Vitamin A Deficiency

Synonyms: Hypovitaminosis A

Vitamin A was the first vitamin identified (McCollum, Davis, 1915) hence given the first letter in the alphabet:

• Vitamin A (retinol) is a fat soluble vitamin, present in liver, milk and eggs.
• Beta-carotene and other provitamin carotenoids occur in green leafy and orange/yellow vegetables and fruits are converted to retinal by small intestine mucosal cells, reduced to retinol, then esterified and stored in the liver (as retinyl palmitate).
• It is transferred round the body as retinol bound to retinol binding protein and prealbumin (transthyretin).
• Retinal is converted to rhodopsin (photoreceptor pigment) in the retina, and is used by other human cells to regulate gene expression and guide differentiation in a variety of other tissues.¹

Primary vitamin A deficiency

• Caused by prolonged dietary deficiency, particularly where rice is the staple food (doesn't contain carotene).
• Vitamin A deficiency occurs with protein-energy malnutrition (marasmus or kwashiorkor) mainly because of dietary deficiency (but vitamin A storage and transport are also impaired).

Secondary vitamin A deficiency

• Occurs where there are problems in converting carotene to vitamin A, or reduced absorption, storage, or transport of vitamin A.
• This occurs in coeliac disease, tropical sprue, giardiasis, cystic fibrosis and other pancreatic disease, cirrhosis, duodenal bypass surgery, and bile duct obstruction.

• Rare in the UK,² but extremely common in developing countries especially Africa, Asia and Western Pacific.
• Between 100 and 140 million children are vitamin A deficient, 250,000-500,000 of these children become blind every year, and half of these die within 12 months of losing their sight.
• In pregnant women vitamin A deficiency occurs especially in the last trimester (demand by fetus and mother is highest).³

• Pathognomonic changes occur in the eye (usually bilateral although may be of differing degrees): night blindness, dry eyes, Bitot's spots (foamy patches on the white of the eye)² and keratomalacia (thinning and ultimate ulceration of the cornea - colliquative necrosis).
  Bitot's spots are an important early sign, and can occur without clinical night blindness. If they are recognised and early Vitamin A replacement initiated complications and blindness can be prevented.
• Other less specific changes include:
  • Keratinisation of epithelia in the lung, gastrointestinal and urinary tract.
  • Increased susceptibility to infection.
  • Skin changes (follicular hyperkeratosis) are also common.

• Good animal sources of vitamin A include liver, egg yolks, whole milk, animal butter and whole small fish (with liver intact).
• Animal sources, including vitamin A in breast milk, are more bioavailable than vegetable sources, which include carrots and other orange/yellow fruits and vegetables, and dark green leafy vegetables.³

Drugs

• Oral vitamin A palmitate in oil 20,000 μg (60,000 IU) daily for 2 days and further dose after 7 to 10 days. If vomiting, then an intramuscular form is available.

• Up to the stage of corneal xerosis (X2), prompt treatment can result in full preservation of sight without residual impairment (heals completely within a few weeks).
• In the developing world, because severe degree of vitamin A deficiency is often accompanied by severe generalised malnutrition (PEM), death is the most likely outcome. Mortality in infants with severe vitamin A deficiency is up to 50%.
• Only about 40% of patients with corneal xerophthalmia are alive one year later (25% are totally blind, and the remainder partially blind).