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Reye's Syndrome 118 TIlE NATIONAL MEDICAL JOURNAL OF INDIA VOL. 4, NO.3 production of insulin-like growth factor I (IGF I) mRNA in administration of corticoids: A new and peculiar stimulus of growth hypophysectomized rats and reduces IGF 1 mRNA abundance in hormone secretion in man. J c/in Endocrinol Metab 1990;70:234-7. intact rats. Endocrinology 1989;125:165-71. 22 Freidman M. Strang LB. Effect of long-term corticosteroids and 13 Gourmelen M. Girard F. Binoux M. Serum somatomedin/insulin- corticotrophin on the growth of children. Lancet 1966;1:568-72. like growth factor (IGF) and IGF carrier levels in patients with 23 Norman AP. Sanders S. Effect of corticotrophin on skeletal matura- Cushing's syndrome or receiving glucocorticoid therapy. J C/in tion and linear growth in six patients with severe asthma. Lancet Endocrinol Metab 1982;54:885-92. 1969;1:287-9. 14 Unterman TG. Phillips LS. Glucocorticoid effects on somatomedins 24 Brown DCP. Savacool AM. Letizia CM. A retrospective review of and somatomedin inhibitors. J Clin Endocrinol Metab 1985; the effects of one year of triamcinolone acetonide aerosol treatment 61:618-26. on the growth patterns of asthmatic children. Ann Allergy 1989; 15 Hyams JS. Carey DE. Corticosteroids and growth. J Pediatr 63:47-51. 1988;113:249-54. 25 Littlewood JM. Johnson AW. Edwards PA. Littlewood AE. 16 Hyams JS. Carey DE. Leichtner AM, Goldberg BD. Type I pro- Growth retardation in asthmatic children treated with inhaled collagen as a biochemical marker of growth in children with beclomethasone dipropionate. Lancet 1988;1:115-16. inflammatory bowel disease. J Pediatr 1986;109:619-24. 26 Balfour-Lynn L. Growth retardation in asthmatic children treated 17 Giustina A. Romanelli G. Candrina R. Giustina G. Growth hormone with inhaled beclomethasone dipropionate. Lancet 1988;1:476. deficiency in patients with idiopathic adrenocorticotropin deficiency 27 Moell C. Aronson AS. Selvik G. Growth in rabbits during alternate- resolves during glucocorticoid replacement. J c/in Endocrinol day cortisone injections: Near normal growth on days without Metab Il)Xl);68:120-4. cortisone. Acta Pediatr Scand 1988;77:69:>-8. 18 Nakagawa K. Ishizuka T. Obara T. Matoubara M. Akikawa K. 28 Elders MJ. Wingfield BS. McNatt ML. Clarke 1S. Hughes ER. Dichotomic action of glucocorticoids on growth hormone secretion. Glucocorticoid therapy in children. Effect on somatomedin secretion. Acta Endocrino/ll)87;116:165-71. Am J Dis Child 1975;129:139>-6. 19 Wehrenberg WB. Baird A. Ling N. Potent interaction between 29 Sturge RA. Beardwell C. Hartog M. Wright D. Ansell BM. Cortisol glucocorticoids and growth hormone-releasing factor in vivo. and growth hormone secretion in relation to linear growth. Patients Science 1l)83;111:556--8. with Still's disease on different therapeutic regimens. Br Med J 20 Casanueva FF. Burguera B. Tome MA. et al. Depending on the 1970;3:547-51. time of administration. dexamethasone potentiates or blocks 30 Rudman D. Freides D. Patterson 1H. et al. Diurnal variation in the growth hormone-releasing hormone-induced growth hormone responsiveness of human subjects to human growth hormone. J c/in release in man. Neuroendocrinology 1988;47:46-9. InvestI973;Sl:912-18. 21 Casanueva FF. Burguera B. Muruais C. Dieguez C. Acute Reye's Syndrome S. M. MEHENDALE, K. BANERJEE INTRODUCTION developed countries," its severity has remained In April 1963, Anderson! described a few fatal cases of unexplored in developing countries such as India. childhood encephalopathy in Australia, with post-mortem evidence of swollen brains and fatty liver. A few months EPIDEMIOLOGY later, Reye- encountered cases with similar pathological Reye's syndrome has a worldwide distribution." However, features but who also had raised blood transaminases, a data on the incidence are poor and diagnosis depends very reduced prothrombin time and diminished sugar levels in much on being aware of the disease and searching for it the serum and the cerebrospinal fluid (CSF). In the USA, diligently." It has been described to be a rural and Johnson? described similar cases during the influenza B semi-urban disease," and hence, even in the absence of outbreaks in October 1963. These three reports gave birth supporting data, would be expected to be a major problem to a new clinical entity-' Reye's syndrome'." in the Third World. Reye's syndrome (RS) is an acute, rare and serious In India, cases were first reported in 1969 from multi-system disease which often follows a mild and un- almost all parts of the country except the Eastern remarkable illness.! Although it has been documented region. It has been estimated that as many as 12000 to to be a major cause of neurological death in children in 18000 cases occur in India every year. 9 Sporadic cases have been reported from Vellore, Chandigarh, Bangalore, Bombay and Delhi. 