We read with interest the study on epidemic of Reye’s syndrome(1) and would like to report an interesting epidemiological correlation of the syndrome. During the months of October and November 1999, we had encountered fourteen cases of Reye’s syndrome in Bijnor, a small district of western U.P. situated around 150 km north of Delhi. The district has the dubious distinction of having reported maximum number of paralytic poliomyelitis cases in the country during the current year. Further, it had also witnessed epidemics of viral encephalitis and falciparum malaria from August to November this year. Majorities of the cases of both diseases were confined to the villages and towns situated in and around ‘Kho River’, a large pool of stagnant water, known for high density of mosquito population. The exact etiology of the cases of viral encephalitis could not be established owing to non availability of facilities of viral isolation and serological testing. Though the occurrence of Japanese encephalitis in the region is not common, the environmental factors strongly favor its presence in the community. Interestingly, twelve (86%) out of fourteen children with Reye’s syndrome belonged to the same geographic area which harbored the above-mentioned epidemics.

In our series of fourteen cases of ‘Reye’s syndrome’, the diseased children were from two to fourteen years old and most had rural background. Both the sexes were equally affected. In one case, the older sib had also died of similar illness three days earlier. One child had history of jaundice with unconsciousness two years back. None of the children was given aspirin or any other medicine containing salicylates.

The following clinical criteria were used to diagnose cases of ‘Reye’s syndrome’: (i) Rapid onset of unconsciousness after a short history of fever and vomiting; (ii) Absence of significant fever and jaundice at the time of presentation; (iii) Four to six folds rise in liver enzyme levels (100%), and low serum glucose levels (79%); (iv) Normal cerebrospinal fluid examination; and (v) Absence of malaria parasite from peripheral blood smear examina-tion. Liver biopsy could not be performed due to deranged coagulation profile, and low general condition of the cases. Six (43%) out of fourteen children expired, two (14.3%) recovered and rest (43%) were referred to higher centers. Unlike the study from Chandigarh(1), DDT in place of Malathion is usually used as an anti-mosquito measure in this region.

Reye’s syndrome is an encephalopathy of uncertain etiology. A number of diseases may present a clinical picture resembling Reye’s syndrome. Various viral infections like vari-cella, measles, influenza A and B, adenoviruses have been implicated as cofactors in the pathogenesis of the syndrome(2). The presence of all the three illnesses in the same geographic area, which harbors a high density of mosqui-toes, points to some interesting causative mechanism in the evolution of ‘Reye’s syndrome’. Since the vectors of both falciparum malaria and Japanese encephalitis virus are mosquitoes, can a micro-organism (probably a viral agent), transmitted by a vector (mosquito) be responsidble for priming of liver which later on ingestion of certain drugs (salicylates or other agents) trigger events that lead to the development of full blown features of ‘Reye’s syndrome’? We need more epidemiological studies to confirm this association apart from identifying the exact arthropod borne pathogen.

Vipin M. Vashishtha,
Mangla Hospital, Shakti Chowk,
Bijnor 246 701, India.
E-mail: [email protected]

J.P. Sharma,
District Hospital
Bijnor 246 701, India.

References

1. Ghosh D, Dhadwal D, Aggarwal A, Mitra S, Garg SK, Kumar R et al. Investigation of an epidemic of Reye’s syndrome in Northern Region of India. Indian Pediatr 1999; 36: 1097-1106.

2. Balistreri WF. Reye syndrome and "Reye-like" diseases. In: Nelson Textbook of Pediatrics, 15th edn. Eds. Behrman Re, Kliegman RM, Arwin AM. Philadelphia, W.B. Saunders, 1996; pp 1144-1145.