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

Case report of a dog which possibly was affected with acute pancreatitis and diabetes mellitus. This possibility was verified by post-mortem findings and morbid-anatomical examination. The clinical and pathological findings suggest that the pancreatitis probably followed and possibly was due to the diabetes mellitus.
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PMID:[A case of (acute) pancreatitis]. 670 80

1. Alcohol was the most common cause of pancreatitis, irrespective of sex or age. The acute hemorrhagic necrotizing form could arise after the consumption of no more than 100-450 g of alcohol a day for 7-10 days. Chronic pancreatitis was almost invariably caused by alcohol. 2. While alcohol predominantly (93%) among the under-60s, biliary tract disease and cancer were a major cause (53%) of pancreatitis in the over-60s. 3. Pancreatitis usually followed one of three courses: acute hemorrhagic, acute oedematous (acute pancreatitis) or chronic. 4. Patients who have been treated for alcoholic pancreatitis have a high death rate. The mean age at death was 46 years. 5. Most cases of acute hemorrhagic, necrotizing pancreatitis (92%) occurred as the patient's first attack of pancreatitis. 6. The diagnosis acute hemorrhagic, necrotizing pancreatitis can at present be established only at operation or autopsy. 7. Extensive resection of the pancreas should be avoided in acute hemorrhagic necrotizing pancreatitis because the function of the pancreas was often acceptably restituted once the disorder had subsided. 8. Disturbed sugar regulation was the most common complication in patients who had had pancreatitis. Diabetes mellitus often occurred (29%) and might do so months or years after an attack. 9. Patients with alcoholic pancreatitis were greatly disadvantaged socially (little education, poor jobs and housing) and in the event of a recurrence elicited by alcohol it is suggested that they should be cared for at a department for alcoholics. 10. It is suggested that in chronic pancreatitis the diagnosis should specify any exocrine and endocrine disturbances as well as any morphological changes that have been documented by i.e. ERCP or ultrasound. Studies of pancreatic function and morphology for the classification of pancreatitis should be made no earlier than 6 weeks after clinical signs of pancreatitis have subsided, with abstention from alcohol in the intervals. A classification of this type would contribute to a better follow-up and treatment of patients with chronic pancreatitis and improve the possibility of comparing patient materials.
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PMID:Diagnostic criteria, classification and clinical course in pancreatitis. 676 27

An acute pancreatitis was observed in 2 children belonging to two unrelated families in which a total of 8 kindreds also had pancreatitis. Evolution was so severe that it demanded parenteral feeding and partial pancreatectomy with Wirsung-intestinal shunting. The authors stress: the rarity of this condition (which has a dominant autosomal transmission), the lack of specificity, the severity in which pseudocysts predominate, the further occurrence of both diabetes and external pancreatic deficiency and finally, the risk of pancreatic carcinoma.
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PMID:[Hereditary pancreatitis. Two new kindreds ]. 681 33

Patients with acute pancreatitis were studied by arginine infusion at 48--72 h. 7--10 days, and 18--21 days after onset of their illness. Plasma glucose, insulin, and glucagon values were determined. Acute pancreatitis was characterized by fasting hyperglycemia and hyperglucagonemia, associated with relative hyoinsulinemia. Arginine stimulation early in the disease (48--72 h) demonstrated hyperglycemia and hyperglucagonemia, which normalized by 18--21 days. Both phases of the normal biphasic insulin response to arginine were decreased during the initial arginine infusion. By 18--21 days, although the first phase was completely normal, the second phase of insulin secretion remained depressed. Acute pancreatitis is associated with damage to both the endocrine and exocrine pancreas. Glucose intolerance seen with this disease appears to be the result of hyperglucagonemia and relative hypoinsulinemia. Although the healing process at 3 wk is associated with return of plasma glucose and glucagon concentrations to normal, the impaired second phase insulin secretion persists.
Diabetes 1980 Jan
PMID:The glucose intolerance of acute pancreatitis: hormonal response to arginine. 699 12

Contrast medium concentration in the pancreas as a function of time after intravenous bolus injection was measured in 12 rats with oil-induced acute pancreatitis, 20 rats with Streptozotocin-induced diabetes and 20 rats with subcutaneous granuloma, induced by sponge, whose pancreatic tissue was used as a control. No significant effect of diabetes was observed. Calculated distribution volume and contrast enhancement in the pancreas were increased in pancreatitis relative to diabetes and controls. The increased enhancement was due to a relatively higher accumulation into the extravascular fluid, considered to represent pancreatic oedema. An even more marked and delayed enhancement was observed with the granuloma tissue and exudate, apparently on a similar basis. There appears to be a possibility of differential diagnosis of some pancreatic lesions using contrast enhanced CT.
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PMID:Contrast enhancement pharmacokinetics in experimental pancreatitis, diabetes and subcutaneous granuloma. 700 56