10 However, it is possible that some National Institute of Virology, 20-A Dr Ambedkar Road, cases are misdiagnosed to have acute encephalopathy or Post Box No. 11, Pune 411001, Maharashtra, India heat stroke." S. M. MEHENDALE, K. BANERJEE Two distinct epidemiological patterns of RS have been Correspondence to K. BANERJEE described. It occurs in an epidemic form during or just © The National Medical Journal of India 1991 MEHENDALE, BANERJEE: REU:'S SYNDROME 119 after influenza epidemics and as sporadic cases, probably (CMV), Epstein-Barr virus (EBV), mumps, Coxsackie A in relation to chickenpox or other viral diseases. 7 Therefore, and B, dengue, herpes simplex, respiratory syncytial although cases occur throughout the year, the greatest virus, parainfluenza, rubella, polio and echoviruses have number of cases are seen from December to March, coin- been reported to be associated with RS. Dual viral infec- ciding with peak influenza activity. 12In India, cases have tions are also thought to be important in its causation.' been reported mainly during the summer and in the early monsoon months." Exogenous medication In the USA, a nationwide surveillance was initiated in Four case-control studies conducted between 1980 and 1973 by the Centres for Disease Control (CDC), Atlanta, 1982 in the USA demonstrated an association between RS Georgia and since 1976 there has been a continuous and aspirin consumption during an antecedent illness." ongoing surveillance. 12Up to 1980, approximately 250 to Simultaneous studies in the UK also led the 'Committee 500 cases were reported annually. Since 1981, there has on Safety of Medicines' to corroborate the fact that such been a noticeable fall in the cases reported with 36 cases an association existed." However, most of these studies in 1987 and only 20 cases in 1988. \3 However, it is possible were retrospective and serious objections have been that the estimate is faulty" because reporting of cases is raised about the validity of their conclusions in view of not compulsory, non-fatal cases are likely to be under- their information, selection and confounding biases. diagnosed and certain inborn errors of metabolism are Subsequently a task force was set up which planned and erroneously included. In the UK, the surveillance was executed a pilot study and then the main study, after care- initiated in 1981.15 The annual incidence of RS in the USA ful elimination of errors in the earlier study design. 23The is estimated to be 0.37 to 0.71 cases per 100000 persons association between RS and aspirin was established; but below 18 years of age." It is slightly higher in the UK and its causality was not confirmed. Australia (0.4 to 0.5), and this is 10 times higher than in Salicylates (mainly aspirin), acetaminophen and other European countries suchas Germany." anti-emetics have been incriminated in the causation of Reye's syndrome affects children of all ages with a peak RS.24.25Lovejoy reported a higher mortality in cases of RS between 5 and 15 years." However, since 1980 there has who had consumed higher aspirin doses. Similar conclu- been a decline in cases among children between 5 and sions were reached by Starco and in Ohio and Michigan.' 10 years of age 18although the incidence among children Although the first conclusive evidence of the RS-aspirin below 5 years and children aged 10 to 19 years has been association was provided in 1980, definite action was relatively stable.'? Instances of RS among neonates have taken by the Food and Drugs Administration (FDA) in been rarely reported and diagnosis in adults is based the USA only in 1986. It advised that the drug should mostly on post-mortem examination. carry a 'package label warning'. 26Earlier, in 1980, the US The incidence of RS among females is marginally Surgeon General had merely advised doctors and parents higher-? than in males. Whites are more prone than blacks against the use of aspirin in viral fevers, especially, except among infants in whom the relative risk in blacks influenza and chickenpox? as against whites is 8: 1. Only a population-based prospective study can define the risk of RS attributable to salicylate use; however, AETIOLOGY aspirin should preferably be avoided in the treatment of The aetiology appears to be multifactorial and is not viral fevers. 28 yet fully known. It is probably the result of virus-host interaction influenced by an exogenous agent in a suscep- Genetic predisposition tible individual with the end result being a metabolic Many instances occurred in which families had more than derangement manifesting clinically as RS.15 one member who had RS. Some reports suggested that The following factors are thought to playa role in its metabolic differences existed between the members of causation. such families compared with others. Certain genetic inborn errors of metabolism such as disorders of Antecedent viral infections ureagenesis, branched chain amino acid metabolism and Many viruses have been incriminated, the most common ketogenesis also have clinical and laboratory abnor- being influenza types A and B, and the varicella-zoster malities similar to those of RS.
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