The lifestyle influence on alcoholic pancreatitis versus alcoholic liver disease: a case-control study.

OBJECTIVE: To evaluate the association of lifestyle with the development of alcoholic liver disease (ALD) or alcoholic pancreatitis (AlcP). METHODS: A case-control study was conducted on 80 patients attending a tertiary university hospital, subdivided into three groups: ALD (n = 34), AlcP (n = 21) and a control (CT) group (n = 25) of alcohol abusers without clinical evidence of hepatic or pancreatic disease. Participants were interviewed regarding alcohol consumption, tobacco use and diet. A physical examination was concomitantly performed and we had access to their complementary investigation. RESULTS: We included 10 females and 70 males (mean age 57 ± 10 years). The pure amount of alcohol consumed by the ALD group was significantly higher than the AlcP group, regarding both daily (grams/day) and lifetime (kilograms) consumptions (p = .018 and p = .009, respectively); no statistically significant differences were seen with the CT group. We found no differences regarding the beverage type or drinking outside meals. Smoking was very common in every study group, with higher consumptions and a significantly higher prevalence of ever smokers in the AlcP group, in comparison with ALD and CT patients (p = .033 and p = .036, respectively). There were significant differences in the patients' eating habits before the onset of disease between groups (p < .001), with ALD subjects reporting a less abundant diet and AlcP a more abundant diet in the past; most of the controls had unchanged habits. CONCLUSION: We found differences in lifestyle between ALD and AlcP, not considered sufficient to explain the subjects' susceptibility to one disease or the other.

Microbiologic analysis of peri-pancreatic fluid collected during EUS in patients with pancreatitis: impact on antibiotic therapy.

BACKGROUND: Pancreatitis is a potentially life-threatening condition frequently accompanied by peri-pancreatic fluid collections (PPFC), such as pseudocysts or pancreatic necrosis. Aspiration of PPFCs during EUS interventions for microbiologic analysis is still rarely performed in clinical routine. OBJECTIVE: To evaluate the role of routine microbiologic analysis of PPFCs and its impact on antibiotic therapy in patients with pancreatitis. DESIGN: Prospective, observational, multicenter study. SETTING: Four treatment centers. PATIENTS: A total of 44 consecutive patients who presented for endoscopic treatment of PPFCs were included. INTERVENTION: Concomitantly, PPFC during intervention and concomitant blood cultures were obtained. MAIN OUTCOME MEASUREMENTS: Microbiologic examination of PPFCs and blood samples. RESULTS: Colonization of PPFCs was found in 59% of PPFC cultures, whereas all but 2 concomitant blood cultures showed no microbial growth. Risk factors for a colonization were the presence of necrosis (P = .006), acute pancreatitis (P = .033), leukocytosis (P = .001), elevated C-reactive protein levels (P = .003), fever (P = .02), turbid material (P = .031), and longer hospital stay (P = .003). In 23 patients with fluid colonization despite empiric antibiotic therapy, the treatment had to be adjusted in 18 patients (78%) according to the observed antibiotic susceptibility profile. LIMITATIONS: Contamination cannot be totally excluded. CONCLUSION: The microbiologic colonization of PPFCs in patients with pancreatitis is common. Only the direct microbiologic analysis of PPFCs, but not of blood cultures, is useful to optimize an effective antibiotic therapy in patients with pancreatitis.

Complete spontaneous regression of an extrahepatic portal vein aneurysm.

Primary portal venous aneurysms are rare; however, they are the most common visceral venous aneurysms, and their pathogenesis is not fully understood. Complications include thrombosis, rupture, and mass effect on adjacent structures. The optimal management of these patients is not known. We describe a patient whose large (6-cm) portal vein aneurysm underwent complete spontaneous regression over several years of serial observation. To our knowledge, this observation has not been reported in the English literature.

Clinical profile of calcific and noncalcific chronic pancreatitis in north India.

GOALS: To compare the clinical profile of calcific and noncalcific chronic pancreatitis (CP) in north India. BACKGROUND: The profile of calcific CP has not been adequately studied. STUDY: Detailed demographic data were recorded; hematologic, biochemical, and radiologic investigations were carried out on 225 patients with CP. The patients were divided into calcific and noncalcific groups based on the presence of pancreatic calcification, which was detected on computed tomography. RESULTS: Calcific CP was reported in 46.7% of the patients and noncalcific CP in 53.3%. The mean age, duration of symptoms before presentation, sex ratio, body mass index, and frequency of various symptoms and complications including abdominal pain, ascites, pleural effusion, and segmental portal hypertension was not statistically different between the 2 groups. However, pseudocysts occurred more frequently in noncalcific CP, whereas jaundice because of bile duct stricture, diabetes mellitus, and steatorrhea occurred more frequently in patients with calcific CP (P<0.05). On comparing calcific and noncalcific alcoholic pancreatitis, only steatorrhea was reported more frequently in patients with calcific alcoholic CP. However, pseudocysts and segmental portal hypertension occurred more frequently in noncalcific idiopathic CP, whereas diabetes mellitus occurred more frequently in patients with calcific idiopathic CP (P<0.05). On comparing calcific alcoholic CP with calcific idiopathic CP, we found significantly lower mean age in patients with idiopathic CP and a higher frequency of male patients and pseudocysts in alcoholic CP (P<0.05). CONCLUSION: Calcific CP has a higher frequency of bile duct stricture, diabetes mellitus, and steatorrhea, whereas noncalcific CP has higher frequency of pseudocysts and segmental portal hypertension.

