Hepatitis B core-related antigen monitoring during peginterferon alfa treatment for HBeAg-negative chronic hepatitis B.

Serum Hepatitis B core-related antigen (HBcrAg) level moderately correlates with cccDNA. We examined whether HBcrAg can add value in monitoring the effect of peginterferon (PEG-IFN) therapy for HBeAg-negative chronic hepatitis B (CHB) infection. Thus, serum HBcrAg level was measured in 133 HBeAg-negative, mainly Caucasian CHB patients, treated with 48 weeks of PEG-IFN alfa-2a. We assessed its association with response (ALT normalization & HBV DNA < 2000 IU/mL) at week 72. HBcrAg level strongly correlated with HBV DNA level (r = 0.8, P < 0.001) and weakly with qHBsAg and ALT (both r = 0.2, P = 0.01). At week 48, mean HBcrAg decline was -3.3 log U/mL. Baseline levels were comparable for patients with and without response at week 72 (5.0 vs 4.9 log U/mL, P = 0.59). HBcrAg decline at week 72 differed between patients with and without response (-2.4 vs -1.0 log U/mL, P = 0.001), but no cut-off could be determined. The pattern of decline in responders resembled that of HBV DNA, but HBcrAg decline was weaker (HBcrAg -2.5 log U/mL; HBV DNA: -4.0 log IU/mL, P < 0.001). For early identification of nonresponse, diagnostic accuracy of HBV DNA and qHBsAg decline at week 12 (AUC 0.742, CI-95% [0.0.629-0.855], P < 0.001) did not improve by adding HBcrAg decline (AUC 0.747, CI-95% [0.629-0.855] P < 0.001), nor by replacing HBV DNA decline by HBcrAg decline (AUC 0.754, CI-95% [0.641-0.867], P < 0.001). In conclusion, in Caucasian patients with HBeAg-negative CHB, decline of HBcrAg during PEG-IFN treatment was stronger in patients with treatment response. However, HBcrAg was not superior to HBV DNA and qHBsAg in predicting response during PEG-IFN treatment.

Cryptogenic liver cirrhosis and hepatitis E virus (HEV): Are they related?

INTRODUCTION AND OBJECTIVES: Hepatitis E virus (HEV) is one of the most common causes of acute hepatitis. In recent years, its role in the development of chronic hepatitis and cirrhosis especially in immunosuppressed patients and its wide range of extrahepatic involvement have increased the amount of research on HEV. In this study we aimed to investigate the presence of HEV infection in individuals with cryptogenic cirrhosis. MATERIALS AND METHODS: HEV antibodies were analysed using the Anti HEV enzyme-linked immunosorbent assay (ELISA) kit (anti-HEV ELISA; Diapro Prodiagnostic Bioprobes, Milan, Italy). HEV RNA was isolated with using QIAMP Viral RNA mini kit (QIAGEN, Hilden, Germany). The HEV RNA titre was detected with the Rotor Gene 3000 real time polymerase chain reaction (PCR) system using GenoSen's HEV (Rotor Gene) Quantitative Real Time PCR Kit (Genome Diagnostics Private Limited, the Netherlands). RESULTS: Our study included 21 healthy volunteers (12 males) and 35 cryptogenic cirrhosis patients (19 males). The ages of the patients and the controls were similar (46±12.1 vs. 37.5±9.7years). The mean Child-Pugh score was 8±2.5. The anti HEV immunoglobulin G(IgG) positivity rate was 9.5% and 25.7% in the control and patient groups respectively (p>0.05). HEV RNA positivity was not detected in the control group, but 3 cases (8.6%) in the patient group were positive (p>0.05). The HEV RNA, aspartate aminotransferase (AST) and alanine aminotransferase(ALT) levels for these 3 cases were 326.461copies/mL, 91IU/L and 67IU/L; 480copies/mL, 68IU/L and 36IU/L and 72copies/mL, 42IU/L and 24IU/L respectively. There were positive correlations between HEV RNA levels and AST and ALT levels (p<0.05). CONCLUSIONS: Anti HEVIgG and HEV RNA positivity rates are high in cryptogenic cirrhosis although it is not statistically significant and there is a positive correlation between HEV RNA and aminotransferases.

