Vitamin A deficiency is an endemic nutrition problem throughout much of the developing world, especially affecting the health and survival of infants, young children, and pregnant and lactating women. These age and life-stage groups represent periods when both nutrition stress is high and diet likely to be chronically deficient in vitamin A. Approximately 127 million preschool-aged children and 7 million pregnant women are vitamin A deficient. Health consequences of vitamin A deficiency include mild to severe systemic effects on innate and acquired mechanisms of host resistance to infection and growth, increased burden of infectious morbidity, mild to severe (blinding) stages of xerophthalmia, and increased risk of mortality. These consequences are defined as vitamin A deficiency disorders (VADD). Globally, 4.4 million preschool children have xerophthalmia and 6 million mothers suffer night blindness during pregnancy. Both conditions are associated with increased risk of morbidity and mortality. While reductions of child mortality of 19-54% following vitamin A treatment have been widely reported, more recent work suggests that dosing newborns with vitamin A may, in some settings, lower infant mortality. Among women, one large trial has so far reported a > or = 40% reduction in mortality related to pregnancy with weekly, low-dose vitamin A supplementation. Epidemiologic data on vitamin A deficiency disorders can be useful in planning, designing, and targeting interventions.

https://journals.sagepub.com/doi/pdf/10.1177/15648265030244S204

Vitamin A deficiency disorders in children and women.

Impact of vitamin A on childhood mortality.

Low Retinol-Binding Protein and Vitamin D Levels Are Associated with Severe Outcomes in Children Hospitalized with Lower Respiratory Tract Infection and Respiratory Syncytial Virus or Human Metapneumovirus Detection.

Vitamin A acts in several ways related to respiratory defense mechanism^.^-^ Advanced vitamin A deficiency results in the replacement of the mucous-secreting ciliated epithelium by a squamous epithelium in the respiratory Even mild vitamin A deficiency, however, is able to alter the light-microscopic structures of the tissue and consequently increase the incidence of respiratory infection^.^.' Well-nourished but marginally vitamin A-deficient children were twice as likely to develop respiratory disease as nondeficient controls.s The underlying causes and influencing contributing conditions have been studied widely but are not completely understood. In cases of marginal vitamin A-deficiency, alimentary replenishment of the vitamin A reserves reverses metaplastic changes of the respiratory epithelium and consequently significantly reduces mortality. Metaplastic changes of the respiratory mucosa due to physical or chemical noxae, however, are not altered following moderate vitamin A supply. Experimental data show, however, that retinoic acid in high and unphysiological concentrations has a protective effect against metaplastic changes of the tracheobronchial mucosa induced by cigarette smoke condensate in uivo and in ~i tro.~'* Consequently it may be asked why metaplastic cells due to vitamin A-deficiency redifferentiate following vitamin A supply in a physiological concentration, whereas similar metaplastic cells due to chemical or physical noxae do not or only with high retinoic acid intake.

Biochemical, morphological, and functional aspects of systemic and local vitamin A deficiency in the respiratory tract.

At the World Summit for Children (New York, 1990), a resolution was passed to eliminate vitamin A and iodine deficiencies and significantly reduce iron-deficiency anemia by the year 2000. In respon...

https://journals.sagepub.com/doi/pdf/10.1177/15648265030244S208

Multiple-micronutrient fortification technology development and evaluation: from lab to market.

To estimate the role of vitamin A on ciliated cells we investigated whether ciliated cells undergo any alteration during vitamin A deficiency. The epithelia examined include the ciliated cells of the respiratory tract and the ciliated sensory cells of the inner ear, the tongue, and the olfactory cells. This part of the paper will describe the ciliated epithelium of the tracheobronchial tract and its relation to vitamin A status. During vitamin A deficiency a partial loss of ciliae can be observed before any squamous metaplasia (which usually occurs during longer lasting vitamin A deficiency) develops. The scanning electron microscopic data illustrate the altered surface of the epithelium during vitamin A deficiency better than transmission electron microscopy.

U. Niederauer

Papers

Vitamin A and ciliated cells. I. Respiratory epithelia.