The performance of M and XL probes of FibroScan for the diagnosis of steatosis and fibrosis on a Brazilian nonalcoholic fatty liver disease cohort.

OBJECTIVES: Recently, controlled attenuation parameter (CAP) was incorporated for XL probe. However, its performance through M and XL probes has been scarcely evaluated in nonalcoholic fatty liver disease (NAFLD). The performance of probes regarding transient elastography by Fibroscan is still under debate. AIM: Compare the performance of CAP and transient elastography in NAFLD patients obtained through XL with M probes using histological analysis as gold standard. METHODS: NAFLD patients underwent liver biopsy and FibroScan/CAP with M and XL probes the same day. C-statistic evaluated CAP performance in the identification of moderate/severe (≥33%) and severe (≥66%) steatosis by both probes and transient elastography performance for identification of significant fibrosis (≥F2). RESULTS: Eighty-one patients (74% female; age 54.2 ± 9.9 years; BMI 32.8 ± 5.2/ BMI ≥ 25 92.6%; 96% metabolic syndrome; 60% diabetes mellitus) were included. Mean CAP with M and XL probes was 314 ± 39 and 325 ± 47 dB/m, respectively. The areas under receiver operating characteristic curves (AUROCs) of the M and XL probes for steatosis detection ≥33% were 0.75 (0.64-0.84) and 0.76 (0.65-0.84) (P = 0.95) and for steatosis ≥66% 0.83 (0.73-0.90) and 0.82 (0.71-0.89) (P = 0.73), respectively, with similar performances for both degrees of steatosis. Regarding transient elastography, AUROCs of M and XL probes for ≥F2 were 0.82 (0.71-0.93) and 0.80 (0.69-0.92) (P = 0.66). CONCLUSION: Performance of M and XL probes is similar for the diagnosis of moderate and severe steatosis and significant fibrosis even on a overweight population with NAFLD.

Assessment of the relative dose-response test as indicators of hepatic vitamin A stores in various stages of chronic liver disease.

Hepatic vitamin A stores should be the best early indicator of vitamin A status because more than 90% of total body vitamin A is stored in the liver. The objective of the present study was to evaluate the hepatic vitamin A stores in all stages of chronic liver disease (CLD), including chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC). One hundred forty-four patients (age 55.34 ± 9.38 years) were evaluated in a cross-sectional study. Vitamin A nutrition status was analyzed by serum retinol levels and relative dose-response (RDR) method. Patients with cholestasis were excluded from the sample group. Biochemical, clinical, and anthropometric evaluations were performed. Vitamin A deficiency (VAD) was detected in 51.4% of all patients. Patients with adequate levels of serum retinol presented adequate liver vitamin A reserves; in contrast, nearly half the patients with low serum retinol levels presented adequate levels of retinol in the liver, although none of the patients with hepatitis had this condition. Therefore, the effectiveness of the RDR method for evaluating vitamin A nutrition status was limited in patients with cirrhosis and HCC, perhaps due to the advanced age of these patients, since those in the chronic hepatitis group, who were younger, responded adequately to the test. Thus, the RDR method should be modified when applied to later stages of CLD, considering the time and dose of retinyl palmitate supplementation, as VAD may be a risk factor for the progression of the disease.

Acute kidney injury network criteria as a predictor of hospital mortality in cirrhotic patients with ascites.

BACKGROUND: Acute kidney injury (AKI) is frequent in cirrhotic patients but its best definition is unclear. Recently, the Acute Kidney Injury Network (AKIN) proposed criteria to define AKI. The aims of this study were to apply AKIN criteria to cirrhotic patients with ascites and to evaluate its association to hospital mortality. STUDY: In this retrospective study, cirrhotic patients with ascites admitted to a university hospital in Brazil between November 2003 and December 2007 were included. AKIN criteria were applied in the first 48 hours of hospitalization, considering 2 values of creatinine in this period. Association of AKI at admission and hospital mortality was analyzed. RESULTS: Of the 198 patients in the study, 91 (46%) presented AKI at hospital admission. Overall hospital mortality was 40.4%. Patients without AKI had a hospital mortality rate of 29.9%, whereas the same rate for patients with this complication was 52.7% (odds ratio=2.6; 95% confidence interval, 1.5-4.7; P=0.001). In a logistic regression analysis, 4 variables were independently associated to hospital mortality: infection, hepatic encephalopathy, Child score, and AKI. A receiver operating characteristic curve analysis revealed that the variation in creatinine proposed by AKIN had the best combination of sensitivity and specificity in relation to hospital mortality. CONCLUSIONS: In cirrhotic patients with ascites, prevalence of AKI at hospital admission is high. Patients with renal dysfunction defined by AKIN have significant higher hospital mortality. AKIN criteria are useful in cirrhotic patients with ascites, as it identifies earlier patients with worse prognosis.

Predictors of response to chronic hepatitis C treatment.

Nowadays the standard of care for hepatitis C therapy is based on pegylated interferon alpha and ribavirin (Peg IFN/RBV). This combination has led to a sustained virological response rate (SVR) of 50 to 80% depending on genotype. This is still low, considering the side effects, overall costs and duration of therapy. So far, strategies to foresee SVR have been described such as genotype, fibrosis stage, viral load and gammaglutamyltransferase.In addition, new data has recently been provided on predictive factors of SVR like genetic polymorphism related to race, insulin resistance and viral kinetics. This review aims to discuss these predictive factors of therapy that might help the decision about starting or discontinuing therapy in chronic HCV infected patients.

Prevalence of hepatitis C infection in patients with non-Hodgkin's lymphomas.

Several studies have suggested an association between hepatitis C virus (HCV) and low-grade B-cell non-Hodgkin's lymphomas. The results, however, have been controversial. Italian and Japanese studies have reported a 40% prevalence rate, but the data were not confirmed by English and Canadian studies. We evaluated the prevalence of HCV infection in 109 patients with non-Hodgkin's lymphomas, and compared it with a control group composed of 67 patients with Hodgkin's disease and 31 patients with chronic lymphocytic leukemia. The prevalence of HCV infection was also determined in blood donors. HCV infection was detected using second and third generation anti-HCV ELISA. Positive results were additionally confirmed using Inno-LIA AbIII and/or RNA-HCV by PCR. Immunohistochemical stains were used to determine B or T cell lineage when the morphological analysis was not sufficient for lymphoma classification. HCV infection was detected in 9% of patients with non-Hodgkin's lymphomas, in 2% of patients in the control group (p=0.036), and in 1.2% of blood donors. There was no difference in the prevalence of HCV infection between patients with B or T cell lymphomas. Blood transfusions or previous surgeries, both risk factors for HCV infection, were detected in 90% of the patients with a positive anti-HCV test, in average 17 and 36 years before the diagnosis of lymphoma, respectively. Seventy percent of the patients with non-Hodgkin's lymphomas and a positive anti-HCV test presented evidence of chronic liver disease when the lymphoma was diagnosed. This study suggests the presence of an association between HCV infection and non-Hodgkin's lymphomas in Brazil.