Conversely, isolated genotype II was more frequently found in patients with elevated ALT values and evidence of chronic liver disease (45% vs. 23%; P < .01) and it was progressively more represented in advanced liver disease, such as cirrhosis and HCC.
The association of viremia, elevated serum alanine aminotransferase (ALT) levels, and hepatocyte inflammatory activity in hepatocellular carcinoma (HCC) patients was studied.
Some patients show persistently normal serum alanine aminotransferase (ALT) values, whereas the others show high-ALT values and progress to liver cirrhosis or hepatocellular carcinoma.
In the validation of this Progression score in 9 patients with normal ALT and 25 with HCC, the score was significantly higher in the HCC group (3.1 +/- 1.1 vs. 2.0 +/- 0.9, P =.019).
HCC developed in 31% of 80 patients with consistently abnormal ALT levels and in 4% of 92 patients with intermittently abnormal ALT levels but never in 102 patients with ALT levels consistently normal during 1993-1998.
Among the 88 HCV-RNA-positive patients, 15 (17.0%) had normal alanine aminotransferase levels and abdominal ultrasound, 61 (69.3%) had nonprogressive chronic hepatitis, and 12 (13.7%) had severe liver disease (6 [6.9%] liver cirrhosis, 4 [4.5%] hepatic decompensation, and 2 [2.3%] hepatocellular carcinoma) after a follow-up period of 25 years.
Among the independent factors (sex, age, HCV genotype, HCV-RNA level, effect of interferon therapy, serum alanine aminotransferase before interferon therapy, and histologic stage and grade) tested by Cox proportional-hazards analysis, histologic stage (hepatic fibrosis) before interferon was significantly associated with HCC development (p = 0.01).
They were clinically classified into asymptomatic carriers with normal serum alanine transaminase (ALT) levels and patients with chronic liver disease, such as those with chronic hepatitis (CH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC).
DNA obtained from 141 Spanish patients with HCV infection (48 with alanine aminotransferase levels in the range considered to be normal, 47 with liver cirrhosis, and 46 with hepatocellular carcinomas [HCCs]) and from 116 control subjects were typed for HLA-B, HLA-DRB1, and HLA-DQB1 alleles, as well as for major histocompatibility complex class I chain-related gene A (MICA) transmembrane polymorphism.
Patient age, sex, hepatitis B e antigen (HBeAg) status, alanine aminotransferase (ALT) levels, and basal core promoter mutations did not predictHCC development.
In the multivariate analysis, the presence of T1653, an alanine aminotransferase level of > or = 37 U/L, and a platelet count of < 18 x 10(4) platelets/mm3 were independent predictive values for hepatocellular carcinoma (odds ratio [95% confidence interval], 5.05 [1.56-16.35], 12.56 [3.05-51.77], and 11.5 [3.47-38.21], respectively).
There were significant improvements in hepatic function including serum albumin, aspartate aminotransferase, alanine aminotransferase, indocyanine green test, platelet count and histological activity grade in comparison with those before interferon therapy and at the onset of hepatocellular carcinoma.
The BCP double variants (odds ratio, 1.92 (95% confidence interval, 1.14 to 3.25)) were statistically significantly associated with HCC risk even after adjusting for alanine aminotransferase levels, antibodies against HBV e antigen, HBV genotype, HBV viral load, and other sequence variants.
The results suggest that maintenance of viral load <4.39 log copies/ml was associated with sustained normalization of ALT levels and decreased risk of HCC.
The multivariate analysis indicated that male gender, alpha-fetoprotein (AFP) 20 ng/ml or greater, average serum alanine aminotransferase (ALAT) 80 IU/l or greater and the presence of anti-HBc were independent risk factors for development of HCC (p=0.038, p=0.013, p=0.020 and p=0.001, respectively).
Expression of nuclear HBcAg in cirrhotic liver was significantly associated with higher aspartate aminotransferase levels (P = 0.001), alanine aminotransferase levels (P < 0.001), and alpha-fetoprotein levels (P = 0.002), as well as a shorter duration to develop hepatocellular carcinoma or liver decompensation (Kaplan-Meier method, P = 0.044).
Recent treatment guidelines now recognize the importance of these treatment endpoints in the prevention of end-stage liver disease and hepatocellular carcinoma rather then other surrogate markers such as HBeAg seroconversion and serum alanine aminotransferase normalization, especially in patients who acquired hepatitis B virus infection early in life.
As compared with the HBV-infected subjects without HCC, NFKBIA -826 T and NFKBIA -881AG allelic carriages were only associated with HCC risk in the subjects with HBV genotype C. The association of NFKBIA -881AG allelic carriage with HCC risk was not affected by liver cirrhosis (LC) status, alanine aminotransferase level and hepatitis B e antigen status.
Prospective trials using therapeutic approaches aimed at decreasing ALAT levels are necessary in order to confirm a positive impact of ALAT reduction on the incidence of HCC in patients with HCV-LC.
In patients with positive HCV RNA status following results were found: Alanine aminotransferase was elevated in 27.4%, decompensated liver disease in 2.9% and hepatocellular carcinoma in 0.4%.
Several factors at baseline (male, smoking, alanine aminotransferase, the positivity of HBe antigen and HB core-related antigen, the proportion of HBV DNA ≥ 5 log copies/mL, T1753V mutation, and A1762T/G1764A double mutation) were significantly associated with HCC among HBV mono-infected subjects.
We investigated the predictive factors for alanine aminotransferase (ALT) elevation, antiviral drug use, and hepatocellular carcinoma (HCC) occurrence in HBeAg-negative patients.
Of the patients, 49/255 (19.2%) developed advanced liver diseases (ALDs) (during 5.2 years): 30 patients developed clinically overt cirrhosis, 10 developed hepatocellular carcinoma and 9 developed severe reactivation of a preexisting chronic hepatitis B. Baseline CD4(+) cell count <200 cell/mm(3) (P = 0.013, OR = 6.503), baseline alanine aminotransferase (ALT) elevation (P = 0.011, OR = 14.456), and longer cumulated time with detectable HIV RNA (P = 0.008, OR = 1.814) and HBV DNA (P = 0.014, OR = 1.536) were risk factors for ALDs development, while CD4(+) cell count changes ≥150 cells/mm(3) within 3 months (P = 0.039, OR = 0.049) and the use of lamivudine-based cART (P = 0.030, OR = 0.034) were protective against ALDs development.