In this study, in vivo effectiveness of ascorbic acid (AA), beta carotene (BC) and allicin in HP eradication were evaluated. 210 patients who are HP positive in biopsy were involved in this study. The patients randomised to seven treatment groups (each group consisting of 30 patients). The first group was given standard eradication treatment (lansaprasol 30 mg bid, clarithromycin 500 mg bid, amoxicillin 1 g bid for 14 days). Second group received AA 1000 mg/day in addition to the standard treatment. Third group received only AA 1000 mg/day for 14 days. Fourth group was treated with standard regiment plus 120 mg/day BC. Fifth group was given only BC 120 mg/day for 14 days. Sixth group was given standard regiment and allicin 4200 μg/day. Seventh group received only Allicin 1200 μg/day for 14 days. The eradication was achieved in 20 (66.6 %) in group I, 15 (50 %) in group II, 3 (10 %) in group III, 15 (50 %) in group IV, 0 (0 %) in group V, 27 (90 %) in group VI and 7 (23.3 %) in group VII. Allicin seemed to be potentially effective agent for HP eradication but ascorbic acid, beta caroten was found to be ineffective.

The transabdominal preperitoneal (TAPP) procedure for laparoscopic inguinal hernia mesh repair is being applied with increasing frequency. This technique has an acceptable recurrence rate (0.4-3.9%), but has varying complication rates (1.3-17.4%).1,2 We report the first case of mesh penetration of the colon following laparoscopic TAPP repair, treated with colonoscopy.

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Colorectal cancers are one of the most common malignancies associated with coagulation abnormalities ranging from asymptomatic laboratory changes to massive thromboembolism or hemorrhage. It was previously shown that global fibrinolytic was increased in non-metastatic colorectal cancer. In this study global fibrinolytic capacity was measured in patients with colorectal cancer and metastatic liver disease, which always more commonly displays various coagulation disorders. Nineteen patients with biopsy-proven colorectal cancer, 30 patients with metastatic colorectal cancer, and 20 healthy control subjects were involved into the study. Using standart silicated fibrin pellets and tissue plasminogen activator, fibrinolytic capacity of the plasmas was detected with the amount of d-dimer produced before the reaction was stopped by adding aprotinin to the medium. Mean global fibrinolytic capacity (GFC) was increased to higher levels in patients with metastatic disease compared to levels in non-metastatic disease (p<0.05). Fibrinogen/GFC ratio correlated to the increase of d-dimer levels. Global fibrinolytic capacity was much higher in metastatic disease, reflecting a progression to overt disseminated intravascular coagulation.

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N(G)-Nitro-L-arginine methyl ester hydrochloride (L-NAME) is a non-specific nitric oxide (NO) inhibitor and it has been used to eliminate the role of NO in many studies like animal models for hypertension. In this study, we aimed to investigate whether lisinopril treatment has any biochemical and/or histopathological effect on rat liver tissue in a L-NAME-induced hypertension model. Forty-eight 6-weeks-old male Spraque-Dawley rats were used in the study. The animals used in the study were randomly divided into four equal groups. To induce hypertension, L-NAME was added to drinking water at a concentration of 600 mg/l and each rat was given 75 mg/kg/day of L-NAME for 6 weeks. Tail cuff systolic blood pressure (SBP) was measured at first, third, and sixth weeks. There was a significant difference between the experiment groups and controls. In only lisinopril given and L-NAME plus lisinopril administered groups, each rat was given 10 mg/kg of lisinopril for 6 weeks. At the end of the study, the animals were sacrificed. Blood and tissue samples were collected for biochemical and histopathological analysis. It has been observed that mean NO level was significantly decreased in L-NAME given group (p<0.05). Mean ALT levels were significantly increased in lisinopril and L-NAME plus lisinopril given groups, when compared with the control group (p<0.05). AST levels were in normal range in all groups (p>0.05). Hepatocyte degeneration was prominent in lisinopril given group, whereas mononuclear cell infiltration was significant in L-NAME given groups. Although the beneficial effects in L-NAME-induced hypertension treatment, lisinopril can lead to some unexpected results like hepatocyte degeneration, serum enzyme level elevation, and slight mononuclear cell infiltration.

Aim: To analyze the risk factors of lamivudine treatment failure (LTF) for the long-term use in patients with low viral load (LVL). Material and Methods: In this multicenter study, 548 antiviral naïve noncirrhotic adult patients with LVL (for HBeAg+ patients HBV DNA <10⁹ copies/ml and for HBeAg- patients HBV DNA <10⁷ copies/ml) were enrolled. As a control group, 46 lamivudine-initiated patients with high viral load (HVL) were included. Primary outcome was switching to or adding on another antiviral drug as a consequence of primary nonresponse, partial response, viral breakthrough or adverse events. Secondary outcomes included LTF rates at 1, 2, 3, 4 and 5 years and LTF-related viral and host factors. Results: Among 594 patients, 294 had to change lamivudine at the follow-up. Primary nonresponse, partial response, viral breakthrough or adverse events frequencies were 6.8, 1.6, 64.5 and 0.1%, respectively. Five-year LTF rates were 61.3 and 84.2% in patients with LVL and HVL, respectively. Among patients with LVL, patients with <100,000 copies/ml and ≥100,000 copies/ml had 54.8 and 67.3% LTF rates at the end of the 5th year, respectively. Logistic regression analysis of risk factors showed HBeAg+, hepatic activity index, HBV DNA, virological response at 6 months and duration of follow-up were independent predictors for LTF (p values were 0.001, 0.008, 0.003, 0.020 and 0.003, respectively). Conclusion: Similar to patients with HVL, first-line lamivudine therapy is not efficient for long-term use in patients with LVL. LTF risk is so high even in the absence of worse predictive factors.

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