Intramuscular injections are poorly absorbed and are ineffective in delivering sufficient bioavailable vitamin A. Fortification of food with vitamin A is costly, but can be done in wheat, sugar, and milk. Households may circumvent expensive fortified food by altering dietary habits. Consumption of yellow-orange fruits and vegetables rich in carotenoids, specifically beta-carotene, provides provitamin A precursors that can prevent VAD-related night blindness. However, the conversion of carotene to retinol varies from person to person and bioavailability of carotene in food varies. Infection
Along with poor diet, infection and disease are common in many developing communities. Infection depletes vitamin A reserves which in turn make the affected individual more susceptible to further infection. Increased incidence of xerophthalmia has been observed after an outbreak of measles, with mortality correlated with severity of eye disease. In longitudinal studies of preschool children, susceptibility to disease increased substantially when severe VAD was present.The reason for the increased infection rate in vitamin A deficient individuals is that T-killer cells require the retinol metabolite retinoic acid to proliferate correctly. Retinoic acid is a ligand for nuclear retinoic acid receptors that bind the promoter regions of specific genes, thus activating transcription and stimulating T cell replication. Vitamin A deficiency will often entail deficient retinol intake, resulting in a reduced number of T-cells and lymphocytes, leading to an inadequate immune response and consequently a greater susceptibility to infections. In the presence of dietary deficiency of vitamin A, VAD and infections reciprocally aggravate each other. Causes
In addition to dietary problems, other causes of VAD are known.
As elucidated by Alfred Sommer, even mild, subclinical deficiency can also be a problem, as it may increase childrens risk of developing respiratory and diarrheal infections, decrease growth rate, slow bone development, and decrease likelihood of survival from serious illness.VAD is estimated to affect about one-third of children under the age of five around the world. It is estimated to claim the lives of 670,000 children under five annually. Around 250,000–500,000 children in developing countries become blind each year owing to VAD, with the highest prevalence in Southeast Asia and Africa. According to the World Health Organization (WHO), VAD is under control in the United States, but in developing countries, VAD is a significant concern. Globally, 65% of all children aged 6 to 59 months received two doses of vitamin A in 2013, fully protecting them against VAD (80% in the least developed countries). Signs and symptoms
The most common cause of blindness in developing countries is Vitamin A deficiency. The WHO estimated in 1995 that 13.8 million children had some degree of visual loss related to VAD. Night blindness and its worsened condition, xerophthalmia, are markers of Vitamin A deficiency, collections of keratin in the conjunctiva, known as Bitots spots, and ulceration and necrosis of cornea keratomalacia can be seen. Conjunctival epithelial defects occur around lateral aspect of the limbus in the subclinical stage of VAD. These conjunctival epithelial defects are not visible on a biomicroscope, but they take up black stain and become readily visible after instillation of kajal (surma); this is called "Imtiazs sign".