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.

The clinical significance of JAK2V617F mutation for Philadelphia-negative chronic myeloproliferative neoplasms in patients with splanchnic vein thrombosis.

Polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic myelofibrosis (IMF), collectively known as Philadelphia-negative (Ph-negative) chronic myeloproliferative neoplasms (MPNs), MPNs represent the most common causes of splanchnic vein thrombosis (SVT), including Budd-Chiari syndrome (BCS) and portal vein thrombosis (PVT). The JAK2V617F mutation has been demonstrated in most of the Ph-negative chronic MPNs. The study objective was to assess the diagnostic value of JAK2V617F mutation in patients with SVT in a group of 68 patients with SVT (42 PVT,19 BCS, 7 combined PVT and BCS). By DNA-melting curve analysis, the JAK2V617F mutation was detected in 42.1 % of BCS, 38.1 % of PVT and 71.4 % of combined PVT and BCS groups. Thirteen of 15 (86.6 %) SVT patients with overt MPN and 16 of 53 (30.1 %) SVT patients without overt MPN (patients with either normal blood counts or cytopenias), including 6 of 16 with BCS (37.5 %), 7 of 33 with PVT (21.2 %) and 3 of 4 with combined BCS and PVT (75 %) possessed JAK2V617F mutation. A substantial proportion of patients with SVT were recognized as carriers of the JAK2V617F mutation despite the absence of overt signs of MPN. Receiver Operating Characteristic (ROC) curve analysis determined a platelet count of 190,000 mm(3) (area under the curve; AUC = 0.724, p = 0.002) and a white blood cell (WBC) count of 8,150 mm(3) (AUC = 0.76, p = 0.001) as the best cut-off values for the highest sensitivity and specificity ratios of the JAK2V617F mutation in patients with SVT. A significant positive correlation existed between the JAK2V617F mutational status of SVT patients and the WBC and platelet counts. Our results imply that JAK2V617F mutation screening should be an initial test for MPN in patients with SVT.

Cyclosporine Therapy as a Rescue Treatment in Steroid Refractory Acute Severe Ulcerative Colitis: A Real Life Data From a Tertiary Center.

BACKGROUND: Cyclosporine is a rescue treatment alternative to avoid colectomy in corticosteroid refractory acute severe ulcerative colitis. In this study, we aimed to evaluate the long-term efficacy and safety of cyclosporine therapy in acute severe ulcerative colitis patients. METHODS: Acute severe ulcerative colitis (basal Lichtiger score > 10) patients who did not respond to 40 mg intravenous methylpredniso- lone therapy after 3-5 days were included in the study. The presence of clinical response and remission was assessed at 1st week, 1st, 6th, and 12th month according to the Lichtiger index. RESULTS: In this study, 40 patients, whose steroid refractory acute severe ulcerative colitis and basal Lichtiger score > 10 points were enrolled. The median disease duration was 49.3 months (2-204). All patients received cyclosporine for 132 ± 78 days (7-270). Clinical response was obtained on seventh day in 82.5%. The clinical response rates of the first and sixth months were 72.5% and 62.5%, respectively. A total of 17/40 (42.5%) patients underwent colectomy within 1 year. In the patients who underwent colectomy, the basal LS (14.2 ± 1.9 vs 12.3 ± 1.7) (P = .002) was higher and the basal hemoglobin value (11.8 ± 2.3 vs 10.1 ± 1.5) (P = .037) was lower than those who did not undergo colectomy. CONCLUSION: Our findings suggest that cyclosporine treatment may be successfully and safely used in steroid refractory acute severe ulcerative colitis patients. Cyclosporine is a drug that has recently started to come up again with the introduction of new maintenance treatments. Especially in patients who develop a loss of response to infliximab therapy, or where infliximab therapy is contraindicated, or who have azathioprine intolerance, or are unresponsive.

