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

Alcoholic pancreatitis may be one of the most serious adverse consequences of alcohol abuse. Its diagnosis, as it has for many years, depends primarily on clinical acumen in interpreting properly the symptoms and signs of abdominal distress, buttressed by elevated pancreatic enzymes (amylase and lipase). More recently, the use of computerized tomography (CT) in selected situations has been both of confirmatory and prognostic value. Severity of abnormality by CT correlates reasonably well with a variety of clinical-laboratory clusters (APACHE system, Ranson's criteria, etc.) and aids in therapy. The pathogenesis of alcoholic pancreatitis is not fully defined. The ultimate picture is one of tissue autolysis by activated proteolytic enzymes. The triggers for such activation, however, are still not known. They are represented by three main theories: (1) large duct obstruction and/or increased permeability relative to pancreatic secretion, (2) small duct obstruction due to proteinaceous precipitates, and (3) a direct toxic-metabolic effect of ethanol on pancreatic acinar cells. While not mutually exclusive, we favor the last hypothesis as being most consistent with the effects of ethanol on other organ systems. The direct effects of ethanol and/or its metabolites may be mediated, at least in part, via oxidative stress or the generation of fatty acid ethyl esters. Autolysis (regardless of proximate mechanism(s)) leads to inflammation likely mediated via release of various cytokines. It also should be appreciated that "acute" pancreatitis (the topic of this chapter) likely represents an acute process within a chronic pancreatic exposure and injury from alcoholic abuse. The key question of why pancreatitis develops in only a small number of alcohol abusers is not resolved. Therapy depends on the severity of alcoholic pancreatitis, which is defined by clinical-laboratory and often CT criteria. Mild pancreatitis usually resolves acutely with alcohol abstention and supportive therapy. Severe pancreatitis has a significant morbidity and mortality, mainly related to the degree of pancreatic necrosis and infection. It requires meticulous combined medical-surgical care.
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PMID:Alcohol and the pancreas. 975 42

Acute pancreatitis is only rarely the first presentation of a cystic neoplasm of the pancreas. Mucinous cystadenomas have not been reported to be a cause of acute pancreatitis; however, we present two cases of mucinous cystadenoma of the pancreas which have caused acute pancreatitis. Both patients (female) presented acute abdominal pain, with serum amylase elevation and ultrasound scan (US) and computed tomography (CT) evidence of moderate pancreatitis, which resolved with medical treatment; fluid collection in the distal pancreas had been misinterpreted as a pseudocyst. There was no history of alcohol abuse or gallstone disease. After distal pancreatectomy the diagnosis of mucinous cystadenoma was confirmed; in one case a large pseudocyst was associated with this diagnosis. Pre-operative differential diagnosis between inflammatory and neoplastic cysts is difficult, especially when the patient's first presentation is due to an episode of acute pancreatitis. A neoplastic cyst should be considered when acute pancreatitis attacks occur in non-alcoholic women, who do not have gallstone disease.
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PMID:Mucinous cystadenoma of the pancreas as a cause of acute pancreatitis. 995 36

Although heavy alcohol intake is known to be one of the most common causative factors of liver disease, pancreatitis, upper gastrointestinal and neurological disorders, the influence of the drinking pattern is largely unknown. The study investigated the relationship of alcohol-related medical disorders in alcoholics and their drinking pattern. Two hundred and forty-one chronic alcoholics were referred consecutively for detoxification and their drinking pattern was sufficient for them to be included in this study. History of alcohol abuse as well as drinking behaviour in the last 6 months were assessed by a semi-structured interview. Findings included intensive clinical examination with abdominal ultrasound in most subjects. Heavy drinking with frequent inebriation was most often found in our sample (44.4%), whereas continuous heavy alcohol consumption without intoxication (33.6%), and an episodic drinking style (22.0%) were less frequent. The heavy drinkers suffered more often from pancreatitis, oesophageal varices, polyneuropathy or erectile dysfunction than episodic drinkers. They also showed more upper gastrointestinal disorders, although the estimated life-time alcohol intake was comparable to continuous drinkers. No difference relating to withdrawal delirium or seizures could be found between the groups of alcoholics. Frequent heavy drinkers showed a trend to more alcohol-related medical disorders than alcoholics with a different drinking pattern, although they were younger and their estimated life-time alcohol intake was comparable to that of continuous drinkers. Thus, the drinking pattern, particularly frequent inebriation, has an influence on the occurrence of alcohol-related disorders.
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PMID:Drinking pattern and alcohol-related medical disorders. 1041 7

