Tran Huy A
Department of Clinical Chemistry, Hunter Area Pathology Service, John Hunter Hospital, New South Wales, Australia.
Endocr Pract. 2006 May-Jun;12(3):288-93. doi: 10.4158/EP.12.3.288.
To report a case of resistance to thyroid hormone compounded by autoimmune primary hypothyroidism and to discuss the unusual pattern of results of thyroid function tests.
A clinical case history is presented and illustrated with laboratory findings. The difficulty of monitoring the patient's response to levothyroxine supplement is also discussed, and relevant issues are addressed, including reviews of the literature.
A 45-year-old woman presented with longstanding and nonspecific symptoms of general anxiety and lethargy. Clinically, she was assessed to be euthyroid with no goiter. Her thyrotropin (thyroid-stimulating hormone or TSH) level was 43.6 (1/4)IU/mL, free thyroxine was 27.6 pmol/L, and free triiodothyronine was 7.8 pmol/L. Her anti-thyroid peroxidase titer was 1:102,400. Primary hypothyroidism was diagnosed, and treatment with 50 (1/4)g of levothyroxine daily was initiated, with progressive dose escalation. The patient, however, had thyrotoxic symptoms when her TSH was rendered "normal." The patient then discontinued her levothyroxine therapy, with a consequent elevation of her TSH level to 170.8 (1/4)IU/mL in conjunction with severe lethargy and lassitude. Biochemical evidence of metabolic disturbances was also present at the time, with hypercholesterolemia and elevated creatine kinase concentration. Rechallenge with levothyroxine resulted in considerable improvement in her biochemical findings and symptoms.
This patient has an interesting combination of autoimmune primary hypothyroidism and resistance to thyroid hormone. Levothyroxine replacement therapy was complicated by the nonspecificity of symptoms and the lack of an established TSH target value in this condition. Consideration should be given to using the affected family members' mean TSH level, when available, as a target guide for replacement therapy.
报告一例合并自身免疫性原发性甲状腺功能减退症的甲状腺激素抵抗病例,并探讨甲状腺功能检查结果的异常模式。
呈现临床病例病史并辅以实验室检查结果说明。还讨论了监测患者对左甲状腺素补充剂反应的困难,并阐述了相关问题,包括文献综述。
一名45岁女性出现长期存在的非特异性全身焦虑和乏力症状。临床评估显示她甲状腺功能正常,无甲状腺肿大。她的促甲状腺激素(甲状腺刺激激素或TSH)水平为43.6(¼)IU/mL,游离甲状腺素为27.6 pmol/L,游离三碘甲状腺原氨酸为7.8 pmol/L。她的抗甲状腺过氧化物酶滴度为1:102,400。诊断为原发性甲状腺功能减退症,开始每日服用50(¼)μg左甲状腺素,并逐渐增加剂量。然而,当她TSH水平恢复“正常”时,患者出现甲状腺毒症症状。随后患者停用左甲状腺素治疗,结果TSH水平升高至170.8(¼)IU/mL,同时伴有严重的乏力和倦怠。当时还存在代谢紊乱的生化证据,即高胆固醇血症和肌酸激酶浓度升高。重新使用左甲状腺素治疗后,她的生化检查结果和症状有了显著改善。
该患者患有自身免疫性原发性甲状腺功能减退症和甲状腺激素抵抗这一有趣的组合。左甲状腺素替代治疗因症状的非特异性以及在这种情况下缺乏既定的TSH目标值而变得复杂。如有可能,应考虑将受影响家庭成员的平均TSH水平作为替代治疗的目标指南。