Public Health

Evidence brief: Biomarkers of chronic liver disease and their determinants in northern Ethiopia: Evaluating the synergistic impact of HBV and Schistosoma mansoni and the contribution of metabolic and lifestyle factors to liver injury

A sourced PLOS One study, published 2026-06-22. Read the researchers’ findings, methods and context, with links to connected African health evidence.

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Illustrative stock photograph from Unsplash. It does not depict the reported event, study participants or a confirmed Kenyan facility. Source: https://images.unsplash.com/photo-1576091160550-2173dba999ef

Published in PLOS One on 2026-06-22, this study is presented as an attributed evidence briefing. The excerpts below are the original researchers’ words, reproduced under their Creative Commons Attribution licence. Health Signal has selected the abstract and, where needed, opening background paragraphs; the complete methods, results, limitations and references remain in the linked paper.

Original authors: Gessessew Bugssa, Nega Berhe, Girmay Medhin, Shevanti Nayagam, Tilahun Teklehaymanot, Asgeir Johannessen, Seth Domfeh

Source: PLOS One • DOI 10.1371/journal.pone.0352266

Read the complete primary study ↗ · Creative Commons Attribution licence

From the researchers

Abstract

Liver diseases are a major global health concern, affecting over 1.5 billion people and ranking among the leading causes of death. Sub-Saharan Africa carries a high burden, yet the underlying etiology of chronic liver disease is poorly described. The aim of this study was to assess biomarkers of chronic liver disease and their determinants in Northern Ethiopia.

A community-based cross-sectional study was conducted between December 2019 and June 2020 among randomly selected participants aged 5 years or older in Alamata district of Tigray region. Socio-demographic, behavioral, and clinical factors were collected via structured questionnaires; blood was tested for liver function biomarkers and Hepatitis B Virus (HBV) and stool samples for S.mansoni infection. Liver function biomarkers’ abnormalities were defined based on age and sex-specific thresholds. Multivariable hierarchical logistic regression analysis was performed to identify predictors of abnormal alanine aminotransferase (ALT) and adjusted odds ratios (AOR) with 95% confidence intervals (CI) were reported.

A total of 767 participants were included, with a median age of 27 years (5–80 years); 53.1% were female and 67.5% resided in rural areas. The prevalence of HBV and S.mansoni infection was 5.9%, and 26.6%, respectively. Overall, 23.5% of participants had abnormal liver function biomarker with 7.3%, 14.2%, 9,4%, and 8.0% had elevated aspartate aminotransferase(AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total bilirubin levels, respectively. Besides, the De Ritis, aspartate to alanine (AAR) ratio revealed a median of 0.96(IQR:0.62–1.74), with 51% (79/155) of the participants presented with an AAR < 1.0, and 21.3% of participants exhibited an AAR > 2.0. Moreover, the R value depicted the patterns of liver injury with 90(52.0%) participants exhibited R-value below 2(cholestatic injury), whereas 44(22.43%), and 39(22.54%) of the participants were found to have R-values between 2 and 5(mixed injury), and R > 5(hepatocellular injury), respectively. The hierarchical modeling depicted that the infectious domain accounted for the largest portion of model variance (change in Nagelkerke R-squared (ΔR2) =0.157, p < .001). Accordingly, the model demonstrated that several determinants of hepatocellular injury led by significant synergistic interaction between HBV and S. mansoni co-infection conferred a 19.7-fold increase in the odds of elevated ALT (aOR:19.7; 95%CI:5.50, 70.6; p < .001), significantly higher than mono-infections of HBV (aOR:13.7; 95%CI: 5.82, 32.04; p < .001) or S. mansoni (aOR:3.4;95% CI:2.5; 5.51, p < .001). Beyond the infectious synergy, khat chewing (aOR:4.1, 95%CI:2.21, 7.58), and diabetes mellitus (aOR:4.01, 95%CI:1.55–10.36); p = .004) were confirmed as significant independent predictors, each associated with a four-fold increase in likelihood of having elevated ALT.

Reading this evidence

Use the full paper to check the study design, participant selection, comparator and outcome definitions before drawing a practical conclusion. An association does not by itself show cause and effect. A reported performance measure needs its denominator and uncertainty. A finding from a particular facility, sample or time period should retain that scope when it is discussed elsewhere.

This briefing makes the source accessible within the wider public health desk. It does not assess an individual patient or certify a product. When considering relevance to another health system, examine the original authors’ account of context and limitations, then seek local implementation evidence. The related reporting below provides other studies to read alongside this one; it is a topic connection, rather than a claim that their results are directly comparable.

© 2026 Gessessew Bugssa, Nega Berhe, Girmay Medhin, Shevanti Nayagam, Tilahun Teklehaymanot, Asgeir Johannessen, Seth Domfeh. Excerpts reproduced under CC BY. Selection, formatting and contextual notes by Health Signal. The researchers are the authors of the source study, not members of Health Signal’s staff.

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Health Signal Editorial Desk

Health Signal’s publication desk curates source-based health analysis and attributed research briefings. Study authors and originating institutions are credited within each article. Preparation used AI assistance; source and licence checks do not constitute independent replication or clinical endorsement.

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