Anticoagulant therapy and Budd-Chiari syndrome: is it successful?

BACKGROUND/AIMS: Anticoagulant therapy is an accepted treatment for Budd-Chiari syndrome (BCS). However, the natural course of untreated patients is unclear. We aimed to evaluate the efficacy of anticoagulant therapy on survival in BCS. METHODOLOGY: Between 1995 and 2007, 45 patients diagnosed with BCS based on the clinical, biochemical, radiological and histological findings were retrospectively evaluated with respect to underlying disease, therapeutic interventions, complications and overall outcome. Complications and survival during the follow-up period were compared in between anticoagulant treated and untreated cases. RESULTS: Mean patient age was 34.4 +/- 11.8 years and 46.7% (21) of them were male. Median followup time was 24 months (6-132); 8.9% of patients were diagnosed as acute, 31.1% as subacute and 60% as chronic BCS according to disease duration. Centrilobular necrosis was found in 16 of 36 biopsy performed patients. Etiological factors were detected in 60% of patients and 40% of them were cryptogenic. Twenty four of them received anticoagulant therapy, the remaining 21 were followed-up with supportive medical therapy. Five patients who had shunt operation were excluded for survival analyses. Complications were similar between treated and untreated cases (p>0.05). There was a positive correlation between survival and centrilobular necrosis (r=0.376, p=0.037). The mean survival periods were 95.5 months (%95 CI 73-117 months) and 72.5 months (%95 CI 42-103 months) in anticoagulant treated and untreated patients, respectively (p>0.246). CONCLUSION: Most patients with BCS are admitted to hospital at the chronic stage and more than half of them have underlying thrombotic risk factor. In our study, no beneficial effects of anticoagulant therapy were observed on the survival and complications of liver disease.

Effect of proton pump inhibitor (PPI) treatment in obstructive sleep apnea syndrome: an esophageal impedance-pHmetry study.

BACKGROUND/AIMS: There is an increasing interest for a link between gastroesophageal reflux (GER) and obstructive sleep apnea syndrome (OSAS). There is no study in the literature which examines the relationship between OSAS and esophageal functions in adults with impedance. We first evaluated the role of reflux in OSAS with simultaneous polysomnography and impedance-pHmetry and then investigated whether the effect of proton pump inhibitor (PPI) treatment changes in these parameters. METHODOLOGY: Twenty two OSAS patients who had applied to sleep laboratory between September 2007 and May 2008 were consecutively enrolled to the study. Twenty four hours esophageal impedance study was performed during polysomnographic recording. At least 50% of all apneas in patients must proceed with a reflux event in 2 minute intervals in order to be considered reflux related apnea patient. RESULTS: Pathologic reflux episodes were determined in 20 patients (8 were weakly acidic, 12 were acidic). Reflux dependent apnea was found in 6 patients. There was endoscopically esophagitis in all reflux related apnea patients. There was a negative correlation between initial mean SaO2 and gas reflux events at night (p=0.004, r =-0.588) and mixed reflux events at night (p=0.02, r=0.493). There was a statistically significant regression of AHI (apnea hypopnea index) after 3-months PPI treatment (p=0.012). CONCLUSIONS: Reflux may trigger apnea in some of the OSAS patients. Therefore, each OSAS patient must be inquired about esophageal and extraesophageal symptoms of reflux.

Second-line levofloxacin-based triple therapy's efficiency for Helicobacter pylori eradication in patients with peptic ulcer.

