(2)由于患者在低血糖症发作时儿茶酚胺呈代偿性升高,人们质疑是否真的存在 IPH。但是,IPH 很可能存在病因与发病机制的不均一性。有些可能与神经-内分泌调节功能障碍、胰岛素敏感性增加和胰高血糖素受体降调节及受体敏感性降低有关;另一部分患者可能是迷走神经紧张性增高,使胃排空加速及胰岛素分泌稍多所致;而症状较重伴餐后血糖降低者,应深入探讨其发病是否与胰源性非胰岛素瘤低血糖综合征(Hypoglycemic syndrome of pancreatic non insulinoma,NIPHS)有某种联系。
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