围为0.5-3.0%)。他于1998年12月短暂发展为甲状腺功能减退,1999年2月为甲状腺功能亢进。甲状腺功能减退时,TBII,TSAb和TSBAb分别为74.3%,769%和95.9%。为了研究他的甲状腺状态波动的机制,我们连续评估了血清中的细胞因子(TNF-α,IFN-γ,IL-1β,IL-2,IL-4)和ICAM-1(sICAM- 1)以及IFN治疗前后两种类型的TSH受体抗体(TRAb),TSAb和TSBAb的活性。在随访期间,细胞因子或sICAM-1没有特征性变化。短暂性甲状腺功能减退状态可以用两种可能的机制来解释:一种可能是由于TRAb的刺激性和阻断性之间的平衡发生转移,另一种可能是由于IFN治疗期间发生的破坏性甲状腺炎的并发症。

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