OBJECTIVES: First-line standard eradication efficacy with lansoprazole, amoxicillin and clarithromycin regressed over 10 years. The aim of this study was to evaluate the efficacy and tolerability of a levofloxacin-based regimen in patients with peptic ulcer after failure of the standard first-line H.pylori eradication therapy in a country with a high rate of infection. METHODS: A total of 91 peptic ulcer patients who were diagnosed H.pylori positive proven by rapid urease test and histology between November 2005 to March 2008 were given lansoprazole 30 mg bid, amoxicillin 1 g bid and clarithromycin 500 mg bid (LAC) for 14 days. After three months from the first line eradication treatment omeprazole 20 mg bid, levofloxacin 500 mg bid, amoxicillin 1 g bid (OLA) 7 day treatment regimen was recommended as a second-line therapy for 37 patients who failed at first-line standard triple therapy. RESULTS: Eradication rates for LAC regimen were found to be 57.14% (52/91) for intention to treat and 58.42% (52/89) for per protocol analysis. Eradication rates for OLA regimen were found to be 37.83% (14/37) for ITT and 41.17% (14/34) for PP analysis. CONCLUSION: OLA regimen eradication rate was successful only in 40% of patients who failed in the first-line eradication. New eradication treatment strategies must be performed, at least in Turkey.

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

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.

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). METHODS: Quantitative and semi-quantitative ultrastructural evaluations were performed on liver biopsies from 23 patients, 10 with NAFL and 13 with NASH. RESULTS: No statistically significant difference was noted between NAFL and NASH patients in ultrastructural features of hepatocytes including megamitochondria, intramitochondrial crystalline inclusions, mitochondrial matrix granules, foamy cytoplasmic appearance, electron-lucent and glycogen-containing nuclear regions, lipofuscin granules, or an increased frequency of vesicles containing electron-dense material in peribiliary Golgi zone; however, the mitochondrial diameter was significantly higher in the NASH patients. Intercellular distance and microvilli between hepatocytes, collagen and electron-dense material accumulation in the space of Disse, electron-dense material accumulation and microvillus density in bile canaliculi did not differ significantly between the groups. CONCLUSIONS: Our data show that, although NAFL and NASH can be distinguished by their distinct light microscopic features, ultrastructural characteristics are similar, which suggests that NAFL may also have the potential to progress to fibrosis and cirrhosis like NASH.

Decreased prohepcidin levels in patients with HBV-related liver disease: relation with ferritin levels.

BACKGROUND: Levels of prohepcidin, a homeostatic regulator of iron absorption, are altered in chronic hepatitis C and liver cirrhosis. However, data on the potential alterations of prohepcidin in patients with HBV-related liver disease are scarce. We investigated whether serum prohepcidin is related to iron overload and perenchymal dysfuction in HBV-related liver disease. METHODS: Three groups of subjects were studied: 66 patients with chronic hepatitis B, 32 patients with HBV-related cirrhosis, and 42 healthy controls without evidence of liver disease. Serum levels of prohepcidin were determined by enzyme-linked immunosorbent assay. RESULTS: Serum prohepcidin levels were significantly lower in patients with HBV-related cirrhosis (175.85 ± 71.5 ng/ml) than in patients with chronic hepatitis B (209.02 ± 62.7 ng/ml P < 0.05) and controls (222.4 ± 128.4 ng/ml, P < 0.05). After adjustment for potential confounders, prohepcidin was found to be an independent predictor of ferritin levels in multiple linear regression analysis (ß = -1.10, t = -3.11, P < 0.01). CONCLUSION: These results demonstrate that prohepcidin levels are reduced in patients with HBV-related cirrhosis and are an independent correlate of serum ferritin.

The treatment of acute liver failure with fractionated plasma separation and adsorption system: Experience in 85 applications.

