Vitamin A Deficiency, Symptoms & Treatment

Presentation Notes on Vitamin A disorder / Diseases (Skin, Hair Loss, Night Blindness, Oral Structure & Tung) Causes, Diagnosis & Treatment Dose in India in word/ .ppt Format  

Clinical manifestation of deficiency of vitamin A :

Vitamin A deficiency may be caused by a decreased dietary intake, however, this is usually seen in very severe malnutrition. It may also occur secondary to fat malabsorption.

In the eye symptoms are progressive. The earliest sign of deficiency is a loss of sensitivity to green light, followed by impairment to adaptation to dim light, followed by night blindness. This is reversible.

More prolonged deficiency leads to xerophthalmia : keratinization of the cornea and conjunctiva and skin and blindness. If untreated, keratomalacia develops, causing corneal ulceration and formation of opaque scar tissue (cataracts); this causes irreversible blindness.

Vitamin A is intimately involved with differentiation of epithelium., and experimentally produced deficiencies have retarded epithelization, closure of wounds, the rate of collagen synthesis and the cross-linking of newly formed collagen.

In the skin, decreased epithelial cell turnover produces:
  • Thickening and dryness of skin due to hyperkeratosis
  • Impaired mucosal function
Vitamin A also has an important role in differentiation of immune system cells, and mild deficiency leads to increased susceptibility to infectious disease.

Vitamin A deficiency is rarely seen in developed countries because liver stores are sufficient to last 3-4 yrs. It is commonly found in children of developing countries, such as India and parts of South-East Asia, where about 500000 children each year are blinded as a result of vitamin A deficiency.

 Deficiencies of vitamin A during early development have been reported to induce eye defects, dental and craniofacial abnormalities such as cleft lip and palate, and abnormalities of genitourinary tract and skeletal systems.                 


Animal studies have shown vit. A to be indispensable to the proper growth and development of periodontium, teeth, salivary gland, and oral epithelium. In humans, the teeth are less sensitive to vit. A deficiency, although some studies suggest that it can exacerbate existing periodontitis. ( Dorsky 2001, Nizel 1989 )

In the periodontium : Little information is available regarding the effects of vitamin A deficiency on the oral structures in humans. Several epidemiologic studies have failed to demonstrate any relation between this vitamin and periodontal dis­ease in humans.

In experimental animals, vitamin A deficiency results in hyperkeratosis and hyperplasia of the gingiva with a tendency for increased periodontal pocket formation. The following periodontal changes have been reported in vitamin A-deficient rats: hyperplasia and hyperkeratinization of the gingival epithelium with proliferation of the junctional epithelium and retardation of gingival wound healing. In the presence of local factors, vita­min A-deficient rats develop periodontal pockets that are deeper than those in animals not deficient in vitamin A and exhibit associated epithelial hyperkeratosis.

In the teeth : In rodents, vitamin A deficiency can slow down and even completely stop the growth of the incisor teeth. Accompanying this growth retardation is a disturbance in differentiation and function of ameloblasts ; therefore, enamel formation is interfered with. This interference produces hypoplastic (incompletely developed) and chalky white incisors. Also, disorders of the labial and lingual odontoblasts occur, producing a thick, regular labial dentin with interglobular spaces and a thin, atubular lingual dentin.

Crowding of the teeth and stunting and thickening of the tooth roots can also be seen in vitamin A-deficient animals.

In the salivary glands : The atrophy of salivary glands resulting from a vitamin A deficiency will reduce salivary flow and consequently increase caries.

In the oral mucous membranes : Because vitamin A deficiency is associated with epithelial metaplasia and hyperkeratinization, it has been postulated that oral leukoplakia (thickened white patches on mucous membranes) might response to  large doses of vitamin A.

Cleft lip and palate : During early development, both a deficiency and high doses of vitamin A have been reported to induce cleft lip and palate.

Diagnosis and treatment :
It is usually on the basis of above clinical features. The following can also be measured:
  • Plasma concentration of vitamin A and retinol binding protein
  • The response to replacement therapy
Urgent treatment with vitamin A (as retinol palmitate) orally or 1M prevents blindness. If the deficiency is severe and has already caused keratomalacia, eyesight cannot be restored.

Vitamin A is also used to treat a number of skin problems, including acne, psoriasis.

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