What is clinical vitamin A deficiency?
Clinical vitamin A deficiency (VAD) is a severe condition characterized by low serum retinol levels and depleted body stores of vitamin A. The clinical stage manifests with observable symptoms, primarily affecting the eyes. Vitamin A is an essential nutrient that the body cannot produce and must be obtained from diet or supplements. Severe deficiency is indicated by serum retinol levels below 0.35 µmol/L.
Causes of clinical VAD
Clinical VAD stems from either insufficient dietary intake or problems with the body's handling of vitamin A.
- Dietary insufficiency: A lack of vitamin A-rich foods in the diet is a major cause in many regions.
- Fat malabsorption: Conditions like cystic fibrosis, chronic diarrhea, celiac disease, and certain surgeries hinder the absorption of fat-soluble vitamin A.
- Liver disorders: Liver diseases, such as cirrhosis, impair the liver's ability to store vitamin A.
- Increased demand: Groups like young children and pregnant or breastfeeding women have higher needs, increasing their risk.
- Infections: Illnesses, particularly measles and diarrhea, can deplete vitamin A reserves.
Symptoms and clinical manifestations
Symptoms are categorized as ocular (eye-related) and non-ocular, with ocular signs known collectively as xerophthalmia.
Ocular signs (Xerophthalmia)
- Night Blindness (Nyctalopia): Often the first symptom, causing difficulty seeing in low light.
- Conjunctival Xerosis: The membrane covering the eye becomes dry and thickened.
- Bitot's Spots: Foamy, whitish-gray patches appear on the conjunctiva.
- Corneal Xerosis: The cornea becomes dry and hazy.
- Keratomalacia: Severe dryness leads to corneal softening, ulceration, and potential irreversible blindness.
Non-ocular signs
- Dry, scaly skin (Phrynoderma): Skin becomes dry and rough, with potential follicular hyperkeratosis.
- Impaired immunity: Weakens the immune system, increasing susceptibility to infections.
- Delayed growth: Can stunt growth in children.
- Reproductive issues: Can contribute to infertility.
Diagnosis of clinical VAD
Diagnosis is primarily clinical, based on patient history and physical examination, especially of the eyes and skin. While serum retinol levels can be measured, they may only be low in advanced stages due to liver stores. An empirical trial with vitamin A supplements can also be diagnostic. Specialized tests for impaired dark adaptation may be used.
Comparison of ocular vitamin A deficiency stages
| Stage | Key Clinical Sign | Characteristic Description | Reversibility | Public Health Significance |
|---|---|---|---|---|
| Night Blindness (XN) | Impaired dark adaptation | Difficulty seeing in low light; earliest sign. | Fully reversible. | Indicates a mild to moderate problem in populations. |
| Bitot's Spots (X1B) | Foamy patches on conjunctiva | Keratinized growths on the conjunctiva. | Reversible, though spots may persist. | Indicates a moderate to severe problem in populations. |
| Corneal Xerosis (X2) | Dry, hazy cornea | Drying and thickening of the cornea. | Partially or fully reversible. | Indicates a severe public health problem. |
| Keratomalacia (X3A/B) | Corneal ulcers/softening | Ulceration and softening of the cornea. | May lead to irreversible blindness. | Indicates a severe public health problem with high mortality. |
Management and prevention
Management involves addressing the deficiency with appropriate strategies. These strategies can reverse night blindness and dry eyes, but may not restore vision if corneal scarring has occurred. Prevention involves dietary diversification, food fortification, and programs aimed at addressing deficiency in at-risk populations. The World Health Organization website offers more information on global efforts.
What are the key distinctions between subclinical and clinical vitamin A deficiency?
Subclinical VAD: Low serum retinol levels without visible clinical signs. Clinical VAD: Severe deficiency presenting with overt symptoms like night blindness and xerophthalmia.