INTRODUCTION: Artificial liver support systems represent a potential useful option for the treatment of liver failure. The outcomes of patients treated with the fractionated plasma separation and adsorption (FPSA) system are presented. PATIENTS AND METHODS: FPSA was performed 85 times for 27 patients (median 3 treatments/patient) with liver failure [85.2% acute liver failure (ALF) and 14.8% acute-on-chronic liver failure] using the Prometheus 4008H (Fresenius Medical Care) unit. Citrate was used for anticoagulation. A variety of clinical and biochemical parameters were assessed. Comparisons between pretreatment and post-treatment data were performed using paired t-test. RESULTS: The 85 sessions had a mean duration of 6 h. There were significant decreases in total bilirubin (13.18 +/- 9.46 mg/dL vs. 9.76 +/- 7.05 mg/dL; P < 0.0001), ammonia (167.6 +/- 75 mg/dL vs. 120 +/- 43.8 mg/dL; P < 0.0001), blood urea nitrogen (BUN; 12.55 +/- 13.03 mg/dL vs. 8.18 +/- 8.15 mg/dL; P < 0.0001), creatinine (0.54 +/- 0.47 mg/dL vs. 0.46 +/- 0.37 mg/dL; P = 0.0022) levels, and in pH (7.48 +/- 0.05 vs. 7.44 +/- 0.08; P = 0.0045). Four patients (14.8%) received liver transplantation after the treatments; in nine patients, transplantation was not necessary anymore (33%); the remaining 14 patients did not receive a transplantation because they were either not appropriate candidates or no organ was available. Overall survival was 48.1% (4 transplanted and 9 treated patients). No hematological complications related to FPSA were observed. CONCLUSIONS: FPSA system is a safe and effective detoxification method for patients with liver dysfunction, including ALF. The system is useful as a symptomatic treatment before liver transplantation; in up to 1/3 of the cases, it can even be used as a sole method of treatment.

Prevalence and virological features of occult hepatitis B virus infection in female sex workers who work uncontrolled in Turkey.

BACKGROUND: There is little information about the prevalence of occult hepatitis B virus infection (OHBVI). We have investigated the prevalence and virological features of OHBVI among female sex workers (FSWs) in Istanbul. METHODS: Hepatitis B surface antigen (HBsAg) was tested in FSWs who work uncontrolled and were admitted to Venereal Diseases Hospital. HBV DNA and anti-HBs were investigated in all the HBsAg-negative cases. Hepatitis B envelope (HBe) antigen, anti-HBe, anti-hepatitis B core (HBc) antigen, HBV genotype, S gene and precore (PC)/basic core promoter (BCP) mutations were determined in HBV DNA-positive sera. RESULTS: Two hundred and eighty-six volunteers were enrolled and 32.5% (n=93) of them had anti-HBs positivity. HBV DNA (range 30-209 copy/ml) was positive in 11 anti-HBs-negative and two anti-HBs-positive cases. The prevalence of OHBVI was 4.5% (13/286). Anti-HBc was positive in 77% (10/13) of those with OHBVI and anti-HBe positivity was 53.8% (7/13). Only genotype D was present in all occult HBV-infected cases. One PC (G1896A) and one BCP (T1762/A1764) mutation was found, but S gene mutation was not detected in any of the samples. CONCLUSION: In this population, OHBVI may have a negligible role in the horizontal transmission because of a very low viral load, and PC and core promoter mutations are very rare.

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 Child's B and 11 Child's 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.

A case of Aeromonas hydrophila enteritis in the course of ulcerative colitis.

A 24-year-old man with a previous diagnosis of ulcerative pancolitis presented with severe malabsorption with watery diarrhea, malaise, and weight loss. Physical examination revealed paleness, hypotension, tachycardia, edema, ascites, and left-sided pleural effusion. Laboratory analysis revealed hypoalbuminemia and hypocalcemia. Further examination revealed that malabsorption was related to Aeromanas hydrophila infection. Clinical improvement was observed upon oral ciprofloxacin treatment. No clinical or laboratory activation of ulcerative colitis was detected during this infection.

Somatostatin and propranolol to treat small-for-size syndrome that occurred despite splenic artery ligation.

