The patient was a 41-year-old
Abstract. According to the diagnostic criteria for adrenal preclinical Cushing's syndrome (PreCS) established by a group headed by the Ministry of Health, Labor and Welfare (MHLW), low-and high-dose dexamethasone suppression tests (DSTs) must be performed to prove autonomous cortisol secretion, i.e., ³3 mg/dL serum cortisol following 1-mg DST administration, and ³1 mg/dL serum cortisol following 8-mg DST administration. However, discrepancies have been documented in the results of low-and high-dose DSTs. We therefore investigated the validity of the DST for diagnosing PreCS by performing 1-mg and 8-mg DSTs in 39 patients with adrenal incidentaloma, but no characteristic Cushingoid symptoms. In about half of these patients (20/39, 51.3%), high-dose DST was positive but low-dose was negative, and one or more of the other abnormalities of hypothalamus-pituitary-adrenal axis dysfunction was seen in 75% of these patients. Furthermore, no significant difference in incidence of glucose intolerance and hypertension was noted in patients with positive high-dose DST and negative low-dose DST compared with patients with positive low-and high-dose DST. Under the current MHLW diagnostic criteria, patients with positive high-dose DST and negative low-dose DST are not diagnosed with PreCS, but some of these patients should be. Discrepancies in the results of low-and high-dose DSTs appear attributable to the current cutoff values, and further investigations are necessary to resolve these discrepancies.
Abstract. To investigate the role of ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, in diabetic gastroparesis, we evaluated the plasma ghrelin profile during the oral glucose tolerance test in 55 patients with diabetes (men/women: 36/19, mean ± SE of age: 55.1 ± 1.7 years) with or without gastroparesis (diagnosed by the 13 Cacetate breath test). We also further examined cardiac autonomic neuropathy by assessing 24-hour variation of the R-R interval in randomly selected 32 patients with diabetes (men/women: 23/9, mean ± SE of age: 54.2 ± 2.5 years), and evaluated the influence of autonomic neuropathy on ghrelin. The fasting plasma ghrelin level was significantly lower in diabetes mellitus with gastroparesis than in healthy controls (7.9 ± 0.7 fmol/ml versus 16.6 ± 5.3 fmol/ml, p = 0.006). Patients with diabetes with gastroparesis showed no decrease of plasma ghrelin after glucose loading, unlike patients without gastroparesis or healthy controls. Diabetes mellitus with autonomic neuropathy, but not those without it, also showed no decrease of plasma ghrelin after glucose loading. Diabetic gastroparesis may be related to ghrelin-associated neurohormonal abnormalities, but the pathophysiological meaning of this abnormal ghrelin response needs further clarification.
Abstract. a 73-year-old woman was admitted to our department for treatment of diabetes (plasma glucose 289 mg/dl, hba 1C 7.1%, and glycated albumin 34.9%). she displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (Nme), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml). Thus, we suspected a glucagonoma causing secondary diabetes. however, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma. her Nme improved markedly after intravenous infusion of amino acids, and her plasma glucose was controlled reasonably well by intensive insulin therapy. however, her general condition deteriorated and she died on day 57 after hospitalization. at autopsy, the only tumor detected was the liver mass. This was a large solid tumor (8×6×5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe. based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases. since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver. Correspondence to: Takuyuki kaTabami, m.d., division of metabolism and endocrinology, department of medicine, st. marianna university school of medicine, 2-16-1 sugao, miyamaeku, kawasaki 216-8511, Japan. e-mail: t2kataba@marianna-u.ac.jp NEUROENDOCRINE tumors (NeTs) are diagnosed on the basis of typical histological findings and the diagnosis is confirmed by diffuse positive staining for neuroendocrine cell markers [1]. NeTs are not only found in endocrine glands, but can occur throughout the body, including the gastrointestinal tract, lungs, and liver. Glucagonoma is one of the NeTs, and it almost always arises from the islets of the pancreas, with extrapancreatic tumors accounting for less than 1% of all cases [2]. Primary hepatic glucagonoma has not been reported before. here we present an extremely rare case of primary malignant hepatic glucagonoma that was confirmed at autopsy. Case ReportThe patient was a 73-year-old woman. at the age of 63 years, distal gastrectomy (billroth ii) was performed at another hospital, but we could not obtain any information with regard to the underlying disease. she had a history of heart failure at the age of 64 years. since then, a liver mass had been found (suspected hemangioma) and myelodysplastic syndrome had occurred at 71 years of age. diabetes mellitus had been diagnosed at our hospital when she was aged 69 years, but she had been followed without any anti-diabetic therapy. since her postprandial glucose level increased to 379 mg/dl, she was admitted to our ward for the treatment of diabetes when she was 73 years old.Physical examination on admission, she was very lean (bmi 12.0 kg/m 2 ). blood pressure was normal (116/89 mmhg), heart rate NOTE
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