Tumor-associated osteomalacia rickets: Also known as tumor-associated osteomalacia, tumor-associated hypophosphatemic osteomalacia rickets has similar clinical features to hypophosphatemic vitamin D-resistant rickets osteomalacia. It was first reported by Prader in 1959 in a case of an 11-year-old girl who developed severe rickets and low blood phosphorus and high urine phosphorus with giant cell tumor of the rib cage within a year, and the rickets resolved after removal of the tumor, and nearly 100 cases have been reported to date. Associated tumors can occur in adults and children and can be located in soft tissue or bone, most commonly benign tumors of mesodermal tissue. Nuovo et al. counted 372 cases and found that bone tumors accounted for 56.3%, half of which were located in the long bones, followed by cranial and including mandibular, paranasal sinus, septal sinus bone tumors; 43.05% were soft tissue tumors, mostly in the lower extremities, and can be located in the skin tumors are mostly benign, including hemangiomas, angiosarcomas, fibrovascular tumors, mesenchymal tumors of bone, multiple neurofibromas, chondromas, giant cell tumors osteoblastomas and Non-neoplastic diseases (fibrous dysplasia and malignant multiple myeloma, breast cancer prostate cancer, oat cell carcinoma, etc.). Most tumors are small averaging 1 to 4 cm minimum of 0.5 cm and up to 15 cm maximum. Clinical features are progressive hypophosphatasia rickets and osteochondrosis rickets and osteochondrosis in previously healthy children or adults may also be progressive in radiological features. Patients present with severe muscle weakness, proximal myopathy, pain in the low back, chest ribs and feet, and may present with pelvic spine limb deformities and pathological fractures. Laboratory tests: normal blood calcium low blood phosphorus, increased urinary phosphorus, normal PTH and calcitonin, normal 25-(0H)D3, often decreased 1,25-(0H)2D3 increased blood alkaline phosphatase, increased urinary HOP, and also reported amino aciduria glycosuria. Rickets osteomalacia and tumor manifestations can occur simultaneously or several years apart. In rickets, osteochondrosis can occur l to 13 years earlier than tumor detection, with an average of 5 years, so some of the previously diagnosed idiopathic and sporadic osteochondrosis rickets may be tumorigenic osteochondrosis rickets. The pathogenesis of this disease is still not well understood. Most scholars believe that it may be due to the release of a factor or substance from the tumor that acts directly on the renal proximal tubule to inhibit phosphorus absorption, resulting in lower blood phosphorus and increased urinary phosphorus. It has also been found that extracts from tumor cells can directly inhibit lα-hydroxylase activity in the kidney, while intracellular cAMP is not elevated, suggesting that this substance is different from PTH, etc. Many case reports have also confirmed abnormalities in vitamin D and a decrease in 25-(OH)D3. Recent studies have also shown that the extract of these tumors is a peptide substance, non-lipid soluble, non-heat resistant to tryptic hydrolysis, with a molecular weight of 8-25 kD, which can inhibit Na-P cotransport on the brush border of proximal renal tubular epithelial cells to reabsorb phosphorus, and also alter the function of proximal renal tubules, thus causing a series of pathological changes. In conclusion, it is important for many clinical tumors to be associated with rickets osteochondrosis, and this damage should be carefully sought in the diagnosis of hypophosphorus-resistant rickets osteochondrosis. Excision of these tumors rickets and osteochondrosis can be cured without treatment. When no tumor is found or when malignant tumors cannot be removed, both phosphorus and alfacalcidol supplementation are required at the same dose and in the same way as in X-linked familial hypophosphatemia.