Vitamin A deficiency can result from inadequate intake, fat malabsorption, or liver disorders. Deficiency impairs immunity and hematopoiesis and causes rashes and typical ocular effects (eg, xerophthalmia, night blindness). Diagnosis is based on typical ocular findings and low vitamin A
Vitamin A is required for the formation of rhodopsin, a photoreceptor pigment in the retina (see table Sources, Functions, and Effects of Vitamins). Vitamin A helps maintain epithelial tissues and is important for lysosome stability and glycoprotein synthesis.
Dietary sources of preformed vitamin A include fish liver oils, liver, egg yolks, butter, and vitamin A–fortified dairy products. Beta-carotene and other provitamin carotenoids, contained in green leafy and yellow vegetables, carrots, and deep- or bright-colored fruits, are converted to vitamin A. Carotenoids are absorbed better from vegetables when they are cooked or homogenized and served with some fat (eg, oils). Normally, the liver stores 80 to 90% of the body’s vitamin A. To use vitamin A, the body releases it into the circulation bound to prealbumin (transthyretin) and retinol-binding protein.
Retinol activity equivalents (RAE) were developed because provitamin A carotenoids have less vitamin A activity than preformed vitamin A; 1 mcg retinol = 3.33 units.
Synthetic vitamin analogs (retinoids) are being used increasingly in dermatology. The possible protective role of beta-carotene and retinoids against some epithelial cancers is under study, but beta-carotene and retinoids are not recommended for prevention of cancer or cardiovascular disease (1). However, risk of certain cancers (eg, lung cancer) (2) and cardiovascular risk (3) may be increased after beta-carotene supplementation.
(See also Overview of Vitamins.)
References
1. Moyer VA; U.S. Preventive Services Task Force. Vitamin, mineral, and multivitamin supplements for the primary prevention of cardiovascular disease and cancer: U.S. Preventive services Task Force recommendation statement. Ann Intern Med. 2014;160(8):558-564. doi:10.7326/M14-0198
2. O'Connor EA, Evans CV, Ivlev I, et al. Vitamin and Mineral Supplements for the Primary Prevention of Cardiovascular Disease and Cancer: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2022;327(23):2334-2347. doi:10.1001/jama.2021.15650
3. Yang J, Zhang Y, Na X, Zhao A. β-Carotene Supplementation and Risk of Cardiovascular Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Nutrients. 2022;14(6):1284. Published 2022 Mar 18. doi:10.3390/nu14061284
Etiology of Vitamin A Deficiency
Primary vitamin A deficiency is usually caused by
Prolonged dietary deprivation
This deficiency is endemic in areas such as southern and eastern Asia, where rice, devoid of beta-carotene, is the staple food. Xerophthalmia due to primary deficiency is a common cause of blindness among young children in countries with high rates of food insecurity.
Secondary vitamin A deficiency may be due to
Decreased bioavailability of provitamin A carotenoids
Interference with absorption, storage, or transport of vitamin A
Interference with absorption or storage is likely in celiac disease, cystic fibrosis, pancreatic insufficiency, duodenal bypass, chronic diarrhea, bile duct obstruction, giardiasis, and cirrhosis. Vitamin A deficiency is common in prolonged protein-energy undernutrition not only because the diet is deficient but also because vitamin A storage and transport is defective.
Symptoms and Signs of Vitamin A Deficiency
Photo courtesy of the Nutrition Program via the Public Health Image Library of the Centers for Disease Control and Prevention.
Impaired dark adaptation of the eyes, which can lead to night blindness, is an early symptom of vitamin A deficiency. Xerophthalmia (which is nearly pathognomonic) results from keratinization of the eyes. It involves drying (xerosis) and thickening of the conjunctivae and corneas. Superficial foamy patches composed of epithelial debris and secretions on the exposed bulbar conjunctiva (Bitot spots) develop. In advanced deficiency, the cornea becomes hazy and can develop erosions, which can lead to its destruction (keratomalacia).
Keratinization of the skin and of the mucous membranes in the respiratory, gastrointestinal, and urinary tracts can occur. Drying, scaling, and follicular thickening of the skin and respiratory infections can result.
Immunity is generally impaired.
The younger the patient, the more severe are the effects of vitamin A deficiency. Growth retardation and infections are common among children. Mortality rate can exceed 50% in children with severe vitamin A deficiency (1).
Symptoms and signs reference
Diagnosis of Vitamin A Deficiency
Ocular findings suggest vitamin A deficiency. Dark adaptation can be impaired in other disorders (eg, zinc deficiency, retinitis pigmentosa, severe refractive errors, cataracts, diabetic retinopathy). If dark adaptation is impaired, rod scotometry and electroretinography are done to determine whether vitamin A deficiency is the cause.
Serum levels of retinol are measured. Normal range is 28 to 86 mcg/dL (1 to 3 mcmol/L). However, levels decrease only after the deficiency is advanced because the liver contains large stores of vitamin A. Also, decreased levels may result from acute infection, which causes retinol-binding protein and transthyretin (also called prealbumin) levels to decrease transiently.
Treatment of Vitamin A Deficiency
Dietary deficiency of vitamin A
Supplementation is also given to patients with measles because vitamin A deficiency is a risk factor for severe measles
≥ 12 months (including adults): 200,000 IU (60,000 mcg RAE)
6 to 11 months: 100,000 IU (30,000 mcg RAE)
< 6 months: 50,000 IU (15,000 mcg RAE)
The dose is given orally once a day for 2 days, with a third dose at least 2 weeks later.
Infants born to mothers with HIV infection should receive 50,000 IU (15,000 mcg RAE) within 48 hours of birth. Prolonged daily administration of large doses, especially to infants, must be avoided because toxicity may result (1).
For pregnant or breastfeeding women, prophylactic or therapeutic doses should not exceed 10,000 IU (3000 mcg RAE)/day to avoid possible damage to the fetus or infant.
Reference
1. Annan RA. Vitamin A supplementation and disease progression in HIV-infected adults. Accessed July 30, 2024.
Prevention of Vitamin A Deficiency
vitamin A in formula feedings.
< 6 months can be given a one-time dose of 50,000 IU (15,000 mcg RAE), and those aged 6 to 12 months can be given a one-time dose of 100,000 IU (30,000 mcg RAE).
Key Points
Vitamin A deficiency usually results from dietary deficiency, as occurs in areas where rice, devoid of beta-carotene, is the staple food, but it may result from disorders that interfere with the absorption, storage, or transport of vitamin A.
Ocular findings include impaired night vision (early), conjunctival deposits, and keratomalacia.
In children with severe deficiency, growth is slowed and risk of infection is increased.
Diagnose based on ocular findings and serum retinol levels.
