Pathologic femur fracture due to a brown tumor in a patient with secondary hyperparathyroidism and vitamin D-resistant rickets

Am J Kidney Dis. 2013 Feb;61(2):337-41. doi: 10.1053/j.ajkd.2012.06.028. Epub 2012 Sep 6.

Abstract

Vitamin D-resistant rickets is the common clinical outcome of multiple genetic mutations that alter the regulation of phosphorus and vitamin D metabolism, mainly through their effects on fibroblast growth factor 23 (FGF-23). These diseases typically present in childhood with the classic physical examination finding of nutritional rickets, such as genu varum/valgum and rachitic rosary. Treatment, which is aimed at improving severe bone disease with vitamin D and phosphorus supplementation, can cause secondary hyperparathyroidism and/or kidney failure from nephrocalcinosis over the life of the patient. Although FGF-23 has been shown to downregulate parathyroid hormone in vitro, its effect on parathyroid secretion in disease states such as chronic kidney disease and X-linked hypophosphatemic rickets is unclear because elevations in FGF-23 and parathyroid hormone levels characterize both of these disease states. We describe a case of vitamin D-resistant rickets that presented with a femur fracture through a brown tumor. Radiographs show the combination of severe bony abnormalities associated with both long-standing hyperparathyroidism and vitamin D-resistant rickets.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Bone Neoplasms / complications*
  • Drug Resistance
  • Female
  • Femoral Fractures / etiology*
  • Fibroblast Growth Factor-23
  • Fractures, Spontaneous / etiology*
  • Humans
  • Hyperparathyroidism, Secondary / complications*
  • Rickets / complications*
  • Rickets / drug therapy
  • Vitamin D / therapeutic use

Substances

  • FGF23 protein, human
  • Vitamin D
  • Fibroblast Growth Factor-23