Xerophthalmia and vitamin A status

The existence of 'fat-soluble A' has been known for over 80 years. But until recently clinicians were almost wholly absorbed by the ocular changes accompanying deficiency (xerophthalmia), and scientists with the vitamin's metabolic role in the rhodopsin cycle. The past two decades have witnessed a revolution in clinical and scientific concerns. Xerophthalmia is now recognized as a late manifestation of severe deficiency rather than of early, mild deficiency; as the mechanism responsible for half or more of all measles-associated blindness; and as the cause of half a million or more cases of pediatric blindness worldwide. Milder deficiency increases the severity of infectious morbidity, exacerbates iron deficiency anemia, retards growth, and is responsible for one to three million childhood deaths each year. Scientists are now busy unraveling vitamin A-dependent gene regulation to explain the myriad manifestations accompanying deficiency, while clinicians are designing and supervising programs to improve vitamin A status in over 60 countries, up from only three countries two decades ago. Control of vitamin A deficiency is now a major health challenge and goal of both UNICEF and the World Health Organization (WHO). Reaching that goal requires better parameters for assessing vitamin A status, increased understanding of metabolic pathways responsible for corneal dissolution (keratomalacia) and the molecular and cellular basis by which vitamin A status mediates resistance to infection. These issues are detailed elsewhere.