کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2791569 | 1154956 | 2015 | 14 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Complications of vitamin D deficiency from the foetus to the infant: One cause, one prevention, but who's responsibility? Complications of vitamin D deficiency from the foetus to the infant: One cause, one prevention, but who's responsibility?](/preview/png/2791569.png)
Calcium and phosphorus represent building material for bones. The supplier of these bone minerals is the hormone calcitriol, which originates from vitamin D, itself made by sunshine in human skin. Requirement for bone minerals is highest during phases of rapid growth, and no one grows faster than the foetus and the infant, making them particularly vulnerable. Deprivation of calcium, whether through low calcium intake or low vitamin D, leads to serious health consequences throughout life, such as hypocalcaemic seizures, dilated cardiomyopathy, skeletal myopathy, congenital and infantile rickets, and osteomalacia. These 5 conditions are often summarised as ‘symptomatic vitamin D deficiency’, are fully reversible but also fully preventable. However, the increasing prevalence of rickets and osteomalacia, and the deaths from hypocalcaemic cardiomyopathy, demand action from global health care providers. Clarification of medical and parental responsibilities is a prerequisite to deliver successful prevention programmes. The foetus and infant have the human right to be protected against harm, and vitamin D supplementation has the same public health priority as vaccinations.
Journal: Best Practice & Research Clinical Endocrinology & Metabolism - Volume 29, Issue 3, June 2015, Pages 385–398