Dermatologic Manifestations of Vitamin A Deficiency Clinical Presentation
- Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD more...
Avitaminosis A generally accompanies states of severe malnutrition, such as kwashiorkor and marasmus, and may be suspected in individuals with an unusual susceptibility to infectious diseases, such as measles. Note the following:
Impaired vision, particularly at night: Because of the essential role of vitamin A in photoreceptor function, night blindness is the earliest and most common symptom of its deficiency.
Xerophthalmia: VAD may produce xerophthalmia. Its ocular manifestations include conjunctival and corneal xerosis (drying), keratomalacia (corneal necrosis/ulceration), nyctalopia (night blindness), and Bitot spots (conjunctival lesions).  Maternal night blindness is common during pregnancy in poor countries. Maternal night blindness during pregnancy has been associated with low birthweight, morbidity, and poor growth in South India. 
Dry, thickened skin (toad skin)
Recent history of biliopancreatic diversion bariatric surgery, with phrynoderma and ocular symptoms rarely noted [14, 15]
The most distinctive clinical features of VAD are present in the ocular system; however, numerous skin findings have also been reported.
Conjunctival xerosis is typically found on the temporal, interpalpebral, and bulbar conjunctivae. Characteristically, it is seen as a dry, granular patch that can exhibit thickening, wrinkling, loss of pigmentation, and transparency.
Bitot spots are triangular, perilimbal, gray plaques of keratinized conjunctival debris overlying an area of conjunctival xerosis.
Xerophthalmia results from instability of the precorneal tear film, which can lead to a dull corneal appearance and a superficial punctate keratopathy noted with the use of fluorescein.
Corneal ulcerations can be partial or full thickness. Keratomalacia is a full-thickness liquefactive necrosis of the cornea. Clinically, it is a sharply demarcated lesion with an opaque, grayish yellow appearance. The stroma can slough, either leaving a descemetocele or, in severe cases, causing perforation and loss of the anterior chamber.
Generalized xerosis with fine wrinkles and scales may be present.
Phrynoderma (follicular hyperkeratosis) is characterized by red-brown follicular papules that are approximately 2-6 mm in diameter, with a central keratotic spinous plug. These lesions are usually found clustered around the bony prominences of the elbows and the knees, although they may extend up the thighs and the arms.
VAD occurs where diets contain insufficient amounts of vitamin A for growth and development, physiological functions, and periods of added stress due to illness.
Avitaminosis A is often diagnosed in persons with alcoholism who are malnourished and in patients who are chronically ill with intestinal malabsorption disorders, such as sprue, bypass surgery, cystic fibrosis, pancreatitis, metastatic cancer, regional enteritis, and chronic gastroenteritis. Other patients with avitaminosis A include those with liver disease that causes abnormal or decreased storage of vitamin A. Patients receiving total parenteral nutrition can also show signs and symptoms of avitaminosis A secondary to loss of vitamin A with prolonged use.
Avitaminosis A is a problem wherever the combination of vitamin A and protein deficiency exists. In developed countries, VAD is a rare condition. However, it is a problem of enormous magnitude worldwide, particularly in the underdeveloped regions of Asia, where the diet often consists of little more than rice. Avitaminosis A is fairly well controlled in much of Latin America and the Caribbean, with the exception of Haiti, where the incidence is as high as that in some Asian countries. Some reports suggest that the prevalence of xerophthalmia in parts of Africa may be as high as that found in Southeast Asia, whereas in other areas, particularly West Africa, the prevalence is lower, mostly because the red palm oil widely used for cooking is a good source of vitamin A supplementation. In endemic countries, the disease is largely confined to lower socioeconomic groups who cannot afford vitamin A–rich foods.
Women of childbearing age are at high risk of VAD and its consequences because of increased vitamin A requirements during pregnancy and lactation. Their newborns, having been vitamin A depleted, require vitamin A supplements. Otherwise, after the initial 4-6 months of breastfeeding, the babies are likely to develop VAD.
Infections, such as measles, may precipitate a child into clinical VAD.[17, 18]
VAD can be assumed to have profound effects because vitamin A supplementation reduces child mortality and severe morbidity in underdeveloped countries. Vitamin A supplementation enhances infants' immune responses to hepatitis B vaccine.
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