Long-term bone mineral density changes after surgical cure of patients with tumor-induced osteomalacia

Colangelo, Luciano; Pepe, Jessica; Nieddu, Luciano; Sonato, Chiara; Scillitani, Alfredo; Diacinti, Davide; Angelozzi, Maurizio; Cipriani, Cristiana; Minisola, Salvatore

doi:10.1007/s00198-020-05369-1

Cited by 31 publications

(28 citation statements)

References 19 publications

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“…The physical and emotional status of the patient showed marked improvement. Bone density will be measured again on month 18 post-operation and we expect an improvement of BMD at both lumbar and femoral sites similar to the results reported by Colangelo L. et al This is the consequence of huge mineralization of a large amount of osteoid tissue after resolution of the disease [14]. The patient will be followed up closely in the upcoming years concerning serum and urine calcium, phosphate and FGF23 levels, which will be monitored.…”

Section: Discussionsupporting

confidence: 66%

The Difficult Diagnosis of Hypophosphatemic Rickets-A Review of 8 Clinical Cases

Borissovа¹,

Vlahov²,

Fukumoto³

et al. 2020

CMR

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Section: Discussionsupporting

confidence: 66%

The Difficult Diagnosis of Hypophosphatemic Rickets-A Review of 8 Clinical Cases

Borissovа¹,

Vlahov²,

Fukumoto³

et al. 2020

CMR

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“…Targeted studies are therefore needed to better identify prevalence of osteomalacia in relation to other forms of skeletal alterations. hydrxyvitamin-D should be aimed at maintaining >30 ng/mL (1,30) and PTH levels within Furthermore, depending on the amount of osteoid accumulation, a striking increase in bone mineral density is observed, as seen after cure of osteomalacia with diseases causing osteomalacia of different aetiology (31) .…”

Section: Chronic Kidney Disease (Also See Section 93)mentioning

confidence: 99%

“…Furthermore, depending on the amount of osteoid accumulation, a striking increase in BMD is observed, as seen after cure of osteomalacia in other conditions. (31) Therapy consists of daily oral doses of vitamin D in the range of 800 to 1200 IU. Another schedule entails administration of 50 000 IU of native vitamin D weekly for 8 to 12 weeks, followed by a maintenance dose of 1000 to 2000 IU daily.…”

Section: Treatmentmentioning

confidence: 99%

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Osteomalacia and Vitamin D Status: A Clinical Update 2020

et al. 2020

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Historically, rickets and osteomalacia have been synonymous with vitamin D deficiency dating back to the 17th century. The term osteomalacia, which literally means soft bone, was traditionally applied to characteristic radiologically or histologically documented skeletal disease and not just to clinical or biochemical abnormalities. Osteomalacia results from impaired mineralization of bone that can manifest in several types, which differ from one another by the relationships of osteoid (ie, unmineralized bone matrix) thickness both with osteoid surface and mineral apposition rate. Osteomalacia related to vitamin D deficiency evolves in three stages. The initial stage is characterized by normal serum levels of calcium and phosphate and elevated alkaline phosphatase, PTH, and 1,25-dihydroxyvitamin D [1,25(OH) 2 D]-the latter a consequence of increased PTH. In the second stage, serum calcium and often phosphate levels usually decline, and both serum PTH and alkaline phosphatase values increase further. However, serum 1,25 (OH) 2 D returns to normal or low values depending on the concentration of its substrate, 25-hydroxyvitamin D (25OHD; the best available index of vitamin D nutrition) and the degree of PTH elevation. In the final stage, hypocalcemia and hypophosphatemia are invariably low with further exacerbation of secondary hyperparathyroidism. The exact,or even an approximate, prevalence of osteomalacia caused by vitamin D deficiency is difficult to estimate, most likely it is underrecognized or misdiagnosed as osteoporosis. Signs and symptoms include diffuse bone, muscle weakness, and characteristic fracture pattern, often referred to as pseudofractures, involving ribs, scapulae, pubic rami, proximal femurs, and codfish-type vertebrae. The goal of therapy of vitamin D-deficiency osteomalacia is to alleviate symptoms, promote fracture healing, restore bone strength, and improve quality of life while correcting biochemical abnormalities. There is a need for better understanding of the epidemiology of osteomalacia. Simplified tools validated by concurrent bone histology should be developed to help clinicians promptly diagnose osteomalacia.

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“…Una volta individuata la sede, la resezione della neoplasia causa della malattia rappresenta la cura definitiva; infatti, alla guarigione consegue la normalizzazione dei parametri biochimici, la riparazione delle fratture, l'incremento dei valori densitometrici [2] e, infine, il miglioramento della qualità di vita dei pazienti.…”

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Burosumab nel trattamento della osteomalacia indotta da neoplasia

Minisola

2021

L'Endocrinologo

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Long-term bone mineral density changes after surgical cure of patients with tumor-induced osteomalacia

Cited by 31 publications

References 19 publications

The Difficult Diagnosis of Hypophosphatemic Rickets-A Review of 8 Clinical Cases

The Difficult Diagnosis of Hypophosphatemic Rickets-A Review of 8 Clinical Cases

Osteomalacia and Vitamin D Status: A Clinical Update 2020

Burosumab nel trattamento della osteomalacia indotta da neoplasia

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