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

Secondary hyperlipidaemia is common and occurs frequently in disorders such as obesity, alcoholism, diabetes mellitus, hypothyroidism, liver and renal diseases and as a side-effect of drug therapy, particularly for hypertension. Its management may be important to prevent complications such as coronary heart disease and acute pancreatitis. Its study provides many fascinating insights into lipoprotein pathophysiology.
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PMID:Secondary hyperlipidaemia. 210 Jun 85

In 14 nonobese patients after acute pancreatitis and with normal oral glucose tolerance, the response of insulin, C-peptide, and pancreatic glucagon after 100 g of oral glucose was assessed. The curves of insulin and C-peptide were significantly raised compared with those of controls, and no difference was found between the response of patients with a negative (n = 8) and a positive (n = 6) family history of type II diabetes. The curves of pancreatic glucagon did not differ from those found in controls. Our results indicate that a normal response to glucose after recovery from an attack of acute pancreatitis is maintained at the cost of increased insulin secretion.
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PMID:Endocrine pancreatic secretion in patients after acute pancreatitis. 218 59

The study aimed at evaluating an incidence of diabetes mellitus and carbohydrate tolerance disorders as well as insulinemia in patients with the history of the acute pancreatitis. Baseline glycemia was determined in 50 patients with a history of the acute pancreatitis and in 15 healthy individuals (aged between 18 and 65 years). Blood sugar was then determined 30, 60, 90 and 180 minutes following loading with 75 g of glucose. Fasting insulinemia and that following loading with 75 g glucose were determined at the same time period. Diabetes mellitus was diagnosed in 6 patients (12%) whereas carbohydrate tolerance in 4 patients (8%). A decrease in insulin response to carbohydrates was noted in 36 patients (72%) with a history of the acute pancreatitis in comparison with the control group. The obtained results suggest that the acute pancreatitis significantly decreases endocrine functioning of the pancreas. Therefore, metabolism of carbohydrates should be checked particularly in the individuals with a history of the acute pancreatitis without the symptoms of both diabetes mellitus and sugar tolerance disorders but with the signs of decreased insulin response to carbohydrates.
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PMID:[Diagnosis of diabetes mellitus and disorders of glucose tolerance in patients after acute pancreatitis]. 225 52

To study incidence and cause of hyperamylasemia in various diseases, serum amylase was determined in 1371 consecutive patients and subsequent isoamylase analysis was carried out in 91 hyperamylasemic sera. Hyperamylasemia was observed in various diseases: acute pancreatitis (5/5), chronic pancreatitis (0/3), mumps (3/3), cerebrovascular diseases (2/39), respiratory diseases (6/69), heart diseases (5/89), liver diseases (16/101), cholelithiasis (0/13), diabetes mellitus (2/66), peptic ulcer (0/46), other digestive diseases (0/33), malignant tumor (9/249), renal failure (21/25), intraabdominal surgery (9/35), extraabdominal surgery (2/20), trauma (1/23), and miscellaneous (10/552). Salivary type hyperamylasemia due to dominant increase of salivary type isoamylase occurred in over half of the hyperamylasemic patients. Knowledge of hyperamylasemia in various diseases and routine isoamylase analysis of hyperamylasemic sera would enhance diagnostic accuracy and exclude unnecessary treatment of pancreatitis solely because of the presence of hyperamylasemia.
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PMID:Clinical value of routine isoamylase analysis of hyperamylasemia. 242 26

The clinical case of a 67-year-old woman admitted for abdominal pain whose interpretation created difficulties but which corresponded substantially to the pain encountered in intestinal occlusion associated with diabetes mellitus and increase in amylasemia is reported. After decrease, 48 hours after hospitalization, necropsy revealed extensive acute pancreatitis associated with infarction of the small bowel to occlusion of the superior mesenteric artery.
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PMID:[An association of acute pancreatitis and intestinal infarct due to superior mesenteric artery occlusion]. 247 24

