Erdem Koçak

Mean platelet volume as a fibrosis marker in patients with chronic hepatitis B

Introduction: Many noninvasive tests have been studied for the diagnosis and determining the liver fibrosis score (LFS). In this study, we aimed to research the correlation of mean platelet volume (MPV) and stage of liver fibrosis in patients with chronic hepatitis B (CHB). Patients and Methods: Fifty‐nine patients with CHB were enrolled retrospectively into the study. Age–sex matched 25 healthy subjects were used as control group. The following data were obtained from computerized patient registry database: HBV‐DNA level, hepatitis B e‐antigen seropositivity, liver enzymes and function tests, white blood cell count, platelet count, hemoglobin, histological activity index, LFS, and MPV. Patients were divided into two groups: patients without significant fibrosis (F0, F1, or F2) (Group 1) and patients with advanced fibrosis (F3, F4) (Group 2). Results: A statistically significant increase in MPV was seen in patients with CHB compared with healthy controls (8.49±0.84 fl vs.7.65±0.42 fl, P<0.001). Receiver operating characteristic curve analysis suggested that the optimum MPV level cut‐off points for CHB was 8.0 fl, with sensitivity, specificity, PPV, and NPV of 68, 76, 86, and 50%, respectively. MPV levels were significantly higher in Group 2 (8.91±0.94 fl, P: 0.009) compared with Group 1 (8.32±0.74 fl). ROC curve analysis suggested that the optimum MPV level cut‐off points for Group 2 was 8.45 fl, with sensitivity, specificity, positive and negative predictive value of 77, 59, 45, and 85%, respectively. Multivariable logistic regression model, which consisted of HAI, ALT, HBV‐DNA, platelet count, and MPV, was performed. We showed that MPV was independently associated with advanced fibrosis (P: 0.031). Conclusion: We suggest that MPV might help in the assessment of fibrosis in CHB. It should not be considered a stand‐alone test for this use owing to nonspecificity with other diseases. J. Clin. Lab. Anal. 25:162–165, 2011.

Diagnostic and prognostic role of serum glypican 3 in patients with hepatocellular carcinoma

α‐Feto protein (AFP) is the widely used tumor marker in the diagnosis of hepatocellular carcinoma (HCC). The aim of this study was to assess the diagnostic and prognostic validity of a novel marker, serum Glypican‐3 (GPC3) and to compare AFP in patients with HCC. One hundred and twenty‐eight patients (75 patients with HCC, 55 patients with cirrhosis, and 28 healthy controls) were included in this study. Cut‐off value of GPC3 was 3.9 pg/ml. AFP was divided into four subgroups, according to cut‐off values with 13, 20, 100, and 200 ng/ml. Sensitivity, specificity, and positive and negative predictive values of GPC3 and AFP13, AFP20, AFP100, AFP200 subgroups and also GPC3+AFP13, GPC3+AFP20, GPC3+AFP100, GPC3+AFP200 combinations were compared. Serum GPC3 levels were significantly higher in patients with HCC and cirrhosis compared with control subjects (P<0.05). The median serum GPC3 levels were 3.9 pg/ml in controls, 5.51 pg/ml in patients with cirrhosis, and 5.13 pg/ml in those with HCC. The median serum AFP levels were 1.37 ng/ml in controls, 2.32 ng/ml in cirrhotics, and 50.65 ng/ml in HCC patients. The sensitivity, specificity, and positive and negative predictive values of GPC3 was 61.33, 41.82, 58.97, and 44.43%, respectively. The values for AFP were 68.57, 94.55, 94.12, and 70.27%, respectively. There was no correlation between GPC3 levels and prognostic parameters. GPC3 is not a useful diagnostic and prognostic marker for HCC. J. Clin. Lab. Anal. 25:350–353, 2011.

Acute therapy with intravenous omeprazole on caustic esophageal injury: a prospective case series.

