Schnabel D, Haffner D
Pädiatrische Endokrinologie und Diabetologie, Otto-Huebner-Centrum für Kinder- und Jugendmedizin, Charité, CVK--Universitätsmedizin Berlin.
Orthopade. 2005 Jul;34(7):703-14; quiz 715-6. doi: 10.1007/s00132-005-0825-6.
Rickets is caused by deficient mineralization at the level of growth plate and is usually due to a decreased serum calcium/phosphate product. Although the diagnosis of rickets can usually be suspected on the basis of a clinical examination (bone deformities in legs, impaired growth), radiological examination and detailed biochemical work-up are necessary to elucidate the etiology of the underlying disease. It is important to differentiate between calcipenic/vitamin deficient and phosphopenic rickets. The former is due to vitamin D deficiency, and the ultimate cause of this usually lies in altered vitamin D supply; however, impaired synthesis of or resistance to the actions of vitamin D can also be a cause. Phosphopenic rickets is usually related to impaired phosphate reabsorption in the proximal renal tubule. Both calcipenic and phosphopenic rickets can be acquired or hereditary in origin.
佝偻病是由生长板处矿化不足引起的,通常是由于血清钙/磷乘积降低所致。虽然佝偻病的诊断通常可根据临床检查(腿部骨骼畸形、生长发育受损)怀疑,但仍需要进行放射学检查和详细的生化检查以明确潜在疾病的病因。区分钙缺乏/维生素缺乏性佝偻病和磷缺乏性佝偻病很重要。前者是由于维生素D缺乏,其根本原因通常在于维生素D供应改变;然而,维生素D合成受损或对其作用产生抵抗也可能是病因。磷缺乏性佝偻病通常与近端肾小管磷重吸收受损有关。钙缺乏性和磷缺乏性佝偻病都可能是后天获得性的或遗传性的。