CD133+ stem cell mobilization after partial hepatectomy depends on resection extent and underlying disease.

BACKGROUND: Bone marrow stem cells (BMSC) can participate to liver regeneration. However, conflicting results have been reported on this topic in patients undergoing liver resection. AIMS: To assess the impact of liver resection extent and presence of underlying liver disease in modulating BMSC mobilization. METHODS: We enrolled 29 patients undergoing liver resection of different extents, 5 surgical controls and 10 blood donors. Circulating CD133+ BMSC were measured by flow cytometry at different time-points after surgery. The hepatic commitment of mobilized BMSC was investigated by polymerase chain reaction. Liver specimens were collected during surgery for histopathological analysis. Hepatocyte growth factor and granulocyte-colony stimulating factor serum levels were measured by enzyme-linked immunosorbent assay. RESULTS: BMSC mobilization was found in patients undergoing major liver resection, especially in the presence of underlying disease. Ductular reactions were noted in patients with chronic hepatopathy and the hepatic progenitor-like cells expressed CD133, NCAM, cytokeratin-19, and alpha-fetoprotein. Hepatocyte growth factor and granulocyte-colony stimulating factor levels increased following liver resection and the contemporaneous presence of liver disease was associated with their highest raise. CONCLUSIONS: Liver repair is mainly an endogenous process. BMSC become important in case of extensive resection, especially in the presence of underlying hepatopathy and hepatic progenitor-like cells activation. Hepatocyte growth factor and granulocyte-colony stimulating factor seem to be involved in the dynamics underlying hepatic regeneration and BMSC recruitment.

Portal vein thrombosis: insight into physiopathology, diagnosis, and treatment.

Portal vein thrombosis (PVT) is a relatively common complication in patients with liver cirrhosis, but might also occur in absence of an overt liver disease. Several causes, either local or systemic, might play an important role in PVT pathogenesis. Frequently, more than one risk factor could be identified; however, occasionally no single factor is discernable. Clinical examination, laboratory investigations, and imaging are helpful to provide a quick diagnosis, as prompt treatment might greatly affect a patient's outcome. In this review, we analyze the physiopathological mechanisms of PVT development, together with the hemodynamic and functional alterations related to this condition. Moreover, we describe the principal factors most frequently involved in PVT development and the recent knowledge concerning diagnostic and therapeutic procedures. Finally, we analyze the implications of PVT in the setting of liver transplantation and its possible influence on patients' future prognoses.

Peginterferon alfa-2b and ribavirin in patients with hepatitis C virus and decompensated cirrhosis: a controlled study.

BACKGROUND/AIM: To evaluate long-term outcomes in decompensated HCV-related cirrhotic patients treated with antiviral therapy. METHODS: Of 129 eligible patients, 66 received peginterferon alfa-2b and ribavirin for 24 weeks, and 63 were controls. Survival and recurrence of liver failure events after therapy were main outcomes. RESULTS: Therapy was tolerated by 27 patients, dose reduced in 26 for toxicity, and discontinued in 13 for intolerance. End-of-therapy and sustained virological response (SVR) rates were 82.6% and 43.5% for HCV 2/3 patients, and 30.2% and 7.0% for HCV 1/4 patients. During therapy, odds ratios for severe infections or deaths due to infection were 2.95 (95% C.I. 0.93-9.3) and 1.97 (95% C.I. 0.40-9.51) in treated patients as compared with controls. During a follow-up of 30 months off-therapy, decompensated events occurred in 52, 33, and 3 of controls, non-responders, and SVR patients. Odds ratios for ascites, encephalopathy, and oesophageal bleeding in treated patients significantly decreased as compared with controls. Annualized incidence of death was 2.34, 1.91, and 0 per 1000 patient-years, respectively, in controls, non-responders, and SVR patients. Survival curves showed early separation of SVR patients from both non-responders and controls at approximately 6 months. CONCLUSIONS: In decompensated cirrhotics, HCV clearance by therapy is life-saving and reduces disease progression.

Effects of a single, short intravenous dose of acetyl-L-carnitine on pattern-reversal visual-evoked potentials in cirrhotic patients with hepatic encephalopathy.

1. In animals and in cultured neurons, L-carnitine and acetyl-L-carnitine (ALCAR) have been shown to counteract some of the toxic effects of ammonia. In order to detect similar properties in humans, we studied neuronal function after ALCAR administration in cirrhotics with hepatic encephalopathy (HE). 2. Eighteen cirrhotic patients with persistent HE and hyperammonaemia were investigated in the present study and six subjects with a prior transient ischaemic attack were used as controls. 3. The prominent positive component that occurs approximately 100 msec after the pattern reversal (P100) latencies of visual-evoked potentials were used to evaluate neuronal function. At first, the P100 latency was measured in six cirrhotic patients with HE and in the six controls before the administration of 0.5 g ALCAR in 50 mL isotonic saline (infusion rate 10 mL/min) and 15, 30, 60 and 90 min later. 4. A significant reduction in P100 latencies was identified 30 min after ALCAR infusion in HE patients, whereas no differences were observed in controls. 5. Thereafter, the P100 latency was evaluated in the 12 other cirrhotic patients with HE only before and 30 min after ALCAR infusion. The mean of the P100 latencies measured in these subjects was significantly shorter after ALCAR infusion compared with values obtained before ALCAR administration (mean (+/-SD) 130.78 +/- 5.50 vs 136.08 +/- 6.45 msec, respectively; P = 0.0013). 6. The present study suggests that a single intravenous dose of ALCAR may transiently improve neuronal function in cirrhotic patients with persistent HE and hyperammonaemia.