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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the prognosis and prognostic factors of chronic pancreatitis, 84 patients with alcoholic chronic pancreatitis and 51 with nonalcoholic chronic pancreatitis have been followed for 1-21 years (average of 7.1 years). The follow-up period was defined as the period from diagnosis to death in those who died and to the present in those still alive. The following conclusions were obtained. (1) Patients with alcoholic chronic pancreatitis showed a significantly higher mortality rate (26.2%) and cancer death rate (8.3%) than the age- and sex-matched population. In patients with nonalcoholic chronic pancreatitis, however, the difference did not reach the level of statistical significance, although both rates tended to be higher. (2) Patients with alcoholic chronic pancreatitis showed a significantly poorer prognosis than those with nonalcoholic chronic pancreatitis. (3) Frequent causes of death in chronic pancreatitis were cancer (11 cases) and diabetes-associated conditions (renal failure in three cases, intractable pneumonia in one, hypoglycemic shock in two, and myocardial infarction in two). Death directly from pancreatitis was observed in four. (4) Unfavorable prognostic factors in alcoholic chronic pancreatitis included heavy drinking, continuance of drinking after diagnosis, smoking, insulin-dependent diabetes, and an advanced age. In nonalcoholic chronic pancreatitis, however, patients' age was the only significant prognostic factor; smoking did not reach the level of statistical significance, although it tended to lead to a poorer prognosis.
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PMID:Prognosis and prognostic factors in chronic pancreatitis. 292 Jun 51

It has been shown recently that longterm but not short term heavy drinking of alcohol frequently results in increased serum activities of pancreatic enzymes suggesting subclinical pancreatic injury. Serum pancreatitis associated protein (PAP) is a novel protein, whose synthesis in the acinar cells and release into serum is specifically induced by acute pancreatic damage. This study was performed to further characterise the alcohol induced subclinical pancreatic injury by using serum PAP measurements. Three groups were studied: (1) control group (n = 25), (2) short term drinking group (n = 20), who consumed 2.0 g of ethanol per kg body weight during four hours, and (3) longterm drinking group (n = 32), who were admitted to withdrawal clinic after a median 30 months heavy drinking period. Serum PAP concentration was low in the control group (8 (5 to 12) micrograms/l, geometric mean (95% confidence intervals)). In the short term drinking group serum PAP was in the range of the control group values during 56 hours after drinking. Longterm drinking induced at least a 10-fold increase in serum PAP, the highest concentrations being seen on day 2 after drinking had ended (106 (61 to 184) micrograms/l). The patients did not develop abdominal symptoms, increased blood white cell count, or increased serum C reactive protein concentration. These results further support the suggestion that heavy longterm drinking often induces subclinical pancreatic damage, but not clinical pancreatitis.
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PMID:Increased serum pancreatitis associated protein (PAP) concentration after longterm alcohol consumption: further evidence for regular subclinical pancreatic damage after heavy drinking? 789 Feb 13

Postemetic spontaneous rupture of the esophagus is an intrathoracic disaster which is generally lethal if untreated. The tragedy seems to strike more often than commonly suspected. The current literature review focuses on publications since 1980 and includes the retrospective review of 18 additional patients treated in our hospital for spontaneous rupture of the esophagus. Frequently, a wide variety of unspecific symptoms has led to the mistaken diagnosis of an acute abdomen, pancreatitis or cardiac arrest. About 40% of the patients with spontaneous rupture of the esophagus presented a history of alcoholism or heavy drinking and 41% suffered from gastroduodenal ulcer disease. Pain (83%) and vomiting (79%) often associated with dyspnea (39%) and shock (32%) are the major symptoms. This unspecific symptomatology delayed the correct diagnosis of the Boerhaave's syndrome and resulted in a significant complication rate. The mortality rate associated with Boerhaave's syndrome was 50% from the first successful surgical repair in 1947 by Barrett to 1980. After 1980, however, the mortality rate dropped to 31%, because of earlier diagnosis, surgical repair and improvement in intensive care. When surgery is delayed, the prognosis of patients with spontaneous rupture of the esophagus is in general severe.
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PMID:Boerhaave's syndrome: analysis of the literature and report of 18 new cases. 907 78

