672, P < 0.0001). Optimal cutoff

of FibroScan values were 6.1 kPa for ≥ F1, 6.3 kPa for ≥ F2, 8.9 kPa for ≥ F3 and 12.0 kPa for F4. Study 2: For Group A, the baseline median FibroScan value was 8.2 kPa. FibroScan values significantly decreased annually for 3 years after the start of NA treatment (6.4 kPa, 5.8 kPa and 5.3 kPa at years 1, 2 and 3, respectively). For Group B, the FibroScan values did not significantly improve over the 3 years after the start of NA treatment. Conclusions:  Liver stiffness, measured by transient elastography, of chronic hepatitis B patients treated with NA showed a rapid decline in the first 3 years followed by a more steady transition for from 3 to 5 years irrespective of long term virological effect. “
“Ascites is the accumulation of fluid in the peritoneal find more cavity. The main causes of ascites in the West are cirrhosis, right heart failure, and peritoneal malignancy. In the first two causes, the source of fluid is the hepatic sinusoid as a result of an elevated sinusoidal hydrostatic pressure, either because the liver architecture is distorted (cirrhosis) or there is a back-up of fluid (and pressure) into the sinusoid (right heart failure). In the

case of peritoneal malignancy, the source of ascites is infiltrated and obliterated peritoneal lymphatics. A careful history, physical examination, and routine laboratory tests can direct the clinician to H 89 chemical structure the etiology of ascites. A diagnostic paracentesis should always be performed in a patient with new-onset ascites to help establish the source of ascites. The serum–ascites albumin gradient correlates with hepatic sinusoidal pressure and will be elevated in ascites secondary to cirrhosis

and right heart failure. Ascites protein levels inversely correlate with leakiness of the sinusoid and will therefore be decreased in cirrhosis (when the sinusoid is less leaky). Low protein ascites is at risk of infection and therefore obtaining a cell count in cirrhotic ascites is important to rule out spontaneous bacterial peritonitis. “
“Aim:  We conducted this prospective study to elucidate the long-term outcome and incidence of hepatocellular carcinoma (HCC) development after nucleos(t)ide analog (NA) treatment in patients with chronic hepatitis B (CHB) or cirrhosis. Methods:  selleck chemicals CHB or cirrhosis patients without past NA treatment or HCC were started on entecavir (ETV) or lamivudine (LVD), and prospectively followed up with monthly blood tests, and with abdominal imaging every 6 months in CHB and every 3 months in cirrhosis patients. Results:  A total of 256 subjects with CHB (n = 194) or cirrhosis (n = 62) received ETV (n = 129) or LVD (n = 127) for 4.25 years (range: 0.41–10.0). After NA treatment, serum HBV DNA, alanine aminotransferase and α-fetoprotein (AFP) dropped significantly, along with significant increases in serum albumin and prothrombin time.