Gungor Boztas

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.

Hypogonadism is not related to the etiology of liver cirrhosis

We investigated the clinical and laboratory findings of hypogonadism and feminization in male patients with viral or alcoholic cirrhosis to determine whether chronic liver disease plays a primary role in the development of sexual dysfunction and hormonal changes. Two groups of male patients with liver cirrhosis (23 alcoholic, 33 viral) age-and Childs gradematched, and 20 age-matched healthy men, as a control group, were included in this study. Clinical signs of hypogonadism and feminization were examined in the cirrhotic patients. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, free testosterone, estradiol, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin were estimated in all groups. Seminal fluid was also analyzed in 7 alcoholic and 15 viral cirrhotics. Serum levels of estradiol, androstenedione, and sex hormone-binding globulin were significantly higher, and free testosterone and dehydroepiandrosterone sulfate levels were significantly lower in both groups of cirrhotics compared with the control group. Childs C patients in both groups of cirrhotics were found to have higher estradiol and lower free testosterone levels than childs A and B patients. Alcoholic and viral cirrhotics had markedly reduced sperm motility and density. The differences between alcoholic and viral cirrhotic patients in the clinical signs of hypogonadism, serum levels of sex steroids, and the results of seminal fluid analysis were not statistically significant. These findings suggest that liver cirrhosis per se, independent of etiology, causes hypogonadism and feminization, and that the degree of hypogonadism and feminization correlates well with the severity of liver failure.

Solitary pancreatic tuberculosis in immunocompetent patients mimicking pancreatic carcinoma

Abstract In this study, two cases of biopsy‐proven pancreatic tuberculosis are reported. The patients presented with fever, anorexia, fatigue, abdominal pain and weight loss. A differential diagnosis of fever of unknown origin was conducted. Computed tomography (CT) revealed a cystic mass image in the pancreatic head in one patient, and a hypodense lesion in the pancreatic head in the other. The first patient was diagnosed by a wedge biopsy specimen obtained in the exploratory laparotomy. The other patient was diagnosed by percutaneous fine‐needle aspiration biopsy. Both patients were successfully treated with quadruple antituberculous therapy for 12 months. We concluded that especially in young patients who present with a mass in the pancreas, pancreatic tuberculosis should be considered among the differential diagnoses, particularly in developing countries and immunosuppressed individuals.

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.

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.

Spontaneous ascitic infection in different cirrhotic groups: prevalence, risk factors and the efficacy of cefotaxime therapy.

Objective: To investigate the prevalence of spontaneous ascitic infection (SAI) in different cirrhotic groups, the risk factors for development of SAI, and the efficacy of cefotaxime therapy. Design: A prospective study. Setting: In‐patient clinic of a university hospital. Patients: Eighty cirrhotic patients with ascites were assigned to four groups: hepatitis B or D virus‐related 34, alcoholic 18, hepatitis C virus‐related 14, miscellaneous 14. Interventions: Paracentesis was performed on 80 patients during 92 consecutive hospitalizations. Ascitic fluid was cultured by the method of bedside inoculation of blood culture bottles with ascites. The patients with SAI were treated with cefotaxime (2g, three times daily, intravenously) for 5 days. Main outcome measures: Frequency of SAI in cirrhotic groups; clinical, bacteriological and biochemical findings of SAI; rate of recovery from infection. Results: Twenty SAI episodes (22%) were found in 16 patients; 8 episodes were spontaneous bacterial peritonitis, 2 bacterascites, and 10 culture‐negative neutrocytic ascites. SAI occurred more frequently in patients with hepatitis B or D virus‐related liver cirrhosis (32%) than in the alcoholic (6%, P<0.05), hepatitis C virus‐related (14%) or miscellaneous (14%) cirrhotic groups. In multivariate analysis, independent predictive factors associated with the development of SAI are chronic hepatitis B virus infection, ascitic fluid total protein and serum bilirubin. Escherichia coli was obtained in 5 of 10 positive ascitic fluid cultures. Cure of the infection was achieved in 95% of episodes. Hospitalization mortality rate in infected patients was 20%. Conclusion: Spontaneous ascitic infection occurs in approximately 20% of cirrhotic patients hospitalized with ascites. The patients with low ascitic protein concentration, high serum bilirubin level or hepatitis B virus cirrhosis are more predisposed to SAI. Cefotaxime may be an effective first‐choice antibiotic for ascitic fluid infection.

