Zeynel Mungan

Tuberculous peritonitis--reports of 26 cases, detailing diagnostic and therapeutic problems.

Objective To evaluate the clinical presentation, biochemical (ascites and serum) and laparoscopic findings, and to assess the efficacy of triple anti-tuberculous therapy without rifampicin for 6 months in patients with tuberculous peritonitis. Methods Twenty-six tuberculous peritonitis patients (11 male, 15 female) with a mean age of 34.8 ± 3.4 years (range 14–77) were assessed with regard to diagnostic and therapeutic features. Results The most common symptoms and signs were abdominal pain (92.3%) and ascites (96.2%), respectively. Tuberculin skin test (TST) was positive in all patients. An abnormal chest radiography suggestive of previous tuberculosis was present in five patients (19.2%), and two patients (7.7%) had extra-peritoneal (cerebral, pericardial) active tuberculous involvement. In 24 of the 25 patients who underwent laparoscopy with directed biopsy, whitish nodules suggested tuberculous peritonitis; 76% of the biopsy specimens revealed caseating, 20% non-caseating granulomatous inflammation, and 4% non-specific findings. The ascitic fluid of one patient (3.8%) was positive for acid-resistant bacilli, and culture was positive in two patients (7.7%). Twenty-four of the patients were treated for 6 months with isoniazid, streptomycin (total dose 40 g) and pyrazinamide (for the first 2 months and then substituted with ethambutol). Eighteen patients also received methyl prednisolone, initially 20 mg/day, for 1 month. The follow-up period was 19 ± 1.7 months after the end of therapy (range 6–36). Ascites and abdominal pain abated earlier in patients on steroid therapy. All but two of the 24 patients responded to treatment. Conclusion Non-invasive tests such as acid-fast stain and culture of the ascitic fluid are usually insufficient, hence invasive laparoscopy and peritoneal biopsy are necessary for the diagnosis of tuberculous peritonitis if non-invasive tests such as ascites adenosine deaminase activity measurement are not easily available. Triple therapy without rifampicin for 6 months is sufficient to treat tuberculous peritonitis.

Hepatopulmonary syndrome in noncirrhotic portal hypertensive patients.

Hepatopulmonary syndrome has yet not been sufficiently assessed in noncirrhotic portal hypertension. The prevalence of hepatopulmonary syndrome was determined in 31 consecutive patients with noncirrhotic portal hypertension (19 idiopathic portal hypertension, 7 portal vein thrombosis, 5 congenital hepatic fibrosis) and 46 patients with liver cirrhosis. Contrast echocardiography was carried out in all patients. Macroaggregated albumin lung perfusion scans were performed in patients with positive contrast echocardiogram. Hepatopulmonary syndrome was detected in 5 (10.8%) cirrhotic and 3 (9.7%) noncirrhotic portal hypertensive patients (2 idiopathic portal hypertension, 1 portal vein thrombosis). All patients with hepatopulmonary syndrome had an increased shunt fraction (13–62%) and a decreased diffusion capacity of carbon monoxide (40–79%), and 7 of them were hypoxemic (PaO2, 31.6–69.8 mm Hg). These findings show that hepatopulmonary syndrome may occur in both liver cirrhosis and noncirrhotic portal hypertension and that portal hypertension is the predominant etiopathogenic factor related to hepatopulmonary syndrome.

Heterotopic gastric mucosa in the cervical esophagus (inlet patch): Endoscopic prevalence, histological and clinical characteristics

Background and Aim:  Heterotopic gastric mucosal patch, which has a 0.1–10% frequency, is encountered when the cervical esophagus is examined carefully during endoscopy. In this study, we aimed to determine the prevalence of the patch in the cervical esophagus, to identify its macroscopic and histological characteristics and to evaluate demographic and clinical features.

