Many non-invasive tests have been studied for diagnosis and determining the activation degree of inflammatory bowel disease (IBD). Nevertheless, an ideal test has not been found yet. Mean platelet volume (MPV) is influenced by the inflammation. In a few study, decreased platelet volume have been reported in IBD. The aim of this study is to determine whether platelet volume would be useful in ulcerative colitis (UC) activity. Additionally we have analyzed overall accuracy of MPV in disease activity and compared with other inflammatory markers. A total of 61 UC patients (male/female : 41/20), and 27 healthy subjects (male/female : 18/9) were enrolled into the study. For all subjects following tests were performed; ESR, CRP, white blood cell count and mean platelet volume. A statistically significant decrease in MPV was noted in patients with UC (8.29 +/- 1.02 fL) compared with healthy controls (8.65 +/- 0.79 fL). MPV of active UC (8.06 +/- 1.19 fL) patients were significantly lower than that of inactive UC (8.45 +/- 0.87 fL). Overall accuracy of MPV in determination of active UC was 71% (with sensitivity 67%, specificity 73%). A negative correlation was found between MPV and endoscopic activity index (r : -0.358 p : 0.005). In UC, MPV did not correlate with ESR, CRP and white blood cell. Our study showed that MPV reduced in UC, particularly in patients with active UC. Decreased MPV may be an indicator for increased disease activity in patients with UC.

Left-sided portal hypertension is a rare clinical syndrome which may lead to bleeding from isolated gastric varices. Pancreatic disease is the most common etiology. Left-sided portal hypertension should be considered in the presence of gastrointestinal bleeding with normal liver function and unexplained splenomegaly. It may be difficult to diagnose this entity both endoscopically and radiologically. While splenectomy is the treatment of choice for cases complicated by variceal bleeding, there is no consensus on the treatment of asymptomatic patients. The prognosis of left-sided portal hypertension mainly depends on the underlying etiology.

Steatosis in chronic hepatitis B appears to be a result of metabolic factors of the host rather than the effect of viruses. Steatosis is unrelated to the HAI and degree of fibrosis, which are considered as the histological indicators of liver damage.

Our aim was to analyze patients diagnosed with left-sided portal hypertension prospectively and to document the complications at follow-up. Twenty-four patients with isolated splenic vein thrombosis (diagnosed by ultrasonography or angiography or intraoperatively) and/or isolated fundal varices (diagnosed by endoscopy or endosonography) were involved in this study. Demographics, clinical presentation, diagnostic and therapeutic procedures, and morbidity and mortality were recorded in their follow-up. There were 11 and 13 left-sided portal hypertension cases associated with pancreatic diseases and nonpancreatic disorders, respectively. Chronic abdominal pain and gastrointestinal bleeding were the two most common complaints. All patients except one had isolated esophageal (2 cases) or fundal (21 cases) varices. Thirteen patients had splenomegaly on ultrasonography. On Doppler sonography, the splenic vein could be evaluated in 21 of the 24 patients (9 and 6 had complete and partial occlusion, respectively, and 6 had patent blood flow). Urgent intervention with therapeutic endoscopy and splenectomy was performed for two patients each. Medical therapy was begun for three patients according to the underlying diseases. Three patients underwent elective surgery. Two patients were lost to follow-up after the first visit and the mean follow-up of the remaining 22 patients after diagnosis of left-sided portal hypertension was 20 months. Only one patient (with pancreas cancer) had gastrointestinal bleeding at follow-up. All patients with pancreas and gastric cancer died within 2-12 months. Left-sided portal hypertension has various etiologies. It may be difficult to diagnose this entity both endoscopically and radiologically. Treatment should be directed at the underlying diseases. Recurrent hemorrhage due to left-sided portal hypertension is not usual and the prognosis depends mainly on the underlying etiology.

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.