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 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

15 to 30% of the patients with chronic pancreatitis develop an inflammatory mass in the pancreatic head. The leading symptoms of these patients are severe upper abdominal pain and complications of the surrounding organs. From 1969 to 1995, 380 patients were treated with a duodenumpreserving pancreatic head resection. The cause of the disease was alcohol abuse in 81%. 93% of the patients suffered from severe pain with recurrent pain attacks. CT-scan revealed enlargement of the pancreatic head (> 4 cm in diameter) in 79% of the patients. 83% of the patients had an impaired exocrine pancreatic function; 48% of the patients had an impaired glucose tolerance or were diabetic. The hospital mortality was 0.8%; 5% of all patients had to be reoperated. The mean duration of the hospitalization was 13.9 days. 89% of the patients showed an unchanged endocrine function in the early postoperative course. The glucose metabolism was improved in 9%, 2% had a deteriorated function. The duodenum-preserving pancreatic head resection is a procedure with a low postoperative mortality and morbidity without deterioration of the endocrine pancreatic function.
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PMID:[Duodenum preserving pancreatic head resection in chronic pancreatitis with inflammatory tumor in the pancreas head]. 904 35

Haemorrhage via the pancreatic duct, a rare cause of upper gastrointestinal bleeding (GIB), often poses a diagnostic dilemma. We analysed our experience with 10 patients (8 men, 2 women; mean age 44 years, range 34-62) treated during a 12 year period. All had a history of alcohol abuse and presented with major upper GIB requiring a median of 8 units (range 2-40) blood transfusion. Nine had upper abdominal pain at the time of admission and nine had a history of pancreatitis. Upper gastroduodenal endoscopy (median 4; range 1-9), was diagnostic in only one. Side-viewing endoscopy showed bleeding from the pancreatic duct in 7 of 8 patients. Visceral aneurysms were demonstrated in 7 of 9 patients in whom coeliac angiography was carried out: (splenic artery 4, gastroduodenal artery 2, and pancreaticoduodenal artery 1). Two of 4 selective embolisations were successful. Six patients underwent distal pancreatectomy, 1 had gastroduodenal artery ligation and 1 died of coagulopathy following a total pancreatectomy. Pancreatic duct haemorrhage should be considered in patients with unexplained recurrent upper GIB, alcohol abuse and epigastric pain, particularly in those with established chronic pancreatitis. Selective angiography is essential for diagnosis and management. For bleeding sites in the head of the pancreas, embolisation should be attempted to avoid major resection. Distal pancreatectomy is preferred for splenic artery lesions.
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PMID:Diagnostic pitfalls and therapeutic strategies in the treatment of pancreatic duct haemorrhage. 929 83

We report a case of intra-gallbladder hemorrhage secondary to blunt abdominal trauma in a patient with liver cirrhosis. A 58-year-old man was admitted to a local hospital with persistent right upper quadrant abdominal pain. Anemia was detected, and computed tomography (CT) revealed a high-density mass in the gallbladder lumen. He was transferred to our hospital because a gallbladder tumor was suspected. He had a history of habitual alcohol abuse and had sustained blunt abdominal trauma in the right upper quadrant 29 days before admission to our hospital (4 days before to the admission local hospital). The intra-gallbladder high-density mass depicted on the CT scan, observed as non-shadowing low-level echoes, was deemed to represent a blood clot on ultrasonography (US) performed 31 days after the trauma. US-guided percutaneous transhepatic gallbladder aspiration and cholecystography confirmed the presence of an old blood clot in the lumen. Because of the patient's persistent pain, a cholecystectomy was performed. The distended gallbladder was filled with old clotted blood.
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PMID:Posttraumatic intra-gallbladder hemorrhage in a patient with liver cirrhosis. 1063 49

