Hepatocarcinoma with tumor thrombus occupying the right atrium and portal vein in a patient with hereditary hemochromatosis and liver cirrhosis

We present the case of a 46-year old patient with Child-Pugh class C cirrhosis with MEDL-Score 16, and hepatocellular carcinoma invading the inferior vena cava and the right atrium. The etiology of cirrhosis is type 1 hereditary hemochromatosis with positive HFE C282Y/C282Y and H63D/H63D mutations. A systematic review of the literature was performed and only 30 cases of hepatocellular carcinoma with tumor thrombosis extending into the right atrium have been described. To our knowledge, this is the first case that evidences the presence in hereditary hemochromatosis of hepatocellular carcinoma with atypical invasion into the right atrium. Screening of patients with a family history of hereditary hemochromatosis allows detection of the disease in the asymptomatic phase, allowing initiation of early therapy and improved prognosis

Immune and Inflammatory Pathways in Non-Alcoholic Steatohepatitis (NASH). An update

Non-alcoholic steatohepatitis (NASH), also known as fatty liver disease (FLD), is a major public health problem. It is considered to be the hepatic manifestation of the metabolic syndrome. Chronic inflammation of the liver is an essential key in the progression from simple hepatic steatosis to steatohepatitis, the evolutionary stage of fatty liver disease. Moreover, the innate immune system plays a crucial role in the progression of hepatic inflammation. For this reason, it is of utmost importance to elucidate the connections between immune mechanisms, Toll-like receptor cytokine signalling, in order to find new effective treatments. Further studies are necessary to test theories presented in this paper. The elucidation of mechanisms underlying the progression of hepatic steatosis towards steatohepatitis is essential for the development of useful diagnosis and treatment for medical practice

Thrombocytopenia in end-stage renal disease and chronic viral hepatitis B or C

Objectives. We evaluated platelet counts in end-stage renal disease and chronic viral hepatitis. Materials and Methods. We studied 70 patients with end-stage renal disease and chronic viral hepatitis and compared them to a control group of 45 patients without hepatitis. Results. The presence of viral hepatitis was associated with a higher prevalence of thrombocytopenia. Correlations between age, C-reactive protein, liver stiffness measurement, and platelet count were observed. C-reactive protein levels \u3e 10 mg/dl were associated with a lower risk of thrombocytopenia in patients with end-stage renal disease and chronic viral hepatitis, yet age \u3e 60 years, dialysis vintage \u3e 10 years, aspartate and alanine aminotransferase levels \u3e 20 IU/L, albumin levels \u3c 3.5 g/dl, and fibrosis stage ≥ 3 were not related. Conclusions. Chronic viral hepatitis leads to a higher prevalence of thrombocytopenia. Platelet counts in these patients begin to decrease significantly once liver fibrosis reaches stage III

Immune and Inflammatory Pathways in Non-Alcoholic Steatohepatitis (NASH). An update

Non-alcoholic steatohepatitis (NASH), also known as fatty liver disease (FLD), is a major public health problem. It is considered to be the hepatic manifestation of the metabolic syndrome. Chronic inflammation of the liver is an essential key in the progression from simple hepatic steatosis to steatohepatitis, the evolutionary stage of fatty liver disease. Moreover, the innate immune system plays a crucial role in the progression of hepatic inflammation. For this reason, it is of utmost importance to elucidate the connections between immune mechanisms, Toll-like receptor cytokine signalling, in order to find new effective treatments. Further studies are necessary to test theories presented in this paper. The elucidation of mechanisms underlying the progression of hepatic steatosis towards steatohepatitis is essential for the development of useful diagnosis and treatment for medical practice

Thrombocytopenia in end-stage renal disease and chronic viral hepatitis B or C

Objectives. We evaluated platelet counts in end-stage renal disease and chronic viral hepatitis. Materials and Methods. We studied 70 patients with end-stage renal disease and chronic viral hepatitis and compared them to a control group of 45 patients without hepatitis. Results. The presence of viral hepatitis was associated with a higher prevalence of thrombocytopenia. Correlations between age, C-reactive protein, liver stiffness measurement, and platelet count were observed. C-reactive protein levels \u3e 10 mg/dl were associated with a lower risk of thrombocytopenia in patients with end-stage renal disease and chronic viral hepatitis, yet age \u3e 60 years, dialysis vintage \u3e 10 years, aspartate and alanine aminotransferase levels \u3e 20 IU/L, albumin levels \u3c 3.5 g/dl, and fibrosis stage ≥ 3 were not related. Conclusions. Chronic viral hepatitis leads to a higher prevalence of thrombocytopenia. Platelet counts in these patients begin to decrease significantly once liver fibrosis reaches stage III

Hepatocarcinoma with tumor thrombus occupying the right atrium and portal vein in a patient with hereditary hemochromatosis and liver cirrhosis

