Immerman S C, Sener S F, Khandekar J D
Arch Surg. 1982 Jul;117(7):905-8. doi: 10.1001/archsurg.1982.01380310025006.
We treated four patients who had hypoglycemia and nonpancreatic tumors. Two had pleural mesothelioma, one had primary fibrosarcoma of the liver, and one had pheochromocytoma metastatic to the liver. We propose four mechanisms for this syndrome: (1) insulin or insulin-like activity produced by the tumor, (2) decreased gluconeogenesis, (3) disruption of glucagon metabolism, and (4) increased utilization of glucose by the tumor. The local effects of the tumor in hepatic parenchyma may also play an important role. The important diagnostic tests are an insulin-glucose ratio, to rule out insulinoma, and fasting glucose levels. An assay of nonsuppressible insulin-like activity can be performed and is of investigative interest, but does not aid in individual patient therapy. Treatment consists of control of the tumor.
我们治疗了4例患有低血糖症和非胰腺肿瘤的患者。其中2例患有胸膜间皮瘤，1例患有肝脏原发性纤维肉瘤，1例患有转移至肝脏的嗜铬细胞瘤。我们提出了该综合征的四种机制：（1）肿瘤产生胰岛素或胰岛素样活性；（2）糖异生减少；（3）胰高血糖素代谢紊乱；（4）肿瘤对葡萄糖的利用增加。肿瘤在肝实质中的局部作用也可能起重要作用。重要的诊断检查是胰岛素-葡萄糖比值，以排除胰岛素瘤，以及空腹血糖水平。可进行不可抑制的胰岛素样活性测定，这具有研究意义，但对个体患者的治疗并无帮助。治疗包括控制肿瘤。
