Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case report is presented of a 38-year-old alcoholic welfare patient. Drainage of a pancreatic abscess, which had to be repeated, pyloromyotomy, cholecystectomy and sphincterotomy were undertaken in 1972 at another hospital. He was admitted on the present occasion because of weight loss, severe attacks of pain and diabetes. At operation multiple necrotic areas were found in the pancreas, with many stones in the parenchymatous tissue and in the main pancreatic duct and one large stone close to the pailla acting like a valve. Sub-total duodenopancreatectomy, resection of the pyloric region of the stomach, retrocolic hepaticojejunostomy and gastroenteroanastomosis was performed. The postoperative recovery took place without complications. 5 days after discharge the patient died in a hypoglycaemic coma at another hospital. He had administered 400 U. insulin to himself whilst in a drunken state. A short description is given of the aetiology and pathogenesis of calcifying pancreatitis. The choice of the surgical technique depends on the operative findings and the aim of therapy. Attention is called to the increase in late mortality in patients with pancreatectomy who do not abstain from alcohol.
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PMID:[Fatal outcome of a case with calcifying alcoholic pancreatitis (author's transl)]. 97 84

Thirteen patients with pancreatic diabetes caused by calcifying pancreatitis were divided into 2 groups; 5 with diabetic autonomic neuropathy [AN(+) group] and 8 without [AN(-) group]. They were subjected to an insulin-induced hypoglycemic stress test to evaluate their blood pancreatic glucagon, adrenalin, and cortisol responses. When a blood glucose level below 45 mg/100 ml was defined to be hypoglycemia, all the patients in the AN(-) group exhibited peripheral adrenalin responses, with a significant increase (mean, 19.0 times the basal level) in the blood adrenalin level. Among the AN(+) group, on the other hand, central nervous symptoms became evident rather than the peripheral adrenalin response (the blood adrenalin level hardly exceeded the basal level). With the exception of a single patient, none exhibited responses in the blood pancreatic glucagon levels. Only one patient showed a minimal cortisol response but the remaining 12 reacted normally in the cortisol release. The findings are summarized as follows: in pancreatic diabetes, insulin-induced hypoglycemia causes little change in pancreatic glucagon secretion; when the condition is complicated with autonomic neuropathy, central nervous symptoms develop while the blood adrenalin level hardly increases. These findings indicated that patients with pancreatic diabetes complicated with diabetic autonomic neuropathy have a risk of lapsing into an acute hypoglycemic coma and difficulty in recovering from the hypoglycemic state.
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PMID:Decreased counterregulatory hormone responses to insulin-induced hypoglycemia in patients with pancreatic diabetes having autonomic neuropathy. 773 13