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)

In an effort to establish diagnostic criteria for rejection and recurrent disease in transplanted pancreas, a comparative study was performed based on clinical diagnosis. Clinical rejection was diagnosed in patients who had decreased urinary amylase or increased blood glucose; they were treated for rejection and improved. A clinical diagnosis of recurrent diabetes was made in syngeneic transplant recipients with islet dysfunction. In addition, two control groups were used--nontransplant, nondiabetic pancreatitis patients and pretransplant normal biopsies from patients in the study. Morphologically, tissues were assessed for acinar inflammation, ductal changes, islet and nerve inflammation, and vascular changes. Immunohistochemical staining for insulin and glucagon was also performed to quantitate differences between the groups. Vascular changes (endothelialitis, vasculitis, obliterative endarteritis) were specific for rejection. Also, rejection was characterized by a lymphocytic or mixed infiltrate that involved the ducts. Recurrent diabetes was characterized by selective loss of beta cells with isletitis. Leukocyte common antigen and UCHL1 staining was helpful in identifying islet inflammation. An insulin/glucagon ratio of less than 1.0 appears to be specific for recurrent disease and in the absence of isletitis is a reasonable method for detecting recurrent disease at an early stage.
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PMID:Pancreas transplant pathology. A morphologic, immunohistochemical, and electron microscopic comparison of allogeneic grafts with rejection, syngeneic grafts, and chronic pancreatitis. 199 30

Eight patients with giant cell arteritis (6 with Horton's disease and 2 with polymyalgia rheumatica) were investigated for abnormalities in glycoregulation, previously reported in Horton's disease, using oral glucose tolerance tests with measurement of insulinaemia and C-peptide response to glucagon to evaluate pancreatic function. The results were compared with those obtained in an age and weight matched population of patients with inflammatory syndromes of other origins. All patients with giant cell arteritis had abnormal glucose tolerance tests, with diabetes mellitus in 6 and impaired glucose tolerance in 2. Insulinaemias at all stages of the test, insulin response areas and basal C-peptide values were elevated; C-peptide response to glucagon was normal. Similar results were observed in patients with other inflammatory syndromes. It is concluded that glycoregulation disorders are not incidental in giant cell arteritis, that the normal pancreatic function seems to exclude immune pancreatic vasculitis, and that the abnormal glycoregulation is probably due to insulin-resistance. Since these abnormalities cannot be explained by the patients' advanced age alone, the part played by the inflammatory syndrome, which was common to both groups, is discussed. Its responsibility for inducing insulin-resistance may account for the fact that corticosteroids, which are rapidly effective against giant cell arteritis, normalise oral glucose tolerance tests.
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PMID:[Glycoregulation disorders in giant-cell arteritis]. 316 17

The autopsy findings in a 58 year old female with the typical glucagonoma syndrome with heart muscle hypertrophy are described. Despite remission of a skin rash and hyperglucagonemia following removal of metastatic liver tumors, the patient died of massive cerebral hemorrhage caused by uncontrolled hypertension and septic cerebral angiitis. On the basis of surgical and autopsy materials, the tumors in the pancreas and liver were defined as malignant glucagonoma by histological, histochemical, immunohistochemical, and ultrastructural studies. The pathohistological changes in several organs that might be related to the hypersecretion of pancreatic glucagon are discussed.
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PMID:A postmortem study of malignant glucagonoma with heart muscle hypertrophy, including chemical, histochemical, immunohistological and ultrastructural observations. 627 84