A population-based case-control study investigated pancreas cancer in relation to consumption of alcoholic beverages, tobacco smoking and pancreatitis, utilizing historical proxy data for 662 decedent Finnish pancreas cancer cases and 1770 cancer controls. Tobacco smoking increased the risk, with an attributable case fraction of 0.27. The data are consistent with a joint effect of early and late stage carcinogens in tobacco smoke. Consumption of distilled beverages did not increase risk, but heavy drinking of wine or beer did. History of pancreatitis was a strong risk factor.
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PMID:Pancreas cancer, tobacco smoking and consumption of alcoholic beverages: a case-control study. 917 54

The intake of larger quantities of alcoholic beverages leads to manifold functional disturbances and organ injury in the upper gastrointestinal tract. These damaging effects of alcohol are frequently the cause of complaints, such as heart burn, symptoms of dyspepsia and diarrhoea. Examples of more pronounced organ injury which can occur even following a single episode of heavy drinking are tears in the mucosa at the junction of the esophagus and the stomach (Mallory-Weiss-lesion) and hemorrhagic erosions in the stomach and/or the duodenum which may lead to massive bleeding. In the small intestine alcohol abuse interferes with the absorption of glucose, amino acids, lipids, water, sodium and vitamins (especially thiamine and folic acid). This inhibition of absorption of nutrients may contribute to nutritional deficiencies frequently observed in alcoholics. Acute alcohol ingestion can also damage the mucosa in the upper region of the small intestine and may lead to the disruption of the tips of the villi. Chronic alcohol abuse increases markedly the prevalence of bacterial overgrowth in the small intestine. The findings of human and animal studies suggest that the mucosal injury together with bacterial overgrowth favour the following sequence of events: Alcohol induced mucosal injury in the small intestine increases the permeability of the mucosa to macromolecules, such as endotoxin and/or other bacterial toxins, into the blood or lymph. This results in the release of potentially toxic cytokines and other mediators like Kupfer cells and other phagocytes. These cytokines and other mediators, in turn, exert multiple injurious effects on the microcirculation and membranes. The result is cell damage and even cell death (apoptosis, necrosis) in the liver and other organs. Chronic alcohol abuse is one of the most important risk factors for the development of cancers of the tongue, larynx, pharynx and esophagus. In many countries alcohol abuse is the most important cause for the development of chronic pancreatitis. In the initial phase the disease is frequently characterised by episodes of 'acute' pancreatitis. These episodes develop only on the basis of prolonged alcohol abuse leading to subclinical damage of the gland. The latter is found in about 20-50% of patients with chronic alcohol abuse while the clinically overt pancreatitis is observed in only 1%-3% of alcoholics. Despite numerous studies performed in animal experiments and man the pathogenesis of alcoholic pancreatitis until now has not been clarified.
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PMID:[Alcohol, the gastrointestinal tract and pancreas]. 1080 79

Aneurysms and pseudoaneurysms of the gastroduodenal artery are rare with less then 50 cases reported. Most frequently they are one of the consequences of pancreatitis much rarer duodenal ulcer or operative trauma during gastrectomy for duodenal ulcer or choledochotomy. We report on a 47 year-old man, chronic heavy alcohol consumer in whom a chronic postbulbar duodenal ulcer destroyed much of the back wall of the duodenum, eroded gastroduodenal artery causing pseudoaneurysm but without noticeable gastrointestinal bleeding. The patient had jaundice of obstructive type and elevated amilase. After Billroth II gastrectomy, suture of the gastroduodenal artery, cholecystectomy and T tube drainage of the common bile duct the patient developed intestinal obstruction caused by two interintestinal abscesses so that he had to be reoperated. After that he had a successful recovery, his general health greatly improved, he gained 15 kg in weight but two years after surgery he again started with heavy drinking and soon died due to serious brain damage. The case is rare and unusual at least for few reasons: First, the pseudoaneurysm was caused by duodenal ulcer. Second, a serious gastrointestinal bleeding did not take place. Third, the pseudoaneurysm was diagnosed by Doppler ultrasonography while angiography failed to opacify it due to thrombosis of the artery.
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PMID:[Pseudoaneurysm of gastroduodenal artery due to duodenal ulcer causing jaundice and interstitial pancreatitis but not bleeding]. 1530 14

