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

Prevention of vascular disease and acute pancreatitis is the goal of hyperlipidemia treatment. The risk of coronary heart disease (CHD) increases with increasing plasma cholesterol levels because low-density lipoprotein (LDL), the major carrier of cholesterol in the plasma, is atherogenic. High-density lipoprotein (HDL), especially the HDL2 subfraction, protects against CHD. Hypertriglyceridemia, although not an independent risk factor for CHD, is generally accompanied by low HDL cholesterol (HDLch), which may predispose to CHD. Reducing plasma LDL and raising HDL levels are thus goals in preventing CHD. Serum LDL levels may be lowered by reducing saturated fat and cholesterol intake; weight loss may decrease LDL but is more effective in lowering plasma triglycerides and raising HDLch. The percent of total calories from polyunsaturated, monounsaturated, and saturated fats should be less than 10%, up to 10-15%, and less than 10%, respectively. High cholesterol intake increases the flux of cholesterol, which may be harmful to arterial walls, but beyond a certain point does not increase plasma cholesterol levels. Some diets change the composition rather than the level of LDL and apoproteins. Weight reduction and maintenance are the most effective dietary measures to lower plasma triglycerides; omega-3 fatty acids (fish oils) have shown promise in reducing triglyceride but not cholesterol levels. Substitution of starch for sugar lowered triglyceride levels toward normal in hypertriglyceridemia patients. Fasting triglyceride levels rise in all individuals fed high-carbohydrate diets, but the high levels persist in hypertriglyceridemia patients. Weight loss, cessation of cigarette smoking, increased physical activity, good control of diabetes, and moderate alcohol use all raise HDLch levels. Vitamin E deficiency causes neurological sequelae in children with severe malabsorption problems due to abetalipoproteinemia or cholestatic liver disease.
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PMID:Nutritional management of plasma lipid disorders. 255 90

The purpose of this study was to ascertain the influence of acute pancreatitis upon the course of chronic pancreatitis, its complications, the need for surgical treatment, and mortality, in alcoholic men. The studied population was composed of 222 men; 110 had never had acute pancreatitis and 112 had presented at least once with acute pancreatitis. The cumulative probability to have a first bout of acute pancreatitis was 41.5 percent, 2 years after the onset of chronic pancreatitis. There was no difference in follow-up but clinical onset of chronic pancreatitis was earlier in the "acute pancreatitis" group. There was no difference in the prevalence of biliary strictures, non-alcoholic hepatic disease or need for surgery. On the contrary, diabetes mellitus, alcoholic hepatic disease were less frequent and pseudocysts were more frequent in the "acute pancreatitis" group. We observed 56 deaths. The comparison of mortality and cumulative survival rates showed a lower mortality in the "acute pancreatitis" group (p less than 0.02 and 0.05, respectively). The main causes of death were alcohol-related hepatic disease, postoperative mortality, and carcinoma Alcoholic cirrhosis was more frequent in patients who died in the "no acute pancreatitis" group. We conclude that: a) acute pancreatitis is an early complication of chronic pancreatitis in one case out of two; b) clinical onset of chronic pancreatitis occurs earlier in patients who presented with acute pancreatitis; c) need for surgery is not different; d) alcoholic hepatic disease is more frequent in the "no acute pancreatitis" group; e) mortality is lower in the "acute pancreatitis" group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Influence of bouts of acute pancreatitis on the course of chronic alcoholic pancreatitis in man]. 262 83

