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The most common cause of osteomalacia is a deficiency of vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet. [10] The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level. [11]
Mapping of several bone diseases onto levels of vitamin D (calcidiol) in the blood [6] Normal bone vs. osteoporosis. Vitamin D deficiency is typically diagnosed by measuring the concentration of the 25-hydroxyvitamin D in the blood, which is the most accurate measure of stores of vitamin D in the body.
Maternal deficiencies may be the cause of overt bone disease from before birth and impairment of bone quality after birth. [20] [21] The primary cause of congenital rickets is vitamin D deficiency in the mother's blood. [21] Vitamin D ensures that serum phosphate and calcium levels are sufficient to facilitate the mineralization of bone. [22]
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Maternal vitamin D deficiency can cause fetal bone defects from before birth and impairment of bone quality after birth. [83] [84] Rickets typically appear between 3 and 18 months of age. [85] This condition can be caused by vitamin D, calcium or phosphorus deficiency. [86]
Vitamin deficiency is the condition of a long-term lack of a vitamin. When caused by not enough vitamin intake it is classified as a primary deficiency, whereas when due to an underlying disorder such as malabsorption it is called a secondary deficiency. An underlying disorder can have 2 main causes:
Vitamin B12 deficiency symptoms . Vitamin B12 deficiency has a few hallmark symptoms, according to doctors: Lack of energy. Mental fatigue. Nausea, vomiting, or diarrhea. Lack of appetite. Weight loss
X-linked hypophosphatemia (XLH) is an X-linked dominant form of rickets (or osteomalacia) that differs from most cases of dietary deficiency rickets in that vitamin D supplementation does not cure it. It can cause bone deformity including short stature and genu varum (bow-leggedness).