Xerophthalmia corneal

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

Because of the potential teratogenic effects of high-dose vitamin A, caution must be taken in the treatment of severe vitamin A deficiency among pregnant women as well as women of reproductive age. Women of reproductive age should be treated with 200,000 IU only when they display active corneal xerophthalmia. For... 

Although rarely encountered in developed countries, vitamin A deficiency remains a global public health problem. The current World Health Organization recommendation for vitamin A treatment in children 1 year of age and older who are at risk (see Table 17-3) is one 200,000 lU oral dose every 3 to 6 months for prophylaxis, and three such doses for treatment and prevention of xerophthalmia. Animal studies (rat model) have shown some improvement in corneal epithelial fimction with topical vitamin A supplementation. In human trials, evidence is contradictory regarding the beneficial role of topical vitamin A application. The apparent mechanism is reduction of inflammatory components. 

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. 

Because of controversy regarding the specificity and sensitivity of the conjunctival changes, some investigators have based the clinical assessment of the prevalence of xerophthalmia only on the appearance of corneal signs. From the preceding discussion, it is obvious that except for a punctate keratopathy, corneal involvement is a late manifestation and would far under assess the prevalence of hypovitaminosis A, and even of xerophthalmia. 

Corneal scars may be indicative of past severe vitamin A deficiency but they may be due to other etiologies as well. When observed, a careful history must be taken for evidence of trauma rather than xerophthalmia as causative. The prevalence of scars that partially or totally obstruct vision (see Fig. 12) are associated with high mortality rates and thus underestimate the prevalence of xerophthalmia when they are used as the sole clinical indicator of hypovitaminosis A prevalence. The reason for the high mortality is likely a combination of factors associated with being blind and living under circumstances of deprivation, e.g., accidents, family neglect, and continued undemutrition and exposure. 

The best documented data on the prevalence and incidence of xerophthalmia in east Asia comes from Indonesia. A major nationwide cross-sectional ocular survey of 36,000 preschool-aged children living in 250 sample sites was conducted in the late 1970s (Sommer, 1982a). In addition, a longitudinal study of approximately 5000 rural preschool children examined every 3-4 months for 2 years was carried out. The risk of developing corneal xerophthalmia before age 5 was 2% and of noncomeal involvement was 52% (WHO, 1982). For the entire... 

Table XIV Oomen, 1971 McLaren era/., 1965a Sommer era/., 1975a, 1976). Measles, though prevalent in developed countries, is not reported to be a blinding disease in such countries. There is substantial literature that documents the association shown in Table XIV between malnutrition and xerophthalmia. A controversy has developed in the medical literature, therefore, as to whether vitamin A deficiency is the primary cause of keratomalacia, with intercurrent measles as a precipitating factor (Oomen, 1971 Sauter, 1976 Franken, 1974), or whether measles can cause blinding corneal disease in a malnourished child in the absence of vitamin A deficiency (Frederique et aL, 1969).

Apart from this, carotenoids are also important in immune system activity and intercellular communication [64, 65]. Deficiency of carotenoids results in clinical signs of conjunctiva and corneal aberrations including xerophthalmia, night blindness, and keratomalacia [66]. The increasing requirement of carotenoids in the food, cosmetic, and pharmaceutical industries makes them ideal candidates for enhancement and manipulation. The carotenoids market has reached, in 2010, an estimated US 1.2 billion, but it is expected to reach 1.4 billion in 2018, with a compound annual growth rate of 2.3 [67]. 

Children with xerophthalmia and measles should be treated immediately with oral, high-potency vitamin A (200,000 lU) according to WHO and IVACG guidelines (Table 5) and provided other supportive nutritional and medical therapy as indicated. Corneal lesions should be topically treated with a suitable antibiotic (e.g., tetracycline or chloramphenicol) to prevent bacterial infection. Corneal xerophthalmia typically improves with VA treatment within 1 week, with complete resolution within 4 weeks. 

For women of reproductive age, give 200,000111 only for corneal xerophthalmia on days 1, 2 and 14 for night biindness or Bitot s spots, give 10,000 lU per day or 25,0001U per week for >3 months. 

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