Vitamin cornea

On a vitamin A-deficient diet, mucus-secreting tissues become keratinized. This condition tends to occur in the trachea, the skin, the saUvary glands, the cornea, and the testes. When this occurs in the cornea, it can be followed by blindness. Vitamin A deficiency is the principal cause of blindness in the very young. This problem is particularly acute in the third world (8). 

Injury (either physical or chemical) to the comeal endothelial cells has a marked efiect on occular function as these cells are responsible for maintaining the thickness and clarity of the cornea, yet they cannot be replaced if damaged. Immunohistochemical studies have revealed that enzymatic antioxidant defences, SOD, CAT and GSHPx, are similarly distributed in the corneal epithelium and endothelium (Rao etal., 1985 Attala et d., 1987, 1988). Other antioxidants include ascorbate, carotenoids and vitamin E (Fleath, 1962). 

A deficiency of vitamin A results in night blindness. A chronic deficiency results in a thickening of membranes in the cornea which, if untreated, can lead to blindness through perforation of the cornea and loss of the lens. It is estimated that half a million children develop blindness due to vitamin A deficiency every year. Refeeding malnourished children can produce a deficiency of vitamin A (see below). 

Riboflavin (vitamin B2) is found in liver, milk, meat, green vegetables, cereals and mushrooms. It is active in the form of two coenzymes, flavin mononucleotide and flavin adenine dinucleotide. As a coenzyme for proton transfer in the respiratory chain it is indispensable for energy-release from carbohydrates, lipids and proteins. Riboflavin deficiency only occurs in combination with deficiencies of other members of the vitamin B family. The symptoms of such deficiency consist of angular stomatitis, lesions of the cornea, dermatoses and normochromic normocytic anaemia. 

Avitaminosis A results in the loss of night vision nyctalopia). Furthermore, the removal of vitamin A from the diet causes the cornea of the eye to dry out xerophthalmia). However, excessive intake of vitamin A can result in severe and even fatal toxicity. 

Substances that guarantee the chemical and mechanical stability of the cornea are mostly collagen type I and X that are mainly made of proline and hydroxy-proline. Other substances that are present in a considerable amount are proteins (pK between 5.3 and 9), vitamin C (pK = 4.2), bicarbonate, glutathione, and lactate. (For more details about pK refer to Chap. 3, Sect. 3.2.4.1)... 

All tissues are retinoid targets, as all cell types have at least one form of nuclear retinoid receptor. In adults, the most significant targets include cornea, skin, epithelia of the lungs and trachea, and the immune system. RA regulates the synthesis of proteins essential for growth or differentiation. Excessive vitamin A can cause birth defects, and pregnant women are advised not to use the retinoid creams that have been developed for treatment of severe acne. 

Impotence Night blindness Retardation of growth Xerophthalmia Increased visuel threshold Dryness of cornea Yes FAT-SOLUBLE p-Carotene not acutely toxic, but supplementation is hot recommended Excess vitamin A can increase incidence of fractures... 

Other vitamins, including B12, have also been included in artificial tear formulations. NutraTear (Aqueous Pharma) contains vitamin B12, but the effects of this nutrient have not been well documented. B12, which is needed for normal cell growth, cannot be synthesized by the body. It may protect the eye from oxidative free radicals and has been found to increase the healing rate of denuded epithelium in rabbit cornea. Controlled clinical studies regarding the clinical efficacy of this and other nutrient products in patients with OSD are presently lacking. 

An analogue of vitamin A, isotretinoin (Accutane), or 13-c/s-retinoic acid, is used for control of severe recalcitrant cystic acne and other keratinizing dermatoses (also see Isotretinoin under Drugs Affecting the Cornea and Lens, above). 

DEFICIENCY Vitamin A deficiency results in night blindness and xerophthalmia (dry cornea and conjunctiva, sometimes with ulceration of the cornea). Nonocular changes may also occur dry skin and mucous membranes. Deficiency may result from poor dietary intake, or poor absorption, as from bowel disease, or a defect in bile flow that causes fet malabsorption. Poor protein intake may result in a reduced level of the transport protein that carries vitamin A in the blood stream. 

Band keratopathy has been reported in patients taking vitamin D (23), as have calcium deposits in the cornea and the conjunctiva (24). 

Vitamin A deficiency occurs with the chronic consumption of a vitamin A-deficient diet or during a prolonged starvation. The first symptom is nightblindness. This is followed by damage to the cornea. The nightblindness is reversible, but comeal... 

Severe riboflavin deficiency is known as ariboflavinosis. Its major symptoms include cheilosis,. seborrheic dermatitis, and vascularization of the cornea. Ariboflavinosis occurs in chronic alcoholism in combination with other vitamin deficiencies. It has also resulted from phenothiazine, tricyclic antidepressant, and probenecid therapy. Riboflavin has no pharmacological action and is relatively nontoxic. The only approved indication is in the treatment and prevention of ariboflavinosis. 

Two retinoids, retinoic acid and retinal, appear to have most of the biochemical functions attributed to vitamin A Retinoic acid is required for cell differentiation and is the ligand for two families of nuclear receptors, RAR . y and RXR 0 y. These receptors are part of a family of superreceptors that include the steroid hormones and cholecalciferol. Vitamin A deficiency can lead to a variety of symptoms depending on the age of the deficient person. The most serious syndrome is keratomalacia, which results in desiccation, ulceration, and xerophthalmia of the cornea and conjunctiva. It is one of the leading causes of blindness in infants and children. 

Nutritional vitamin A deficiency causes xerophthalmia, a progressive disease characterized by night blindness, xerosis (dryness), and keratomalacia (comeal thinning), which may lead to perforation xerophthalmia may be reversed with vitamin A therapy. However, rapid, irreversible blindness ensues once the cornea perforates. Vitamin A also is involved in epithelial differentiation and may have some role in corneal epithelial wound healing. There is no evidence to support using topical vitamin A for keratoconjunctivitis sicca in the absence of a nutritional deficiency. 

Among the changes attributed to vitamin A deficiency, only those affecting the eye can be related to vitamin A deficiency without hesitation. In the eye, the vitamin A deficiency leads to a decrease in the amount of pigment in the rods and cones of the retina, causing nyctalopia, or night blindness, and alterations of the epithelia, cornea, and conjunctiva. 

Interesting observations have been made on the corneas of vitamin A-deficient mice. The corneas contain mitochondria that in vitamin A carency become progressively loaded with electron-dense material. 

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