Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Traumatic injury frequently follows alcohol abuse. Between October 1, 1988 and January 31, 1992, 2,219 patients were admitted to the Trauma Service at the University Medical Center of Eastern Carolina-Pitt County. Of the 1,602 who were tested for serum ethanol, 685 (43%) were found to have measurable levels. Thirty-seven patients had alcohol withdrawal and were treated with intravenous ethanol; 34 were male (21 black, 13 white) and 3 female (1 black, 2 white), with an average age of 46 years. Those who had withdrawal had an average serum ethanol level, on presentation, of 239 mg/dL (N = 34). Fourteen patients were involved in motor vehicle crashes, seven were pedestrians struck by cars, and the remaining 16 had various traumatic mechanisms of injury. The most common injuries were long-bone fractures and blunt abdominal trauma. The length of ethanol therapy averaged 4 days. A majority of patients had a favorable response to treatment. Relative contraindications to i.v. ethanol therapy were CNS trauma, liver disease, and pancreatitis. i.v. ethanol is a safe and effective method of alcohol detoxification in the trauma patient.
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PMID:Intravenous ethanol for alcohol detoxification in trauma patients. 828 18

In a population of 716 patients with end-stage renal disease (ESRD), 46 patients (6.4%) were identified as having pancreatitis. Pancreatitis was significantly more common in those with alcohol abuse, systemic lupus erythematosus (SLE), and polycystic kidney disease. It was not significantly associated with hyperlipidemia, biliary tract disease, or hypercalcemia. Acute pancreatitis occurring before the patient developed ESRD was mainly alcohol-related and did not appear to be a significant risk factor for future episodes of pancreatitis during dialysis. Chronic calcific pancreatitis diagnosed before ESRD was almost invariably due to alcohol abuse, and tended to be a marker for recurrent acute exacerbation after development of ESRD, whether alcohol consumption continued or not. Pancreatitis occurring for the first time after ESRD in patients on dialysis was generally benign, and was usually accompanied by an uneventful recovery and few recurrent episodes. However, a significant elevation of the calcium x phosphate product was observed in these patients, occurring in about half the patients without any known precipitating factor. After kidney transplantation, the development of pancreatitis was associated with higher morbidity and mortality. Chronic calcific pancreatitis diagnosed after ESRD occurred only in patients with SLE; reported here for the first time, it may be a manifestation of long-standing disease, chronic steroid therapy, or both.
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PMID:Pancreatitis in patients with end-stage renal disease. 830 63

Indications as to which patients should undergo cholecystectomy remain, at least in part, a matter of controversy. In 1987, a panel of nine Israeli physicians from different specialties established a list of indications for the performance of cholecystectomy based on the literature available at the time. The panel agreed that cholecystectomy was appropriate for 59 indications and that it was inappropriate for 58. The major indications for surgery were biliary colic and acute cholecystitis. Patients who were asymptomatic or had vague symptoms were not recommended to undergo surgery unless they had stones in the common bile duct and were less than 71 years of age. Patients with pancreatitis were recommended for surgery if they had stones in the common bile duct and did not have a history of alcohol abuse. Performing a cholecystectomy at the same time as abdominal surgery was being performed for other reasons was indicated only if the patient was symptomatic from his gall-stones.
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PMID:The agreed indications and contra-indications for cholecystectomy. 845 92