The ingestion of caustic substances may result in significant esophageal injury. There is no standard treatment protocol for esophageal injury and most patients are treated with a proton pump inhibitor or H2 antagonist. However, there is no clinical study evaluating the efficacy of omeprazole for caustic esophageal injury. A prospective study of 13 adult patients (>18 years of age) who were admitted to our hospital for caustic ingestion between May 2010 and June 2010 was conducted. Mucosal damage was graded using a modified endoscopic classification described by Zargar et al. Patients were treated with a proton pump inhibitor and maintained without oral intake until their condition was considered stable. Patients received omeprazole 80 mg in bolus IV, followed by continuous infusion of 8 mg/hour for 72 hours. A control endoscopy was performed 72 hours after admission. There was significant difference regarding endoscopic healing between the before and after omeprazole infusion (P = 0.004). There was no hospital mortality at the follow-up. Omeprazole may effectively be used in the acute phase treatment of caustic esophagus injuries.

Beneficial effects of Ankaferd Blood Stopper on caustic esophageal injuries: an experimental model

Ankaferd Blood Stopper (ABS) is an herbal extract that enhances mucosal healing. The aim of this study was to investigate the efficacy of ABS on the healing of the esophagus and prevention of stricture development after esophageal caustic injuries in rats. The study included 50 rats. Rats were divided into five groups: group 1 (no injury, sham surgery), group 2 (injury + no ABS + study after 2 weeks of injury), group 3 (injury + ABS + study after 2 weeks of injury), group 4 (injury + no ABS + study after 4 weeks of injury), and group 5 (injury + ABS + study after 4 weeks of injury). Standard esophageal burn injury was created by applying 50% NaOH solution to distal esophagus of about 1.5 cm. To rats in the sham group, isotonic solution was given instead of NaOH. ABS (2 mL/day) was given via oral route to group 3 and 5 rats. Fourteen days (group 2 and 3) and 28 days (group 4 and 5) later, all the live rats were killed. The distal esophageal segments of all rats were removed and divided into two equal parts for biochemical and histopathological examination. Mortality rate, weight changes, inflammation, stenosis index (SI), and biochemical measurements were evaluated. The SI was found as 0.31 ± 0.03 in group 1, 0.533 ± 0.240 in group 2, 0.568 ± 0.371 in group 3, 0.523 ± 0.164 in group 4, and 0.28 ± 0.03 in group 5. The SI and inflammation in ABS-treatment group 5 was significantly lower than that in non-treatment group 4 (P= 0.005). There were no significant differences between inflammation and SI among other groups. The mortality rate was 14.2% in group 1, 37.5% in untreated group 2, 14.2% in ABS-treated group 3, 80% in untreated group 4, and 33.3% in ABS-treated group 5. The mortality rate in group 4 was significantly higher than other groups (P= 0.025). Decrease rates in mean body weights of the groups were as follows: group 1, 1%; group 2, 15%; group 3, 14%; group 4, 46%; and group 5, 15%. Biochemical tests other than albumin and creatinine were comparable among the groups. Treatment with ABS prevents inflammation, scar formation, weight loss, and mortality in esophageal caustic injuries. Additional studies to evaluate the clinical benefits of ABS in esophageal caustic injury are recommended.

A novel appetite peptide, nesfatin-1 in patients with non-alcoholic fatty liver disease

Abstract Background and aims. Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver pathology worldwide and is strongly associated with obesity and insulin-resistance and food intake. Nesfatin-1 is a new peptide that controls appetite and food intake. The objective of this research was to examine the serum concentrations of nesfatin-1 in NAFLD. Material and methods. Thirty NAFLD patients who had elevated liver enzymes and 40 age- and sex-matched healthy subjects were included in this study. NAFLD was diagnosed and graded with the findings of liver ultrasound scan. Nesfatin-1 concentrations were measured using an ELISA method and the relationship between nesfatin-1 and metabolic parameters were investigated. The subjects were divided into two groups according to their body mass index (≥ 30 and < 30) and nesfatin-1 concentrations were examined between both groups. Results. Serum nesfatin-1 concentrations in NAFLD patients were lower than healthy controls (0.26 ± 0.14 ng/ml, 0.38 ± 0.18 ng/ml, respectively, and p = 0.008). We found a negative correlation between nesfatin-1 and fasting glucose and body mass index. In obese subjects, serum nesfatin-1 concentrations were significantly lower when compared with non-obese subjects (0.26 ± 0.12 ng/ml, 0.37 ± 0.19 ng/ml, respectively; p = 0.014). In addition, we showed that nesfatin-1 concentrations in subjects with insulin resistance were significantly lower in comparison with insulin-sensitive ones (0.27 ± 0.17 ng/ml, 0.38 ± 0.17 ng/ml, respectively; p = 0.015). Conclusion. Our study has shown that nesfatin-1 concentrations were reduced in NAFLD. The results of this study indicate that nesfatin-1 may have a significant role in NAFLD.

