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Glucagon receptor gene mutations with hyperglucagonemia but without the glucagonoma syndrome

World Journal of Gastrointestinal Surgery 2015年第4期7卷 60-66页

作者： Helen C Miller Mark Kidd Irvin M Modlin patrizia cohen Roberto Dina Panagiotis Drymousis Panagiotis Vlavianos Günter Klöppel Andrea Frilling Department of Surgery and Cancer Imperial College LondonLondon W12 0HSUnited Kingdom Department of Surgery Yale UniversityNew HavenCT 06510United States Emeritus Yale University School of MedicineNew HavenCT 06510United States Department of Histopathology Imperial College LondonLondon W12 0HSUnited Kingdom Department of Gastroenterology Imperial College LondonLondon W12 0HSUnited Kingdom Department of Pathology Technical University of Munich81675 MunichGermany

Pancreatic neoplasms producing exclusively glucagon associated with glucagon cell hyperplasia of the islets and not related to hereditary endocrine syndromes have been recently described. They represent a novel entity within the panel of non-syndromic disorders associated with hyperglucagonemia. This case report describes a 36-year-old female with a 10 years history of nonspecific abdominal pain. No underlying cause was evident despite extensive diagnostic work-up. More recently she was diagnosed with gall bladder stones. Abdominal ultrasound, computerised tomography and magnetic resonance imaging revealed no pathologic findings apart from cholelithiasis. Endoscopic ultrasound revealed a 5.5 mm pancreatic lesion. Fine needle aspiration showed cells focally expressing chromogranin, suggestive but not diagnostic of a low grade neuroendocrine tumor. Octreo Scan was negative. Serum glucagon was elevated to 66 pmol/L(normal: 0-50 pmol/L). Other gut hormones, chromogranin A and chromogranin B were normal. Cholecystectomy and enucleation of the pancreatic lesion were undertaken. Postoperatively, abdominal symptoms resolved and serum glucagon dropped to 7 pmol/L. Although H and E staining confirmed normal pancreatic tissue, immunohistochemistry was initially thought to be suggestive of alpha cell hyperplasia. A count of glucagon positive cells from 5 islets, compared to 5 islets from 5 normal pancreata indicated that islet size and glucagon cell ratios were increased, however still within the wide range of normal physiological findings. Glucagon receptor gene(GCGR) sequencing revealed a heterozygous deletion,K349_G359del and 4 missense mutations. This case may potentially represent a progenitor stage of glucagon cell adenomatosis with hyperglucagonemia in the absence of glucagonoma syndrome. The identification of novel GCGR mutations suggests that these may represent the underlying cause of this condition.

关键词： Hyperglucagonemia Glucagon receptorgene Mutation Adenomatosis Pancreas

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内毒素腹腔内注射诱发小鼠肠套叠的实验研究

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华夏医学 1999年第1期12卷 12-14页

作者：林中 M.HANANI P.cohen 桂林医学院附属医院消化内科以色列希伯来大学医学院HADASSAH医院

报告了一种新型的内毒素肠套叠动物模型，并对其发病机理进行了初步探索。结果发现：给小鼠腹腔内注射内毒素，肠套叠诱发率为２３．８％，内毒素最佳剂量是１２ｍｇ／ｋｇ，肠套叠形成高峰时间在６～１２ｈ。内毒素使肠传递时间延长，... 详细信息

报告了一种新型的内毒素肠套叠动物模型，并对其发病机理进行了初步探索。结果发现：给小鼠腹腔内注射内毒素，肠套叠诱发率为２３．８％，内毒素最佳剂量是１２ｍｇ／ｋｇ，肠套叠形成高峰时间在６～１２ｈ。内毒素使肠传递时间延长，一氧化氮合成酶抑制剂Ｌ－ＮＡＭＥ降低肠套叠诱发率。实验结果提示：内毒素可诱发肠套叠，其发病机理与肠动力紊乱有关。该动物模型可为研究肠套叠的病因，发病机理及治疗提供帮助。

关键词：肠套叠内毒素一氧化氮小鼠

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