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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of endocrine pancreatic tumour secreting the 2 antagonistic peptides that regulate growth hormone, somatostatin and somatocrinin, is reported. Such tumours are extremely rare and only one other case has been published so far, although pancreatic malignant tumours frequently secrete several hormones. In our patient, the association of diabetes with steatorrhoea, hypochlorhydria, anaemia and biliary lithiasis suggested hypersecretion of somatostatin. Acromegaly, suggested by clinical signs, was confirmed by an excess of growth hormone and somatomedin, and pre-operative somatrocrinin assay confirmed its extra-pituitary origin. Finally, the presence of hyperparathyroidism due to parathyroid gland hyperplasia and of a Recklinghausen disease constituted a multiple endocrine neoplasia syndrome. The significance and implications of this double secretion in vivo are discussed.
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PMID:[Endocrine pancreatic tumor secreting somatostatin and somatocrinin]. 286 53

A 60 year old man developed steatorrhoea, weight loss, mild diabetes mellitus, labile hypertension and limb cramps. Raised plasma concentrations of catecholamines, particularly noradrenaline and a computed tomography-scan showing an adrenal tumour strongly suggested a pheochromocytoma. Adrenoreceptor blockade reversed the symptoms, decreased faecal fat, and increased duodenal trypsin to normal concentrations. After adrenalectomy the patient was asymptomatic and there was no steatorrhoea. The blood glucose concentrations became normal. Immunocytochemistry revealed the tumour cells to store large amounts of enkephalin and somatostatin reactive material and moderate amounts of immunoreactive beta-endorphin and dynorphin.
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PMID:A mixed endocrine adrenal tumour causing steatorrhoea. 289 May 60

Massive retroperitoneal necrosis may follow life-threatening acute pancreatitis. At delayed operation, the surgeon may not be able to delineate dead pancreas from dead adipose tissue. The question arises: has "gloved hand" debridement resulted in pancreatectomy? The histologists report only "necrotic debris, of uncertain origin." To obtain objective data, pancreatography was performed in 13 patients, 10 weeks to 23 months after onset of massive pancreatic necrosis. Each patient had required delayed laparotomy for debridement and external drainage at some earlier stage of their illness. Pancreatography was correlated with the clinical assessment of diabetes and steatorrhea. Except in specific cases involving internal fistulae, pancreatography has not been previously reported in such patients. The results demonstrate that the main pancreatic duct usually maintained its normal length and configuration. Necrosis or stricture of the main duct, if it occurred, was more likely to be followed by diabetes. Steatorrhea was clinically detected in a single patient only. The necrotic tissue, up to several kilograms in wet weight, is largely dead adipose tissue. The pancreas, especially its head, is resistant to necrosis, much more resistant than is the retroperitoneal fat.
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PMID:Pancreatography after recovery from massive pancreatic necrosis. 291 Feb 13

We describe a patient with a small somatostatinoma of the papilla of Vater without clinical evidence for diabetes mellitus, diarrhea, steatorrhea, or cholelithiasis, showing normal plasma basal levels for somatostatinlike immunoreactivity. The diagnosis was based on histologic and immunohistochemical analysis of tumor tissue and hypersomatostatinemia induced by the calcium-pentagastrin test. Before removal of the tumor both diagnostic tests recommended for the detection of a somatostatinoma, a tolbutamide test and a calcium-pentagastrin test, were performed. Whereas the calcium-pentagastrin test provoked a markedly elevated plasma somatostatin level in association with a depressed plasma neurotensin level, the tolbutamide test surprisingly did not. After removal of the tumor the calcium-pentagastrin test no longer induced hypersomatostatinemia. Further studies are needed to determine whether the calcium-pentagastrin test is a more reliable diagnostic test than the tolbutamide test in somatostatinomas with normal plasma basal levels.
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PMID:Comparative diagnostic value of the calcium-pentagastrin test versus the tolbutamide test in a patient with a somatostatinoma. 302 98

Fat replacement of the exocrine pancreas is a rare cause of exocrine pancreatic failure. We report two adult patients (a 25-year-old woman and a 63-year-old man) with weight loss and massive steatorrhea in whom abdominal computed tomograms were diagnostic of pancreatic lipomatosis. In both patients, oral pancreatic enzyme replacement in association with cimetidine led to a marked reduction of steatorrhea and weight gain. Pancreatic lipomatosis should be suspected in cases of severe exocrine pancreatic insufficiency in the absence of abdominal pain and diabetes. Computed tomogram scanning should lead to an increasing detection rate of this unusual condition.
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PMID:Lipomatosis of the pancreas: an unusual cause of massive steatorrhea. 318 86

