Prospective Evaluation of Liver Stiffness Using Transient Elastography in Alcoholic Patients Following Abstinence.

AIMS: Fibroscan® is a non-invasive method to evaluate liver stiffness (LS), however, its accuracy in alcohol-related liver diseases (ALD) especially with respect to active or stopped alcohol drinking is largely unknown. We prospectively evaluated the LS changes in patients with ALD following alcohol withdrawal. METHODS: Sixty-four patients were evaluated by FibroScan® and lab tests at baseline and after 4 weeks of abstinence. RESULTS: At baseline, 21 patients (33%) had an abnormal LS (> 7 kPa) and 32 patients (50%) had abnormal liver function tests. More specifically, 3 and 11 subjects had a LS higher than 9.6 kPa and 12.5 kPa, respectively. The LS significantly declined in abstinent from 9.2 ± 10.1 (M±SD) at the baseline to 6.9 ± 6.1 kPa at 4 weeks (P = 0.03), respectively, while did not change significantly in drinkers. In addition, 80% of abstainers had a significant LS reduction (-2.6 ± 5.5 kPa), compared to drinkers (2.2 ± 3.6 kPa) (P = 0.004). After 6 months, 27 patients accepted a further evaluation: 22 abstinent and 5 relapsed to drink. At the final evaluation, only 4 out of 22 abstainers had still a LS higher than 7 kPa. CONCLUSIONS: During active drinking LS is probably overestimated by Fibroscan® in ALD, since 1 month after abstinence it is dramatically reduced, especially in subjects with baseline values higher than 7 kPa. SHORT SUMMARY: We prospectively evaluated liver stiffness by Fibroscan® in patients with alcohol-related liver disease at baseline and following abstinence. After 1 month of abstinence, the LS is dramatically reduced, especially when values are greater than 7 kPa and transaminase elevated at baseline.

Genetic determinants in hepatitis C virus-associated mixed cryoglobulinemia: role of polymorphic variants of BAFF promoter and Fcγ receptors.

OBJECTIVE: Mixed cryoglobulinemia (MC) is a hepatitis C virus (HCV)-related immune complex disorder. Only some HCV-infected patients develop MC, which suggests that the genetic background of the host plays a key role. This study was undertaken to evaluate the contribution of host genetic factors in the pathogenesis of HCV-associated MC (HCV-MC) by analyzing allelic variants of low-affinity Fcγ receptor (FcγR) genes and BAFF promoter. METHODS: FcγR polymorphisms (FCGR2A 131 R/H, FCGR2B 232 I/T, FCGR3A 176 V/F, and FCGR3B NA1/NA2) and BAFF promoter polymorphism -871 C/T were analyzed in 102 patients with HCV-MC and 108 patients with HCV without MC, using polymerase chain reaction-based techniques. RESULTS: A higher prevalence of -871 T/T homozygosity (31% versus 16%; P = 0.001) and a greater frequency of T alleles of the BAFF promoter (80% versus 57%; P = 0.004) were found in the HCV-MC group than in the HCV group. A significant increase in serum BAFF concentration was significantly associated with the higher frequency of the T allele in HCV-MC (mean ± SD 4.12 ± 1.29 versus 2.09 ± 0.81 ng/ml; P < 0.0005). The distribution of the FcγR genotypes was not significantly different. In the 21 HCV-MC patients treated with rituximab, the response was strictly related to F allele homozygosity (significantly reduced in 5 of 5 patients with the FCGR3A F/F genotype versus 4 of 16 with V/V or V/F; P < 0.0005). CONCLUSION: These results indicate the importance of host genetic background in the development of HCV-MC, suggesting that mechanisms enhancing Ig production and B cell survival may play a relevant role. Genetic FcγR variants seem to be crucial to the effectiveness of rituximab therapy.