Liver Fatty Acid-binding Protein Is A Diagnostic Marker to Detect Liver Injury Due to Chronic Hepatitis C Infection

BACKGROUND AND AIMS Liver fatty acid-binding protein (L-FABP) is a small molecule. The aim of this study was to examine L-FABP levels and to detect its diagnostic value in chronic hepatitis C (CHC). METHODS We studied 22 patients with CHC and 20 healthy control subjects. Patients with persistently elevated serum aminotransferases and positive HCV RNA were included in the study. Patients with CHC underwent percutaneous liver biopsy. Serum level of L-FABP was determined by ELISA method. RESULTS Patients with CHC had significantly increased levels of L-FABP compared to controls. A strong correlation between serum L-FABP concentrations and aspartate aminotransferases, alanine aminotransferases, HCV RNA levels and hepatic inflammation was found. When a cut-off value was 29,000 pg/mL for L-FABP, sensitivity and specificity were 75 and 100%, respectively. Positive and negative predictive values for L-FABP were 100 and 78%, respectively. CONCLUSIONS Serum L-FABP is used as a new diagnostic marker to detect liver injury.

Clinical Trial: Transcutaneous Interferential Electrical Stimulation in Individuals with Irritable Bowel Syndrome – A Prospective Double-Blind Randomized Study

Background: The exact etiology of irritable bowel syndrome (IBS) remains unclear. Curative treatment is not available and current treatment modalities are mainly directed against the predominant symptoms. There are a few studies reporting the beneficial effects of transcutaneous electrical stimulation in patients with chronic constipation, gastroparesis, and functional dyspepsia. Aim: To investigate whether transcutaneous electrical stimulation is an effective procedure in IBS patients. Methods: IBS patients were randomly placed in vacuum interferential current (IFC) and placebo groups. Both treatments consisted of 12 sessions administered over 4 weeks. Symptoms due to IBS were documented via questionnaires, including the IBS Global Assessment of Improvement Scale, numeric rating scales, visual analogue scale, and IBS Quality of Life Scale at the beginning of, end of, and 1 month after the treatment. Results: Patients in the therapy (29 cases) and placebo (29 cases) groups were homogeneous with respect to demographic data and gastrointestinal system symptoms. When compared to the beginning scores, severity of abdominal discomfort, bloating, and abdominal distension and rumbling improved significantly in either interference or placebo groups at both the end of treatment and 1 month after treatment. In the IFC group, severity of symptoms continued to decrease significantly at 1 month after treatment when compared to scores at just the end of treatment, whereas in the placebo group severity of these symptoms did not change significantly on numeric severity scales. Also, the visual analogue scale of the first month after treatment continued to decrease significantly when compared to the level at the end of treatment in the IFC group. Total quality score increased significantly in the IFC group. Conclusions: Vacuum IFC therapy can significantly improve symptoms and quality of life in patients with IBS. It may represent a novel treatment modality for drug-refractory IBS patients.

Oxidative Stress Might Play a Role in Low Serum Vitamin D Associated Liver Fibrosis Among Patients with Autoimmune Hepatitis

