Mustafa Güçlü

A Recent Evaluation of Empirical Cephalosporin Treatment and Antibiotic Resistance of Changing Bacterial Profiles in Spontaneous Bacterial Peritonitis

The aim of this research is to evaluate the recent changes in microorganisms causing spontaneous bacterial peritonitis in cirrhotic patients, antibiotic resistance, and response to empirical cephalosporin therapy. A total of 218 patients with ascites secondary to cirrhosis were enrolled. Parenteral cefotaxime or cefepime was given to patients who had a neutrophil count of 250/mm3 or more or a positive bacterial culture of ascitic fluid. Antibiotic failure was defined by an absence of clinical improvement and an insufficient decrease in neutrophil count of ascites (<25% of initial value) by the third day of therapy. Of all the patients, 44.6% had culture-negative neutrocytic ascites, 24.8% had spontaneous bacterial peritonitis, and 10.1% had monomicrobial nonneutrocytic bacterascites. Growth in culture was observed in 76 patients (34.9%). The two most common isolated bacteria were Escherichia coli (33.8%) and coagulase-negative Staphylococcus (CoNS; 19.7%). The two cephalosporins were effective against E. coli (82%) and but not against CoNS (44%), while levofloxacin showed reasonable activity against both E. coli (71%) and CoNS (90%) in vitro. We confirmed a recent increased incidence of spontaneous bacterial peritonitis caused by Gram-positive bacteria. Levofloxacin seems to be a good alternative treatment for patients with uncomplicated spontaneous ascites infections.

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.

Methylenetetrahydrofolate Reductase C677T Mutation and Nonalcoholic Fatty Liver Disease

A mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is known as one of the causes of hyperhomocyteinemia. The oxidation products of homocysteine can initiate lipid peroxidation, which has a central role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). We aimed to assess the possible role of the MTHFR C677T mutation in the progression of simple steatosis to an advanced form of NAFLD. Thirty-four patients with NAFLD diagnosed by histologic analysis and 282 healthy controls were included in the study. The discrimination of nonalcoholic steatohepatitis (NASH) from another NAFLD was made by NAFLD activity score (NAS), and a NAS≥5 was considered NASH. Patients with either NASH or nonalcoholic fatty liver (NAFL) and controls were evaluated for frequency of the MTHFR C677T mutation. The frequency of the MTHFR C677T mutation was 53.5% (CT, 44.7%; TT, 8.9%) in controls and 41.5% (CT, 37.7%; TT, 3.8%) in patients (odds ratio [OR], 0.62; 95% confidence interval [CI], 0.34–1.12). There was no statistical difference in the frequency of this genotype between patients with NAFL and those with NASH (36% [CT, 28%; TT, 8%] vs 46.4% [CT, 46.4; TT, 0%]; OR, 0.65; 95% CI, 0.22–1.96). According to this study, the MTHFR C677T mutation does not seem to be a risk factor for the progression of NAFL to NASH.

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.