Aspirin and Reye's syndrome. A reappraisal.

Abstract

Reye's syndrome occurs in children and is characterised by an encephalopathic illness combined with fatty degeneration of the liver. Early case reports of similar illnesses appeared in the literature (Brain et al. 1929; Johnson et al. 1963), but it was first clearly defined by Reye and his colleagues at the Royal Alexandra Hospital for Children, Sydney, Australia; of the 21 children reported, 17 died and were found to have fatty degeneration of the liver and other viscera (Reye et al. 1963). This syndrome is now known to occur after an infectious illness, typically chickenpox or influenza A or B (Sullivan-Bolyai & Corey 1981). Severe vomiting is followed by drowsiness which may progress to deep coma; there is no jaundice but the serum transaminase levels and blood ammonia are raised. In severe cases there may be hypoglycaemia and low prothrombin levels . There are microvesicular fatty changes in the liver and electron microscopy reveals mitochondrial abnormalities in hepatocytes and cerebral neurons (Partin et al. 1971). The yearly incidence of Reye's syndrome in the US has varied between 1.5 and 8.8 per million population under 18 (Centers for Disease Control 1986). Mild cases have been described and may be diagnosed at the earliest stage of vomiting, hepatic dysfunction and minimal encephalopathy following an infectious illness (Lichtenstein et al. 1983). Reported mortality has varied between 20% and 80%; it is thought that early diagnosis and prompt institution of measures designed to reduce cerebral oedema will increase the chances of survival (Hurwitz et al. 1982). The first suggestion that this illness might be linked to aspirin came in 1965 when attention was drawn to the similarity between Reye's syndrome and aspirin poisoning (Giles 1965). Other possible causative factors which have been suggested include aflatoxins (Nelson et al. 1980; Ryan et al. 1979), pesticides (Crocker & Bagnall 1981) and emulsifiers (Crocker et al. 1986).