Non-islet cell tumor-induced hypoglycemia associated with macronodular pulmonary metastases from poorly differentiated thyroid carcinoma.

Non-islet cell tumor-induced hypoglycemia associated with macronodular pulmonary metastases from poorly differentiated thyroid carcinoma.
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DOI:
10.1089/thy.2013.0141
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发表时间:
2014
期刊:
Thyroid : official journal of the American Thyroid Association
影响因子:
--
通讯作者:
T. Morioka;K. Ohba;H. Morita;G. Takahashi;H. Uchida;A. Matsushita;S. Sasaki;Y. Oki;T. Suda;K. Kakudo;A. Yoshino
T. Morioka;K. Ohba;H. Morita;G. Takahashi;H. Uchida;A. Matsushita;S. Sasaki;Y. Oki;T. Suda;K. Kakudo;A. Yoshino
中科院分区:
其他
文献类型:
--
作者:
T. Morioka;K. Ohba;H. Morita;G. Takahashi;H. Uchida;A. Matsushita;S. Sasaki;Y. Oki;T. Suda;K. Kakudo;A. Yoshino

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背景:非胰岛细胞肿瘤诱导性低血糖(NICTh)是空腹低血糖的主要原因,其原因是高相对分子质量的胰岛素样生长因子-II(IGF-II)分泌过多,称为“大”IGF-II。据我们所知,目前仅有两例与NicTh相关的甲状腺癌病例被记录在案。患者发现我们报告了一例72岁的女性,她被带到急诊科,意识受损。患者有低分化甲状腺癌(PDTC)肺转移的病史,自最初治疗以来已有12年。实验室测试显示,即使检测不到免疫反应性胰岛素、IGF-I和生长激素(GH),血糖水平也有所下降。CT扫描显示肺大结节状转移灶,体积估计为456ml。生化数据和成像结果都表明是NicTh。对分离的血清样本进行的Western印迹分析结果显示,大IGF-II的表达增加,这是诊断NicTh的重要指标。由于巨大的肺转移瘤被认为是不能手术的,所以对储存的福尔马林固定的石蜡包埋组织进行了免疫组织化学分析。分析表明,肿瘤细胞IGF-II和甲状腺球蛋白均为阳性。全身CT检查排除肺外转移灶。一项回顾显示,糖化血红蛋白水平逐渐降低,同时估计的肺转移灶体积增加。这些结果表明,NicTh是由PDTC的肺转移引起的。结论我们在此描述了第三例与甲状腺癌相关的NICTh病例。这也是第一例报道甲状腺癌患者血清中有大量IGF-II的病例。
BACKGROUND Non-islet cell tumor-induced hypoglycemia (NICTH), a major cause of fasting hypoglycemia, is caused by the overproduction of incompletely processed, high molecular-weight insulin-like growth factor-II (IGF-II), termed "big" IGF-II. To the best of our knowledge, only two cases of thyroid carcinoma associated with NICTH have been documented. PATIENT FINDINGS We report the case of a 72-year-old woman who was brought to the emergency department with impaired consciousness. The patient had a history of pulmonary metastases from poorly differentiated thyroid carcinoma (PDTC), spanning 12 years since initial treatment. Laboratory tests showed decreased plasma glucose levels even though immunoreactive insulin, IGF-I, and growth hormone (GH) were undetectable. Computed tomography (CT) scan revealed macronodular pulmonary metastases the estimated volume of which was 456 mL. Both the biochemical data and imaging results suggested NICTH. The results of Western blot analysis performed on a fractionated serum sample showed an increased expression of big IGF-II, an important indicator in the diagnosis of NICTH. Because the massive pulmonary metastases were considered inoperable, immunohistochemical analysis of stored formalin-fixed, paraffin-embedded tissues was performed. The analysis revealed that the tumor cells were positive for both IGF-II and thyroglobulin. A whole-body CT excluded extrapulmonary metastatic lesions. A retrospective review revealed a gradual decrease in glycohemoglobin levels accompanied by an increase in the estimated volume of pulmonary metastases. These findings suggested that NICTH had been caused by pulmonary metastases from PDTC. CONCLUSIONS We describe here the third reported case of NICTH associated with thyroid carcinoma. This is also the first case reporting big IGF-II in the serum of a patient with thyroid carcinoma.