Increased deposition of the extracellular matrix components, particularly collagen, is a central phenomenon in liver fibrosis. Stellate cells, the central mediators in the pathogenesis of fibrosis are activated by free radicals, and synthesize collagen. Melatonin is a potent physiological scavenger of hydroxyl radicals. Melatonin has also been shown to be involved in the inhibitory regulation of collagen content in tissues. At present, no effective treatment of liver fibrosis is available for clinical use. We aimed to test the effects of melatonin on dimethylnitrosamine (DMN)-induced liver damage in rats. Wistar albino rats were injected with DMN intraperitoneally. Following a single dose of 40 mg/kg DMN, either saline (DMN) or 100 mg/kg daily melatonin was administered for 14 days. In other rats, physiologic saline or melatonin were injected for 14 days, following a single injection of saline as control. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. Malondialdehyde (MDA), an end product of lipid peroxidation, and glutathione (GSH) and superoxide dismutase (SOD) levels were evaluated in blood and tissue homogenates. DMN caused hepatic fibrotic changes, whereas melatonin suppressed these changes in five of 14 rats (P < 0.05). DMN administration resulted in increased hydroxyproline and MDA levels, and decreased GSH and SOD levels, whereas melatonin reversed these effects. When melatonin was administered alone, no significant changes in biochemical parameters were noted. In conclusion, the present study suggests that melatonin functions as a potent fibrosuppressant and antioxidant, and may be a therapeutic choice.

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Summary Background Results are conflicting with respect to the renal effects of anti‐viral agents used for hepatitis B virus infection. Aim To compare short and long‐term renal effects in real‐life settings and to determine risk factors for renal impairment during treatment. Methods 2221 treatment‐naïve patients were enrolled. Among these, 895 (302 lamivudine, 27 telbivudine, 282 entecavir, 273 tenofovir and 11 adefovir initiated patients) had ‘repeated measures’ of creatinine (baseline, 1st, 6th, 12th and 24th month of treatment). Telbivudine and adefovir groups were excluded from further analysis because of the low number of patients. We calculated the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) formula at each time point. Hypophosphataemia was also recorded. Risk factors for renal impairment were analysed. Results Tenofovir caused a decline in GFR at each time point when compared to baseline levels. However, lamivudine and entecavir did not change GFR. GFR‐shifting from ≥90 to 60–89 mL/min/1.73 m2 was comparable among groups. The proportion of patients whose baseline creatinine increased more than 25% was comparable among all anti‐virals. GFR showed a decline in patients who switched from entecavir to tenofovir. One patient with compensated cirrhosis needed to change from tenofovir because of renal safety. Seven and three patients developed transient hypophosphataemia in the tenofovir and lamivudine groups, respectively. Conclusions Although tenofovir caused a decline in GFR, differences between the anti‐viral agents do not appear to be so impressive. In patients with and without renal risk factors at baseline, there is no impact of anti‐virals, including tenofovir.

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This study showed that an increased FE(NO) level may be used for identifying patients with IBD who need further pulmonary evaluation.

Objectives: Obesity is defined as a risk factor for carpal tunnel syndrome (CTS). In this study, the presence or absence of recovery in median nerve conduction velocities after weight loss in obese patients was assessed in order to determine whether excess weight or other factors influence the higher prevalence of CTS in obese patients. Methods: Patients with body mass indexes (BMIs) ≧30 were included in the study. CTS symptoms, age, gender, height, body weight, and concomitant diseases were evaluated. Nerve conduction studies (NCS) were obtained on one upper extremity. All patients were included in dietetic programs. Three months later, NCS were repeated and compared with the first NCS. Results: BMIs were statistically significantly lower on the second visits 3 months later (p = 0.0001). No statistically significant difference was observed in the second NCS of electromyographically diagnosed cases with CTS (p > 0.05). Conclusion: We expected a recovery in median nerve conduction velocities in patients with CTS after weight loss. In the literature, even in untreated cases with CTS, spontaneous improvements in second NCS have been reported. This finding suggests that factors other than excess body weight may be influential in the higher prevalence of CTS in obese patients. A more detailed, genetic-factor-targeted investigation may prove more beneficial to clarify this issue.

Anti-HCV was found positive in 2% of the spouses. None of the seronegative spouses developed seroconversion in the 3-yr follow-up period. This is the first study that stresses the importance of the total number of sexual intercourse in sexual transmission (p= 0.055). Our results of special monogamous group with very limited risk factors support the role of number of total sexual intercourse in HCV transmission. However, the seroprevalence rate of the spouses was still within the upper limit of our country population.