The Foot That Broke Both Hips: A Case Report and Literature Review of Tumor-Induced Osteomalacia

Table 1

Differential diagnoses of hypophosphatemia.

Decreased absorption	Increased excretion	Intercellular shifts
Poor dietary intake	Hyperparathyroidism: primary and secondary	Insulin effect, i.e., during refeeding syndrome
Inhibition of absorption due to medications including phosphate binders, anticonvulsants, antacids, etc.	Hereditary hypophosphatemic rickets: XLHR (mutations in PHEX gene), ADHR (mutations in FGF23 gene), ARHR (mutations in DMP1 gene), HHRH (mutations in sodium phosphate transporter 2c)	Respiratory alkalosis
Malabsorption syndromes, i.e., celiac disease, Crohn’s, nontropical sprue, etc.	Fanconi syndrome: inherited versus acquired, i.e., heavy metal induced, chemotherapeutic agents, monoclonal gammopathies, etc.	Hungry bone syndrome
Vitamin D deficiency or resistance: dietary, lack of sunlight, excess fluoride, etc.	Tumor-induced osteomalacia	Increased metabolism: blast crisis, thyrotoxicosis

FGF23, fibroblast growth factor 23; XLHR, X-linked hypophosphatemic rickets; ADHR, autosomal dominant hypophosphatemic rickets; ARHR, autosomal recessive hypophosphatemic rickets; HHRH, hereditary hypophosphatemic rickets with hypercalciuria.