Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the study was to determine (a) the frequency and cause of mortality in patients with chronic pancreatitis; (b) the cumulative survival rates corrected by comparison of patients with a matched French population; and (c) the factors associated with mortality by a unidimensional and multidimensional analysis. The study population consisted of 240 patients (men = 208, women = 32; alcoholic = 210, nonalcoholic = 30) followed for a mean time of 8.7 yr. The status of the patients (dead or alive) was recorded in February 1987. Mean age at onset of chronic pancreatitis was 41.5 yr. Fifty-seven patients died. Mean age at time of death was 52.3 yr. "Overmortality" after 20 yr of course was 35.8% in comparison with a matched French population (p less than 0.0001). Chronic pancreatitis was the direct cause of death for only 19.3% of patients. The main causes of death have been alcoholic hepatopathy (n = 10), cancer (n = 9), postoperative mortality (n = 8). Unidimensional analysis of mortality rates showed that male sex (p less than 0.03), surgery (p less than 0.007), hepatopathy (p less than 0.01), diabetes mellitus (p less than 0.02), and absence of attack of acute pancreatitis (p less than 0.02) were associated with mortality. Multidimensional analysis showed that the following variables were linked with mortality: in a first model including the totality of the study population: surgery (p less than 0.006), hepatopathy (p less than 0.008), no attack of acute pancreatitis (p less than 0.03), male sex (p less than 0.03); in a second model excluding cirrhosis: surgery (p less than 0.001), male sex (p less than 0.06), diabetes mellitus (p less than 0.09). Nevertheless, surgery did not seem to interfere with long-term mortality. The lower mortality of patients with attacks of acute pancreatitis suggests a favorable influence for alcohol abstinence.
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PMID:Mortality factors associated with chronic pancreatitis. Unidimensional and multidimensional analysis of a medical-surgical series of 240 patients. 292 60

The D variant of encephalomyocarditis virus (EMCV-D) induces a diabetes mellitus-like disease in male SJL/J mice. Other inbred strains, while resistant to the diabetogenic effect, exhibit strikingly different responses to this virus. In these studies, infection of diabetes resistant C3H mice with the D variant produces massive acute pancreatitis with little apparent direct islet cell involvement. This exocrine tropism is not altered when C3H mice with an inherent macrophage defect are infected, and appears to be a gender-specific phenomenon, with female C3H mice resistant to this exocrine involvement. Long-term infection of both male and female C3H mice does not change their response to the virus. Castration of male C3H mice, using a protocol that has been reported to block the diabetogenic effect of this virus, does not alter the development of this acinar lesion. The B variant of EMCV does not induce acinar destruction, nor is it diabetogenic. However, preinfection with the B variant 3 days prior to infection with the D variant does protect against the development of the exocrine lesion. Coinfection with equal doses of the two variants also protects against this lesion, as does coinfection with a lower dose of B variant. Therefore, the host response that is generated against the B variant appears to be responsible for this protection from D variant exocrine destruction. Due to the short time frame, it is unlikely that this protection is the result of an antibody response. Rather, this data is more consistent with an interferon response generated against the B variant that would inhibit replication of the D variant.
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PMID:Altered pathogenesis in encephalomyocarditis virus (D variant)-infected diabetes-susceptible and resistant strains of mice. 301 7

From the clinical use of RIA-gnost trypsin kit, the following results were obtained. 1. Standard curve showed a steep and good curve was shown. 2. Incubation: The condition for the first incubation was set at the room temperature for 10-24 hours and that for the second incubation at the room temperature for 3-5 hours. With these settings, satisfactory results were obtained. 3. Reproducibility and recovery: The C.V. of the reproducibility and the recovery were considered superior, and the values were below 10% and +/- 3%, respectively. 4. Correlation between trypsin and serum elestase-1: An excellent positive correlation (coefficient of correlation r = 0.889) was shown. 5. Serum trypsin concentration of normal and pancreatic diseases: The normal range was from 100 to 500 ng/ml. Acute pancreatitis rose obviously. Diabetes mellitus and chronic pancreatitis was below 500 ng/ml and the pancreatic cancer showed a tendency to scatter in the range of 50-1,250 ng/ml. The above results indicated that serum trypsin can be easily measured with high precision by using this method. Thus the method is considered useful for the diagnosis of pancreatic diseases.
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PMID:[Clinical usefulness of a trypsin radioimmunoassay kit]. 322 76

