Читать книгу The SAGE Encyclopedia of Stem Cell Research - Группа авторов - Страница 178

Rickets is a defective mineralization of bones before epiphyseal closure in humans due to deficiency of or impaired metabolism of vitamin D, phosphorus, or calcium. It is a disease of the growing bone and is unique to children and young adults. The primary cause is a vitamin D deficiency, but rarely, a dietary deficiency of calcium or phosphorus can also cause rickets. In a vitamin D deficiency state, hypocalcemia development leads to the production and secretion of excessive parathyroid hormone. This, in turn, causes a greater renal phosphorus loss. The excessive parathyroid hormone causes the decreased calcium levels to rise to normal values and the ALP, which is produced due to the overactive osteoblast cells, leaks into the ECF, causing elevation to very high levels. Also, recent studies have shown a correlation with increased fibroblast growth factor 23 and the development of rickets. Rickets leads to skeletal deformity and short stature. In females, pelvic distortion from rickets can cause problems with childbirth. Respiratory failure is a severe consequence. Thickening of the skull, frontal bossing, greenstick fractures, rickety myopathy, tetany, uncalcified osteoid at the metaphases, and weight-bearing deformities are all common clinical features.