Vitamin A deficiency (VAD) is usually caused by:
(i) Prolonged dietary deprivation, and is endemic in areas where foods lacking in carotene are staple. An example is southern and east Asia, where rice is the main dietary component.
(ii) Secondary VAD may be caused by inadequate conversion of carotene to vitamin A, or to interference with absorption, storage, or transport of vitamin A. This may occur with conditions such as celiac disease, cystic fibrosis, and pancreatic disease.
(iii) VAD is common in protein-energy malnutrition (PEM), which retards growth and development. Transport of vitamin A from the liver to the tissues relies upon production of retinol-binding protein (RBP). In protein deficiency there is insufficient RBP synthesized by the liver, which means that less retinol enters the bloodstream and less vitamin A.

Primary vitamin A deficiency (xerophthalmia)-VAD results in blindness in 350 000 children every year.
Night Blindness-the retinal form of vitamin A is an active component of the photosensitive pigment in rods and cones. In the rods, retinal is found associated with opsin in the form of the visual pigment, rhodopsin. When exposed to light, rhodopsin is broken down into retinal and opsin, a process known as bleaching. The reformation of rhodopsin requires a fresh supply of vitamin A. Vitamin A deficiency causes incomplete reformation of rhodopsin. This leads to poor dark adaptation, also known as night blindness.
Conjunctival xerosis-drying of the conjunctiva results from damage to the secretory function of mucus membranes and proliferation of basal cells.

Bitot’s spots- occur on the bulbar conjunctiva, most commonly temporally and usually confined to the interpalpebral fissure. They are classically triangular, although in practice many shapes are found. They consist of keratinized epithelial debris which most often have a punctate granular appearance.

Corneal xerosis-early stages of corneal involvement my present as haziness and dryness of the cornea, with small erosions or punctuate superficial infiltrations. Without intervention, the keratopathy progresses to epithelial defects, stromal oedema, and keratinisation in the interpalpebral fissure. Further progression results in ulceration of partial or full thickness, with potential for bacterial infection.

Keratomalacia consists of rapid liquefactive necrosis of the cornea. The cornea becomes a gelatinous mass. In severe cases loss of the anterior chamber and extrusion of the lens may occur.

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