Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most, if not all, of the glucagon-producing tumours of the pancreas are malignant. For this reason an early diagnosis is essential. The glucagonoma syndrome is associated with a skin rash, stomatitis, anaemia, glucose-intolerance, hypoaminoacidaemia, weight loss, elevated sedimentation rate and hyperglucagonaemia. The more important and constant findings are the skin lesion, the low level of aminoacids in the blood and the increased glucagon concentrations. The skin lesion is not pathognomonic, but any therapy-resistant bullous dermatosis which microscopically is characterized by epidermal changes should alert the clinician to suspect a glucagonoma. The syndrome can be proved by demonstration of hyperglucagonaemia and a pancreatic tumour.
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PMID:Possible entries to the diagnosis of a glucagon-producing tumour. 22 89

A 34-year-old man presented with classic glucagonoma syndrome manifested by weight loss, dermatitis, stomatitis, anemia, and mild diabetes mellitus. The diagnosis of glucagonoma was made by light and electron microscopic demonstration of a metastatic alpha cell carcinoma in a liver biopsy specimen. Plasma glucagon concentration was abnormally high. The patient also had symptoms and signs of involvement of the central nervous system. Radionuclide and CAT scans of the brain, negative CSF cytology and myelography excluded the possibility of metastases or other space-occupying lesions. Glucagon was demonstrated in the CSF. We postulate that the neurologic symptoms were due to direct or indirect effect of this hormone on the brain. Following therapy with streptozotocin and 5-fluorouracil, the patient had a subjective and objective clinical and hormonal remission of his disease including amelioration of his neurological impairment.
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PMID:Neurologic involvement in glucagonoma syndrome: response to combination chemotherapy with 5-fluorouracil and streptozotocin. 22 32

A 66-year-old male patient with non-insulin-dependent diabetes of probably 20 years' duration presented with necrolytic migratory erythema, stomatitis, anemia and weight loss. Plasma-glucagon concentration measured with Unger's antibody 30-K was 8500 pg/ml, representing a hundredfold elevation. Two thirds consisted of high molecular glucagon fractions (10 000--40 000 Dalton). This may be an important index for detection of glucagonoma with endocrine activity. After excision of the glucagonoma the clinical syndrome was reversed and the patient recovered completely. Histological and histochemical investigation confirmed that the tumor was a glucagonoma. Despite complete removal of the tumor and a normal plasma glucagon concentration, the diabetes remained unchanged. Excessive hyperglucagonemia does not appear to play a primary role in the pathogenesis of this patient's diabetes.
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PMID:[The course of diabetes and clinical findings in glucagonoma]. 52 94

A number of hemodynamic, pharmacologic, and metabolic interventions were found to change the extent of acute ischemic injury of the myocardium and subsequent necrosis following experimental coronary artery occlusion. Reduction in myocardial damage occurred by decreasing myocardial oxygen demands (beta-adrenergic blocking agents, intra-aortic balloon counterpulsation, nitroglycerin, decreasing afterload in hypertensive patients, inhibition of lipolysis, and digitalis in the failing heart); by increasing myocardial oxygen supply either directly (coronary artery reperfusion or elevating arterial pO2), or through collateral vessels (evevation of coronary perfusion pressure by alpha adrenergic agonists, intra-aortic balloon counterpulsation); or by increasing plasma osmolality (manitol, hypertonic glucose); presumably by augmenting anaerobi metabolism (glucose-insulin-potassium, hypertonic glucoxe insulin potassium, hypertonic glucose); by enhancing transport to the ischemic zone of substrates utilized in energy production (hyaluronidase); by protecting against autolytic and heterolytic damage (hydrocortisone, cobra venom factor, aprotinin). Augmentation of myocardial ischemic damage occurred as a consequence of increasing myocardial oxygen requirements (isoproterenol, glucagon, ouabain, bretylium tosylate, tachycardia); by decreasing myocardial oxygen supply either directly (hypoxia, anemia), through reduction of collateral flow (hemorrhagic hypotension, minoxidil), or by decreasing substrate availability (hypoglycemia). Pilot studies have been carried out in patients with hyaluronidase, nitroglycerin intra-aortic balloon counterpulsation, beta-blocking agents and Arfonad and have shown that these interventions may also reduce myocardial damage, which suggests that the concept of reduction in infarct size following coronary occlusion is applicable clinically.
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PMID:Effects of metabolic and pharmacologic interventions on myocardial infarct size following coronary occlusion. 76 15

Several studies have demonstrated the efficacy of cyclosporin A in modifying the initial course of Type 1 (insulin-dependent) diabetes mellitus in older children and adults but none have reported the effects in very young children. We treated 14 newly-diagnosed Type 1 diabetic patients aged 22 months to 95 months with cyclosporin A. Mean insulin dose at entry was 0.7 +/- 0.07 IU.kg-1.day-1. Initial cyclosporin A dose was 10 mg.kg-1.day-1. Insulin dose reached a nadir of 0.13 IU.kg-1.day-1 by 180 days. Mean glucagon-stimulated connecting peptide levels were maximal at 6 months (0.75 nmol/l) and were maintained while on cyclosporin A. Insulin was discontinued in four patients for 4, 12, 15 and 30 months respectively. In five other patients the insulin dose was less than 0.15 IU.kg-1.day-1 for at least 3 months. Glycated haemoglobin levels for all patients were within the normal range. Side effects included anorexia, stomach pains, poor weight gain, hypertrichosis, gum hyperplasia, mild anaemia and elevated creatinine. All patients have now discontinued cyclosporin A and all but one have been followed for 5 years after discontinuation. Reasons for discontinuing cyclosporin A included exposure to chicken pox (varicella), non-resolving otitis media, incomplete or no response and relapse. All side effects have resolved since the treatment was discontinued. Following discontinuation of cyclosporin A insulin requirements and glycated hemoglobin levels increased while glucagon-stimulated connecting peptide levels declined dramatically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporin A treatment of young children with newly-diagnosed type 1 (insulin-dependent) diabetes mellitus. London Diabetes Study Group. 139 85

