Vitamin A deficiency (VAD) or hypovitaminosis A is a lack of vitamin A in blood and tissues. It is common in poorer countries, especially among children and women of reproductive age, but is rarely seen in more developed countries. Vitamin A plays a major role in phototransduction, so this deficiency impairs vision, often presenting with nyctalopia (night blindness). In more severe VAD cases, it can progress to xerophthalmia, keratomalacia, and complete blindness. Vitamin A deficiency is the leading cause of preventable childhood blindness worldwide and is a major cause of childhood mortality. Each year, approximately 250,000 to 500,000 malnourished children in the developing world go blind from a VAD, with about half of whom dying within a year of losing their sight. Addressing VAD has been a critical focus of global health initiatives, including Sustainable Development Goal 2: to end hunger, achieve food security and improved nutrition and promote sustainable agriculture. In pregnant women, VAD is associated with a high prevalence of night blindness and poor maternal health outcomes including an increased risk of maternal mortality and complications during pregnancy and lactation. VAD also affects the immune system and diminishes the body's ability to fight infections. In countries where children are not immunized, VAD is linked to higher fatality rates from infectious diseases such as measles. Even mild, subclinical deficiency can also be a problem, as it may increase children's risk of developing respiratory and diarrheal infections, decrease growth, impair bone development, and reduce their likelihood of surviving serious illnesses. Globally, VAD is estimated to affect about one-third of children under the age of five, causing an estimated 670,000 deaths in children under five annually. It is most prevalent in sub-Saharan Africa (48 percent) and South Asia (44 percent). Although VAD is well-managed in many high income nations, it remains a significant concern in resource-poor settings. Public health interventions, such as vitamin A supplementation, reached 59% of targeted children in 2022, highlighting the ongoing need for comprehensive efforts to combat VAD.
Signs and symptoms Vitamin A deficiency is the most common cause of blindness in developing countries. 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 Bitot's 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 "Imtiaz's sign".
Night blindness A process called dark adaptation typically causes an increase in photopigment amounts in response to low levels of illumination. This occurs to an enormous magnitude, increasing light sensitivity by up to 100,000 times its sensitivity in normal daylight conditions. VAD affects vision by inhibiting the production of rhodopsin, the photopigment responsible for sensing low-light situations. Rhodopsin is found in the retina and is composed of retinal (an active form of vitamin A) and opsin (a protein). Night blindness caused by VAD has been associated with the loss of goblet cells in the conjunctiva, a membrane covering the outer surface of the eye. Goblet cells are responsible for secretion of mucus, and their absence results in xerophthalmia, a condition where the eyes fail to produce tears. Dead epithelial and microbial cells accumulate on the conjunctiva and form debris that can lead to infection and possibly blindness. Decreasing night blindness requires the improvement of vitamin A status in at-risk populations. Supplements and fortification of food have been shown to be effective interventions. Supplement treatment for night blindness includes massive doses of vitamin A (200,000 IU) in the form of retinyl palmitate to be taken by mouth, which is administered two to four times a year. 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. While VAD can make measles worse, Vitamin A supplements do not prevent measles, high doses may be dangerous, and vaccines remain the most effective way to prevent the disease. The reason for the increased infection rate in vitamin A deficient individuals is that killer T-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.
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