We have already reported that renal glycine amidinotransferase (GAT) activity decreases in the course of renal damage, however, the inability of the kidney to synthesize guanidinoacetic acid (GAA) may be compensated by the pancreas in a more advanced stage of renal failure, and that in diabetes mellitus, the production of GAA is decreased from the period without renal dysfunction, and the extrarenal production of GAA is also decreased. In order to elucidate the significance of GAA synthesis in the pancreas, the author measured serum concentration of GAA, creatine, and the renal and pancreatic GAT activity in control, streptozotocin (STZ)-induced diabetic, insulin-treated diabetic, and ethionine-induced acute pancreatitis rats. The serum GAA concentration was depressed in untreated diabetic rats (21.5 +/- 2.5 micrograms/dl) compared with the level in controls (85.5 +/- 10.1 micrograms/dl), and was restored to control level by insulin treatment (66.2 +/- 7.3 micrograms/dl). The renal and pancreatic GAT activities were depressed in untreated diabetic rats compared with the level in controls and the latter was restored (625.2 +/- 96.2 micrograms/g.tissue/h) by insulin treatment. The positive correlation was observed between pancreatic GAT activity and serum GAA concentration. The serum GAA concentration was significantly higher in acute pancreatitis rats (716.0 +/- 223.7 micrograms/dl) compared with the level in controls, although the renal and pancreatic GAT activities were lower in acute pancreatitis rats compared with the level in controls. These results indicate that in STZ-induced diabetic rats, depressed pancreatic GAT activity was ameliorated by insulin treatment, consequently the level of serum GAA was restored and that GAA might be released from the acinar pancreas, resulting in higher concentration of serum GAA in acute pancreatitis rats. GAA may be synthesized in the acinar pancreas, and insulin can directly regulate the function of acinar pancreas including GAA synthesis.
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PMID:[Study of impaired metabolism of guanidinoacetic acid in uremia--the compensatory role of the pancreas in guanidinoacetic acid synthesis]. 268 30

Diabetic lipemia with and without acute pancreatitis in chronic alcoholism. A report of 4 cases. Diabetic lipemia was observed in 4 chronic alcoholic men after ingestion of high doses of alcohol and/or sugar-rich beverages, including one patient who was treated for insulin-dependent diabetes. None had a previous history of serum lipid disturbances. All had marked hyperglycemia, hyperosmolality and hypertriglyceridemia (mean: 60.8 mmol/l), 2 of undetermined type and 2 of type IV with eruptive xanthomas. Factitious hyponatremia was present in 3 cases, but true serum sodium was normal (138 mmol/l) or elevated (154, 156, 182 mmol/l) after correction. Three patients developed acute pancreatitis ascribed to high serum triglyceride levels and/or to alcohol ingestion. Serum and urine amylase activity was inhibited by hypertriglyceridemia. The diagnosis of pancreatitis was assessed twice by echography and computed tomographic scan, and once by tomographic scan and an elevation of the amylase on creatinine clearance ratio. It is likely that hypertriglyceridemia predisposed these patients to develop pancreatitis, alcoholism being a precipitating factor. We suggest that the diagnosis of acute pancreatitis should be systematically considered in any case of diabetic lipemia without true hyponatremia.
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PMID:[Diabetic hyperlipemia with or without acute pancreatitis in patients with chronic alcoholism. A study of 4 cases]. 274 Jun 61

We tested the new radioimmunoassay method of serum phospholipase A2 (PLA2). In healthy individuals, serum PLA2 concentrations were 301 +/- 65.6 ng/dl (mean +/- SD), and in patients with acute pancreatitis, significant elevations of serum PLA2 concentrations were observed. In clinical course of acute pancreatitis, serum PLA2 was maintained high level more longer than serum amylase and elastase 1. In patients with chronic pancreatitis, serum PLA2 concentration were low at a stage of severe exocrine dysfunction, and high at a stage of acute exacerbation. In patients with pancreatic cancer, serum PLA2 concentration were changed in accord with severity of disease states. After endoscopic retrograde pancreatography, serum PLA2 levels immediately elevated significantly, and returned to basal levels 24 hours later. Serum PLA2 concentrations were within normal range in patients with other malignant tumors, diabetes mellitus, chronic liver diseases, and hypertension, whereas in patients with chronic renal failure serum PLA2 concentrations were elevated. These results suggest that measurement of serum PLA2 can be clinically useful for diagnosis of pancreatitis and monitoring of mild and severe stage of pancreatitis.
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PMID:[Clinical studies of serum phospholipase A2 immunoreactivity]. 279 50

Although tumour metastases to the pancreas and peripancreatic lymph nodes are found commonly at necropsy in cases of small cell carcinoma of lung, tumour-induced acute pancreatitis is described rarely. A case of metastasis-associated necrotising pancreatitis with the unusual presentation of epigastric pain followed by diabetes is described here. Patients (particularly cigarette smokers) with none of the conventional risk factors for acute pancreatitis merit chest radiography and if indicated prompt cytotoxic treatment.
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PMID:Necrotising pancreatitis and diabetes associated with disseminated small cell carcinoma of lung. 285 1