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

Chronic pancreatitis is characterized by progressive and irreversible loss of pancreatic exocrine and endocrine function. In the majority of cases, particularly in Western populations, the disease is associated with alcohol abuse. The major complications of chronic pancreatitis include abdominal pain, malabsorption, and diabetes. Of these, pain is the most difficult to treat and is therefore the most frustrating symptom for both the patient and the physician. While analgesics form the cornerstone of pain therapy, a number of other treatment modalities (inhibition of pancreatic secretion, antioxidants, and surgery) have also been described. Unfortunately, the efficacy of these modalities is difficult to assess, principally because of the lack of properly controlled clinical trials. Replacement of pancreatic enzymes (particularly lipase) in the gut is the mainstay of treatment for malabsorption; the recent discovery of a bacterial lipase (with high lipolytic activity and resistance to degradation in gastric and duodenal juice) represents an important advance that may significantly increase the efficacy of enzyme replacement therapy by replacing the easily degradable porcine lipase found in existing enzyme preparations. Diabetes secondary to chronic pancreatitis is difficult to control and its course is often complicated by hypoglycaemic attacks. Therefore, it is essential that caution is exercised when treating this condition with insulin. This paper reviews recent research and prevailing concepts regarding the three major complications of chronic pancreatitis noted above. A comprehensive discussion of current opinion on clinical issues relating to the other known complications of chronic pancreatitis such as pseudocysts, venous thromboses, biliary and duodenal obstruction, biliary cirrhosis, and pancreatic cancer is also presented.
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PMID:Chronic pancreatitis: complications and management. 1050 49

Nonalcoholic steatohepatitis (NASH) is a histological diagnosis applied to a constellation of liver biopsy findings that develop in the absence of alcohol abuse. Steatosis, a mixed cellular inflammatory infiltrate across the lobule, evidence of hepatocyte injury and fibrosis are the findings that can be seen. This entity is often identified during evaluation of elevated aminotransferases after exclusion of viral, metabolic and other causes of liver disease. Obesity is a major risk factor for NASH. The role of diabetes is less certain, although evidence is accumulating that hyperinsulinism may play an important pathophysiological role. Patients sometimes suffer from right upper quadrant abdominal pain and fatigue; examination may reveal centripetal obesity and hepatomegaly. Although patients are often discovered because of persistent aminotransferase elevations, these enzymes can be normal in NASH. When they are elevated, the alanine aminotransferase level is typically significantly greater than the aspartate aminotransferase level. This can be particularly helpful for excluding occult alcohol abuse. Imaging studies identify hepatic steatosis when the amount of fat in the liver is significant; however, imaging does not distinguish benign steatosis from NASH. Ultimately a liver biopsy is needed to diagnose NASH. The biopsy may be useful for establishing prognosis based on the presence or absence of fibrosis and for excluding other unexpected causes of liver enzyme elevations. Weight loss is the mainstay of treatment for obese patients. About 15% to 40% of NASH patients develop fibrosis; how many of these cases progress to cirrhosis is unknown, but about 1% of liver transplants are performed with a pretransplant diagnosis of NASH.
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PMID:Nonalcoholic steatohepatitis: an evolving diagnosis. 1079 85

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

A seriously ill patient with cirrhosis and resistant ascites from hepatitis C and alcohol abuse abruptly deteriorated. He developed encephalopathic changes, abdominal pain and tenderness and was suspected of having spontaneous bacterial peritonitis. The peritoneal fluid contained many granulocytes and Steptococcus salivarius was isolated from the fluid.
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PMID:Spontaneous bacterial peritonitis from Streptococcus salivarius in a compromised host. 1238 78

Patients with chronic pancreatitis may suffer from maldigestion and malnutrition. Longstanding inflammation and fibrosis in the gland can destroy exocrine tissue, leading to inadequate delivery of digestive enzymes to the duodenum in the prandial and postprandial period and subsequent maldigestion. Maldigestion is augmented by inadequate bicarbonate delivery to the duodenum, with secondary inactivation of enzymes and bile acids by gastric acid. Abdominal pain, sitophobia, nausea, vomiting, postprandial satiety, and on-going alcohol abuse may contribute to poor oral intake. Gastric dysmotility and mechanical gastric outlet obstruction from fibrosis in the pancreatic head may contribute to malnutrition and clinical decline. Patients with chronic pancreatitis may at times experience profound steatorrhea and weight loss. In this article, we examine the natural history of exocrine insufficiency in chronic pancreatitis, outline the important nutritional issues in these patients, review the methods of diagnosis of maldigestion, and discuss the approach to therapy.
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PMID:Chronic pancreatitis and maldigestion. 1246 5


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