Since the publication of the American Association for the Study of Liver Diseases (AASLD) practice guidelines on the management of hepatocellular carcinoma (HCC) in 2005, new information has emerged that requires that the guidelines be updated. The full version of the new guidelines is available on the AASLD Web site at http://www.aasld.org/practiceguidelines/ Documents/Bookmarked%20Practice%20Guidelines/ HCCUpdate2010.pdf. Here, we briefly describe only new or changed recommendations.

/pdf/aasld-practice-guideline-management-of-hepatocellular-51bocalv0r.pdf

AASLD PRACTICE GUIDELINE Management of Hepatocellular Carcinoma: An Update

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.20933

Management of hepatocellular carcinoma.

Clinical Management of Hepatocellular Carcinoma. Conclusions of the Barcelona-2000 EASL Conference

https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.29913

Diagnosis, Staging, and Management of Hepatocellular Carcinoma: 2018 Practice Guidance by the American Association for the Study of Liver Diseases

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1053/jhep.2003.50195

Des-gamma carboxyprothrombin can differentiate hepatocellular carcinoma from nonmalignant chronic liver disease in american patients☆

Plasma des-γ-carboxyprothrombin in the early stage of hepatocellular carcinoma

To clarify the natural history of hepatitis B virus (HBV)-associated liver cirrhosis, the clinical, laboratory and histological features of 174 untreated hepatitis B surface antigen (HBsAg)-positive cirrhotics were analysed, with a mean follow-up period of 34 months (range 8–135 months) after liver biopsy. Male patients were predominant (86.8%) and the mean age of the whole group was 45 years, s.d. = 12 (range 15–82 years). Serum HBeAg and HBV-DNA positivity were 38.9% and 31.8%, respectively. The calculated annual rate of spontaneous HBeAg seroconversion was 6.4% which was significantly lower than that (12%) of patients with HBeAg-positive chronic active hepatitis (CAH). Superinfection by δ-agent was rare, and anti-δ antibody was detected in only 1.7% of them. The occurrence rate of hepatocellular carcinoma in the whole group was 5.7%/year which was not higher than that of HBsAg-negative cirrhotics (6.2%/year). Serial liver biopsy showed that in the late evolution of cirrhosis, hepatitic activity tended to decline. Active cirrhosis may represent the intermediate stage between CAH and inactive liver cirrhosis. The 5-year survival probability rate of the patients belonging to Child's functional classes A, B and C was 83.4% (s.d. = 5.7), 79.2% (s.d. = 9.4) and 30.9% (s.d. = 14.3), respectively. Most patients were in a well-compensated state on entry into the study and remained stable for several years after diagnosis. Major causes of death include massive variceal bleeding, hepatic failure and/or hepatorenal syndrome, infection and hepatocellular carcinoma.

Natural history of hepatitis B surface antigen‐positive cirrhosis in Taiwan: A clinicopathological study

T cell clones specific for hepatitis B core (HBcAg) and e (HBeAg) antigens of hepatitis B virus (HBV) were generated from liver infiltrates of HBeAg-positive patients. Analyzed with a panel of overlapping synthetic peptides spanning the complete sequences of HBcAg and HBeAg, eight clones responded specifically to the e2 peptide (PAYRPPNAPIL; amino acid residues 130–140 of HBcAg and HBeAg), which was doubly restricted by class I and II molecules. A preferential usage of the T cell receptor (TCR) α chain variable (Vα) gene was found: Vα12.1 for five HLA-Cw9(3)-restricted cytotoxic T lymphocyte (CTL) clones, and Vα7.1 for three other HLA-DRw52-restricted type 1 helper T cell (Th1) clones. Although heterogeneous in the usage of TCR α chain joining region (Jα) segments, their junctional-region sequences revealed conserved hydrophilic serine residues in seven of the eight e2-specific T cell clones. Single alanine substitution of the centrally located and the only hydrophilic asparagine residue of e2 peptide abrogated T cell responsiveness. The nonstimulatory e2 analogue could competitively inhibit e2-specific responses. These results demonstrate that both CTL and Th1 clones recognizing a determinant of HBcAg and HBeAg are present in the liver of chronic hepatitis B patients. The preferential Vα gene usage and the expression of conserved residues in junctional-region sequences of TCRα chains by viral-peptide-specific, intrahepatic T cells may provide a T cell mechanism of HBV immunopathogenesis.

Characterization of T Cell Clones Specific to a Determinant of Hepatitis B Virus Core and e Antigens in Chronic Type B Hepatitis: Implication for a T Cell Mechanism of HBV Immunopathogenesis.

T cell clones (TCC) were generated from liver infiltrates of chronic hepatitis B patients. Examined with a panel of overlapping synthetic peptides spanning the entire sequences of HBcAg and HBeAg, eight clones had a specific response to the e2 peptide (amino acid residues 130–140 of HBcAg and HBeAg). Analyzed by polymerase chain reaction (PCR) using specific oligonucleotide primers of T-cell receptor (TCR) genes, these eight clones preferred usage of TCR α-chain variable gene (Vα): Vα 12.1 for five HLA-Cw9(3)-restricted cytotoxic T lymphocyte (CTL) clones, and Vα 7.1 for other three HLA-DRw52-restricted type 1 helper T cell (Th1) clones. A conserved hydrophilic serine residue was also found in junction sequences (CDR3) of TCR α-chain. A single alanine substitution of the centrally located and the only hydrophilic asparagine residue of e2 peptide abroagated T cell responsiveness. The nonstimulatory e2-analogue could competitively inhibit the e2-specific responses. These results demonstrate that both CTL and Thl cells, recognizing a determinant of HBcAg and HBeAg, are present in the liver of patients with chronic type B hepatitis. The preferential Vα usage and the expression of conserved residues in CDR3 of TCR α-chain by viral peptide-specific, intrahepatic T cells may provide a T-cell mechanism of HBV immunopathogenesis.

Peptide Recognition and Competition, T Cell Receptor Usage, and HLA Restriction Elements of T Cell Clones Specific to a Determinant of Hepatitis B Virus Core and e Antigens in Chronic Type B Hepatitis

Sun-Lung Tsai

Papers

Plasma des-γ-carboxyprothrombin in the early stage of hepatocellular carcinoma

Natural history of hepatitis B surface antigen‐positive cirrhosis in Taiwan: A clinicopathological study

Characterization of T Cell Clones Specific to a Determinant of Hepatitis B Virus Core and e Antigens in Chronic Type B Hepatitis: Implication for a T Cell Mechanism of HBV Immunopathogenesis.

Peptide Recognition and Competition, T Cell Receptor Usage, and HLA Restriction Elements of T Cell Clones Specific to a Determinant of Hepatitis B Virus Core and e Antigens in Chronic Type B Hepatitis