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Protein synthesis and degradation are particularly sensitive to malnutrition and catabolic states. Intracellular protein degradation is determined by the conformation, molecular weight, isoelectric point, and carbohydrate content of the proteins. ATP-stimulated endoproteases appear to catalyse the rate-limiting steps. In the liver, proteolysis is reduced by amino acids and/or insulin, whereas glucagon stimulates protein degradation, probably due to depletion of intracellular gluconeogenic amino acids. In the muscle, protein degradation is promoted by interleukin-1 and inhibited by Ep-475, which specifically inactivates cathepsin B,H, and L. Myofibrillar alkaline proteinase activity increases postoperatively and in patients suffering from malignant tumors, whereas normal proteinase values were observed in these patients following total parenteral nutrition. Increased alkaline proteinase activity is also observed in diabetes mellitus and is normalized by insulin. Extracellular proteolysis has been reported in patients with hypercatabolic acute renal failure and in patients with sepsis or acute pancreatitis. Plasma fractions obtained from hypercatabolic patients with postoperative acute renal failure were proteolytic. Plasma proteinase activity decreases during hemodialysis due to elimination of a metallo-proteinase. Plasma alpha 2-macroglobulin decreases in patients with acute renal failure and also during acute pancreatitis. Proteolytic degradation of parathyroid hormone by sera obtained from patients with acute pancreatitis has been observed. Also, there is a decrease of high molecular weight kininogen during experimental acute pancreatitis. Granulocyte elastase increases postoperatively, mainly in patients with sepsis. Sepsis also causes increased proteolytic activity in the urine. In conclusion, intracellular protein degradation can supply important precursors for hepatic and renal gluconeogenesis during malnutrition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proteinases in catabolism and malnutrition. 331

The operation of total pancreatectomy is performed rarely. Its role in the management of patients with chronic pancreatitis remains to be elucidated. We have reviewed our series of 29 total pancreatectomies for benign disease [14 women median age 39 years; 15 men median age 34 years]. Twelve underwent standard total pancreatectomy, in 17 duodenum preserving total pancreatectomy (DPTP) was performed. There was one death (mortality 3.4%). In no patient was the total pancreatectomy the first operative procedure. The patients were compared with age and sex matched diabetic control subjects selected on a best fit basis from the diabetic clinic database. The aetiology of the pancreatitis was idiopathic nine, pancreas divisum nine, alcohol eight and other causes three. The indication for surgery was pain 27, acute pancreatitis one and cholangitis with pancreatitis one. The complications of the procedures were mainly caused by infection [wound three, chest six and central line sepsis four] and in two there was a leak from the duodenum; no patient required re-operation. The postoperative stay [standard total, median 21 days (range 13-98) DPTP median 31 days (range 17-49)] has lengthened over the period due to greater attention to analgesic, diabetic and enzyme deficiency control before discharge. In standard total pancreatectomy there were five major hypoglycaemic episodes with only two in 17 DPTP patients. The per cent ideal body weight, the insulin requirement and the HbAl compared less well in standard total pancreatectomy group compared with controls than did DPTP. With both groups large doses of enzyme replacement were required, and this proved of importance in diabetic control. Our experience with total pancreatectomy suggests that pain will be improved in over 80% of patients and that the results of surgery will improve with prolonged follow up provided attention is given to analgesic abuse, enzyme deficiency and diabetes.
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PMID:Total pancreatectomy for chronic pancreatitis. 335 68

An unusual case of diabetes secondary to acute pancreatitis in a boy with end-stage renal failure receiving continuous ambulatory peritoneal dialysis (CAPD) is described. A hyperglycaemic, hyperosmolar pre-coma developed, aggravated by associated hypercalcaemia. The glucose content of the dialysis fluid contributed to the hyperglycaemia, which settled as the pancreatitis resolved and lower glucose concentration dialysis fluid was used. Our experience suggests that pancreatic dysfunction should be considered where significant hyperglycaemia occurs during peritoneal dialysis.
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PMID:Non-ketotic hyperosmolar diabetic pre-coma due to pancreatitis in a boy on continuous ambulatory peritoneal dialysis. 354 Jun 93

In the absence of ductal ectasia there is no adequate alternative to pancreatectomy for severe chronic pancreatitis. A personal series of 30 such patients operated upon between 1977 and 1984 included 16 with distal pancreatectomy, 6 with proximal pancreatectomy and 12 with total pancreatectomy; 4 patients progressed from distal to total resection after an interval of 15-28 months. The mean age was 39 years with a male preponderance of 77 per cent. The main aetiological agents were chronic alcoholism (63 per cent) and previous acute pancreatitis (23 per cent). One patient died after total pancreatectomy, giving a 30-day mortality rate for all resections of 3 per cent. Postoperative complications necessitated reoperation in 10 per cent, and there have been 5 late deaths (17 per cent). Among 27 patients followed for a median of 4.5 years, pain relief has been good in 16, fair in 8 and poor in 3 (11 per cent). Proximal pancreatectomy has proved superior to distal pancreatectomy with regard to analgesia and the avoidance of diabetes. Although technically demanding, total pancreatectomy has improved symptoms substantially in 9 of 10 patients surviving for a minimum of 18 months.
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PMID:Resection in chronic pancreatitis. 366 47

Mild to moderate hypertriglyceridemia is not associated with specific signs or symptoms in either IDDM or NIDDM. However, symptoms of the "chylomicronemia syndrome," including abdominal pain and acute pancreatitis, can occur when poorly controlled diabetes is present in a patient with a familial form of hyperlipidemia. The low-carbohydrate, high-fat diet that was commonly recommended for diabetics during past years may have contributed to the elevated plasma LDL levels in some individuals. Such "diabetic diets" may also have played a role in the predisposition of diabetics toward atherosclerotic complications.
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PMID:Hyperlipidemia: forestalling complications in older diabetics. 388 43

A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.
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PMID:Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. 389


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