Introduction Hypoxic hepatopathy (HH) is a common entity in hospital with impaired hepatic perfusion secondary to transient altered cardio pulmonary haemodynamics, manifesting with sharp rise of transaminases with perfusion injury rarely requiring transplantation. Transaminases are non-specific index of reperfusion injury (IR). HSP are reperfusion signal proteins represent sheer stress. HSP-70 is one of specific signals of IR impacts on specific target. This study evaluates the utility of a novel marker of HILI.
Methods Sixty (n=60) patients were recruited from Hospital. Group A control (n=20) Group B (n=20) HILI, GroupC (n=20) Acute Hepatitis [(Tylenol 8/20 (40%), Acute hepatitis B 8/20 (40%) herpes simplex 1/20 (5%) EBV 1/20 (5%) acute hepatitis A 1/20 (5%) unknown 1/20 (5%)]. All groups underwent serial blood levels of HSP70, Liver and renal functions, MELD score, SOFA score, from day 0, 4, 7 and 10. Exclusion; Cardio respiratory failure, Renal failure, Acute alcoholic hepatitis, sepsis, organ transplant haemolytic Syndromes, CVA, MELD >20, MAP <90.
Conclusion Results: Group A; HSP 70 was normal. Group B was intermediate on day 0 and very high on day 4, 7 and reverting back to lower levels on day 10. Group C had a low level (mildly elevated) of HSP-70 on all days with the exception of the Tylenol group where it was intermediate levels. Conclusion: HSP-70 is a relevant surrogate marker for hypoxia induced hepatopathy. HSP-70 levels strongly correlated with HILI and poorly with Tylenol induced liver injury. But negatively with other non-vascular liver injuries. Larger study needed to validate this finding.
Competing interests None declared.
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