Background: Nucleos(t)ide analogues withdrawal may improve HBsAg loss rates. However, conditions to select patients are not well established. Aims: to evaluate the impact of HBsAg kinetics before treatment interruption on post-treatment response. Methods: Longitudinal, ambispective study in non-cirrhotic chronic hepatitis B HBeAg-negative patients, analysing on-treatment and post-treatment HBsAg kinetics. On-treatment HBsAg kinetics diagnostic accuracy (AUROC) to identify HBsAg loss was evaluated. Results: 52 HBeAg-negative patients stopped treatment after 8.2 years, and 6 (11.5%) achieved HBsAg loss one year after withdrawal. Multivariate analysis showed that on-treatment HBsAg kinetics was related to HBsAg loss (OR = 0.10; 95%CI = 0.016-0.632; p = 0.014) with a high diagnostic accuracy (AUROC = 0.935). A significant HBsAg decline ≥1 log10 IU/mL showed a positive and negative predictive value of 50% and of 97.6%, respectively. After treatment interruption, HBsAg decline speed (log10 IU/mL/year) accelerated in patients treated > 6 years (from -0.06 to -0.20, p < 0.05) and remained stable in treated < 6 years (from -0.12 to -0.12 p = ns). Conclusions: On-treatment HBsAg kinetics can predict post-treatment HBsAg loss rate. Half of patients with a significant HBsAg decline can eliminate HBsAg the first year after withdrawal. Post-treatment HB-sAg decline is faster not only in patients who lost the HBsAg but also in those who remain HBsAgpositive.
Abnormal liver function tests (A‐LFTs) during admission for coronavirus disease‐19 (COVID‐19) are frequent, but its evolution after COVID‐19 resolution remains unexplored. We evaluated factors related to A‐LFTs during COVID‐19 and assessed the liver outcome after patients' discharge. This is a observational study including: (1) retrospective analysis of variables related to A‐LFTs during COVID‐19; and (2) follow‐up evaluation with blood test, transient elastography and liver biopsy in those with persistent A‐LFTs. A‐LFTs were defined according to CTCAEv4.0. Among 595 patients, 366 (61.5%) showed A‐LFTs. The ratio of partial pressure of oxygen and inspired oxygen fraction (P/F) below 200, ferritin ≥1000 ng/mL, male gender and antibiotic and immunomodulatory treatments were related to A‐LFTs. Follow‐up evaluation was performed in 153 individuals. Persistent A‐LFTs at follow‐up was similar in patients with/without A‐LFTs during admission (14.1% vs. 4.9%, p = 0.104). Fifteen (93%) and 58 (39%) patients with/without A‐LFTs at follow‐up showed metabolic fatty liver disease criteria (p < 0.001), which were histologically confirmed. In conclusion, A‐LFTs during COVID‐19 were related to infection severity. Abnormalities remitted at follow‐up in >80% of patients, and no correlation between A‐LFTs at admission and at follow‐up was found. Most patients with A‐LFTs at follow‐up had non‐invasive and histologically proven fatty liver disease.
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