Exploration of association between litchi consumption and seasonal acute encephalopathy syndrome
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In this hospital-based surveillance and nested age-matched case-control study, authors performed laboratory investigations to assess potential infectious and non-infectious causes of acute neurological illness in children (age d”15 y) who were admitted with new-onset seizures or altered sensorium to two hospitals in Muzaffarpur, India. Age-matched controls were residents of same area who were admitted to the same hospitals for a non-neurologic illness within seven days of the date of admission of the case. Clinical specimens (blood, cerebrospinal fluid, and urine) and environmental specimens (litchi fruits) were tested for evidence of infectious pathogens, pesticides, toxic metals, and other non-infectious causes, including presence of hypoglycin A or methylenecyclopropylglycine (MCPG)–naturally occurring fruit-based toxins that cause hypoglycemia and metabolic derangement. Out of 390 patients meeting the case definition admitted to the two referral hospitals, 122 (31%) died. On admission, 204 (62%) of 327 had blood glucose concentration d”70 mg/dL. In comparison of 104 cases with 104 age-matched controls, litchi consumption (matched odds ratio [mOR] 9.6; 95% CI 3.6, 24) and absence of an evening meal (mOR 2.2; 95% CI 1.2, 4.3) in the 24 h preceding illness onset were associated with illness. The absence of an evening meal significantly modified the effect of eating litchis on illness (OR 7.8; 95% CI 3.3, 18.8 without evening meal; and OR 3.6; 95% CI 1.1, 11.1 with an evening meal). Metabolites of hypoglycin A, MCPG, or both were detected in 48 (66%) of 73 urine specimens from cases and none from 15 controls; 72 (90%) of 80 case-patient specimens had abnormal plasma acylcarnitine profiles, consistent with severe disruption of fatty acid metabolism. In 36 litchi arils tested, hypoglycin A concentrations ranged from 12.4 μg/g to 152.0 μg /g, and MCPG ranged from 44.9 μg/g to 220.0 μg/g. Authors concluded that outbreak of acute encephalopathy in Muzaffarpur was associated with both hypoglycin A and MCPG toxicity.
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