Is portal hypertensive enteropathy an important additional cause of blood loss in portal hypertensive patients

Abstract Objective. Recently, mucosal changes of small bowel were defined by developing new imaging techniques including capsule endoscopy (CE) in portal hypertensive patients. However, the clinical impact of these changes is unknown. In this study, we aimed to determine the additional cause of blood loss in portal hypertensive patients. Material and methods. A total of 444 portal hypertensive patients, hospitalized in our clinic between 2005 and 2007, were evaluated. Patients with obscure bleeding were enrolled to this prospective case–control study. CE was performed in 21 patients who met inclusion criteria. Gastroscopy, colonoscopy and computerized tomography/small bowel enema were performed in all patients. Results. Fourteen cirrhotic and seven noncirrhotic portal hypertensive patients were enrolled to this study. Mean age of patients was 47.9 ± 15.6 years, and 13 of 21 were male. Small bowel varices were found in 7 patients (1 active bleeding) and other mucosal abnormalities in 10 patients (vascular ectasia, erosion and edema, 1 active bleeding). Although two of them were normal, jejunal malignant mass was found in two patients (1 active bleeding). Of 21 patients, 19 (90.5%) patients had portal hypertensive abnormalities (including varices). However, ileal varices rate was 57.1% (4 patients) in noncirrhotic portal hypertensive patients and 21.4% (3 patients) in cirrhotics. Conclusion. Ninety percent of patients had portal hypertensive abnormalities in small bowel and one-third of them had small bowel varices. Small bowel varices and vascular ectasia were the main causes of obscure bleeding in portal hypertensive patients.

Etiological factors of duodenal and gastric ulcers.

BACKGROUND/AIMS We aimed to determine the etiology of patients with duodenal and gastric ulcers. METHODS 140 patients diagnosed with peptic ulcer between April 2002-2009 were enrolled in this prospective study. Two biopsy specimens were collected from the antrum and corpus for histology and one for rapid urease testing, and stool samples were analyzed for Helicobacter pylori antigen. Serum calcium and gastrin levels were also analyzed. RESULTS 82 (58%) patients were male, with a median age of 47.70±15.03 years (range: 16-92). The ulcer was located in the duodenum in 96 patients, stomach in 40, and both duodenum and stomach in 4. The rates of patients positive for Helicobacter pylori antigen in stool, positive in urease testing and positive for Helicobacter pylori presence in antral and corpus samples were 48%, 52%, 67%, and 60%, respectively. 107 (76%) patients were positive for Helicobacter pylori in one of the test methods. 64 (46%) patients had a history of nonsteroidal antiinflammatory drug use within the last month. Mean levels of calcium and gastrin were 9.29±0.40 (7.90-10.20) and 73.96±89.88 (12.86-562.50), respectively. Gastrin level was correlated to inflammatory activity (p<0.05). 19 (13.6%) of the patients were negative for Helicobacter pylori, nonsteroidal anti- inflammatory drug use and hypersecretory illness, and were classified as idiopathic. CONCLUSIONS The most common cause of duodenal and gastric ulcer was Helicobacter pylori, and it was responsible for three-fourths of the cases. About half of the patients had a history of nonsteroidal antiinflammatory drug use, and nonsteroidal antiinflammatory drug and Helicobacter pylori were both responsible for the ulcer in three-fourths of these patients. In about one-tenth of the patients, nonsteroidal antiinflammatory drug use was the cause of ulcer alone, and about one-tenth of the ulcers were classified as idiopathic.