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Distinct mechanisms of hypoglycaemia in patients with somatostatin‐secreting neuroendocrine tumours

机译:生长抑素分泌型神经内分泌肿瘤患者低血糖的独特机制

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Introduction Somatostatin‐secreting neuroendocrine tumours may present with diabetes, cholelithiasis and steatorrhoea. In addition, hypoglycaemia has been associated with somatostatinomas. However, the mechanism of hypoglycaemia in patients with somatostatinomas has not been well characterized. Methods We describe two patients with recurrent neuroglycopenic episodes caused by somatostatin‐secreting neuroendocrine tumours in the liver, detected by abdominal CTs and whole‐body octreotide scintigraphy scans and confirmed by biopsy. Results Pancreatic islet hyperplasia and co‐secretion of insulin (in addition to somatostatin) from tumour cells, respectively, have been characterized as completely distinct mechanisms of hypoglycaemia at both the functional and morphological levels in these two patients. Conclusions Hypoglycaemia may be caused by different mechanisms in patients with somatostatinomas.
机译:简介分泌促生长素抑制素的神经内分泌肿瘤可能与糖尿病,胆石症和硬脑膜炎有关。此外,低血糖症与生长抑素瘤有关。但是,尚没有很好的表征生长抑素瘤患者低血糖的机制。方法我们描述了两名由生长激素抑制素分泌的神经内分泌肿瘤在肝脏中引起的反复性神经糖尿发作的患者,这些患者通过腹部CT和全身奥曲肽闪烁显像扫描得以检测并经活检证实。结果在这两名患者中,胰岛增生和从肿瘤细胞中胰岛素共分泌(除生长抑素外)分别被认为是功能性和形态学上低血糖的完全不同的机制。结论低血糖症可能是由生长抑素瘤患者的不同机制引起的。

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