Scheuba C, Kaserer K, Moritz A, Drosten R, Vierhapper H, Bieglmayer C, Haas O A, Niederle B
Department of Surgery, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
Endocr Relat Cancer. 2009 Mar;16(1):243-53. doi: 10.1677/ERC-08-0059. Epub 2008 Nov 5.
'Calcitonin screening' is not accepted as the standard of care in daily practice. The clinical and surgical consequences of 'calcitonin screening' in a series of patients with mildly elevated basal calcitonin and pentagastrin stimulated calcitonin levels are presented. 260 patients with elevated basal (>10 pg/ml) and stimulated calcitonin levels (>100 pg/ml) were enrolled in this prospective study. None of the patients was member of a known medullary thyroid carcinoma family. Thyroidectomy and bilateral central and lateral neck dissections were performed. Testing for the presence of germ-line mutations was performed in all patients. Histological and immunohistochemical findings were compared with basal and stimulated calcitonin levels. All patients were subsequently followed biochemically. C-cell hyperplasia (CCH) was found in 126 (49%) and medullary thyroid cancer was found in 134 (51%) patients. RET proto-oncogen mutations were documented in 22 (8%) patients (medullary thyroid cancer:18, CCH:4). In 56 (46%) of 122 patients, sporadic CCH was classified neoplastic ('carcinoma in situ'). Of 97 (72%; 10 with hereditary medullary thyroid cancer) had pT1 (International Union against Cancer recommendations 2002) and 33 (25%) had pT2 or pT3 and 4 (3%) pT4 tumors. Of 39 (29.1%) had lymph node metastases. 106 (79.1%; 15 (38.5%) with lymph node metastases) patients were cured. Evaluation of basal and stimulated calcitonin levels enables the prediction of medullary thyroid cancer. All patients with basal calcitonin >64 pg/ml and stimulated calcitonin >560 pg/ml have medullary thyroid cancer. Medullary thyroid cancer was documented in 20% of patients with basal calcitonin >10 pg/ml but <64 pg/ml and stimulated calcitonin >100 pg/ml but <560 pg/ml.
“降钙素筛查”在日常临床实践中未被视为标准治疗方法。本文介绍了一系列基础降钙素轻度升高且经五肽胃泌素刺激后降钙素水平升高的患者进行“降钙素筛查”后的临床及手术结果。260例基础降钙素水平（>10 pg/ml）和刺激后降钙素水平（>100 pg/ml）升高的患者纳入了这项前瞻性研究。所有患者均非已知甲状腺髓样癌家族成员。患者均接受了甲状腺切除术及双侧中央区和侧颈部淋巴结清扫术。对所有患者进行了生殖系突变检测。将组织学和免疫组化结果与基础及刺激后降钙素水平进行比较。所有患者随后均接受生化随访。126例（49%）患者发现C细胞增生（CCH），134例（51%）患者发现甲状腺髓样癌。22例（8%）患者记录有RET原癌基因突变（甲状腺髓样癌：18例，CCH：4例）。122例患者中有56例（46%）散发性CCH被归类为肿瘤性（“原位癌”）。97例（72%；其中10例为遗传性甲状腺髓样癌）患者为pT1期（2002年国际抗癌联盟推荐标准），33例（25%）为pT2或pT3期，4例（3%）为pT4期肿瘤。39例（29.1%）患者有淋巴结转移。106例（79.1%；其中15例（38.5%）有淋巴结转移）患者治愈。评估基础及刺激后降钙素水平有助于预测甲状腺髓样癌。所有基础降钙素>64 pg/ml且刺激后降钙素>560 pg/ml的患者均患有甲状腺髓样癌。基础降钙素>10 pg/ml但<64 pg/ml且刺激后降钙素>100 pg/ml但<560 pg/ml的患者中，20%被诊断为甲状腺髓样癌。