Determinants of accelerated small intestinal transit in alcohol-related chronic pancreatitis.

Patients with chronic pancreatitis may have abnormal gastrointestinal transit, but the factors underlying these abnormalities are poorly understood. Gastrointestinal transit was assessed, in 40 male outpatients with alcohol-related chronic pancreatitis and 18 controls, by scintigraphy after a liquid meal labeled with (99m)technetium-phytate. Blood and urinary glucose, fecal fat excretion, nutritional status, and cardiovascular autonomic function were determined in all patients. The influence of diabetes mellitus, malabsorption, malnutrition, and autonomic neuropathy on abnormal gastrointestinal transit was assessed by univariate analysis and Bayesian multiple regression analysis. Accelerated gastrointestinal transit was found in 11 patients who showed abnormally rapid arrival of the meal marker to the cecum. Univariate and Bayesian analysis showed that diabetes mellitus and autonomic neuropathy had significant influences on rapid transit, which was not associated with either malabsorption or malnutrition. In conclusion, rapid gastrointestinal transit in patients with alcohol-related chronic pancreatitis is related to diabetes mellitus and autonomic neuropathy.

Splenic Artery Pseudoaneurysm Causing Massive Hematemesis 10 Years After Necrotizing Pancreatitis.

We report a case of a 54-year-old male presenting to a regional hospital with severe hematemesis and hemodynamic instability. His medical history was significant for a previous episode of alcoholic necrotizing pancreatitis and pseudocyst, requiring cystoenterostomy drainage and debridement 10 years prior. He underwent multiple gastroscopies and one emergency laparotomy which failed to definitively treat the bleeding. A splenic artery pseudoaneurysm was diagnosed with computed tomography angiography, adjacent to the previous cystoenterostomy site. The patient was transferred to a major tertiary center with access to interventional radiology and underwent successful embolization of the pseudoaneurysm.

Left colic artery pseudoaneurysm from pancreatitis presenting as upper gastrointestinal hemorrhage.

Visceral pseudoaneurysms resulting from pancreatitis occur in approximately 10% of cases. The present report describes a left colic artery pseudoaneurysm from pancreatitis presenting with active duodenal bleeding. Based on the clinical and endoscopic demonstration of duodenal bleeding, celiac and superior mesenteric arteriograms were initially obtained, and their findings were negative. Repeat arteriography, including an inferior mesenteric artery injection, demonstrated a left colic pseudoaneurysm with rupture into the pancreatic duct and retrograde flow into the duodenum. Because of inconsistent diagnostic yields for arteriography performed for pancreatitis-related bleeding, the authors recommend disciplined interrogation of all three major mesenteric vessels, unbiased by initial endoscopic findings, to reduce false-negative examination results and empiric embolization.

A novel SPINK1 gene mutation, c.206C>T, in a Thai patient with chronic alcoholic pancreatitis.

CONTEXT: The exact mechanism of alcoholic pancreatitis has not yet been clarified. Recent studies suggest that alcohol represents only a risk factor for developing pancreatic inflammation in genetic or environmental susceptible subjects. In this regard, various genes involving an alcohol-metabolizing pathway or pancreatitis protecting factors have been extensively studied in order to identify genetic predisposition to alcoholic pancreatitis. CASE REPORT: A 43-year-old man with a history of heavy alcohol drinking presented with recurrent abdominal pain. Alcoholic pancreatitis was diagnosed and responded well to pancreatic stricture dilatation with stent insertion. Sequencing analysis revealed that he was heterozygous for a novel transition c.206C>T in exon 4 of the SPINK1 gene, resulting in the substitution of threonine for isoleucine at codon 69 (T69I). Evidence supporting its etiologic role includes the alteration of the polarity of the amino acid change, its revolutionary conservation among mammals and its absence in 100 ethnic-matched control alleles. CONCLUSIONS: We identified a novel SPINK1 mutation, c.206C>T (T69I), in a Thai patient with alcoholic pancreatitis. This extends the total number of confirmed SPINK1 mutations and polymorphisms to more than 30. It also supports a previous observation that the SPINK1 gene is a susceptibility locus for alcoholic pancreatitis.

