Jolanta Zuwała-Jagiełło

Picolinic Acid in Patients with Chronic Hepatitis C Infection: A Preliminary Report

Macrophage activation seems to be a feature of chronic liver diseases. Picolinic acid (PA) as a macrophage secondary signal causes the activation of interferon-gamma- (IFN-γ-) prime macrophage and triggers cytokine-driven inflammatory reactions. The rationale for seeking increased PA formation in chronic viral hepatitis is based on the involvement of activated macrophages in chronic viral hepatitis-associated inflammation. The aim of this study was to determine serum PA levels in patients with chronic hepatitis C infection, taking into account the presence of diabetes. We assessed PA and high-sensitivity C-reactive protein (hsCRP) as a marker of inflammation in 51 patients with chronic hepatitis C infection (CHC), both with and without diabetes and 40 controls. Compared with the controls, the patients with CHC showed a significant increase in plasma concentrations of PA and hsCRP (P < 0.01 and P < 0.05, resp.). The values of PA and hsCRP were more elevated in patients with diabetes than without diabetes (both P < 0.01). The positive relationships were between PA and hsCRP levels (P < 0.05) and the presence of diabetes (P < 0.001). We documented that significant elevation in serum PA levels is associated with diabetes prevalence and increased inflammatory response reflected in hsCRP levels in CHC patients.

Diagnostic Challenges in Primary Hepatocellular Carcinoma: Case Reports and Review of the Literature

Hepatocellular carcinoma is the fifth most common malignancy and the third leading mortality cause worldwide. It typically develops secondarily to liver cirrhosis, due to hepatitis B or C infection, alcohol abuse, metabolic disease, and so forth. According to the American Association for the Study of Liver Diseases (AASLD) guidelines, which constitute diagnostic standards, the diagnosis of primary hepatocellular carcinoma (HCC) should be based on contrast-enhanced imaging. Lesion hyperenhancement should be observed throughout the arterial phase, followed by the washout during the venous phase. The diagnosis can also be based on the histopathological evaluation of liver biopsy specimen. Although the standards are clear, we often see patients with advanced HCC in clinical practice, who cannot be offered any effective treatment. Patients with chronic liver disease, presenting with inconclusive and changeable test results, constitute a separate problem. In such cases the diagnostic process is typically long-term and delayed. In this paper we present three case reports where the diagnosis could not be made promptly and the patients died as a result of a delayed diagnostic process.

Increased Circulating Advanced Oxidation Protein Products and High-Sensitive Troponin T in Cirrhotic Patients with Chronic Hepatitis C: A Preliminary Report.

Aim. To investigate the relationship between advanced oxidation protein products (AOPPs) and myocardial injury by comparing the selected biomarker for detecting myocardial injury [high-sensitive troponin T (hs-TnT)] in patients with chronic HCV infection. Methods and Results. Eighty-eight patients with cirrhosis and 40 healthy control subjects were enrolled in the study. Circulating levels of AOPPs-albumin (the ratio of AOPPs to albumin content), hs-TnT, tumor necrosis factor α (TNF-α), and high-sensitivity C-reactive protein (hs-CRP) were assessed. Compared with healthy controls, the cirrhotic patients with chronic HCV infection had higher levels of AOPPs-albumin, which were associated with increased hs-TnT. When the presence of ascites was considered, the plasma levels of AOPPs-albumin were higher, as well as TNF-α. AOPPs-albumin positively correlated with hs-TnT level in all cirrhotic patients with chronic HCV infection and this correlation was stronger in decompensated cirrhotic patients. In multivariate logistic regression analysis, the independent factors associated with the presence of ascites were high AOPPs-albumin levels and elevated hs-TnT levels. Conclusion. The simultaneous monitoring of plasma AOPPs and hs-TnT can be helpful for the alterations in myocardial function control in cirrhotic patients with chronic HCV infection.

