Дефіцит вітаміну К

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.

Ксерофтальмія

Зображення

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).

• Serum retinol levels, clinical evaluation, and response to vitamin A

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.

A therapeutic trial of vitamin A may help confirm the diagnosis.

• Vitamin A

Dietary deficiency of vitamin A is traditionally treated with vitamin A palmitate in oil 60,000 international units (IU) (18,000 mcg RAE) orally once a day for 2 days, followed by 4500 IU orally once a day. If vomiting or malabsorption is present or xerophthalmia is probable, intramuscular supplementation can be given.

Supplementation is also given to patients with measles because vitamin A deficiency is a risk factor for severe measles; treatment with vitamin A can shorten the duration of the disorder and may reduce the severity of symptoms and risk of death. Doses are age-based:

• ≥ 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.

The diet should include dark green leafy vegetables, deep- or bright-colored fruits (eg, papayas, oranges), carrots, and yellow vegetables (eg, squash, pumpkin). Vitamin A–fortified milk and cereals, liver, egg yolks, and fish liver oils are helpful. Carotenoids are absorbed better when consumed with some dietary fat. If milk allergy is suspected in infants, they should be given adequate vitamin A in formula feedings.

In countries with high rates of food insecurity, prophylactic supplements of vitamin A palmitate in oil 200,000 IU (60,000 mcg retinol activity equivalent [RAE]) orally every 6 months are advised for all children between 1 and 5 years of age; infants < 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).