Arif Cosar

Agenesis of the dorsal pancreas in a patient with recurrent acute pancreatitis: case report and review

CASE REPORTA 33-year-old Turkish woman presented with severeepigastric abdominal pain, nausea, and vomiting. Anepisode of acute pancreatitis had occurred 1 year earlier.There also was a history of frequent urinary-tract in-fections over the previous 15 years; a diagnosis ofvesicoureteral reflux was made 3 years earlier. Peritonealdialysis on an ambulatory basis was begun 2 years beforepresentation because of chronic renal failure secondary tochronic pyelonephritis. Noninsulin-dependent diabetesmellitus was diagnosed 1 year before presentation. Upperabdominal tenderness was elicited on examination atadmission. Laboratory test results at admission were thefollowing: serum amylase, 1512 IU/L (normal: 30-110 IU/L); lipase, 1563 IU/L (23-300 IU/L); calcium, 8.9 mg/dL(8.40-10.0 mg/dL); triglycerides, 430 mg/dL (55-175mg/dL); aspartate aminotransferase, 26 IU/L (12-50 IU/L);alanine aminotransferase, 12 IU/L (10-70); gammaglutamyl transferase, 154 IU/L (7-40 IU/L); alkalinephosphatase, 188 IU/L (25-100 IU/L); total bilirubin,0.4 mg/dL (0.4-1.35 mg/dL); direct bilirubin, 0.2 mg/dL(0.10-0.50mg/dL);C-reactiveprotein,96mg/dL(0-6mg/dL);and blood glucose, 333 mg/dL (70-110 mg/dL). Analysisof peritoneal dialysis fluid revealed 10 white blood cellsper high-power field.On transabdominal US, the head of the pancreasappeared as a hypoechoic glandular structure in thenormal location, but the body and the tail were not visible.Afewmillimeter-sizedpolypswerenotedinthegallbladderwall;freeintraperitonealfluidwasattributedtoperitonealdialysis. CT with and without contrast revealed onlya prominent head of the pancreas (Fig. 1). At ERCP, theorifice of the major duodenal papilla was in the normalposition, but careful examination revealed no minorpapilla.Injectionofcontrastmaterialintothemajorpapillademonstrated a short, branching duct that was notconsistent with a normal main pancreatic duct (Fig. 2).MRCP also was obtained in an attempt to visualize thepancreas and bile ducts in greater detail. The head of thepancreas appeared normal on cross-sections, but no otherpancreatic tissue was evident. The scan also revealeda dilated common bile duct and a short main pancreaticductofnormaldiameterintheheadoftheglandbutnoductin the body and the tail (Fig. 3). Triphasic dynamic CTrevealed only the head portion of the pancreas. Based onthecollectiveimagingstudies,adiagnosisofagenesisofthedorsal pancreas was made.With conservative treatment, the clinical status of thepatient and the laboratory parameters of pancreaticinflammation improved rapidly and her overall statushad returned to baseline after 3 days of hospitalization.Blood pressure, fundic examination, and neurologic func-tion remained normal throughout follow-up.

Massive lower gastrointestinal hemorrhage secondary to rectal hemorrhoids in elderly patients receiving anticoagulant therapy: case series.

Hemorrhages secondary to hemorrhoids are common but they are usually occult or oozing type with low amounts. Acute massive rectal hemorrhage is usually originated from upper GI (UGI) bleeding [1]. However, lower GI bleeding (LGI) may occasionally cause massive bleeding. In elderly patients, generally the reasons of colonic hemorrhage are diverticulum (17–40%), arteriovenous malformations (2–30%), colitis (9–21%), colonic neoplasms (11–14%), post-polypectomy, and anorectal pathologies (4–10%) [2]. Colonoscopy is the most important diagnostic tool for determining the focus of bleeding [3]. Generally massive LGI hemorrhage secondary to hemorrhoids has been reported in the literature as case presentations after surgical hemorrhoidectomy and rubber band ligation. Massive hemorrhoidal bleeding without any intervention has not been reported [4]. Case Reports

Atherosclerosis and acetylsalicylic acid are independent risk factors for hemorrhage in patients with gastric or duodenal ulcer

OBJECTIVE Risk factors for hemorrhage due to gastric and/or duodenal ulcer in patients diagnosed by upper gastrointestinal (GI) endoscopy were investigated in the present study. METHODS Medical records of 350 patients (226 males, 124 females) diagnosed as duodenal or gastric ulcers by GI endoscopy in the gastroenterology clinic were scanned retrospectively. Upper GI hemorrhage was detected in 92 patients by upper endoscopic examination. The medical history of non-steroidal anti-inflammatory drugs (NSAIDs) or acetylsalicylic acid (ASA) usage and the presence of coronary artery disease (CAD) were investigated in all patients with or without hemorrhage. Results were evaluated by Chi-square test and logistic regression analysis. RESULTS The mean age of the patients was 50.4 ± 15.7 years (range: 25 to 82 years). Hemorrhage due to gastric or duodenal ulcer was identified in 92 patients (26%). Mean age was 64.6 ± 11.4 years in patients with hemorrhage and 45.7 ± 13.9 years in patients without hemorrhage. ASA usage was more common than NSAID in patients with ulcer hemorrhage (NSAID usage n=35 (40%); ASA usage n=51 (60%); p=0.035). Hemorrhage was reported in 20% of the females and in 28% of the males who have ulcer (p=0.055). Risk factors for hemorrhage were CAD (OR:24.75, 95% CI=1.6-96.7, p=0.001), ASA usage (OR:9.76, 95% CI=2.1-37.5, p=0.021), NSAID usage (OR: 4.72, 95%CI=1.1-16.5, p=0.032), age (OR: 11.59, 95% CI= 2.7-12.1, p=0.001), and male gender (OR: 2.56, 95% CI= 0.8, 9.6, p=0.052). CONCLUSION Advanced age, atherosclerosis, male gender and NSAID administration (particularly aspirin) are the major risk factors of upper GI hemorrhage in patients with gastric and/or duodenal ulcer.

