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Background: Liver involvement in acute dengue infection is frequently observed and sometimes leads to acute liver
failure, with fatal outcomes. Many factors are thought to contribute to liver dysfunction, including hypoxic injury due to
decreased perfusion, direct damage by the virus and immune mediated injury. In this study, we sought to identify the
pattern in the change in liver enzymes throughout the illness and its association with the degree of viraemia, onset
and extent of plasma leakage and inflammatory mediators.
Methods: Serial daily blood samples were obtained from 55 adult patients with acute dengue from the time of
admission to discharge and the liver function tests, viral loads and cytokines were assessed. The onset and extent of fluid
leakage was measured by daily ultrasound examinations and all clinical and laboratory features were serially recorded.
Results: Aspartate transaminase (AST), alanine transaminase (ALT) and gamma glutamyl transferase (GGT) levels were
elevated in patients with dengue infection throughout the illness. The highest AST levels were seen on day 6 of illness
and both AST and GGT levels were significantly higher in patients with severe dengue (SD), when compared to those
with non-severe dengue (NSD) on day 5 and 6 of illness. Three patients with SD had AST and ALT values of >1000/IU in
the absence of any fluid leakage or a rise in the haematocrit (≥20 %). The peak of the AST levels and the lowest serum
albumin levels were seen 24 h before the maximum fluid leakage and 24 h after the peak in viraemia. Both serum IL-10
and IL-17 levels were elevated during early illness and were significantly higher in those with SD when compared to NSD.
Conclusion: Dengue associated liver injury appears to peak around day 6 and 7. Therefore, liver function tests done
at earlier dates might not reflect the extent of liver involvement in acute infection. Since severe liver involvement can
occur in the absence of fluid leakage, after the peak viraemia, and since it is associated with high IL-17 and IL-10 levels,
possible immune mechanisms leading to hepatic damage should be investigated.