Chronic pancreatitis is associated with glucose intolerance and resultant pancreatogenic diabetes. Using the canine pancreatic duct-ligated model of pancreatitis, we serially evaluated pancreatic histology and electron microscopy, tolerance to intravenous and oral glucose, and insulin response to glucose loading. Pancreatic duct ligation caused microscopic evidence of acute pancreatitis at 1 week, progressing to acinar loss and fibrosis consistent with chronic pancreatitis at time periods up to 6 months. The islets of Langerhans showed degranulation early and appeared to be structurally preserved late. Calculated K values indicated a progressive significant deterioration in intravenous glucose tolerance, falling significantly from 3.46 +/- 0.23 basally to 1.51 +/- 0.17 at 6 months after duct ligation (p less than 0.0001). Oral glucose tolerance deteriorated significantly, with the integrated glucose response rising from 23.7 +/- 1.2 g/dl.minute basally to 32.3 +/- 2.8 g/dl.minute at 6 months after duct ligation (p less than 0.05). Integrated insulin response to both intravenous and oral glucose deteriorated with pancreatitis. Pancreatitis-induced glucose intolerance is a consistent feature of this duct-ligated model. Glucose intolerance stabilizes between 4 and 6 months after duct ligation and is associated with pancreatic acinar fibrosis and pancreatic endocrine structural preservation. While the mechanism of altered glucose tolerance may involve mechanical, neural, humoral, or vascular events, our data clearly support the conclusion that pancreatic ductal stenosis with resultant pancreatic fibrosis and chronic pancreatitis is associated with abnormal islet responsiveness leading to circulating insulin deficiency and glucose intolerance, despite histologic and ultrastructural evidence of intact islets of Langerhans.
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PMID:Pancreatic structure and glucose tolerance in a longitudinal study of experimental pancreatitis-induced diabetes. 247 67

Recent longitudinal studies have improved the knowledge of the natural history of chronic pancreatitis. This disease is mainly induced by alcohol abuse. Mean age at onset of the disease is 40 years. First symptoms are generally pain, often related to acute pancreatitis. Over the first five years of course, complications as pseudocysts or common bile duct stenoses can occur, often necessitating surgical treatment. In the late course, the disease becomes less symptomatic but the risk of diabetes mellitus increases. Occurrence of pancreatic calcifications is observed with time in the majority of patients. Chronic pancreatitis is associated with overmortality but the causes of death are mainly extrapancreatic (alcoholic liver disease and cancers). Abnormalities of pancreatic secretion induced by alcohol abuse play an important role in the pathophysiology of the disease: it is possible that the decrease of concentration of the "pancreatic stone protein" promotes formation of calcifications. Direct toxicity of alcohol is another possible factor.
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PMID:[The natural history and physiopathology of chronic pancreatitis]. 248 15

The authors observed 53 cases of diabetic ketoacidosis treated with low doses of insulin. Mean age of the patients was 41 +/- 17 years, duration of diabetes mellitus 7.5 +/- 6.4 years. Ketoacidosis was due to: infections in 36%, other diseases in 7%, and cessation of insulin therapy in 25% of cases. Ketoacidosis was a first sign of diabetes mellitus in 19% of cases while causative factor was not detected in 13% of cases. At the admission to hospital mean blood pH was 7.02 +/- 0.15, mean bicarbonate concentration 6.17 +/- 3.45 mM/l, and glycaemia 40.6 +/- 16.8 mM/l. Therapy of ketoacidosis was complicated by hypopotassemia in 1 patient and transient hypoglycaemia in another patient. Five patients (9.6%) died. Infections, myocardial infarction, acute pancreatitis, pulmonary edema, and disseminated intravascular coagulation were the causes of deaths.
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PMID:[Analysis of the cause of death in diabetic ketoacidosis based on 5 years of personal observation]. 251 62