The glucagonoma syndrome is characterized by elevated serum glucagon, a pancreatic alpha-cell tumor, anemia, hypoaminoacidemia, and necrolytic migratory erythema. Necrolytic migratory erythema may cause marked morbidity and is frequently misdiagnosed. A 42-year-old white woman with a 1 1/2-year history of refractory dermatitis (most severe on the lower extremities) had the glucagonoma syndrome. Her severe morbidity was markedly relieved with the administration of intravenous amino acids. This therapy was successful in controlling the necrolytic migratory erythema through recurrences after somatostatin (SMS 201-995), surgical debulking, and chemotherapy proved inadequate.
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PMID:Treatment of necrolytic migratory erythema in glucagonoma syndrome. 176 71

Attempts have been made to determine the reason for the depletion of glycogen reserves in tumour-bearing rats. The possible roles of anorexia, competition for glucose by the tumour, and lack of hormonal control of glycogen biosynthesis have been investigated. The glycogen content of the liver, skeletal muscle, and brain, and the levels of glucose and the hormones corticosterone, insulin, and glucagon were determined in healthy rats which had been starved for various periods and in tumour-bearing rats carrying the fast-growing Zajdela ascites hepatoma or the slow-growing solid hepatoma 27. It was found that towards the terminal stages of tumour development there was an increase in the content of corticosterone and glucagon in the blood serum and also an increase in the glycogen reserves in skeletal muscle and brain despite the presence of hypoglycaemia and hypo-insulinaemia. There was at this time a sharp fall in the level of liver glycogen. It is shown that neither anorexia nor excessive competition for glucose by the tumour were the main reasons for liver glycogen depletion and hypoglycaemia. A strong correlation was observed, however, between the occurrence of anaemia and the loss of liver glycogen, which suggests that the former may be an important factor in the changes in host tissue observed in response to tumour growth.
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PMID:Factors within the body determining the glycogen reserves in the tissues of rats with transplantable tumours. 177 67

The glucagon-producing pancreatic tumors or glucagonomas are among the rarest forms of islet cell tumors; most are malignant and usually produce a definite clinical syndrome. Mild diabetes mellitus, weight loss, and anemia usually accompany the syndrome. However, only the presence of a peculiar cutaneous rash (necrolytic migratory erythema) and the finding of hyperglucagonemia on assay are reliable diagnostic features of the syndrome. Selective, celiac axis arteriography is the most valuable preoperative technique for localizing these neoplasms and their common liver metastases. Immunohistochemical and ultrastructural examinations are particularly helpful in defining the tumor cell nature (alpha-2 islet cell) and the peptide content (glucagon). When the tumor is benign (less than 30%), complete operative removal results in lasting cure; for malignant forms, surgical therapy is mainly palliative, and adjunctive chemotherapy should be administered. In this report, the importance of clinical recognition and operative and chemotherapeutic responses is illustrated in two patients. In each case, the characteristic dermatitis, diabetes mellitus, weight loss, anemia, and elevated plasmatic glucagon were present. Both patients had their tumors localized by selective angiography and underwent operative removal of the primary pancreatic lesion. In the case of benign glucagonoma, surgical excision was curative. In the malignant one, cytoreductive surgery plus adjunctive chemotherapy (dimethyltriazenomidazole-carboxamide resulted in prolonged survival and significant clinical improvement. Follow-up with serum glucagon assay has been useful in monitoring recurrence.
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PMID:Response of glucagonomas to surgical excision and chemotherapy. Report of two cases and review of the literature. 254 27

Data presented in this study suggest existence of hyperendorphinism in uraemic patients. This hyperendorphinism may be regarded both as a primary beneficial compensatory mechanism counteracting disturbances of the internal environment, while causing secondary harmful side effects, which contribute to the uraemic state. Erythropoietin treatment of uraemic, haemodialyzed patients is followed by marked endocrine alterations (suppression of plasma levels of STH, ACTH, prolactin, glucagon, aldosterone, cortisol and plasma renin activity, elevation of plasma insulin and atrial natriuretic levels, lack of influence on plasma PTH, CT and AVP). It remains to be clarified whether the erythropoietin induced endocrine alterations are due to correction of the existing anaemia or reflect a specific effect of this hormone.
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PMID:Endocrine abnormalities in patients with endstage renal failure. 256 Mar 46

We report a case of pancreatic tumour metastatic to the liver in a patient with insulin-treated diabetes, anaemia, cheilitis, necrolytic migratory erythema, hypokalemia and chronic watery diarrhea, a picture suggesting combined glucagonoma and VIPoma syndromes. Immunocytochemistry of a biopsied hepatic metastatic nodule revealed both glucagon and vasoactive intestinal peptide (VIP) positive cells. Increased plasma glucagon and VIP levels were detected (values of 900 pmol/l and 277 pmol/l respectively). This is the first reported case showing not only immunocytochemical, but also clinical evidence of the combined secretion of these hormones.
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PMID:A combined glucagonoma and VIPoma syndrome. First pathologic and clinical report. 284 62


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