Some recent proposals in management of alcoholic liver disease are discussed focusing on early diagnosis and treatment of alcohol abuse itself, alcoholic hepatitis early mortality, clinical meaning of nutritional therapy, serological approach and treatment of hepatic fibrosis, and problems in liver transplantation for end stage alcoholic liver cirrhosis. CAGE or similar systematized brief questionnaires, and desialylated transferrin/total transferrin ratio as serological marker, seems to be interesting contributions to "hidden" alcohol abuse diagnosis and abstinence control while psycho-social support and voluntary incorporation to self-aid groups are the best weapons to reach persistent abstinence. Corticosteroids seems to improve survival in a selected group of patients with severe alcoholic hepatitis, specially in those presenting encephalopathy but free of GI bleeding, decompensated diabetes, active infections, pancreatitis, and other contraindications or adverse effects of these drugs. Relationship between direct toxicity and nutritional deficiencies in pathogenesis of alcoholic liver injury are not clear enough, but malnutrition is generally present in patients requiring hospitalization, and related to clinical severity; oral, enteral or parenteral nutritional supplementation in this order of preference according to patients condition, associated or not with steroid anabolics, are useful in cases with moderate to severe alcoholic hepatitis or decompensated cirrhosis to eliminate the catabolic state, reaching a better nitrogen balance and liver function tests, without special adverse effects. A special role on liver regeneration is discussed. Antioxidants and supernutrients are special "modern" aspects of nutritional therapy in alcoholic liver disease generally related to the MEOS activation in chronic alcoholism, the excessive production of free radicals, and the depletion of glutathione, membrane phospholipids (specially phosphatidycholine), and vitamin A, E, and C. Natural supplements as soybean polyunsaturated lecithin, with high concentration of phosphatidycholine, or oral supplementation with natural metabolic products depleted from the liver of chronic heavy drinkers, such SAMe, have an interesting rationale based on experimental and clinical findings besides availability and costs. Carotenoids and tocopherols supplementation seems to be an useful tool, but are limited in the case of vitamin A because its special toxicity in chronic alcoholism. Serological markers of metabolism of liver connective tissue are clearly involved in fibrogenesis process and other inflammatory connected events; standardization of laboratory methods surely will result in new possibilities of non-invasive valuation of liver injury, evolution and therapeutic response; special histological damage such as sinusoidal "cappilarization" (type i.v. collagen and laminin), endothelial sinusoidal cell function (seric hyaluronate), or collagenase activity (TIMP-1 or tissue inhibitor of metalloproteinases-1) seems to be valuable by these new technologies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[New suggestions for the management of alcoholic liver diseases]. 852 63

Pancreatitis caused by chylomicronaemia was diagnosed in three patients, two men of 36 and 51 years and a woman of 33 years. All three patients had a combined hyperlipidaemia, with severely elevated levels of triglycerides and cholesterol. Secondary causes of hypertriglyceridaemia such as uncontrolled diabetes mellitus, alcohol abuse, and non-compliance with diet and lipid lowering drug therapy caused aggravation of the lipid disorder. It is important to consider chylomicronaemia as a possible cause of pancreatitis, as treatment of the lipid disorder with diet and, if necessary, drugs can prevent recurrence of pancreatitis.
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PMID:[Acute pancreatitis caused by chylomicronemia syndrome]. 856 9

The clinical spectrum of acute pancreatitis ranges from mild, self-limiting disease of fulminant illness that may rapidly lead to multiple organ failure and death. To identify factors associated with a subsequent severe course and/or high mortality we investigated retrospectively 91 patients admitted to the medical intensive care unit (ICU) with acute pancreatitis during a 2 year period. 67% of the attacks were mild (< or = 1 complication). The overall mortality rate was 9%, whereby 3% of patients with alcoholic and 13% with biliary pancreatitis died. 75% of the patients in the group with a fatal outcome were aged over sixty and 30% in the group with a mild course (p < 0.05). Females with pancreatitis of biliary origin had a mild course in 57% and a severe (> or = 2 complications) or fatal outcome in 43%. In males with alcohol abuse we observed a mild form of pancreatitis in 79% and a severe or fatal course in 21%. The delay between onset of abdominal pain and commencement of treatment in hospital was greater than 12 hours in 70% of all patients studied and there was no association with severity and development of subsequent complications. The median of the acute physiology and chronic health evaluation scoring system (APACHE-III) on the day of admission was 19 in patients with mild disease, which was significantly lower than in patients with severe (40) or fatal acute pancreatitis (53) (p < 0.0001). Serial APACHE-III measurements over 5 days after admission provided further differentiation between mild and severe or fatal cases (p < 0.0001), but no significant difference was observed between survivors with severe course and fatal outcome. In addition, RANSON scores were calculated for comparison with APACHE-III at admission and after 48 hours: concerning the recognition between mild and severe/fatal pancreatitis both scoring systems exhibited similar significant differences on day 1 and day 2. The RANSON scoring system provided further a significant differentiation between survivors with a severe course of pancreatitis when compared to deaths on day 2, whereas the APACHE-III scoring system did not. Advanced age, female sex, biliary obstruction and elevated RANSON and APACHE-III scores are risk factors for an increased rate of life-threatening complications in acute pancreatitis. The daily assessment of such scoring systems may allow the recognition of such patients and may be helpful in the routine clinical management and monitoring of acute pancreatitis.
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PMID:Intensive care management of acute pancreatitis: recognition of patients at high risk of developing severe or fatal complications. 867 61