Dear Editor We have read with great interest the promising article by Efe et al. [1] recently published in your journal. The authors successfully demonstrated the role of Vitamin D in the hepatic fibrotic process and severe inflammation in patients with autoimmune hepatitis (AIH). Moreover, they stated that Vitamin D might be a potential biomarker for predicting treatment response and histological features in AIH. Although the authors discussed comprehensively possible links in this association, we would like to suggest an alternative mechanism relating Vitamin D to liver fibrosis, which we think may be important for a better understanding of the results presented in this study. In their study, the authors give a detailed discussion relating Vitamin D and hepatic fibrosis in AIH. But it seems that the authors mainly attribute the possible connection between these two entities to immunological mechanisms, namely to T cell-mediated hepatic inflammation and liver damage. Although there is growing evidence that low Vitamin D is related to advanced liver fibrosis, the pathophysiological mechanisms still need to be defined. In this context, we think that oxidative stress mechanisms, by directly inducing fibrotic processes, could possibly play a significant role in the eventual outcome. Several studies have reported that low vitamin D levels are associated with increased markers of oxidative/nitrosative stress [2]. Experimental studies also demonstrated that Vitamin D, via interaction with the Vitamin D receptor, protects against oxidative stress and can influence migration, gene expression and proliferation of fibroblasts, and diminishes the inflammatory and fibrogenic activity of hepatic stellate cells [3]. Moreover, it has been shown that Vitamin D has antiproliferative effects in liver fibrosis and that Vitamin D supplementation provides significant protection against oxidative stress-mediated complications and strengthens antioxidant defenses [4–6]. Interface hepatitis is the histological hallmark of AIH, consisting of infiltration of CD4 and CD8 T lymphocytes, plasma cells, and macrophages into the liver parenchyma [7]. There is accumulating evidence that suggests interface hepatitis to be an example of apoptosis rather than a necrosis [8]. Nitric oxide (NO)-dependent modifications may contribute to the activation of intrinsic apoptotic pathways that induce cell death. However, the mechanism by which this pathway is activated in cells exposed to NO is not known [9]. The factors that affect cell-specific sensitivity to NO-mediated apoptosis can be related to several influences, including the redox state within the cells, apoptotic signaling cascade activation, regulation of cell survival, and apoptotic gene expression [10]. Based on these findings, it is reasonable to consider that elevated oxidative stress levels contribute to enhanced inflammation and liver damage in AIH by inducing apoptotic pathways. As discussed above, in addition to the other mechanisms mentioned by the authors, it is reasonable to suggest a potential link between low Vitamin D levels and liver fibrosis via oxidative stress pathways.Understanding the intricacies of Y. Beyazit E. Kocak Department of Gastroenterology, Canakkale State Hospital, Canakkale, Turkey

Alterations of platelet function and coagulation parameters during acute pancreatitis.

Vascular thrombosis and systemic hypercoagulable states are known complications of pancreatitis. Higher levels of mean platelet volume (MPV) have been associated with thrombotic diseases. However, a few studies have investigated the association between acute pancreatitis and MPV. We aimed to investigate whether there is a difference of MPV and coagulation parameters in patients with active and remission in acute pancreatitis. We included 24 consecutive patients with biliary acute pancreatitis and 24 consecutive healthy age-matched and sex-matched controls. Full blood counts and other laboratory tests were collected at onset and remission. The MPV was significantly higher in patients with acute pancreatitis at admission 8.6 ± 1.4 fl than controls 7.6 ± 0.7 fl (P = 0.005). We detected positive correlation between, aspartate aminotransferase, alanine aminotransferase, &ggr;-glutamyltransferase, amylase, lipase, and glucose, BMI, D-dimer and MPV. However, there was negative correlation between progression, thrombocyte counts, hemoglobin and MPV. As a result higher MPV levels in acute pancreatitis may reflect hypercoagulation associated with pancreatitis.

Evaluation of Platelet Distribution Width and Mean Platelet Volume in Patients With Carotid Artery Stenosis

Platelets contribute to the pathogenesis of atherosclerosis. Platelet activation has been linked with increased mean platelet volume (MPV) and platelet distribution width (PDW). We investigated the association between PDW, MPW, and the degree of carotid artery stenosis (CS). Patients (n = 229) were divided into 3 groups according to the North American Symptomatic Carotid Endarterectomy Trial criteria. Demographic and clinical features were collected retrospectively. Correlation analysis showed a positive association between PDW and the degree of CS. However, there was no significant correlation between CS and MPV. Moreover, we observed that PDW and low-density lipoprotein cholesterol were independent predictors of the degree of CS. This study showed that PDW, not MPV, is related to the degree of CS. Platelet distribution width could be a useful biomarker for CS. Whether targeting PDW will be of clinical benefit remains to be established.