Mean platelet volume could be possible biomarker in early diagnosis and monitoring of gastric cancer.

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.

Thrombosis of the portal venous system: a prospective study.

BACKGROUND: Thrombosis in the portal system causes a wide spectrum of clinical pictures. There are few published studies describing the clinical features and consequences of portal venous system thrombosis. We aimed to document presentations and outcomes in patients with thrombosis in the portal and/or splenic veins. PATIENTS AND METHODS: The study included 95 patients who were diagnosed with portal venous system thrombosis in the period September 2001 to April 2006. Demographics, clinical presentation, diagnostic investigation, management, morbidity, and mortality were recorded in their follow-up. RESULTS: Of the 95 patients with portal vein thrombosis (PVT), 35 had isolated PVT (IPVT), 27 had isolated splenic vein thrombosis (ISVT), and 33 had thrombosis in both the portal and splenic veins (PSVT). The mean follow-up periods after diagnosis of IPVT, ISVT, and PSVT were 36, 31, and 32 months, respectively. Abdominal pain and gastrointestinal bleeding were the most common symptoms at presentation in the IPVT and PSVT groups, whereas abdominal pain was the dominant symptom in the ISVT group. During the follow-up period, no bleeding was seen in 26 of the 35 (74%) patients with IPVT, in 23 of the 33 (70%) patients with PSVT, and in 24 of the 27 (89%) patients with ISVT. Biliopathy developed during follow-up in 11 of 35 patients with IPVT, in 1 of 27 with ISVT, and in 5 of 33 with PSVT. In the ISVT group, there were 11 deaths, and one each in the IPVT and PSVT groups. CONCLUSIONS: The etiology of PVT varies in portal and splenic veins. IPVT has a higher morbidity (bleeding and portal biliopathy), whereas ISVT that is not associated with an underlying malignancy has a favorable prognosis.

Serum angiotensin converting enzyme levels in pancreatic diseases.

BACKGROUND/AIMS: Recently, the existence of a local renin angiotensin system (RAS) in the pancreas has been demonstrated in laboratory animals as well as in human. It has been suggested that RAS and angiotensin converting enzyme (ACE) activity increase in diseases involving pancreas tissue. In the present study, we analyzed the relationship between serum ACE levels and pancreas disorders including acute and chronic pancreatitis, and pancreas adenocancer. METHODOLOGY: The study groups comprised 14 cases with acute pancreatitis (male/female: 5/9), 38 chronic pancreatitis patients (male/female: 25/13) and 21 pancreas adenocancer cases (male/female: 11/10). The ACE activity in the sample was determined by comparing the sample reaction rate to that obtained with the ACE calibrator. RESULTS: Serum ACE levels were 38.28 +/- 23.67 U/L (10-108), 43.71 +/- 23.58 UL (7-120), 39.14 +/- 19.31 U/L (5-77) and 38.04 +/- 13.69 U/L for patients with acute pancreatitis, chronic pancreatitis, pancreas cancer and healthy controls respectively. Serum ACE levels were not significantly different among all groups (p>0.05). There was no significant difference regarding ACE levels in patients with metastasis and without metastasis. There was no correlation between ACE levels and tumor size. CONCLUSIONS: Our results showed that serum ACE levels increased in neither benign nor malignant pancreas diseases. However, serum ACE levels may not reflect the actual RAS activity because non-ACE pathways affecting RAS activity have been described. Further studies analyzing non-ACE pathways contributing to RAS activity in human pancreatic disorders are needed.

Effects of urtica dioica extract on experimental acute pancreatitis model in rats.

Acute pancreatitis is the acute inflammation of pancreas and peripancreatic tissues, and distant organs are also affected. The aim of this study was to investigate the effect of Urtica dioica extract (UDE) treatment on cerulein induced acute pancreatitis in rats. Twenty-one Wistar Albino rats were divided into three groups: Control, Pancreatitis, and UDE treatment group. In the control group no procedures were performed. In the pancreatitis and treatment groups, pancreatitis was induced with intraperitoneal injection of cerulein, followed by intraperitoneal injection of 1 ml saline (pancreatitis group) and 1 ml 5.2% UDE (treatment group). Pancreatic tissues were examined histopathologically. Pro-inflammatory cytokines (tumor necrosis factor-α), amylase and markers of apoptosis (M30, M65) were also measured in blood samples. Immunohistochemical staining was performed with Caspase-3 antibody. Histopathological findings in the UDE treatment group were less severe than in the pancreatitis group (5.7 vs 11.7, p = 0.010). TNF-α levels were not statistically different between treated and control groups (63.3 vs. 57.2, p = 0.141). UDE treatment was associated with less apoptosis [determined by M30, caspase-3 index (%)], (1.769 vs. 0.288, p = 0.056; 3% vs. 2.2%, p = 0.224; respectively). UDE treatment of pancreatitis merits further study.

The utility of thrombopoietin in predicting liver fibrosis in chronic hepatitis B.