Clinical predictors of poor outcomes among patients with nonvariceal upper gastrointestinal bleeding in Europe

Aliment Pharmacol Ther 2011; 33: 1225–1233

Are Acquired Hepatocerebral Degeneration and Hepatic Myelopathy Reversible

Background Acquired hepatocerebral degeneration (AHD) and hepatic myelopathy (HM) are rare complications of chronic liver disease and are usually resistant to medical therapy. Materials and Methods The clinical and laboratory findings of 14 male and 2 female patients with AHD or HM were evaluated. Results The prevalence of AHD and HM was 2% inpatient case series in the last 10 years. The median age of the patients (5 Childs B and 11 Childs C) was 48.7 years (28 to 66 y), and the mean known duration of the liver disease was 75 months (24 to 194 mo). The median time of onset of neurologic findings after diagnosis of the liver disease was 14.5 months. Eight patients who had marked spastic paraparesis or tetraparesis were included in the HM group and all others had AHD group. Sixty-nine percent of the patients had a spontaneous or surgical portosystemic shunts, and the remaining dense retroperitoneal collaterals. During the follow-up period of median 29 months (4 to 72 mo), 12 patients died while waiting for liver transplantation, and these patients suffered from the several complications of chronic liver disease more than the living patients. A marked improvement was observed in 2 of the patients (1 with AHD and the other with HM) at 6 and 8 months after the liver transplantation, respectively. Conclusions Our data suggest that liver transplantation had an important effect on the improvement in these patients.

Electron microscopic findings in non-alcoholic fatty liver disease: is there a difference between hepatosteatosis and steatohepatitis?

Background and Aims:  Non‐alcoholic fatty liver disease has long been accepted as benign; however, recent evidence suggests that the disease may progress to cirrhosis and hepatocellular carcinoma, although the natural course of the disease is still unclear. This study was designed to comparatively evaluate electron microscopic features of non‐alcoholic fatty liver (NAFL) and non‐alcoholic steatohepatitis (NASH).

Association of the mefv Gene Variations With Inflammatory Bowel Disease in Turkey

Background: Association of NOD2 (CARD15) gene mutations with inflammatory bowel diseases (IBD) is well known. We herein aimed to investigate the role of familial Mediterranean fever-associated MEFV variations in IBD patients as additional regional-specific risk factor. Study: One hundred thirty-seven (78 female, 56.9%) IBD patients [62 Crohn’s disease (CD), 75 ulcerative colitis (UC)] were enrolled into the study. The diagnosis of all patients was confirmed by colonoscopy, histopathology, and the clinical findings. One hundred one healthy donors’ samples were used as healthy controls. All patients were genotyped for the most common E148Q, M608I, M694V, and V726A variations of the MEFV and R702W, G908R, and 1007fs of the NOD2. Results: The overall MEFV variation frequency was found to be higher in the IBD (25.5%) patients (28% in UC, 22.6% in CD) compared with controls (9.9%, P=0.006). This association was stronger with the penetrant exon 10 variations (M694V, M680I, V726A; odds ratio =4.5, P=0.001). Contribution of M694V was higher compared with the other variations (14.5% in CD, 17.3% in UC and 3% in controls, odds ratio =6.039, 95% confidence intervals, 1.7-20.7, P=0.002). The overall frequency of 3 NOD2 variants in the IBD group was not different from that of controls. Conclusions: The results of this study suggest that the MEFV variations may be an additional susceptibility factor for IBD in certain parts of the world where the carrier rate is high, and the genetic background of the IBD patients may show regional changes.

A novel locus for syndromic chronic idiopathic intestinal pseudo-obstruction maps to chromosome 8q23–q24

Chronic idiopathic intestinal pseudo-obstruction (CIIP) is a rare and severe clinical syndrome characterized by symptoms and signs of intestinal occlusion, in the absence of any mechanical obstruction of the gut lumen. In the attempt to identify the genetic basis of CIIP, we analyzed a Turkish pedigree with a high degree of consanguinity in which three siblings presented with a syndromic form of CIIP. All affected family members were characterized by recurrent, self-limiting subocclusive episodes, long-segment Barrett esophagus, and a variety of minor cardiac valve or septal defects. In some patients full-thickness intestinal biopsy samples were obtained and tissues were processed for immunohistochemistry using antibodies to different markers of the intestinal neuromuscular tract. Full-thickness biopsies of the gut wall showed abnormalities of both the neural and muscular components suggesting an underlying intestinal neuro-myopathy. Blood samples were collected for DNA extraction from each available family member and DNAs were genotyped using 382 microsatellites spanning the entire genome with the aim to take advantage of the homozygosity mapping approach. Linkage analysis identified a new syndromic locus on chromosome 8q23–q24 (multipoint LOD score=5.01). Our data strongly support the presence of a new genetic locus associated with CIIP, long-segment Barrett esophagus, and cardiac involvement on chromosome 8.

