Clinical and basal aspects of anemia during antiviral therapy for hepatitis C

Background and Rationale. Anemia is a major side effect of combination therapy for chronic hepatitis C. In this study, severity, potential risk factors for and potential underlying mechanisms of anemia were evaluated.Patients and methods. 44 chronic hepatitis C patients on interferon-ribavirin treatment were included. Anemia-related parameters were measured before and during treatment. Potential changes in membrane phospholipids composition of erythrocytes of patients on anti-viral treatment and potentially increased erythrocyte susceptibility to osmotic or bile salt induced stress were explored.Results. Anemia was almost universal during treatment, with evidence of hemolysis. Decrease of Hb after six months of therapy was 2.1 ± O.I mmol/L (range -0.6-4.1). Higher pre-treatment Hb, highest ribavirin dose (1S-17.S mg/kg) and lower pre-treatment platelet level were independent risk factors for decrease of Hb. Serum erythropoietin levels increased during treatment with negative correlation to Hb levels at week 12 (r = -0.70, p = 0.002) and 24 (r = -0.72, p = 0.002). Erythrocyte membrane phospholipid composition did not differ between anemic patients and healthy controls. Also, resistance to osmotic or bile salt induced stress was normal in anemic patients. Phosphatidylserine exposure at the outer membrane leaflet did not change upon 24 hrs ex vivo incubation with pharmacological ribavirin concentration.Conclusions. Anemia is almost universal during anti-HCV treatment. The extent of anemia correlates with pre-treatment levels of thrombocytes and Hb and with high ribavirin dosing. Although we found hemolysis as contributing factor, our data do not indicate that altered membrane phospholipids composition is an important factor in pathogenesis of anemia

Impact of Fibroscan® on management of chronic viral hepatitis in clinical practice

Background. Liver stiffness measurement (LSM) using Fibroscan® is an increasingly popular non-invasive me¬thod for quantifying liver fibrosis in patients with chronic viral hepatitis. We aimed to explore potential im¬pact of Fibroscan® on clinical management.Material and methods. 133 patients with chronic hepatitis B (HBV, n = 75) or C (HCV, n = 58) underwent Fibroscan® measurement. LSM results were compared with li-ver biopsy results, ultrasound, and APRI-scores, and the impact of LSM on clinical management was evalua¬ted.Results. LSM results indicated fibrosis stage F0-F1 in 84 patients (63%), F2 in 28 (21%), F3 in 8 (6%), and F4 in 13 patients (10%). Nineteen patients had liver biopsies within one year of LSM. In ten patients, LSM and biopsy showed the same fibrosis stage, in 8 there was one stage difference, and in 1 three stages di¬fference. Ultrasound only showed cirrhosis in three patients, who all exhibited advanced cirrhosis at LSM. There was a statistically significant, but weak correlation between LSM results and APRI scores (r = 0.31, p-value < 0.001). LSM results changed clinical management in 39% of patients (55 cases): in 15 patients antivi¬ral treatment was indicated, in 21 patients surveillance for hepatocellular carcinoma was indicated, and 19 successfully treated hepatitis C patients could be discharged from clinical follow-up in absence of severe fibrosis or cirrhosis.Conclusion. LSM appears to be a valuable non-invasive tool to manage patients with chronic viral hepatitis in clinical practice

Growth and final height after liver transplantation during childhood

Objective: To evaluate the effect of end-stage pediatric liver disease and liver transplantation on growth and final height.Patients and Methods: We evaluated growth at 2 years (n = 101) and 5 years (n = 63) after pediatric liver transplantation (LTx). Twenty-three children reached final height. Height was expressed as a standard deviation score of the target height (z(TH) score) of each patient.Results: At the first 2 years after LTx, the z(TH) score was significantly increased from -1.7 to -1.3 SD (P &lt;0.05). Growth at 2 or 5 years after LTx, expressed as Delta z(TH) score, was positively correlated with pretransplant growth retardation (P &lt;0.05). In comparison with patients with noncholestatic primary liver disease, patients with cholestatic primary liver disease were more severely growth retarded before LTx (z(TH) score -2.0 vs -1.2 SD, P &lt;0.05) and had better growth in the first 2 years after LTx (Delta z(TH) score +0.6 vs -0.1 SD, P &lt;0.05). Twelve of the 23 patients had a final height below -1.3 SD of their target height.Conclusions: Growth retardation is common in children before LTx, particularly in children with an underlying cholestatic disease. After LTx, catch-up growth was partial and was prominent only in cholestatic children who had been severely growth retarded before LTx. After LTx during childhood, similar to 50% of patients reach a final height lower than -1.3 SD of their genetic potential JPGN 47.165-171, 2008.</p

Growth and final height after liver transplantation during childhood

Objective: To evaluate the effect of end-stage pediatric liver disease and liver transplantation on growth and final height. Patients and Methods: We evaluated growth at 2 years (n = 101) and 5 years (n = 63) after pediatric liver transplantation (LTx). Twenty-three children reached final height. Height was expressed as a standard deviation score of the target height (z(TH) score) of each patient. Results: At the first 2 years after LTx, the z(TH) score was significantly increased from -1.7 to -1.3 SD (P <0.05). Growth at 2 or 5 years after LTx, expressed as Delta z(TH) score, was positively correlated with pretransplant growth retardation (P <0.05). In comparison with patients with noncholestatic primary liver disease, patients with cholestatic primary liver disease were more severely growth retarded before LTx (z(TH) score -2.0 vs -1.2 SD, P <0.05) and had better growth in the first 2 years after LTx (Delta z(TH) score +0.6 vs -0.1 SD, P <0.05). Twelve of the 23 patients had a final height below -1.3 SD of their target height. Conclusions: Growth retardation is common in children before LTx, particularly in children with an underlying cholestatic disease. After LTx, catch-up growth was partial and was prominent only in cholestatic children who had been severely growth retarded before LTx. After LTx during childhood, similar to 50% of patients reach a final height lower than -1.3 SD of their genetic potential JPGN 47.165-171, 2008