New therapeutic option with N-acetylcysteine for primary sclerosing cholangitis: two case reports.

Primary sclerosing cholangitis is a progressive, cholestatic hepatic disease of unknown etiology. It is characterized by progressive inflammation, destruction, and fibrosis of the intrahepatic and extrahepatic bile ducts. Several medical therapies have been tried such as penicilamin, colchicine, methatraxate, cyclosporine, tacrolimus, and ursodeoxycholic acid. Treatment with mucolytic agents in excessively high viscosity conditions appears to have an important role. N-acetylcysteine (NAC), as a mucolytic agent, may fascilitate the drainage in partial obstructions by decreasing the mucous viscosity. We suggest that NAC and ursodeoxycholic acid have markedly positive effects on the clinical course of cholangitis and cholestasis when used together by affecting bile viscosity. Here, we present two cases treated with NAC. NAC capsul therapies at 800 mg/day were administered to two patients with primary sclerosing cholangitis. Clinical and laboratory parameters of patients saw significant improvement.

Ultrasonographic evaluation of gallbladder functions in patients with irritable bowel syndrome

Background:  The aim of the present study was to evaluate gallbladder function in irritable bowel syndrome (IBS) patients.

Recurrent hypersplenism caused by giant accessory spleen due to portal hypertension after splenectomia.

Splenectomy is one of the primary choices of treatment in immune thrombocytopenic purpura. However, the disease may relapse despite splenectomy. One of the leading causes of relapse is the presence of accessory spleen, which may become enlarged significantly with underlying pathologies such as presence of portal hypertension. The accessory spleen, which will inevitably enlarge in time, may grow significantly within a short period of time in the presence of portal hypertension and may thus be misdiagnosed as a tumoral mass. Presence of ectopic spleen should be borne in mind in patients diagnosed with immune thrombocytopenic purpura with relapsing hypersplenism following splenectomy. This article discusses a patient developing portal hypertension secondary to chronic liver disease and presenting with a significantly enlarged accessory spleen as well as hypersplenism findings.

Effect of cumulative time of Helicobacter pylori infection on gastric precancerous lesions

Helicobacter pylori is classified as a grade 1 carcinogen affecting more than half of the world’s population (1). In the pathogenesis of intestinal-type non-cardia adenocarcinoma, H. pylori-induced chronic gastric inflammation slowly progresses as a sequence known as Correa’s cascade: non-atrophic gastritis, multifocal atrophic gastritis without intestinal metaplasia, intestinal metaplasia, dysplasia, and ultimately, cancer (2,3). Mucosal atrophy and intestinal metaplasia have been considered precancerous lesions (4). The sequential nature of gastric carcinogenesis presents an opportunity for early detection and intervention to prevent the progression of premalignant lesions. Among individuals with intestinal metaplasia (IM), the risk of progression to gastric cancer may vary by IM type (3).

Autonomic neuropathy and gallbladder motility in patients with liver cirrhosis.

BACKGROUND/AIMS Impaired gallbladder motility has been suggested as a contributor to increased incidence of gallstones in patients with liver cirrhosis. The purpose of this study was to determine gallbladder function and its relation with autonomic neuropathy in liver cirrhosis. MATERIALS AND METHODS Gallbladder function was measured using ultrasonography in 48 patients with liver cirrhosis and in 31 controls. Autonomic neuropathy tests were applied in patients with liver cirrhosis. Patients with liver cirrhosis were analyzed in subgroups according to the severity of disease using the Child-Pugh classification. RESULTS Fasting gallbladder volume was 16.2 mL (range: 2.1 mL-71.9 mL) in patients and 17.6 mL (range: 4.9 mL-76.6 mL) in controls. There were no differences in fasting gallbladder volume among the study groups (p>0.05). Gallbladder ejection fraction was significantly higher in patients compared with controls (84% vs. 65%) (p<0.001). No correlation was found between gallbladder ejection fraction and autonomic neuropathy (p>0.05). CONCLUSION Our results indicate that liver cirrhosis does not impair gallbladder emptying, and that there is no association between gallbladder motility and autonomic neuropathy. Further investigations are required to explain increased gallbladder motility in liver cirrhosis.