We present the case of a 46-year old patient with Child-Pugh class C cirrhosis with MEDL-Score 16, and hepatocellular carcinoma invading the inferior vena cava and the right atrium. The etiology of cirrhosis is type 1 hereditary hemochromatosis with positive HFE C282Y/C282Y and H63D/H63D mutations. A systematic review of the literature was performed and only 30 cases of hepatocellular carcinoma with tumor thrombosis extending into the right atrium have been described. To our knowledge, this is the first case that evidences the presence in hereditary hemochromatosis of hepatocellular carcinoma with atypical invasion into the right atrium. Screening of patients with a family history of hereditary hemochromatosis allows detection of the disease in the asymptomatic phase, allowing initiation of early therapy and improved prognosis

Immune and Inflammatory Pathways in Non-Alcoholic Steatohepatitis (NASH). An update

Non-alcoholic steatohepatitis (NASH), also known as fatty liver disease (FLD), is a major public health problem. It is considered to be the hepatic manifestation of the metabolic syndrome. Chronic inflammation of the liver is an essential key in the progression from simple hepatic steatosis to steatohepatitis, the evolutionary stage of fatty liver disease. Moreover, the innate immune system plays a crucial role in the progression of hepatic inflammation. For this reason, it is of utmost importance to elucidate the connections between immune mechanisms, Toll-like receptor cytokine signalling, in order to find new effective treatments. Further studies are necessary to test theories presented in this paper. The elucidation of mechanisms underlying the progression of hepatic steatosis towards steatohepatitis is essential for the development of useful diagnosis and treatment for medical practice

Thrombocytopenia in end-stage renal disease and chronic viral hepatitis B or C

Objectives. We evaluated platelet counts in end-stage renal disease and chronic viral hepatitis. Materials and Methods. We studied 70 patients with end-stage renal disease and chronic viral hepatitis and compared them to a control group of 45 patients without hepatitis. Results. The presence of viral hepatitis was associated with a higher prevalence of thrombocytopenia. Correlations between age, C-reactive protein, liver stiffness measurement, and platelet count were observed. C-reactive protein levels > 10 mg/dl were associated with a lower risk of thrombocytopenia in patients with end-stage renal disease and chronic viral hepatitis, yet age > 60 years, dialysis vintage > 10 years, aspartate and alanine aminotransferase levels > 20 IU/L, albumin levels < 3.5 g/dl, and fibrosis stage ≥ 3 were not related. Conclusions. Chronic viral hepatitis leads to a higher prevalence of thrombocytopenia. Platelet counts in these patients begin to decrease significantly once liver fibrosis reaches stage III

Salbutamol-mediated effects on arterial parameters: a tool for subclinical atherosclerosis detection in patients with metabolic syndrome submitted to a cardiac rehabilitation program

Introduction. Early detection of atherosclerosis is important in patients with metabolic syndrome (MetS) because cardiovascular diseases are the main cause of mortality in these patients. Cardiac rehabilitation (CR) is one of the best known and studied interventions, which has been shown to be associated with decreased morbidity and mortality of cardiovascular disease. Salbutamol mediated effects on pulse wave represent a practical, valid and reliable non-invasive surrogate marker of subclinical atherosclerosis. Aim of the study We assessed subclinical atherosclerosis in patients with MetS vs. a control group, by measuring aortic pulse wave velocity (PWVAo), the augmentation index and central blood pressure, before and after salbutamol administration, which allows evaluation of the hemodynamic effects of inhaled salbutamol on the arterial parameters. Material and methods We conducted a clinical study on a representative sample of 30 subjects, 67% had metabolic syndrome and 33% did not have metabolic syndrome (control group). We measured all parameters of arterial stiffness: brachial augmentation index (Aixb), aortic augmentation index (Aixao), pulse wave velocity (PWVao), aortic pulse pressure (PPao), central blood pressure (SBPao), before and after administration of two inhalations of Ventolin® (salbutamol). Results The analysis of arterial stiffness parameters (Table 2) showed that PWVao before salbutamol administration was 10.60 m/s in the group with MetS, and 9.11 m/s in the control group, with no significant difference. After salbutamol administration, PWVao was 10.78 m/s in the group with MetS, and significantly lower 8.2 m/s (p=0.008), in the group without MetS. There was a significant difference between the groups regarding PPao (mmHg) before salbutamol (54.040 ± 8.5530, 66.215 ± 15.6326, p=0.03), SBPao (mmHg) before salbutamol (147.14±20.12 vs. 125.34±9.71; p<0.0001) and after salbutamol administration. (138.76±21.97 vs.121.38±8.08; p=0.005). There were no significant differences in brachial Aix (0.03±27.5 vs.- 3.04±29.64, p=NS) and aortic Aix (37.72±14.04 vs.36.11±15; p=NS) between the two groups. Conclusions. Early identification of endothelial dysfunction in subjects with metabolic syndrome is important in order to prescribe an optimal cardiac rehabilitation program