Vitamin A deficiency: night blindness and xerophthalmia

Vitamin A deficiency: night blindness and xerophthalmia

Worldwide, vitamin A deficiency is a major public health problem and the most important preventable cause of blindness; the WHO estimates that some 256 million children under 5 years old show subclinical deficiency and 2.7 million have xerophthalmia.

The earliest signs of clinical deficiency are associ-ated with vision. Initially, there is a loss of sensitivity to green light; this is followed by impairment of the ability to adapt to dim light, then an inability to see at all in dim light: night blindness. More prolonged or severe deficiency leads to the condition called xerophthalmia: keratinization of the cornea, followed by ulceration – irreversible damage to the eye that causes blindness. At the same time there are changes in the skin, with excessive formation of keratinized tissue.

Vitamin A also plays an important role in the dif-ferentiation of immune system cells, and mild defi-ciency, not severe enough to cause any disturbance of vision, leads to increased susceptibility to a variety of infectious diseases. At the same time, the synthesis of RBP is reduced in response to infection (it is a nega-tive acute-phase protein), so that there is a reduction in the circulating concentration of the vitamin, and hence further impairment of immune responses.

Signs of vitamin A deficiency also occur in protein– energy malnutrition, regardless of whether or not the intake of vitamin A is adequate. This is due to impair-ment of the synthesis of plasma RBP; functional vitamin A deficiency can occur secondary to protein– energy malnutrition; even if liver reserves of the vitamin are adequate, it cannot be mobilized.