[Biliary microcrystals in idiopathic acute pancreatitis: clue for occult underlying biliary etiology]. / Microcristais biliares na pancreatite aguda idiopática: indício para etiologia biliar oculta subjacente.

The main causes of pancreatic inflammation worldwide are biliary lithiasis and alcoholism. However, 10 to 30% of patients have been considered to have "idiopathic" acute pancreatitis. Recently, some studies showed that a significant rate of the so called idiopathic pancreatitis are caused by microlithiasis and/or biliary sludge, identified by the presence of cholesterol monohidrate and/or calcium bilirubinate microcrystals in the biliary sediment. In the present study, the analysis of microcrystals from bile obtained during endoscopic retrograde cholangiopancreatography was done in patients with pancreatitis (idiopathic, biliary or alcoholic--20 in each group). Patients with idiopathic pancreatitis and microcrystals in the bile underwent cholecystectomy whenever possible. Those who refused or were inapt to surgery underwent endoscopic sphincterotomy or received continuous therapy with ursodeoxycholic acid. Patients with idiopathic pancreatitis without biliary crystals did not receive any specific treatment. The prevalence of biliary microcrystals in patients with idiopathic pancreatitis (75%) and biliary pancreatitis (90%) was significantly higher than in those with alcoholic pancreatitis (15%). In the identification of the etiology of biliary pancreatitis, the presence of microcrystals had a sensitivity of 90%, specificity of 85%, positive predictive value of 85.7%, negative predictive value of 89.4% and accuracy of 87.5%. In the patients with recurrent idiopathic pancreatitis, with biliary crystals, there was an statistically significant reduction in the number of pancreatitis episodes after specific treatment. In the follow-up of this group during 23.3 +/- 4.8 months, recurrence of pancreatitis occurred only in patients with "persistent biliary factor" (choledocholithiasis and/or persistence of cholesterol monohidrate). All patients with idiopathic pancreatitis who underwent cholecystectomy had chronic cholecystitis. Moreover, cholelithiasis was present in one case. In the ultrassonographic follow-up of the patients with idiopathic acute pancreatitis with microcrystals in the bile, cholelithiasis was detected in one case. In the subgroup of five patients with idiopathic pancreatitis without biliary microcrystals recurrence occurred in one case. Ultrassonographic study during follow-up did not reveal biliary stones in any of these patients. We concluded that the detection of biliary microcrystals in "idiopathic" pancreatitis suggested an underlying biliary etiology, even if occult. What's more, early specific therapeutic procedure (cholecystectomy, endoscopic sphincterotomy or ursodeoxycholic acid) in patients with recurrent idiopathic pancreatitis with microcrystals in the bile reduced significantly the recurrence during the follow-up. Finally, acute pancreatitis (specially recurrent) should not be called idiopathic before the microscopic analysis of the bile, aiming to detect or exclude the presence of microcrystals.

Induction of acute and chronic pancreatitis with the use of the toxin of the scorpion Tityus serrulatus: experimental model in rats.

We observed that the purified venom of the Tityus serrulatus scorpion (T1 fraction), injected i.v. in rats, in a single dose of 0.5 mg/kg, produces: acute pancreatitis, characterized by degranulation and acinar cell vacuolization, necrosis and an inflammatory reaction, 24, 48 and 96 hours after the injection; chronic pancreatitis, characterized by interstitial fibrosis, lymphocyte infiltration, ductal and ductular dilation, acinar cell atrophy, periductal ductular hyperplasia, 20 days after injection: hyperplasia of Langerhans' islets and nesidioblastosis, associated to chronic pancreatitis. The absence of deaths in the experimental group is an interesting finding: the dose used preserved the animals from death and allowed the safe follow-up of the progression of the provoked pancreatitis. The results led us to conclude that the toxin of Tityus serrulatus scorpion is an agent of considerable efficacy in the induction of pancreatitis in rats providing an experimental model of acute and chronic form of this disease.

Asymptomatic hepatopathy is frequent in chronic alcoholic pancreatitis.

BACKGROUND: Chronic ethanol abuse is a common cause of chronic hepatic and pancreatic diseases in Western countries. The objectives of the present study were to determine the occurrence and the clinical evolution during follow-up of asymptomatic hepatic disease in Brazilian alcoholics with chronic pancreatitis whose most important beverage is cachaça, a beverage distilled from sugar cane. PATIENTS-METHODS: Thirty-two patients, mean age 35 years, with a mean daily ethanol intake of 204 g during a mean period of 16 years, presenting with chronic pancreatitis without clinical and laboratory features of hepatocellular failure, were followed up during 34 +/- 8 months after undergoing a percutaneous biopsy of the liver and histological examination. RESULTS: Hepatic injury was observed in 50% of the cases. During the follow-up, only one patient showed clinical or biochemical evidence of hepatic deterioration or complication. CONCLUSIONS: In subjects with a chronic intake of cachaça, the association between asymptomatic alcoholic hepatopathy and chronic alcoholic pancreatitis is frequent (50%). In chronic alcoholic pancreatitis, associated hepatic disease may remain asymptomatic in the majority of the cases and has little influence on the outcome of the patients, at least in a short-term follow-up.

[Glucagonoma: case report and literature review]. / Glucagonoma: relato de caso e revisão de literatura.

Glucagonoma is a neuroendocrine tumor of pancreatic alpha cells manifested by necrolytic migratory erythema, hyperglucagonemia, glucose intolerance, weight loss, anemia and hypopaminoacidemia. We report a case of glucagonoma in a 38 years-old patient diagnosed by the presence of a pancreatic tumor, liver metastasis, weight loss, glucose intolerance, necrolytic migratory erythema, hyperglucagonemia (1400 pg/ml; normal < 200 pg/ml) and histologic demonstration of glucagon and neurospecific enolase by immunocytochemical reaction. Actual therapeutic of glucagonoma includes surgery, chemotherapy, somatostatin or octreotide for control of the symptoms, and more recently alpha-interferon was suggested.

[Current approach to pancreatic necrosis]. / Abordagem atual na necrose pancreática.

The incidence of acute pancreatitis is increasing. Necrosis occurs in 10 to 20% of the cases, and is associated with great morbidity and mortality. The diagnosis of pancreatic necrosis can be suspected clinically and biochemically, and confirmed with imaging methods. A computerized tomography with contrast injection (dynamic pancreatography) is the best diagnostic method. Treatment of pancreatic necrosis is primarily conservative. Prophylactic antibiotic therapy is reserved for the biliary pancreatitis and for severe cases. When pancreatic infection is suspected, computerized tomography or ultrasonic exam guided percutaneous aspirative punction must be performed, with Gram stain and culture of the material aspirated. If bacterial infection is present, adequate antibiotic therapy with good penetration in necrotic tissue must be provided associated with surgical necrosectomy and local washing or open drainage.

[Hereditary pancreatitis]. / Pancreatite hereditária.

Hereditary pancreatitis (HP) is a rare cause of chronic pancreatitis. Recurrent abdominal pain is the most common clinical manifestation, with onset in childhood or adolescence. PURPOSE--Report of a case of HP with atypical presentation and a review of the literature. METHODS--A non-alcoholic patient, without history of abdominal pain, with steatorrhea and malnutrition was investigated. The diagnostic evaluation revealed severe chronic pancreatitis. Two close relatives with early onset calcifying pancreatitis were detected. Epidemiologic and clinical features of HP were reviewed. CONCLUSION--Although uncommon, HP should be regarded in the differential diagnosis of chronic pancreatitis. Familial screening of suspected cases should be routinely performed.