ABSTRACT
Background and aimsTo determine the impact of the COVID-19 pandemic on the population with chronic Hepatitis B virus (HBV) infection under hospital follow-up in the UK, we quantified the coverage and frequency of measurements of biomarkers used for routine surveillance (ALT and HBV viral load). MethodsWe used anonymised electronic health record data from the National Institute for Health Research (NIHR) Health Informatics Collaborative (HIC) pipeline representing five UK NHS Trusts. ResultsWe report significant reductions in surveillance of both biomarkers during the pandemic compared to pre-COVID years, both in terms of the proportion of patients who had [≥]1 measurement annually, and the mean number of measurements per patient. ConclusionsFurther investigation is required to determine whether these disruptions will be associated with increased rates of adverse chronic HBV outcomes.
Subject(s)
COVID-19 , Hepatitis BABSTRACT
Background: COVID-19, the clinical syndrome caused by infection with SARS-CoV-2, has been associated with deranged liver biochemistry in studies from China, Italy and the USA. However, the clinical utility of liver biochemistry as a prognostic marker of outcome for COVID-19 is currently debated. Methods: We extracted routinely collected clinical data from a large teaching hospital in the UK, matching 585 hospitalised SARS-CoV-2 RT-PCR-positive patients to 1165 hospitalised SARS-CoV-2 RT-PCR-negative patients for age, gender, ethnicity and pre-existing comorbidities. Liver biochemistry was compared between groups over time to determine whether derangement was associated with outcome. Results: 26.8% (157/585) of COVID-19 patients died, compared to 11.9% (139/1165) in the non-COVID-19 group (p<0.001). At presentation, a significantly higher proportion of the COVID-19 group had elevated alanine aminotransferase (20.7% vs. 14.6%, p=0.004) and hypoalbuminaemia (58.7% vs. 35.0%, p<0.001), compared to the non-COVID-19 group. Within the COVID-19 group, those with hypoalbuminaemia at presentation had 1.83-fold increased hazards of death compared to those with normal albumin (adjusted hazard ratio [HR] 1.83, 95% CI 1.25-2.67), whilst the hazard of death was ~4-fold higher in those aged [≥]75 years (adjusted HR 3.96, 95% CI 2.59-6.04) and ~3-fold higher in those with pre-existing liver disease (adjusted HR 3.37, 95% CI 1.58-7.16). In the COVID-19 group, alkaline phosphatase increased (R=0.192, p<0.0001) and albumin declined (R=-0.123, p=0.0004) over time in patients who died. We did not find a significant association between other liver biochemistry and death. Conclusion: In this UK population, liver biochemistry is commonly deranged in patients with COVID-19 but only baseline low albumin and a rising alkaline phosphatase over time are prognostic markers for death.