The letter from Drs. Benakappa and Benakappa is interesting and important. They had admitted 269 cases of acute encephalo-pathy during 3 months in 1986, of which at least 124 were diagnosed as Reye’s syndrome. This illustrates the high incidence of Reye’s syndrome in one region at one period of time. Would it be wrong to call it an outbreak? For a spurt in incidence there must have been some common factor, such as a preceding infection or exposure to a toxin. Unfortunately, research to investigate such causative factors are seldom undertaken partly because our institutions are by and large not well equipped for such research and partly because the very diagnosis is often contested and the opportunity for such targeted research is often lost. If Drs Benakappa and Benakappa could do liver biopsies on 104 children with acute encephalopathy, others who see large numbers of cases should be encouraged and emboldened to do liver biopsies on at least a small proportion of cases to confirm or exclude Reye’s syndrome by examining the tissue for microvescicular fat in hepatocytes. The spurt in incidence is unpredictable and often nonrecurring in the same place. If IAP can tie up with the Indian Council of Medical Research, a research protocol can be developed and it may then be applied anywhere when the incidence of Reye’s syndrome is found to be of outbreak proportions. Research is also needed to investigate the cases of encephalopathy not diagnosed as Reye’s syndrome. It will be worthwhile for IAP to develop consensus on diagnostic criteria and treatment modalities for acute encephalopathy syndromes includ-ing Reye’s syndrome. Early detection of cerebral edema and its rapid treatment can drastically reduce case fatality.

T. Jacob John,
439, Civil Supplies Godown Lane,
Kamalakshipuram,
Vellore, TN, 632 002
E - Mail: [email protected]