We report our success with somatostatin and propranolol to treat small-for-size syndrome that occurred despite splenic artery ligation. A 48-year-old woman with cirrhosis due to autoimmune hepatitis underwent living-donor liver transplant; her graft-to-body weight ratio of the right lobe was 0.91%. After arterial reperfusion, portal pressure and flow were 24 cm H20 and 2.22 L/min (ie, 360 mL/100g graft/min), respectively. Following splenic artery ligation, the portal pressure decreased to 16 cm H20 and portal flow to 1.74 L/min (ie, 282 mL/100g graft/min). On the second postoperative day, small-for-size syndrome was diagnosed based on the marked prolongation of prothrombin time (international normalized ratio, 4.4), hyperbilirubinemia (359.1 micromol/L), rapid escalation of transaminases (alanine aminotransferase 2488 U/L, aspartate aminotransferase 1075 U/L) and very high portal flow rate (> 90 cm/sec). Oral propranolol (40 mg/day b.i.d.) and somatostatin infusion (250-microgram bolus followed by perfusion at a rate of 250 microgram/h for 5 days) were started. Prothrombin time and transaminase levels began to decrease the following day, although the bilirubin level increased to 495.9 micromol/L before returning to normal. The patient was discharged in excellent health 5 weeks after surgery. Despite reduction of portal pressure by splenic artery ligation, small-for-size syndrome may develop in patients with persistent high portal flow. To the best of our knowledge, this is the first report of the successful treatment of small-for-size syndrome by somatostatin and propranolol in the clinical setting.

What is the impact of capsule endoscopy in the long term period?

AIM: To assess the clinical impact of capsule endoscopy (CE) in the long-term follow-up period in patients with obscure gastrointestinal bleeding (OGIB). METHODS: One hundred and forty-one patients who applied CE for OGIB between 2009 and 2012 were retrospectively analyzed, and this cohort was then questioned prospectively. Demographic data of the patients were determined via the presence of comorbid diseases, use of non-steroidal anti-inflammatory drugs anticoagulant-antiaggregant agents, previous diagnostic tests for bleeding episodes, CE findings, laboratory tests and outcomes. RESULTS: CE was performed on 141 patients because of OGIB. The capsule was retained in the upper gastrointestinal (GI) system in two of the patients, thus video monitoring was not achieved. There were 139 patients [62% male, median age: 72 years (range: 13-93 years) and a median follow-up duration: 32 mo (range: 6-82 mo)]. The overall diagnostic yield of CE was 84.9%. Rebleeding was determined in 40.3% (56/139) of the patients. The rebleeding rates of patients with positive and negative capsule results at the end of the follow-up were 46.6% (55/118) and 4.8% (1/21), respectively. In the multivariate analysis, usage of NSAIDs, anticoagulant-antiaggregant therapies (OR = 5.8; 95%CI: 1.86-18.27) and vascular ectasia (OR = 6.02; 95%CI: 2.568-14.146) in CE were detected as independent predictors of rebleeding. In the univariate analysis, advanced age, comorbidity, and overt bleeding were detected as predictors of rebleeding. CONCLUSION: CE is a reliable method in the diagnosis of obscure GI bleeding. Negative CE correlated with a significantly lower rebleeding risk in the long-term follow-up period.

Retention during capsule endoscopy: Is it a real problem in routine practice?

OBJECTIVE: This study evaluated the risks and outcomes of capsule retention during capsule endoscopy (CE) for investigating small bowel disease. Capsule retention is the most serious complication of CE. METHODS: Before CE, the gastrointestinal tract was evaluated for blockages with computerized tomography. Analysis of CE was made retrospectively. RESULTS: Capsule endoscopy was used to investigate obscure bleeding (90.2%; n = 324) or other symptoms (9.8%; n = 35). The capsule retention rate was 11/359 (3.1%); it was retained in a malignant lesion area (adenocarcinoma or melanoma) in two patients (18.2%), in the small bowel in an ulcerated area in five patients (45.5%), and in the oesophagus/stomach in four patients (36.4%) due to dysmotility. None of the patients had symptoms of obstruction. CONCLUSIONS: Scanning patients before CE did not predict capsule retention. Retention is a complication of CE, but occurs as a result of the underlying disease. The risk of retention is increased in patients with motility disorders, suspected small bowel ulcers or malignancies.