After the eradication of Helicobacter pylori infection, relapse is a serious problem in Turkey

Eradication of Helicobacter pylori (Hp) infection is strongly recommended in duodenal and gastric ulcer. In developed countries the recurrence rate is low; however, in Turkey, the Hp recurrence rate is suspected to be high as the prevalence of Hp infection is--as high as 70-80% in the asymptomatic population. We planned this study to determine the relapse rate of Hp infection after successful eradication therapy in Turkey. Fifty-two cases including 24 patients with duodenal ulcer and 28 patients with nonulcer dyspepsia were examined in this study. The eradication regimen was omeprazole 20 mg twice daily, clarithromycin 500 mg twice daily, and metronidazole 500 mg three times a day for 1 week. All patients underwent upper gastrointestinal tract endoscopy. At least four samples from antrum and corpus were taken to enable histologic diagnosis of Hp infection. After the eradication therapy, endoscopy was repeated at 1, 3, 6, and 12 months, and Hp-positive patients were dropped from study. With the use of this regimen, the Hp eradication rate was 92.3% (48/52). After the eradication of Hp infection, relapse rates were 6.97%, 27.5%, and 11.11% at 3, 6, and 12 months, respectively. The cumulative relapse rate for 1 year was 41.46%. The results of this study revealed that after the eradication of Hp infection, recurrence is encountered very often as a problem in Turkey. We concluded that hygienic and environmental factors can affect these high relapse rates.

Heterotopic gastric mucosa in the cervical esophagus: could this play a role in the pathogenesis of laryngopharyngeal reflux in a subgroup of patients with posterior laryngitis?

Objective. Acid secretion produced by a heterotopic gastric mucosal patch (HGMP) in the proximal esophagus, instead of gastric acid, may be responsible for laryngopharyngeal reflux (LPR), passing the upper esophageal sphincter. The aim of this study was to investigate the prevalence of HGMP in the proximal esophagus in patients with posterior laryngitis indicating the presence of LPR in comparison with a control group and to elucidate the possible role of this lesion in the pathogenesis of LPR. Material and methods. A total of 36 consecutive patients with posterior laryngitis diagnosed on laryngoscopic examination were enrolled in the study. Esophagoscopy and ambulatory 24-h intra-esophageal dual-probe pH monitoring were performed in all patients. During endoscopy, special attention was paid to the proximal part of the esophagus, and the proximal electrode for pH monitoring was placed in this region under endoscopic view. The control group comprised 660 consecutive patients who had undergone upper gastrointestinal endoscopy for the usual indications. When HGMP was found, biopsies were taken for histological confirmation. Results. HGMP was detected in 5 out of 36 patients. One out of five patients with patches was excluded from the study because the histopathology of this patients patch revealed antral-type mucosa, which is not capable of acid secretion. Thus a total of 35 patients were included in the study, yielding a HGMP prevalence of 11.4% (4/35). Compared with the prevalence of the control group (1.6%), a significant difference was observed (p<0.005). pH monitoring showed that 45.4% of the patients had abnormal proximal acid reflux. All of four HGMP (+) patients with posterior laryngitis revealed significantly higher abnormal proximal reflux compared to the patients without patches (p<0.05). Conclusions. This first preliminary study may suggest that HGMP in the cervical esophagus could play a role in the pathogenesis of LPR, at least in a minor group of patients with posterior laryngitis, depending on its capability to produce acid in situ, although isolated proximal reflux could not be demonstrated. This finding may need to be supported by further studies with larger patient populations and using acid stimulation tests.