[A case of intrahepatic pseudocyst complicating acute pancreatitis].

Although most of pseudocysts as one of complications of pancreatitis occur primarily within the pancreas, the extrapancreatic locations of pseudocysts, especially in the liver, are rare events. With advanced technology of imaging studies including abdominal computed tomography, ultrasonography, and magnetic resonance imaging, their frequency seems to be increasing. We report here a case of left intrahepatic pancreatic pseudocyst following acute pancreatitis. Percutaneous puncture revealed a high level of amylase and lipase in the collection, confirming the diagnosis of intrahepatic pseudocyst. Symptomatic intrahepatic pseudocysts can be managed surgically, transcutaneously or endoscopically, and asymptomatic intrahepatic pseudocysts can be treated conservatively. We report this case with a review of literature.

[Spontaneously reversible portal vein thrombosis complicating acute pancreatits--computed tomographic findings]. / Computertomographische Verlaufsbeobachtungen der spontanen Rückbildung von Portalvenenthrombosen bei akuter Pankreatitis.

Portal vein thrombosis complicating acute pancreatitis is more often diagnosed today due to the improved imaging techniques (computed tomography, ultrasound, nmr). Nevertheless the outcome of recent portal vein thrombosis is ill-known. We report on the computed tomographic findings and clinical course of portal vein thrombosis in two patients suffering from acute pancreatitis. Both patients showed spontaneous recanalization of the thrombosis.

Mass forming chronic pancreatitis mimicking pancreatic cystic neoplasm: A case report.

Mass forming chronic pancreatitis is very rare. Diagnosis could be done by the pathologic findings of focal inflammatory fibrosis without evidence of tumor in pancreas. A 34-year-old man presented with right upper abdominal pain for a few weeks and slightly elevated bilirubin level on clinical findings. Radiological findings of multidetector-row computed tomography, magnetic resonance (MR) imaging with MR cholangiopancreatography and endoscopic ultrasonography revealed focal branch pancreatic duct dilatation with surrounding delayed enhancing solid component at uncinate process and head of pancreas, suggesting branch duct type intraductal papillary mucinous neoplasm. Surgery was done and pathology revealed the focal chronic inflammation, fibrosis, and branch duct dilatation. Herein, I would like to report the first case report of mass forming chronic pancreatitis mimicking pancreatic cystic neoplasm.

[Hepatic portal venous gas associated with acute pancreatitis: reports of two cases and review of literature].

Hepatic portal venous gas (HPVG) is an uncommon disease entity that usually has grave prognosis. It is generally associated with bowel necrosis, and has been reported in a wide variety of conditions such as ulcerative colitis, Crohn's disease, diverticulitis, intestinal ischemia, or infarction. We experienced two cases of HPVG associated with acute pancreatitis. HPVG was found in patients with severe necrotizing pancreatitis and concurrent bowel ischemia. Despite aggressive resuscitation with fluids and broad spectrum antibiotics, each patient developed multiorgan failure, and died within few days. Acute pancreatitis is a potential cause of severe intraabdominal systemic catastrophe. Moreover, HPVG is associated with bowel ischemia in the setting of acute pancreatitis which could lead to rapid aggravation of symptom and complicated clinical course. Therefore, vigilant and aggressive management should be warranted in such condition.

Dual drainage using a percutaneous pancreatic duct technique contributed to resolution of severe acute pancreatitis.

A 66-year-old man was admitted for severe acute alcoholic pancreatitis with infected pancreatic necrosis (IPN). Abdominal computed tomography revealed an inflamed pancreatic head, a dilated main pancreatic duct (MPD), and a large cavity with heterogeneous fluid containing gas adjacent to the pancreatic head, and extending to the pelvis. The cavity was drained percutaneously near the pancreatic head on admission; another tube was inserted into the pelvic cavity on hospital day 3. The drained fluid contained pus with high amylase concentration. Nasopancreatic drainage tube placement was unsuccessfully attempted on hospital day 9. On hospital day 23, percutaneous puncture of the MPD and placement of a pancreatic duct drainage tube was performed. Pancreatography revealed major extravasation from the pancreatic head. The IPN cavity receded; the percutaneous IPN drainage tube was removed on hospital day 58. On hospital day 83, the pancreatic drainage was changed to a transpapillary pancreatic stent, and the patient was discharged. Measuring the amylase concentration of peripancreatic fluid collections can aid in the diagnosis of pancreatic duct disruption; moreover, dual percutaneous necrotic cavity drainage plus pancreatic duct drainage may be essential for treating IPN. If transpapillary drainage tube placement is difficult, percutaneous pancreatic duct drainage may be feasible.