Search

Five and half years male child with one day history of pain abdomen and vomiting who was on aspirin for suspected rheumatoid arthritis presented initially with acute gastritis. Next day, however he developed the signs of encephalopathy with altered liver function.

The authors report two cases of Puttman Reye syndrome: one, classical, involving a young child with a fatal encephalopathy with visceral fatty infiltration, the other, less typical, not showing any signs of visceral fatty degeneration. Both cases were subjected to complete anatomical examination of the brain, revealing marked cerebral oedema, in localised areas or in a laminar distribution, with degenerative changes in the neurones and slight demyelinisation. The authors, on the basis both on the classical appearances of the first case as well as the atypical features of the second, envisage a clinical, anatomical and biological link between the Puttman-Reye syndrome,. Thai encephalopathy and Ekiri, which they consider to represent a single entity.

Patients with Reye's syndrome (RS) whose degree of severity was classified as stage 0 (alert and awake) were compared with patients with a severity classification of stage 1 or greater. The Centers for Disease Control case definition and staging criteria were used. Two hundred twenty-seven patients with RS were investigated by the Ohio Department of Health from Dec 1, 1978, through March 31, 1980. There were 67 identified patients who never exceeded stage 0 and 160 patients classified as stage 1 or greater. Both groups of patients were compared according to demographic features, symptomatology, medication use during the antecedent illness, and laboratory findings during the RS illness. Stage 0 patients were similar to patients at stage 1 or greater in their demographic features, illnesses, medications preceding RS, and results of liver function tests; however, values of serum ammonia, creatine phosphokinase, prothrombin time, and bilirubin increased with RS severity.

Mitochondrial alterations are known to be constantly associated with Reye's syndrome. Fifty-eight liver specimens from 50 patients who fulfilled the clinical and pathologic criteria were examined by electron microscopy. The degree of mitochondrial injury was graded I, II, and III according to the severity of the alteration of mitochondrial matrix. The results correlated well with clinical parameters--specifically initial clinical stage, peak clinical stage, and clinical outcome. Electron microscopic examination of hepatic mitochondria is therefore potentially useful in evaluating Reye's syndrome patients.