About half of the absorbed vitamin A ingested is oxidized and excreted in the feces and urine, and the remainder is stored in the liver as retinol ester. It is released into the plasma for transportation to peripheral tissues after binding with specific protein known as retinol binding protein (RBP). Protein deficiency in severe malnutrition reduces the hepatic synthesis of RBP [15], [16] which is the likely to be the reason for low serum retinol level observed in such children [17-19]. Infectious diseases such as diarrhoea and acute lower respiratory infections including pneumonia are common in malnourished children, which worsen the vitamin A level [20]. Acute infections are also associated with acute phase response and a transient decrease in serum retinol level [21]. This is due to reduced transcription of messenger RNA for RBP, resulting in decreased release of RBP from the liver into the blood [22], [23]. It is likely that liver utilizes all of its available resources for rapid synthesis of proteins that are required for the host defense in acute infection, thereby limiting the synthesis of relatively lesser important ones such as RBP. In severe infection, the increased urinary loss of retinol contributes to the lower serum retinol concentration [24]. Thus the utilization of vitamin A in the peripheral tissue is adversely affected in systemic infections and in protein- energy malnutrition leading to development of features of vitamin A deficiency.