Whether or not AP may progress to the chronic form is controversial. Equally debatable is whether AP caused by alcohol abuse develops in a chronically diseased gland or in a normal pancreas. As for the state of the gland, several postmortem studies have shown that AP may occur after acute alcohol abuse in the normal pancreas. As for progression from acute to chronic pancreatitis, many experimental studies have demonstrated signs of the chronic from of the disease in animals, but these signs were reversible. Some clinical studies have shown that alcohol-induced pancreatitis may progress to chronic pancreatitis. There are, however, presently no predictive parameters indicating when such a progression does or does not occur.
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PMID:Progression from acute to chronic pancreatitis: a physician's view. 1047 Mar 29

Hypertriglyceridaemia is thought to be the aetiology in 3% of patients with acute pancreatitis, often associated with poorly controlled diabetes mellitus or chronic alcohol abuse. However, in patients with non-biliary pancreatitis, chylomicronaemia is an underrated cause of acute pancreatitis. The activity of lipoprotein lipase (LPL) is crucial in removing triglycerides from the plasma; LPL gene mutations combined with secondary alterations in plasma lipoproteins, such as occur in pregnancy, diabetes mellitus, and alcohol abuse can cause severe hypertriglyceridaemia and pancreatitis. Heparin and insulin stimulate LPL activity. During a 12 months' period we consecutively screened all patients with the diagnosis of acute non-biliary pancreatitis for hypertriglyceridaemia, to evaluate the prevalence of hypertriglyceridaemia-induced pancreatitis and to assess the outcome under standardised treatment with intravenous heparin and insulin. Hypertriglyceridaemia-induced pancreatitis was diagnosed in 5 out of 46 patients (11%) with acute pancreatitis. In 2 patients hypertriglyceridaemia was associated with diabetes mellitus, in one patient with pregnancy and in another with chronic alcohol abuse. Four patients had to be referred to the intensive care unit. Plasma concentrations of triglycerides were (median +/- range) 43 mmol/l (14.7 to 80.4); pancreas amylase was 574 U/l (155 to 1606), and lipase was 1003 U/l (330 to 3010). All patients had oedematous pancreatitis demonstrated by CT scan. Treatment with i.v. heparin and i.v. insulin decreased trigylceride levels to less than 10 mmol/l within 2.8 days (1 to 6), the amylase and lipase levels returned to normal after 3 and 4 days respectively, and the abdominal pain was resolved. Hypertriglyceridaemia is a common and under-diagnosed etiology of acute non-biliary pancreatitis. Intravenous heparin and insulin is safe and effective in the treatment of hypertriglyceridaemia-induced pancreatitis. Low fat diet, supplements of (n-3) fatty acids ("fish oil") and fibrates are recommended for long-term maintenance therapy.
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PMID:[Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis]. 1049 50

Percutaneous catheter drainage (PCD) of symptomatic pancreatic pseudocysts under CT radiologic guidance is a valuable adjunct or alternative to operative pseudocyst management. PCD failure is characterized by the development of recurrent pseudocysts or external pancreatic fistulas. The purpose of this study is to define the cause and management of PCD failure patients. A retrospective review and analysis of patients with symptomatic pancreatic pseudocysts managed with PCD who required subsequent operative treatment because of PCD failure was undertaken. There were 23 study patients (18 men, 5 women) with a mean age of 44 years identified over a 13-year time period. Pancreatitis etiology was alcohol abuse in 10, gallstones in 7, pancreas divisum in 3, trauma in 2, and sphincter of Oddi dysfunction in 1. Endoscopic retrograde cholangiopancreatography findings were: 13 genu strictures, 4 main pancreatic duct dilations, 2 head strictures, 1 body stricture, 1 stricture in the tail, 1 intact duct, and 1 unknown. Operations used to manage PCD failures were: lateral pancreaticojejunostomy (LPJ) in 9 patients, Roux-en-Y pancreatic fistula jejunostomy in 7, distal pancreatectomy in 3, caudal pancreatectomy in 2, pancreatoduodenectomy in 1, cyst gastrotomy in 1, and caudal pancreatojejunostomy in 1. Follow-up has ranged from 1 to 13 years (mean, 5 years). Five patients who underwent pancreatic fistula jejunostomy developed recurrent pseudocysts or pancreatitis. There have been no recurrent pseudocysts or fistulas in patients managed with LPJ or pancreatic resection. Genu strictures were the cause of PCD failure in the majority of patients. LPJ is the treatment of choice for genu strictures but may not always be possible because of chronic inflammatory changes. Roux-en-Y pancreatic fistula jejunostomy is an acceptable alternative. Recurrent pseudocysts in the head and body are treated with LPJ with cyst incorporation. Pancreatic resection is appropriate for certain strictures of the head, body, and pancreatic tail. Failure of PCD is associated with an underlying ductal disorder that needs to be defined preoperatively with endoscopic retrograde cholangiopancreatography to select the appropriate operation.
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PMID:Failure of percutaneous catheter drainage of pancreatic pseudocyst. 1075 95