Many noninvasive serum markers have been studied to determine the liver fibrosis score (LFS). In this study, we aimed to investigate the association between thrombopoietin (TPO) levels and the stage of liver fibrosis in patients with chronic hepatitis B (CHB). Seventy-seven patients (64 active and 13 inactive) with CHB were included in this cross-sectional study. Patients were divided into three groups: In group 1, patients with mild or no fibrosis (F0, F1); in group 2, patients with significant fibrosis (F2-F4); and in group 3, inactive CHB carriers. Digital patient records were used to access pre-treatment laboratory findings including HBV DNA, HBeAg, ALT, AST, total bilirubin, PLT, albumin, INR. Liver biopsies were examined by experienced pathologists in our hospital who were blinded to the data of the patients. Serum TPO levels were measured using commercial ELISA kit. Serum TPO levels were significantly lower in patients with active CHB compared with the inactive carriers (528 vs 687.1 p=0.003). There was no statistically significant difference in TPO levels between the patients with and patients without significant fibrosis (568.9 vs 459.8 p=0.367). Correlation analysis with respect to ALT, AST, TPO, HBV-DNA level, platelet count, histological activity index (HAI) and liver fibrosis score was performed. TPO was only weakly positively correlated with AST, ALT and HBV-DNA levels (r=0.269 p=0.018; r=0.341 p=0.002; r=0.308 p=0.006; respectively) and no correlation in TPO with LFS and HAI was found (r=0.140 p=0.270, r=0.162 p=0.201; respectively). TPO was not associated with significant fibrosis (p=0.270). In conclusion, TPO levels were decreased in active CHB patients compared with inactive carriers but there was no correlation between TPO levels and the stage of fibrosis in active CHB.

Serum m 30 levels reflects ulcerative colitis activity.

BACKGROUND: Apoptosis plays a role in epithelial and mucosal injury, which is 1 of the mechanisms in the pathogenesis of ulcerative colitis. Apoptotic cells increase as a result of injured mucosa in ulcerative colitis and serum M 30 levels increase in epithelial cell apoptosis. In this study, we aimed to evaluate the relation between M 30 serum levels and ulcerative colitis activity. METHODS: Eighty patients with ulcerative colitis and 40 healthy controls were enrolled into the study. The patient group consisted of 31 extensive colitis, 30 left-sided colitis, and 19 proctitis. The activity of ulcerative colitis was determined with clinical and endoscopic findings. Serum M 30 levels, acute phase reactants, and biochemical tests were analyzed in all subjects. RESULTS: Serum M 30 levels in patients with active ulcerative colitis were significantly higher when compared with the healthy controls (165.6 ± 60.6 and 129.6 ± 37.4; P = 0.003). Serum M 30 levels in active left-sided colitis patients was significantly higher when compared with patients in remission phase (180.6 ± 58.5, 141.5 ± 35.4; P = 0.044). When we exclude patients with ulcerative proctitis, M 30 levels in active ulcerative colitis patients were significantly higher than that the patients in remission phase (174.0 ± 63.5, 135.0 ± 29.9; P = 0.017). CONCLUSIONS: We found that M 30 levels increase in patients with active ulcerative colitis. Our findings support the role of apoptosis demonstrated by serum M 30 levels in the pathogenesis of active ulcerative colitis.

Detection of an aortoenteric fistula in a patient with intermittent bleeding.

BACKGROUND: A 57-year-old male with an aortobifemoral bypass graft presented to a gastroenterology clinic with a 3-month history of intermittent hematemesis, melena and fever. The patient had received antibiotic therapy 2 months before for the same symptoms; however, following brief regression ( approximately 3 weeks) the symptoms had returned. INVESTIGATIONS: Physical examination; analysis of full blood count; measurement of erythrocyte sedimentation rate, C-reactive protein levels, liver enzymes, electrolytes, renal function, serum cholesterol and serum triglyceride; HIV serology; blood, sputum, urine and stool culture analysis; performance of esophagogastroduodenoscopy, colonoscopy, abdominal ultrasonography and multidetector CT scanning. DIAGNOSIS: Aortoenteric fistula with an inflammatory mass surrounding the aortobifemoral bypass graft. MANAGEMENT: Laparotomy with removal of the aortobifemoral bypass graft, performance of an extra-anatomic right axillofemoral bypass graft and an extra-anatomic right-left femorofemoral bypass graft.

Recurrent pancreatitis in a patient with autosomal-dominant polycystic kidney disease.

Autosomal-dominant polycystic kidney disease is an inherited disorder characterized by multiple cysts in kidneys and other organs. A 63-year-old man was evaluated for the etiology of recurrent pancreatitis and chronic renal failure. Multiple cysts of kidneys, liver, and pancreas and pancreas divisum was diagnosed. Pancreatitis should be included in the differential diagnosis of abdominal pain in patients with ADPKD. Pancreas divisum may be a predisposing factor for acute pancreatitis in these patients.

Report of 24 left-sided portal hypertension cases: a single-center prospective cohort study.

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.