Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status.
Affected children lack the exposure to ultraviolet light necessary for the dermal synthesis of vitamin D and have a poor diet in vitamin D in which the component (high fiber and high cereal) probably contribute to the excessive breakdown of vitamin D.
Symptoms of vitamin D deficiency rickets include restlessness, lack of sleep, slow growth, a delay in crawling, sitting or walking, soft skull bones, swelling of the skull, bead-like nodules where the ribs and their cartilages join, and a delay in the closing of the skull bones.
In adults, the same disorder is called osteomalacia or adult rickets. It is to be distinguished from osteoporosis where bone mass is decreased from hypophosphatemic osteopeniaof premature infants, and from renal osteodystrophy.
The name rickets is from the Old English wrickken, to twist. The more technical medical term, rachitis, which comes from Greek, the spine , was suggested by Francis Glisson in 1650.
Vitamin D deficiency rickets occurs in underprivileged populations throughout the world. It is more common in children of Asian, African-Caribbean and Middle Eastern origin because their skin is darker and needs more sunlight to get enough vitamin D.
Women in United States usually take multivitamins and eat vitamin D dairy foods so rickets and vitamin D deficiency is less a problem than in developing countries and northern Europe.
Vitamin D deficiency and rickets
