Deficiencies due to inadequate intake are commonly seen in the developing countries accompanying PEM. This is not, however, invariable, e.g. vitamin A deficiency is never seen in Jamaica, but is common in PEM in Hyderabad. In the Western World, deficiency of vitamins is rare except in the specific groups shown. The widespread use of vitamins as ‘tonics’ is unnecessary and should be discouraged. Toxicity from excess fat-soluble vitamins is occasionally seen. Fat-soluble vitamins


Vitamin A (retinol) is found in dairy products, liver and fish, but is also formed in the intestinal wall from its precursor f3-carotene found in green leafy vegetables. This is the main source.

Vitamin A deficiency

Since vitamin A is absorbed in a similar way to all lipids, deficiency can be seen in all chronic conditions where there is fat malabsorption. Nevertheless, the clinical features of vitamin A deficiency are rare in most of these malabsorptive conditions. They are normally only seen associated with severe PEM and other multiple deficiencies in developing countries. As a result of multiple deficiencies being present, it is not always clear which nutrient deficiency is responsible for anyone clinical syndrome.


The clinical features of vitamin A deficiency are impaired dark adaptation followed by night blindness. Later, dryness of the conjunctiva and the cornea (xerophthalmia) occurs as a result of keratinization. Bitot’s spots-white plaques of keratinized epithelial cells-are found on the conjunctiva of young children with vitamin A deficiency. These spots can, however, be seen without vitamin A deficiency, possibly due to exposure. Corneal ulceration and dissolution keratomalacia eventually occur; superimposed infection is a frequent accompaniment. Both may lead to blindness. Vitamin A deficiency is a common cause of blindness in developing countries, affecting 250000 children per year. Follicular hyperkeratosis, in which there is thickening and dryness of the skin, is also seen with vitamin A deficiency. It is also sometimes seen without vitamin A deficiency.

Fat-soluble and water-soluble vitamins-reference nutrient intake (RNI) and lower reference nutrient intake (LRNI).
Fat-soluble and water-soluble vitamins-reference nutrient intake (RNI) and lower reference nutrient intake (LRNI).
Some causes of vitamin deficiency in the Western World.
Some causes of vitamin deficiency in the Western


In parts of the world where the deficiency is common, diagnosis is made on the basis of the clinical features and deficiency should always be suspected if any degree of malnutrition is present. Blood levels of vitamin A will usually be low, but the best guide to the diagnosis is a response to replacement therapy.


Urgent treatment with retinol palmitate 50 000 i.u. orally should be given on two successive days. In the presence of vomiting and diarrhoea, vitamin A 50000 i.u. i.m. is given. Associated malnutrition must be treated and superadded bacterial infection should be treated with antibiotics. Referral for specialist ophthalmic treatment is necessary in severe cases.


Most Western diets contain enough dairy products and green vegetables but vitamin A is added to foodstuffs, e.g. margarine, in some countries. Vitamin A is not destroyed by cooking. Education of the population is important; in particular, pregnant women and children should be encouraged to eat green vegetables. Vitamin A, but not {3-carotene, in excess is teratogenic and can possibly cause liver and eNS damage.


Vitamin K is present in many plant foods as phylloquinone (vitamin K,). Intestinal bacteria can synthesize menaquinone (vitamin K2), which may make up an important component of daily requirements. Synthesized vitamin K or that derived from the diet (leafy vegetables) is absorbed in a similar manner to other fat-soluble substances and therefore deficiency occurs with malabsorption of fat. Deficiency is most commonly seen in biliary obstruction, when no bile salts are available to facilitate absorption. Antibacterial drugs also interfere with bacterial synthesis of vitamin K.
Vitamin K is a cofactor necessary for the synthesis of clotting factors (see p. 238) and deficiency will increase the prothrombin time. Vitamin K injection (phytomenadione 10 mg i.m.) is effective treatment for vitamin K malabsorption. (NB An increased prothrombin time due to liver disease does not respond to vitamin K, there being no shortage of vitamin K, just poor liver function.) Phytomenadione (1 mg) was always given to all newborn babies but in the UK this practice is not now universal.


Vitamin E occurs mainly in vegetable oils but is also found in fish. Its role in human nutrition is uncertain but severe deficiency leads to anaemia, haemolysis and muscle disorders as well as central nervous lesions. Deficiency is only seen in patients who are virtually unable to absorb any fat or fat-soluble vitamins, e.g. in biliary atresia. In children with abetalipoproteinaemia the severe neurological deficit (gross ataxia) can be prevented by vitamin E injection. Large doses may prevent coronary artery disease.

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