Miyakawa M, Sato K, Hasegawa M, Nagai A, Sawada T, Tsushima T, Takano K
Department of Internal Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical University, Japan.
Thyroid. 2001 Sep;11(9):883-8. doi: 10.1089/105072501316973154.
A 50-year-old woman who had undergone lung lobectomy because of lung adenocarcinoma presented with thyrotoxicosis, neck swelling, and cervical lymphadenopathy one month after the operation. The total serum triiodothyronine (T3) and thyroxine (T4) levels were markedly elevated to 514 ng/dL and 26.4 microg/dL, respectively, and serum thyrotropin (TSH) was suppressed to less than 0.005 microU/mL. Although the thyroid gland had been normal before surgery, chest computed tomography (CT) scan revealed a markedly enlarged thyroid gland only 1 month after surgery. 123I uptake for 24 hours was suppressed to 4% in the thyroid gland with no uptake elsewhere including the lung. Fine-needle aspiration cytology (FNAC) of the thyroid showed invasion of poorly differentiated adenocarcinoma cells, cytologically identical to the cells obtained from sputum and those infiltrating the resected sections of the lung adenocarcinoma. Immunohistochemical studies of resected lung tissues did not show positive staining for thyroglobulin, carcinoembryonic antigen (CEA), or surfactant protein A. Clinically, the thyrotoxicosis had spontaneously improved, followed by a hypothyroid state with shrinkage of the thyroid gland after chemotherapy. Despite repeated chemotherapy and the administration of thyroxine for hypothyroidism, the patient died of respiratory failure 9 months after the onset of thyrotoxicosis. From these findings and the clinical course, thyroid metastasis, developing subacutely from lung adenocarcinoma, was diagnosed. We speculate that aggressive invasion of tumor cells into the thyroid gland resulted in highly destructive thyrotoxicosis.
一名50岁女性因肺腺癌接受了肺叶切除术，术后1个月出现甲状腺毒症、颈部肿胀和颈部淋巴结病。血清总三碘甲状腺原氨酸（T3）和甲状腺素（T4）水平分别显著升高至514 ng/dL和26.4 μg/dL，血清促甲状腺激素（TSH）被抑制至低于0.005 μU/mL。尽管术前甲状腺正常，但胸部计算机断层扫描（CT）显示术后仅1个月甲状腺就明显肿大。甲状腺24小时123I摄取率被抑制至4%，其他部位包括肺部均无摄取。甲状腺细针穿刺细胞学检查（FNAC）显示有低分化腺癌细胞浸润，细胞学上与痰液中及肺腺癌切除标本中浸润的细胞相同。切除的肺组织免疫组化研究未显示甲状腺球蛋白、癌胚抗原（CEA）或表面活性蛋白A的阳性染色。临床上，甲状腺毒症自发改善，随后在化疗后出现甲状腺功能减退状态且甲状腺缩小。尽管反复化疗并给予甲状腺素治疗甲状腺功能减退，但患者在甲状腺毒症发作9个月后死于呼吸衰竭。根据这些发现及临床病程，诊断为肺腺癌亚急性发生的甲状腺转移。我们推测肿瘤细胞对甲状腺的侵袭性侵犯导致了具有高度破坏性的甲状腺毒症。
