Abstract
Serum biliverdin has been found to be very high in patients with paracetamol-induced hepatic necrosis who die but only slightly raised in those who survive. The rise in nontoxic biliverdin is proportionately greater than that of potentially toxic bilirubin. Studies using rats show that paracetamol or galactosamine induced necrosis or long-standing biliary obstruction cause a reduction in biliverdin reductase activity in the liver. In man, biliverdin accumulation in obstructive jaundice is proportional to the accumulation of bilirubin and this might be accounted for by the accompanying increase in bile acids which impair the reductase activity.
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