Hepatitis B virus treatment in hepatocellular carcinoma patients prolongs survival and reduces the risk of cancer recurrence

Chronic hepatitis B virus (HBV) infection and HBV-related liver disease are estimated to affect about 240 million people worldwide. Now that a vaccine is available, the number of new HBV infection cases has plummeted. Yet, there are still regions with very high incidence of HBV. Hepatocellular carcinoma (HCC) is the fourth to six most common malignancy in men and the ninth most common malignancy in women worldwide. 54% of all HCC cases are HBV-associated, making it the most common cause of cancer worldwide. Hepatitis B therapy prevents progression of chronic hepatitis to cirrhosis and HCC development, but even with the best HBV treatment, such patients are still at risk of HCC. Also in patients after transarterial chemoembolization (TACE), liver resection (hepatectomy) or liver transplant, suppression of hepatitis B virus (HBV) improves patient survival. In this paper we present current possibilities of HCC and HBV treatment, which lead to improved survival and quality of life.

Nutrition principles and recommendations in different types of hepatic encephalopathy

Appropriate nutrition – in terms of both quantity and quality – is not only one of the main life processes. A well-balanced diet including sufficient amounts of minerals and vitamins supports proper human development and functioning from fetal development to very advanced old age; it promotes regeneration after intensive exercise and is a key element for successful treatment of most acute and chronic diseases, including liver diseases.

Elevated circulating endothelial cell-derived microparticle levels in patients with liver cirrhosis: a preliminary report

Aim of the study To determine plausible associations between liver cirrhosis and circulating endothelial cell-derived microparticles (EMPs), vascular endothelial growth factor (VEGF) levels and plasma nitric oxide (NO) metabolites. Material and methods Sixty patients with cirrhosis and 20 healthy control subjects were enrolled in the study. Circulating EMPs from platelet-poor plasma samples were examined by flow cytometry. These microparticles were categorized into endothelial cell-derived activated MPs (EMP-ac) (CD31+ CD42b– AN-V–) and endothelial cell-derived apoptotic MPs (EMP-ap) (CD31+ CD42b– AN-V+). Plasma VEGF levels were measured by enzyme-linked immunosorbent assay. Plasma NO metabolites (NOx–) levels were determined using a Greiss reaction method. Results Compared with the healthy control subjects, the patients with cirrhosis showed a significant increase in plasma levels of both phenotypes of EMPs. When the presence of ascites was considered, the plasma levels of EMP-ap were higher (p < 0.01), as well as NOx– (p < 0.05). EMP-ap positively correlated with VEGF level in all cirrhotic patients and this correlation was stronger in decompensated cirrhotic patients. In multivariate logistic regression analysis, the independent factors associated with the presence of ascites were high EMP-ap levels and elevated VEGF levels. Conclusions Elevated plasma levels of EMP-ap in addition to high levels of VEGF might be considered as valuable parameters for predicting the occurrence of ascites in cirrhotic patients.

Circulating Advanced Oxidation Protein Products, Nε-(Carboxymethyl) Lysine and Pro-Inflammatory Cytokines in Patients with Liver Cirrhosis: Correlations with Clinical Parameters

Patients with chronic liver disease are characterized by hepatic inflammation and the destruction of hepatocytes. Viral antigen-specific cytotoxic T lymphocytes, polyclonal cytokines, immune modulators, and oxidized biomolecules have been shown to induce damage and destruction of hepatocytes in these patients (Tsutsui et al., 2003). The contribution of oxidative stress per se to the chronic inflammatory state has been suggested, and consistent evidence has been afforded that both monocyte/macrophage activation and a defect in antioxidant systems occur early in the course of chronic liver failure and gradually increase with its progression to end-stage liver disease (Kirkham, 2007; Videla, 2009). Oxidative stress lead to formation of glycoxidation products, including advanced glycation endproducts (AGEs among them Ne(carboxymethyl)lysine (CML) is best known), and advanced oxidation protein products (AOPPs). AOPPs can be formed in vitro by exposure of serum albumin to hypochlorous acid. In vivo, plasma AOPPs are mainly carried by albumin and their concentrations are closely correlated with the levels of dityrosine. Within the heterogeneous group of AGEs, Ne-(carboxymethyl)lysine has been identified as a major AGEs in vivo (Reddy et al., 1995). Plasma concentrations of AGEs (closely correlating with AOPPs levels) increase with progression of chronic diseases (Witko-Sarsat et al., 1996; 1998), therefore CML has been considered as liver disease-related biomarker for oxidative stress (Sebekova et al., 2002; Yagmur et al., 2006).