An association between acute pancreatitis and hypertriglyceridemia has long been recognized. The frequency of this association may be as high as 25 per cent. Whether the lipid abnormalities are secondary to acute pancreatitis and therefore temporary or whether they are primary and possibly etiologically involved is unsettled. Most experimental and clinical evidences suggest that hypertriglyceridemia precedes and apparently cause the development of pancreatitis. The mechanism of injury may be mediated through free fatty acids released from the triglycerides. It has recently been identified a group of normotriglyceridemic patients with a previous attack of acute pancreatitis, at least 6 months earlier, who had an impaired clearance of serum triglycerides after an oral fat tolerance test. The clearance of ingested triglycerides was significantly impaired as compared with a control group, irrespective of the presence of diabetes, alcohol consumption or biliary lithiasis. The authors suggested that a triglyceride tolerance test is the only way to detect those patients in whom future attacks of pancreatitis may be precipitated by a diet rich in fat or an alcoholic debauch. In a further study the authors suggested that the abnormal oral fat tolerance test in these patients with previous acute pancreatitis and normotriglyceridemia is secondary to an impaired chylomicron remnants clearance. These findings strongly suggest a relatively common and preexistent defect in lipid metabolism which may be important in the pathogenesis of the disease.
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PMID:[Acute pancreatitis and hypertriglyceridemia]. 248 26

Chronic pancreatitis of biliary origin, frequently located in the cephalic portion of the organ, etiopathogenically dependent on biliary lithiasis, the anatomoclinical evolution of which is complicated by their presence, have a better prognosis, and are usually reversible following therapy of the biliary affections. Persistent chronic pancreatitis proper, usually of the recurrent type, associated with calcification and the development of pancreatic stones, and with pseudocysts, although rare in our country, raise diagnostic difficulties from the standpoint of surgery, and have a reserved prognosis. The authors have evaluated a total of 321 cases hospitalized between 1960 and 1987 with chronic pancreatitis of biliary origin (252 cases--78.5%), and chronic pancreatitis proper, not associated to biliary affections (69 cases--21.5%). Male patients totalled 33.6% of all cases. The authors stress the high frequency of chronic pancreatitis associated to biliary lithiasis (181 cases), in contrast with pancreatitis associated to nonlithiasic cholecystopathies (38 cases), or to postoperative cholecystic disturbances (33 cases). Chronic pancreatitis non-associated to biliary affections totalled 69 cases, of which 24 were of the persistent type, 13 were of the recurrent type, one had calcifications, two had pancreatic stones, four followed acute pancreatitis, six were complicated by pancreatic abscesses, and 9 were complicated by pseudocysts. The duration of biliary and pancreatic disturbances was between 3 and 5 years in 43.9% of the cases, and between 6 and 10 years in 21.3%. Chronic pancreatitis achieves a complex clinical syndrome, the dominant feature being the painful biliopancreatic syndrome associated to obstructive jaundice (42.4%), angiocholitis (47.6%), weight loss (46%), hepatic and renal failure (10.9%), diabetes (8.4%), and a tumoral mass (15.7%). Indirect surgical interventions aimed at suppressing the biliary factor were carried out in 291 patients, with very good results in 56% of the cases, good results in 32%, mediocre in 7%. In 2.4% of the cases surgery failed to improve the condition of the patients. Direct interventions on the pancreas, which consisted either in pancreatic decompression or in exeresis of the gland have been performed in 30 patients. Drainage of pancreatic abscesses was done in 6 patients (2 deaths), cystic-digestive anastomoses were performed in 8 patients, Wirsung-jejunostomy in 3 patients (1 death), cystostomy in one patient, distal pancreatectomy in one patient (deceased), viscerolysis and novocaine infiltration in 11 patients. In the 321 cases of chronic pancreatitis operated by direct and indirect procedures very good
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PMID:[Chronic pancreatitis: anatomico-clinical and surgical therapy characteristics. Our experience with 321 cases]. 252 82


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