The vitamin deficiency may be caused by poor nutrition, a lack of exposure to the sun, or malabsorption syndromes in which the intestines do not adequately absorb nutrients from foods.
Advanced Search ABSTRACT Nutritional rickets remains a public health problem in many countries, despite dramatic declines in the prevalence of the condition in many developed countries since the discoveries of vitamin D and the role of ultraviolet light in prevention.
The disease continues to be problematic among infants in many Vitamin d and nutritional rickets, especially among infants who are exclusively breast-fed, infants and children of dark-skinned immigrants living in temperate climates, infants and their mothers in the Middle East, and infants and children in many developing countries in the tropics and subtropics, such as Nigeria, Ethiopia, Yemen, and Bangladesh.
In sunny countries such as Nigeria, South Africa, and Bangladesh, such factors do not apply. Studies indicated that the disease occurs among older toddlers and children and probably is attributable to low dietary calcium intakes, which are characteristic of cereal-based diets with limited variety and little access to dairy products.
In such situations, calcium supplements alone result in healing of the bone disease. Studies among Asian children and African American toddlers suggested that low dietary calcium intakes result in increased catabolism of vitamin D and the development of vitamin D deficiency and rickets.
Dietary calcium deficiency and vitamin D deficiency represent 2 ends of the spectrum for the pathogenesis of nutritional rickets, with a combination of the 2 in the middle. Despite these developments, rickets remains a major public health problem in many developing countries 2 — 6and its prevalence is reported to be increasing in several developed countries 7 — Until recently, it was generally accepted that nutritional rickets is caused by vitamin D deficiency alone and that dietary calcium deficiency might exacerbate the disease in the presence of vitamin D deficiency but by itself is not responsible for nutritional rickets In the past 25 y, consensus regarding the pathogenesis of nutritional rickets has shifted as studies have suggested that, among older children in developing countries in particular, dietary calcium deficiency plays a pivotal role.
In this article, I review the evidence that nutritional rickets is caused by both vitamin D deficiency and dietary calcium deficiency and that the 2 combine to exacerbate the development of the disease among children.
Factors that have been shown to be important in the pathogenesis of rickets at this age include exclusive breast-feeding, maternal vitamin D deficiency, living in temperate climates, lack of sunlight exposure, and darkly pigmented skin. In the Middle East and other more-tropical climates, social and religious customs that prevent sunlight exposure appear to be important 15 — Specker et al 21 elegantly demonstrated that the vitamin D status of breast-fed infants is correlated with sunlight exposure rather than the vitamin D content of maternal breast milk.
Breast-fed infants are generally protected from vitamin D deficiency rickets during the first few months of life, because vitamin D metabolites, especially hydroxyvitamin D [25 OH D], do cross the placenta, such that neonatal 25 OH D concentrations are approximately two-thirds of maternal values Several studies from the Middle East, North America, and northern Europe have highlighted the prevalence of low circulating concentrations of 25 OH D during pregnancy 23 — Factors found to be important include increased skin pigmentation, immigration from non-European countries to countries of high latitude, limited skin exposure as a result of religious and social customs, and vegetarian diets.
Congenital rickets has been observed in such situations, although its occurrence is rare 28 — 30and neonatal hypocalcemia is more frequent among neonates born to mothers with low 25 OH D concentrations than among those born to mothers with normal vitamin D status Studies from northern Europe and North and South America have highlighted the marked seasonal fluctuations in serum 25 OH D concentrations, with values being lowest in late winter and highest in late summer or early autumn 32 — Several studies have documented spontaneous healing of radiologically evident rickets during the summer months 36 and seasonal fluctuations in serum parathyroid hormone PTH 37 and 1,dihydroxyvitamin D [1,25 OH 2D] 38 concentrations in association with changes in serum 25 OH D concentrations.
Clinical vitamin D deficiency rickets also is well recognized to have seasonal fluctuations in prevalence, with the highest prevalence being in spring and early summer The seasonal changes in 25 OH D concentrations, the lag period between the decrease in 25 OH D concentrations and the development of biochemical, radiologic, or clinical rickets, and the influence of diet on the development of rickets have made it difficult to define a clear division between vitamin D deficiency and sufficiency on the basis of serum 25 OH D concentrations.Read about vitamin D deficiency treatment, causes, symptoms, signs, diagnosis, and daily limits chart.
Depression, thyroid problems, osteoporosis, allergies, and certain cancers have been tied to vitamin D deficiency.
There are two basic types of Vitamin D or are there? A vitamer is defined as a member of a family of chemical related compounds, each with similar molecular structures and each with the ability to function as a unique vitamin. Medscape - Indication-specific dosing for Drisdol, Calciferol (vitamin D), frequency-based adverse effects, comprehensive interactions, contraindications, pregnancy & .
A number of studies have found that higher vitamin D, which the body makes using sunlight, protects against some cancers and illnesses, such as rickets, bone-thinning osteoporosis, and diabetes.
Feb 08, · Although we can find many foods in the supermarket that have been fortified with a synthetic form of vitamin D, there are only a select number of foods that naturally contain vitamin D. As long as calcium and phosphate intake is adequate, adults with osteomalacia and children with uncomplicated rickets can be cured by giving vitamin D 3 40 mcg ( IU) po once/day.
Serum 25(OH)D and 1,25(OH) 2 D begin to increase within 1 or 2 days.
Serum calcium and phosphate increase and serum alkaline phosphatase decreases within about 10 days.