A 52-year-old man, having been treated for 4 months with chlorpropamide for diabetes mellitus type II, developed severe cholestatic hepatitis following a short course of erythromycin ethylsuccinate. Despite prompt withdrawal of both drugs, the cholestatic picture worsened and was associated with morphological evidence of disappearing interlobular bile ducts. After a 2-year course of profound cholestasis complicated by steatorrhea and striking hyperlipidemia, the patient died of ischemic cardiomyopathy. It is believed that this is the first published case of irreversible cholestasis with disappearance of ducts potentially related to a metabolic interaction between erythromycin ethylsuccinate and chlorpropamide.
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PMID:Prolonged cholestasis and disappearance of interlobular bile ducts following chlorpropamide and erythromycin ethylsuccinate. Case of drug interaction? 326 70

Twenty three patients with chronic calcific pancreatitis of the tropics in Northern India were prospectively studied. All had pancreatic calcification and ERCP changes typical of chronic pancreatitis, the most predominant being ductal dilatation which was detected in all patients by both ERCP and by ultrasonography. Pain was present in 19 (83%) patients and diabetes in 11 (48%) patients. Exocrine pancreatic dysfunction was uncommon, steatorrhoea being present in only 9% of patients. Ten of the 11 patients with diabetes required insulin for control and one case was able to be controlled by an oral antidiabetic agent. Two patients developed ketoacidosis during acute episodes of pancreatitis, 3 patients had peripheral neuropathy and one patient had visual changes. Recurrent severe pain was the reason for operation in 7 patients. All had a lateral pancreaticojejunostomy. In order to obtain an objective assessment of pain, a scoring system was developed to grade its severity according to its intensity, frequency and consequences. Six patients who preoperatively had a pain score of 15 or more (out of a maximum score of 24) attained significant relief after the surgery. We feel this scoring system may provide an easy objective assessment of pain in the subsequent follow-up of these patients.
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PMID:Chronic calcific pancreatitis: clinical profile in northern India. 329 40

Controversies in the literature regarding definition, diagnosis, and therapy of chronic pancreatitis may be related in part to differences in the natural history of alcoholic and idiopathic (nonalcoholic) chronic pancreatitis. In order to evaluate this problem the long-term course of 205 patients with alcoholic (85.4% with calcifications) (group A) and 82 patients with idiopathic (nonalcoholic) chronic pancreatitis (76.8% with calcifications) (group B) has been analyzed prospectively since 1963. The patients were studied at regular intervals with particular regard to pain, pancreatic exocrine, and endocrine function and calcifications. The observation time was 2 years or longer in 230 patients with a median observation time of 6.7 years from diagnosis in group A and 10.6 years in group B. In group B over 50% of the cases had primary painless chronic pancreatitis. Progressive deterioration of exocrine and endocrine function was observed in both groups. However, in group A the rate of progression of exocrine dysfunction after diagnosis was more rapid and the incidence of diabetes in relation to marked exocrine insufficiency was much higher than in group B. Steatorrhea preceded diabetes in 56% (group A) and 80% (group B), respectively. Onset of pancreatic calcifications was closely associated with pancreatic exocrine insufficiency in group A in contrast to group B. In addition lasting pain relief occurred spontaneously in about 30% of patients in group B despite a normal exocrine function for 6 years or longer which is in disaccord with the results in alcoholic chronic pancreatitis. In conclusion group A and B have many features in common, in particular the high incidence of pancreatic calcifications and the progressive pancreatic dysfunction. However, the long-term profile of both groups differs in some important aspects, particularly in the clinical pattern and in the rate of progression of pancreatic dysfunction and morphology. These differences should be appreciated in the discussion of problems regarding definition, diagnosis, and surgical therapy of chronic pancreatitis.
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PMID:Differences in the natural history of idiopathic (nonalcoholic) and alcoholic chronic pancreatitis. A comparative long-term study of 287 patients. 362 34

Pain relief and compensatory therapy of exocrine and endocrine pancreatic insufficiency is the aim of conservative treatment of chronic pancreatitis. Pain relief may be achieved by analgetics, dietary restrictions, alcohol abstinence, enzyme substitution, and operative procedures. Decompensated exocrine pancreatic insufficiency, i.e. steatorrhea, is a late complication of chronic pancreatitis. It requires diet, vitamin, and enzyme replacement. Failure of the latter may be due to inactivation of the enzymes by gastric acid. Finally, diabetes mellitus, secondary to chronic pancreatitis, is managed with diet and insulin. Pancreatogenic diabetes responds only for a short period, if at all, to oral antidiabetics.
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PMID:Conservative treatment of chronic pancreatitis. 365 Jan 83

Data presented here showed that oxalate loading test--a technique for diagnosis of steatorrhoea is not applicable if the patient is also suffering with diabetes. In vitro experiments showed that sugar interferes in oxalate assay.
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PMID:Oxalate loading test for screening steatorrhoea in diabetics. 368 30


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