A fatal case of acute pancreatitis is reported. On account of difficulty in eating caused by persistent dysphagia and heartburn, the clinical condition of a 39-year-old man who had been a heavy drinker deteriorated rapidly. He was taken to a hospital in an ambulance in an unconscious state. Based on the endoscopic examination and blood chemistry data, the diagnosis of hemorrhagic esophagitis and hepatic failure was made. Treatment including fluid infusion was unsuccessful and he died on the second hospital day. Based on a strong suspicion that the pathologic change in the esophagus may have been chemical esophagitis caused by corrosives of some type, the police ordered an administrative autopsy. The postmortem examination revealed marked necrosis in the pancreas and in the abdominal fatty tissue including the omentum and the mesentery. The necrotic areas in the pancreas were accompanied by only a slight degree of hemorrhage. The cause of death was diagnosed as acute pancreatitis. The pathologic change in the esophagus was identified as Candida esophagitis. Alcohol abuse and malnutrition caused by esophagitis were both considered to be factors which lead to the acute fatal pancreatitis.
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PMID:Death caused by undiagnosed acute pancreatitis. 869 55

In the 108 patients with diabetes (75 men and 33 women between the ages of 15 and 86 years) hospitalized in the Internal Medicine Department of the Libreville Hospital Center between January 1, 1989 and December 31, 1991, 53 were easily classified, 12 being due to alcohol-induced chronic calcific pancreatitis, two to insulin-dependent diabetes, and 39 to non-insulin-dependent diabetes. Fifty-five patients treated with insulin were not immediately classifiable including 11 who were obese and probably should not have required insulin. In the remaining 44 patients who were not overweight, the youngest often presented features comparable to those observed in patients with chronic calcific pancreatitis except with regard to calcification. Most of the older patients were women in whom diagnosis was coincidental. These findings indicate that authentic insulin-dependent diabetes is uncommon, that non-insulin-dependent diabetes are frequent, and that the endocrine pancreas is particularly susceptible to alcohol abuse.
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PMID:[Types of sugar diabetes encountered in internal medicine in Gabon]. 876 94

The association between acute pancreatitis and severe hypertriglyceridemia has long been recognized. We report two cases of severe primary hypertriglyceridemia (types 1 and V) with recurrent acute pancreatitis. In both patients, observance of appropriate diet and drug therapy was insufficient. Recurrent episodes of pancreatitis were precipitated by dietary fat or alcohol abuse. A plasmapheresis was performed every 4 weeks to decrease the incidence of pancreatitis. It appears that plasmapheresis is a safe and highly effective method for quickly removing serum triglycerides. Moreover, plasma-pheresis may be useful for preventing acute pancreatitis.
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PMID:Prevention of recurrent acute pancreatitis in patients with severe hypertriglyceridemia: value of regular plasmapheresis. 878 40

Chronic pancreatitis is characterized by inflammation and fibrosis leading to tissue destruction; in industrialized nations, alcohol abuse is the cause of 70-80% of cases of pancreatitis in adults. The purpose of the current work was to determine whether free radical adducts are produced by the pancreas during the early phases of chronic exposure to ethanol. Accordingly, rats were chronically fed ethanol using the model of continuous enteral infusion developed by Tsukamoto et al.[Am. J. Physiol. 247: R595-R599 (1984)]. Histological evaluation revealed only mild acinar steatosis and spotty necrosis after 4 weeks of alcohol treatment; the pancreatic enzymes lipase and amylase were not elevated. Furthermore, no fibrosis was detected, nor were there differences in pancreatic collagen alpha 1(l) mRNA levels between the dietary control and ethanol-treated groups. After 4 weeks, rats were injected with the spin trap alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (1 g/kg intravenously), and pancreatic secretions were collected over a 4-hr period. A six-line free radical adduct spectrum indicative of a carboncentered free radical was detected in pancreatic secretions and in Folch extracts of pancreatic tissue by electron spin resonance spectroscopy. Control experiments ruled out ex vivo radical formation. This study represents the first detection of radical adducts in pancreatic secretions. When [13C]ethanol (3 g/kg intragastrically) was administered, a definitive 12-line spectrum was detected in pancreatic secretions, demonstrating that the alpha-hydroxyethyl radical adduct was formed in the pancreas from [13C]ethanol. Interestingly, only a six-line signal was detected in tissue extracts under these conditions. Free radicals, therefore, are formed in the pancreas during the early phases of chronic alcohol intake in rats before the development of overt pathology.
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PMID:Detection of alpha-hydroxyethyl free radical adducts in the pancreas after chronic exposure to alcohol in the rat. 879 7


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