Predictors of treatment requirement in HBeAg-negative chronic hepatitis B patients with persistently normal alanine aminotransferase and high serum HBV DNA levels.

OBJECTIVES: Serum alanine aminotransferase (ALT) is a controversial marker for disease monitoring in hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) patients. The aim of this study was to determine the fibrosis stage and histological activity index (HAI) in HBeAg-negative CHB patients with persistently normal ALT (PNALT) and high serum HBV DNA (≥2000 IU/ml) and to investigate clinical risk factors for the requirement of treatment through the examination of liver biopsy specimens. METHODS: HBeAg-negative CHB patients with PNALT (≤40 IU/l) and high serum HBV DNA (≥2000 IU/ml) were included. HBV fibrosis stage and HAI were scored according to the Ishak system. Multivariate logistic regression analysis was used to estimate the independent risk factors for fibrosis stage ≥2 and/or HAI ≥6. Receiver operating characteristic curve analysis was used to determine an optimal age cut-off for liver biopsy. RESULTS: A total 120 patients were enrolled. These patients had a mean HBV DNA level of 123680±494500 IU/ml; the HBV DNA load was 2000-20000 IU/ml in 68 patients (56.6%) and ≥20000 IU/ml in 52 (43.4%). Eighteen patients (15%) had moderate-to-severe histological activity (HAI ≥6). Forty-three patients (35.9%) had a fibrosis stage ≥2. Forty-eight patients (40%) had a fibrosis stage ≥2 and/or HAI ≥6. On multivariate logistic regression analysis, independent variables associated with fibrosis stage ≥2 and/or HAI ≥6 included age and HBV DNA viral load. Patients with HBV DNA 2000-20000 IU/ml were more likely to require treatment compared to those with a viral load ≥20000 IU/ml. The optimal age cut-off to predict fibrosis stage ≥2 and/or HAI ≥6 was 46 years. CONCLUSIONS: Significant liver damage was detected in 40% of CHB patients with PNALT and high HBV DNA upon biopsy. Age and HBV DNA viral load were independent predictors of significant liver damage. A biopsy to determine the degree of liver damage is advisable for CHB patients older than 46 years.

Gastroesophageal reflux in asymptomatic obese subjects: An esophageal impedance-pH study.

AIM: To investigate the relationship between reflux and body mass index (BMI) in the asymptomatic obese population using the impedance-pH technique. METHODS: Gastroesophageal reflux is frequent in the obese population. However, the relationship between acid reflux and BMI in asymptomatic obese people is unclear. Forty-six obese (BMI > 25 kg/m(2)) people were enrolled in this prospective study. We evaluated the demographic findings and 24-h impedance pH values of the whole group. Gas, acid (pH < 4), weak acid (pH = 4-7) and weak alkaline (pH ≥ 7) reflux parameters were analyzed. RESULTS: The mean age of patients was 49.47 ± 12.24 years, and half of them were men. The mean BMI was 30.64 ± 3.95 kg/m(2) (25.14-45.58 kg/m(2)). BMI of 23 was over 30 kg/m(2). Seventeen patients had a comorbidity (hypertension, diabetes mellitus, or ischemic heart disease). Endoscopic examination revealed esophagitis in 13 of the 28 subjects (10 Grade A, 3 Grade B). The subjects were divided into two groups according to BMI (< 30 and > 30 kg/m(2)). Demographic and endoscopic findings, and impedance results were similar in these two groups. However, there was a positive correlation between BMI and total and supine pH < 4 episodes (P = 0.002, r = 0.414; P = 0.000, r = 0.542), pH < 4 reflux time (P = 0.015, r = 0.319; P = 0.003, r = 0.403), and DeMeester score (P = 0.012, r = 0.333). CONCLUSION: Acid reflux is correlated with BMI in asymptomatic obese individuals.