There are two types of natural vitamin A, namely A1 and A2. A1 is also known as retinol, while A2 is called 3-dehydroretinol, with only half the activity of A1. Vitamin A is oxidized in the body to retinal, a derivative with special physiological functions for dark adaptation. Retinol often forms retinyl esters with fatty acids and is found in animal foods such as liver, kidney, milk, and eggs, with liver being the richest source. Plants do not contain vitamin A but contain carotenoids, which have vitamin A activity, with β-carotene being the most important. After absorption, β-carotene can be catalyzed by intestinal enzymes to produce two molecules of retinal, which are then reduced to retinol. This reaction is reversible, allowing storage in the form of alcohol or utilization in the eye as an aldehyde. β-carotene is abundant in dark green or red-yellow vegetables and fruits. Both vitamin A and β-carotene are fat-soluble, easily oxidized by air, and can be destroyed by ultraviolet light. After absorption, they are transported via lymphatic vessels and taken up and stored by the liver. The main functions of vitamin A are to maintain visual function and the integrity of cell membranes. It participates in the formation of rhodopsin in retinal rod cells, which detects dim light, and also supports the normal metabolism of skin, mucous membranes, and corneal epithelial cells. Additionally, vitamin A plays a role in maintaining normal growth, reproduction, and immune function. The daily dietary supply of vitamin A is 200 μg RE (retinol equivalents) for infants and 300–800 μg RE for children. (1 μg RE = 1 μg retinol = 6 μg β-carotene; 0.167 μg RE = 1 μg β-carotene; 0.3 μg RE = 1 IU of vitamin A).

(I) Medical History 1. Long-term history of low vitamin A, low carotenoid, and low-fat dietary intake. 2. Long-term intravenous nutrition without vitamin A supplementation. 3. History of intestinal vitamin A absorption disorders, such as chronic diarrhea, hepatobiliary, and pancreatic diseases. 4. History of diseases that increase vitamin A excretion or consumption, such as cancer, urinary tract diseases, and chronic infectious diseases. 5. History of low protein intake (which may lead to insufficient carrier proteins, resulting in decreased plasma vitamin A levels). 6. History of hypothyroidism or diabetes (may impair the conversion of carotenoids to vitamin A, leading to decreased plasma vitamin A levels). 7. Vitamin A deficiency due to zinc deficiency, preventing the body from utilizing vitamin A, etc. (II) Clinical Manifestations Ocular symptoms appear earliest. Older children may first exhibit night blindness, while infants, due to difficulty in objective assessment, may present with dry eyes, reduced tearing, photophobia, and loss of luster in the conjunctiva and cornea. Dry, soap-like patches (Bitot spots) may appear on the conjunctiva near the cornea. Disease progression can lead to corneal opacity, softening, ulceration, and ultimately perforation and blindness. Dry skin and follicular keratosis may also be observed, commonly on the extensor surfaces of the limbs, buttocks, and shoulders. Mucosal changes may predispose to respiratory infections and pyuria. (III) Diagnostic Tests 1. The most sensitive method for older children is detecting reduced dark adaptation ability. 2. Decreased plasma vitamin A levels (normal range: infants 20–50 μg/dL; children and adults 30–225 μg/dL). 3. Fresh midstream urine epithelial cell count >3/mm³, or excessive epithelial keratinocytes observed under high-power microscopy in urine sediment. 4. Microscopic examination of conjunctival or vaginal smears obtained with saline-moistened swabs may reveal keratinized epithelial cells.

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﹝Treatment﹞

(1) General Treatment: Improve diet by adding liver, kidney, eggs, dairy, and dark-colored vegetables and fruits. Treat the underlying disease. (2) Vitamin A Therapy: For mild cases, oral vitamin A supplementation at 5,000 IU/(kg·d). For severe cases—such as those with serious eye symptoms, rapid progression, or concurrent diarrhea or liver disease—administer 50,000 IU/d of vitamin A for 5 days, then reduce to 25,000 IU/d, either orally or intramuscularly, until recovery. Symptoms usually improve significantly after 2–3 injections. Night blindness may improve within hours, while skin symptoms resolve more slowly, taking about 1–2 months. Reduce the dosage appropriately after symptom improvement to avoid toxicity. (3) Eye Care: Rinse eyes with boric acid solution and apply antibiotic eye drops to prevent infection. For corneal ulcers, instill 1% atropine to dilate the pupil and prevent iris prolapse or adhesions.

bubble_chart Prevention

Children under 6 years old should be provided with foods rich in vitamin A and carotene. Premature infants should be supplemented with 700 IU/d of vitamin A (equivalent to 210 μg/d RE) early. For children over 6 years old, if their diet is diverse, vitamin A needs can generally be met. Children prone to vitamin A deficiency due to illnesses (such as measles, chronic diarrhea, or long-term infectious wasting diseases) should be promptly supplemented with 3,000–5,000 IU/d of vitamin A (equivalent to 900–1,500 μg/d RE), with timely dose reduction to avoid toxicity.