Measurement of serum concentration of trypsin by RIA-Gnost Trypsin kit (Hoechst-Japan) was evaluated. The clinical usefulness of measuring serum trypsin level in diabetic patients was assessed. The measurement of trypsin using the radioimmunoassay (RIA) kit revealed good precision and reproducibility with intraassay error ranging from 3.6 to 5.5% in C.V. corresponding to mean trypsin concentration of 236.5-838.7 ng/ml and interassay error ranging from 8.1 to 11.1%. Tests for recovery and dilution were satisfactory for clinical use. Clinical materials included 35 normal subjects, 88 diabetics, 22 patients with liver diseases, 3 with acute pancreatitis, 7 with chronic pancreatitis and 3 with chronic renal failure. Serum trypsin concentration in normal controls was 157.6 +/- 59.9 ng/ml (m + 1 S.D.). Diabetic patients treated with diet therapy alone revealed serum trypsin level of 203.6 +/- 74.8 ng/ml (n = 50). In diabetics treated with sulfonil urea serum trypsin was 171.3 +/- 83.0 ng/ml (n = 25). In patients receiving insulin serum trypsin level was 90.5 +/- 49.0 ng/ml (n = 13). In patients with liver diseases, acute pancreatitis, chronic pancreatitis and chronic renal failure serum trypsin concentration were 236.9 +/- 88.0, 520.1 +/- 80.0, 113.0 +/- 75.6, and 2557 +/- 2771 respectively. Our results may indicate impaired pancreatic exocrine function in patients with severe diabetes mellitus. Increased serum trypsin level in diabetics treated with diet therapy may be due to stimulated excretion of trypsin resulted from restricted food intake. However, further study in larger number of patients is needed.
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PMID:[Evaluation of measuring serum trypsin by radioimmunoassay and clinical application for the study on the exocrine function in diabetics (author's transl)]. 708 13

A 59-year-old patient with acute pancreatitis is described, whose treatment was complicated by concomitant diabetes mellitus and arterial hypertension. He received propranolol and insulin without subsequent problems; however, when the insulin was changed to chlorpropamide, a significant increase in blood sugar occurred. It was postulated that this increase in blood sugar was due to an antagonistic action of propranolol at the pancreatic level which interfered with the action of chlorpropamide.
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PMID:Hyperglycemia associated with propranolol and chlorpropamide coadministration. 724 36

The cases of 380 patients with pancreatitis were analyzed retrospectively. There were 237 men (62%) and 143 women (38%). Etiologic factors included: alcoholism, 62%; biliary lithiasis, 16.6%; idiopathic, 12%; miscellaneous, 7%; and trauma, 2.4%. Acute pancreatitis occurred in 279 patients (73%); 189 (67%) were treated nonoperatively, 90 (33%) underwent operation; electively in 43 and urgently in 47. Postoperatively, one patient (2.3%) died in the elective group and 14 (30%) in the emergency group. Chronic pancreatitis occurred in 101 patients. Their pertinent findings were: alcoholism in 78%, biliary lithiasis in 8%, absence of abdominal pain in 15%, diabetes in 40%, and jaundice in 20%. Fifty patients were treated without operation; 43 were alcoholics, 17 of them died in the follow-up period. Fifty-one patients, 36 of them alcoholics, underwent a variety of operations, with three deaths (6%); 21 were improved after operation. It was concluded that 30% of patients with acute pancreatitis require operation, mainly to correct biliary lithiasis. Emergency operations dictated by relentless deterioration or uncertain diagnosis had a high operative mortality (30%), particularly in patients with necrotizing or hemorrhagic pancreatitis. Operative treatment for chronic pancreatitis was most effective when directed toward specific goals, including pseudocysts, obstructed pancreatic or common bile ducts. Operations done without specific anatomical objectives were often therapeutic failures.
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PMID:Evaluation and treatment of acute and chronic pancreatitis. A review of 380 cases. 738 28

The levels of serum secretory component (SC) were measured in 147 patients with digestive disease. Decreased levels were found patients with acute hepatitis, HBs-antigen associated chronic hepatitis, HBs-antigen associated liver cirrhosis and hepatoma. Normal levels were observed in patients with diabetes mellitus, gastric cancer and colonic carcinoma. Elevated levels were found in patients with cholecystitis, obstructive jaundice and acute pancreatitis. The serum SC level in almost all disease groups showed no correlation with immunoglobulin levels.
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PMID:Studies on secretory component in digestive disease. III. Levels of serum secretory component in digestive disease. 743 18

During August 1989-August 1994 at the referral-based obstetric practice of MacKay Memorial Hospital in Taipei, Taiwan, obstetricians saw 8 pregnant women with acute pancreatitis. All but 1 patient had gallstones and/or hyperlipidemia. None had ever been diagnosed with pancreatitis or gallstones in the past. None suffered from alcoholism. One woman was lost to follow-up at 33 weeks gestation. No pregnant woman died. Magnesium sulfate and nifedipine controlled preterm labor in 2 patients. Two women underwent cesarean section (fetal distress and elective). Pancreatitis struck all but 1 during the 3rd trimester of pregnancy. One woman presented at 23 weeks gestation with loss of consciousness, abnormally low volume of circulating plasma in the body, upper gastrointestinal bleeding, and a dead fetus. She also had diabetes mellitus which had gone untreated for 2 years. After spontaneous delivery of the dead fetus, she developed metabolic encephalopathy, sepsis, respiratory distress, and acute renal failure. She completely recovered and left the hospital 62 days after arriving. Physicians instituted conservative treatment for pancreatitis and a fat-restricted diet for hyperlipidemia. Labor was induced in 3 women after determining fetal lung maturity. Pancreatitis symptoms diminished after delivery. At 2 weeks postpartum, they underwent cholecystectomy. In fact, all but 3 women underwent cholecystectomy. Five patients had a fever greater than 38 degrees Celsius upon admission. Three patients were jaundiced. All 8 patients experienced nausea and/or vomiting and abdominal pain. Six women had low serum calcium levels. Only 1 had a serum lactic dehydrogenase level above 350 IU/L. Primiparous women were just as likely to develop pancreatitis during pregnancy as multiparous women. These findings suggest that early diagnosis and prompt treatment of acute pancreatitis are essential to a favorable outcome.
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PMID:Acute pancreatitis in pregnancy. 766 Jul 65


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