Rickets in the growing child or adolescent and osteomalacia in the adult develop in a variety of clinical situations and have in common an absence or delay in the mineralization of growth cartilage and in newly formed bone collagen. Classically, deficiency of vitamin D, which is essential for the absorption of dietary calcium, has been the major cause. However, rickets is also seen as a result of hereditary defects in critical vitamin D signaling molecules. Disturbances of phosphate metabolism can also lead to signs of rickets and osteomalacia, notably X-linked hypophosphatemic rickets, and oncogenic osteomalacia. Extrarenal synthesis of 1,25-dihydroxyvitamin D, such as that associated with granulomatous disease, can also lead to disturbances in calcium metabolism, with associated skeletal and nonskeletal changes.
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Osteomalacia: A Challenging Diagnosis Adverse Event Associated with Intravenous Ferric Carboxymaltose-A Case Report.
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Dysregulated FGF23 production is a demonstrated cause of hypophosphatemia and osteomalacia. Diseases associated with these conditions include phosphaturic mesenchymal tumor (PMT) causing tumor induced osteomalacia, various forms of rickets, and fibrous dysplasia (FD). Coexistence of 2 conditions that can increase FGF23 concentrations is rare.
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Article Synopsis
- Hypophosphatemic osteomalacia is a rare condition marked by low phosphate levels, which can occur due to genetic or acquired factors, and a case study discusses its management and prognosis when caused by specific antiviral drugs.
- A 55-year-old man with chronic hepatitis B experienced symptoms like chest pain and fatigue after switching from adefovir to tenofovir, leading to the diagnosis of drug-induced hypophosphatemic osteomalacia.
- Treatment included stopping the problematic drugs, switching to entecavir, and recommending dietary changes and supplements, which resulted in improved phosphate levels and resolution of symptoms.
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