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.

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The risk of stent migration is higher in BBS compared with in MBS. The cases with multiple stents had significantly lower stent migration. In BBS, long stent, proximal and postcholecystectomy strictures were associated with distal migration, while short stent, distal and non-postcholecystectomy strictures were associated with proximal migration.

Gastric cancer is the fourth most frequent cancer and the second cause of cancer-related deaths worldwide. The early diagnosis of gastric cancer is fundamental in decreasing the mortality rates. It has been shown that MPV level is a sign of inflammation in hepatocellular carcinoma and pancreatic adenocarcinoma. The aim of this study is to examine whether MPV would be a useful inflammatory marker for differentiating gastric cancer patients from healthy controls. Thirty-one gastric cancer patients and 31 age-sexes matched healthy subjects included into the study. Patients with hypertension, hematological and renal disease, heart failure, chronic infection, hepatic disorder and other cancer were excluded from the study. MPV level was significantly higher in pre-operative gastric cancer patients compared to healthy subjects (8.31 fL vs. 7.85; p: 0.007). ROC analysis suggested 8.25 fL as the cut-off value for MPV (AUC: 0.717, sensitivity: 61%, specificity: 81%). Surgical tumor resection resulted in a significant decrease in MPV level (8.31 fL vs. 7.55 fL; p: 0.001). No significant difference was found in MPV level between the post-operative group and control subjects. We did not find statistically significant difference between MPV and TNM stages. In conclusion, changes in MPV values may be used as an easily available biomarker for monitoring the healthy patients for GC risk and may prompt physicians to make an early diagnosis of GC.

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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.

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Our results suggest that serum TGF-β1, TIMP-1, fetuin-A, and FGF21 are not useful for the assessment of the extent of liver fibrosis in CHB in this patient group. However, APRI, FIB-4, and Forn's index have a better diagnostic value in patients with significant fibrosis than in those with no/minimal fibrosis.