Unhealthy alcohol use is among the leading causes of morbidity and mortality in the United States. Among military personnel, service members between the ages 18 and 25 had a 27.3% prevalence of heavy drinking in the previous 30 days, compared to 15.3% among civilians in the same age group. In the civilian world, > 100 million patients are treated in U.S. emergency departments (ED) annually; 7.9% of these visits are alcohol related. Alcohol is associated with a broad range of health consequences that may ultimately present in the ED setting: traumatic injuries (e.g., motor vehicle crashes, intentional violence, falls); environmental injuries (e.g., frostbite); cardiovascular problems (e.g., hypertension, dilated cardiomyopathy); gastrointestinal disorders (e.g., hepatitis, pancreatitis, gastrointestinal bleeding); neurological problems (e.g., encephalopathy, alcohol withdrawal, withdrawal seizures), as well as psychological problems (e.g., depression, suicide). Seminal work has been done to create behavioral interventions for at-risk drinkers. These motivational interventions have been found to be successful in encouraging clients to change their risky behaviors. We present such a technique, called the Brief Negotiated Interview as performed in a civilian ED setting, in hopes of adapting it for use in the military context. Military health care providers could easily adapt this technique to help reduce risky levels of alcohol consumption among service members, retirees, or military dependents.
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PMID:Brief interventions to reduce harmful alcohol use among military personnel: lessons learned from the civilian experience. 1680 38

Only a small proportion of heavy drinking individuals develop pancreatitis. The environmental and host cofactors shown to have an association with alcoholic pancreatitis are smoking and race. The known genetic variations and polymorphisms do not seem to play an important role in alcoholic pancreatitis. Newer developments in the understanding of complex disorders allow clinicians to understand better the role of cofactors and interactions between known and yet unknown environmental and genetic factors in causing alcoholic pancreatitis.
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PMID:Alcohol-associated pancreatitis. 1753 76

In order to provide a more precise quantification of the association between alcohol consumption and pancreatic cancer risk, we performed a meta-analysis of relevant dose-risk results. We conducted a PubMed search of all case-control (N=21) and cohort (N=11) studies published up to March 2009. We computed summary relative risk (RR) estimates using either fixed- or, in the presence of heterogeneity, random-effects models. The pooled RR was 0.92 (95% confidence interval, 95% CI, 0.86-0.97) for <3 drinks/day and 1.22 (95% CI, 1.12-1.34) for > or = 3 drinks/day. The increased risk for heavy drinking was similar in women and men, but apparently stronger in cohort studies (RR=1.29), in studies with high quality index (RR=1.30), and did not appear to be explained by residual confounding by either history of pancreatitis or tobacco smoking. This meta-analysis provides strong evidence for the absence of a role of moderate drinking in pancreatic carcinogenesis, coupled to an increased risk for heavy alcohol drinking. Given the moderate increase in risk and the low prevalence of heavy drinkers in most populations, alcohol appears to be responsible only for a small fraction of all pancreatic cancers.
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PMID:Alcohol drinking and pancreatic cancer risk: a meta-analysis of the dose-risk relation. 1981 41

We review the current evidence for associations of several medical conditions with risk of pancreatic cancer, including allergies, pancreatitis, gall bladder disease, cholecystectomy, ulcers, gastrectomy, appendectomy, and tonsillectomy. There are consistent findings of reduced risk associated with presence of self-reported allergies, particularly hay fever but not asthma; data on other allergies are limited and inconclusive. Several studies provide evidence that patients with pancreatic cancer are more likely than comparison groups to report pancreatitis. Those studies that investigated the time between onset of pancreatitis and diagnosis of pancreatic cancer found that risk estimates declined with longer periods of time; however, increased risks were noted for long-term pancreatitis, indicating that this condition is both a risk factor and a sign of early disease. Increased risk was reported in association with cholelithiasis, but the few studies that considered time before diagnosis of cancer did not find increased risk for cholelithiasis diagnosed in the more distant past. There is weak evidence that cholecystectomy 2 or more years before cancer diagnosis is related to risk, but this is based on only a few studies. There is no consistent association between ulcers and risk, while gastrectomy may increase risk. Overall, study of these conditions, particularly those that are rare, presents methodologic challenges. Time between diagnoses is likely to be important but is not considered in most studies. Lack of adequate control in several studies for risk factors such as smoking and heavy alcohol use also makes it difficult to draw firm conclusions about these results.
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PMID:Selected medical conditions and risk of pancreatic cancer. 2216 33


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