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

Chronic pancreatitis (CP) is characterized by irreversible morphological and functional alterations of the pancreas presenting clinically with upper abdominal pain as well as exocrine and endocrine insufficiencies. CP is morphologically characterized by pancreatic head enlargement, calcifications of the parenchyma, cysts, and pancreatic stones. The most common etiological factor of CP in Western industrialized countries is alcohol abuse; less common factors include hereditary pancreatitis, CP due to metabolic disturbances, CP due to pancreas divisum or duodenal wall cysts, and idiopathic CP. The molecular alterations leading to the chronic inflammatory process are nor completely understood. Research during the last years, however, has elucidated that a number of growth factors and their receptors are overexpressed in CP, which is thought to contribute to the high degree of pancreatic fibrosis and to the proliferative potential of ductular cells in this disorder. In addition, gene mutations have been detected in a subgroup of CP samples underscoring the pre-malignant potential of CP. In this review we will summarize our current knowledge about pathogenic and molecular aspects of CP.
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PMID:Chronic pancreatitis: pathogenesis and molecular aspects. 1082 17

Chronic pancreatitis is a dynamic disease characterized on one side by a progressive destruction of the pancreatic parenchyma and change in the architecture of the gland and on the other by the impairment of its function. Diagnosis of chronic pancreatitis may be a quite easy or a very difficult attempt according to the severity and evolutive stage of disease. In fact, while most patients presents with a typical history of alcohol abuse, recurrent abdominal pain and steatorrhea, in the late stage of disease it is not rare to see patients with symptoms and signs which may be not typical for pancreatitis. A large number of morphological and functional methods has been developed to allow an easy and early diagnosis of disease. However, while in the advanced stages of disease, where pancreatic insufficiency, calcifications, or pseudocysts are present, diagnosis is easy and most of the procedures show high sensitivity and specificity, in the early disease the degree of pancreatic dysfunction and structural change are too small to be detected by current methods. The present article aims to evaluate the different morphological and functional methods with their advantages and shortcomings, as well as to establish their role in the diagnostic assessment of chronic pancreatitis.
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PMID:Chronic pancreatitis: diagnosis and staging. 1082 20

Acute pancreatitis is a disorder that has numerous causes and an obscure pathogenesis. Bile duct stones and alcohol abuse together account for about 80% of acute pancreatitis. Most episodes of biliary pancreatitis are associated with transient impaction of the stone in the ampulla (that causes obstruction of the pancreatic duct, with ductal hypertension) or passage of the stone though and into the duodenum. Other causes of acute pancreatitis are various toxins, drugs, other obstructive causes (such as malignancy or fibrotic sphincter of Oddi), metabolic abnormalities, trauma, ischemia, infection, autoimmune diseases, etc. In 10% of cases of acute pancreatitis, no underlying cause can be identified; this is idiopathic pancreatitis. Occult biliary microlithiasis may be the cause of two thirds of the cases of "idiopathic" acute pancreatitis. Intra-acinar activation of trypsinogen plays a central role in the pathogenesis of acute pancreatitis, resulting in subsequent activation of other proteases causing the subsequent cell damage. Ischemia/reperfusion injury is increasingly recognized as a common and important mechanism in the pathogenesis of acute pancreatitis and especially in the progression from mild edematous to severe necrotizing form. Increased intracellular calcium concentration also mediates acinar cell damage. Oxygen-derived free radicals and many cytokines (e.g., interleukin [IL]-1, IL-6, IL-8, tumor necrosis factor-alpha, platelet activating factor) are considered to be principal mediators in the transformation of acute pancreatitis from a local inflammatory process into a multiorgan illness.
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PMID:Etiology and pathogenesis of acute pancreatitis: current concepts. 1087 61


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