This article is aimed at reviewing and analyzing studies that are related to the possible therapeutic use of a potent and ubiquitously-distributed hormone--somato-statin (SS-14), and its analogues. Administration of these substances has provided beneficial effects in treating acromegaly, gastro-intestinal hemorrhagic and hypersecretory disorders, acute pancreatitis, diabetes mellitus, and certain types of cancer. Further studies with SS-14-analogues might provide new therapies for treating certain life-threatening disorders of man.
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PMID:Pharmacological studies of somatostatin and somatostatin-analogues: therapeutic advances and perspectives. 288 Feb 72

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

The purpose of this study was to determine the incidence of death as the initial manifestation of cholelithiasis. Records of patients who died or underwent cholecystectomy for gallstone-related disease at Duke University Medical Center between 1976 and 1985 were reviewed. Thirty patients died, six of whom (20%) had previous episodes of biliary pain and stone documentation. Twenty-four (80%) were asymptomatic (three with previous incidental diagnosis of cholelithiasis). Reason for admission included acute cholecystitis (nine), pancreatitis (eight), biliary pain (six), cholangitis (four), jaundice (one), and endocarditis (one). Three patients died of gallstone complications without surgical intervention; one patient had renal failure and two had septicemia. Other causes of death were: sepsis (seven patients), cardiac failure (six), pulmonary complications (four), renal failure (three), cerebrovascular accident (three), liver failure (two), pancreatitis (one), and gastrointestinal bleeding (one). During this period, 1731 cholecystectomies were performed without mortality. In this group, the patients were younger (50 +/- 8 years vs. 64 +/- 13 years, p less than 0.001), and had a lower incidence of cirrhosis (p less than 0.001) and diabetes (p less than 0.002). The sex ratio was inverted (p less than 0.001). This study demonstrates that death from gallstones is uncommon (three cases per year), as is death from their initial clinical manifestation (1.2%). The risk of death is two- and ninefold higher in patients with acute cholecystitis or acute pancreatitis. Age, cirrhosis, and diabetes are important determinants of outcome.
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PMID:Deaths from gallstones. Incidence and associated clinical factors. 291 58

Hypertriglyceridemic patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased risk of coronary heart disease (CHD) and acute pancreatitis. To examine the potential of hypolipidemic drugs for therapy of lipoprotein abnormalities in NIDDM, 10 patients maintaining marked (plasma triglycerides greater than 500 mg/dl) and 6 with moderate (plasma triglycerides 250-500 mg/dl) hypertriglyceridemia, despite good glycemic control, were studied in two phases. In the first phase, gemfibrozil alone (600 mg twice daily) was compared with a placebo, and in the second phase a combination of gemfibrozil and lovastatin (20 mg twice daily) was compared with gemfibrozil alone in a randomized, double-blind, placebo-controlled crossover study. In markedly hypertriglyceridemic patients, gemfibrozil reduced plasma triglycerides by 52% and very-low-density lipoprotein cholesterol (VLDL-chol) by 55% and increased high-density lipoprotein cholesterol by 23% compared with a placebo. However, low-density lipoprotein cholesterol (LDL-chol) levels increased (42%), and LDL apolipoprotein B (apoB) levels remained unchanged. Addition of lovastatin to gemfibrozil effectively reduced total cholesterol (25%), LDL-chol (30%), and LDL-apoB (19%). Lovastatin further reduced plasma triglycerides (11%) and VLDL-chol (27%). However, in moderately hypertriglyceridemic patients, gemfibrozil or the combination therapy did not seem to offer benefits over the previously reported study with lovastatin alone. Glycemic control was maintained throughout the study. In conclusion, the beneficial effects of the combination therapy on lipoprotein levels in markedly hypertriglyceridemic NIDDM patients could decrease the risk of development of both acute pancreatitis and CHD.
Diabetes 1989 Mar
PMID:Gemfibrozil alone and in combination with lovastatin for treatment of hypertriglyceridemia in NIDDM. 291 1


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