Thiamine deficiency in exclusive breastfed infants with encephalopathy attending Govind Ballabh Panth children hospital, Srinagar
DOI:
https://doi.org/10.18203/2349-3291.ijcp20230736Keywords:
Thiamine levels, Breastfed infants, Shock, Encephalopathy, Metabolic acidosisAbstract
Background: Thiamine deficiency (TD) has historically affected countries and populations consuming milled white rice. TD in infants can have an acute presentation of encephalopathy with shock with severe metabolic acidosis and death sometimes, if not promptly treated with an intravenous dose of thiamine. Aim was to study the biochemical deficiency of thiamine in exclusively breastfed infants presenting with encephalopathy and compare them with age-matched controls and to study their clinical course and short-term outcome (till discharge).
Methods: After dividing infants into four groups based on age in days: (31-60 days; 13 in cases and 8 in controls; 61-90; 4 in cases and 3 in controls; 91-120 days; 2 in cases and none in controls; and >120 days 4 each in cases and controls. This study primarily included the selection of case/control subjects. Two case-control analyses were conducted. In the first one, blood thiamine levels were compared between infants with encephalopathy and without encephalopathy. In the second one, breast milk thiamine levels were compared between infants with encephalopathy and without encephalopathy. Student's independent t test was used for statistical analysis.
Results: Out of 38 infants, 23 had presented with encephalopathy, and 15 were healthy taken as controls. The mean blood levels of thiamine in infants with encephalopathy in cases were 17.29 nmol/l with a standard deviation of 8.86: the levels ranged between 13.47 and 21.13. The mean value of controls was 51.31, with a standard deviation of 25.52 ranging between 23.25 and 124.7. The p<0.001 and was considered statistically significant. The ROC analysis of the data obtained from thiamine levels obtained in the study 'patient's blood compared with the control group.
Conclusions: TD can be clinically and biochemically attributed to presentation of infants with acute encephalopathy.
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