"Osteomalacia"

Osteomalacia Osteomalacia - Symptoms, diagnosis and treatment | BMJ Best PracticeSkip to main contentSkip to search * English (US)EnglishPortuguês * Log in * Personal account * Access through your institution(Open Athens) * Subscribe * Access through your institution * Log in * English (US)EnglishPortuguês HomeSearchSearchHome * About usOverviewWhat is BMJ Best Practice?Our historyKey plate cartilage in children, resulting in skeletal deformities and growth retardation. Rickets and osteomalacia are different manifestations of the same underlying pathological process. History and examKey diagnostic factors * older age * vitamin D and calcium deficient diets * lack of sunlight exposure * fractures * malabsorption syndromes * diffuse bone pain and tenderness * proximal muscle weakness

Ferric carboxymaltose (Ferinject): risk of symptomatic hypophosphataemia leading to osteomalacia and fractures Ferric carboxymaltose (Ferinject▼): risk of symptomatic hypophosphataemia leading to osteomalacia and fractures - GOV.UK Skip to main content Cookies on GOV.UKWe use some essential cookies to make this website work.We’d like to set additional cookies to understand how you use GOV.UK (COVID-19) * Find a job * Check benefits and financial support you can get * Universal Credit account: sign in 1. Home 2. Drug Safety Update Ferric carboxymaltose (Ferinject▼): risk of symptomatic hypophosphataemia leading to osteomalacia and fractures Monitor serum phosphate levels in patients treated with multiple high-dose administrations, or those on long-term treatment, and in those

Glucose Metabolic Abnormalities and Their Interaction With Defective Phosphate Homeostasis in Tumor-induced Osteomalacia. Phosphate homeostasis was compromised in tumor-induced osteomalacia (TIO) due to increased fibroblast growth factor 23 (FGF23) secretion. Nevertheless, the glucose metabolic profile in TIO patients has not been investigated. This work aimed to clarify the glucose metabolic

Orthopedic surgical treatment of osteomalacia induced by culprit soft tissue tumor in the hip region: a single-center retrospective study. Due to its occult position, complex anatomical structure, and spatial relationships, the causative tumor of Tumor-Induced Osteomalacia (TIO) in the hip region is quite difficult to detect and qualitatively diagnose in clinical practice. In this regard

Tumor-induced rickets/osteomalacia (TIO): diagnostic pitfalls and therapeutic options. A 10-year-old girl developed bilateral gonalgia and waddling gait. Biochemical and imaging studies showed hypophosphatemia with impaired proximal tubular phosphate reabsorption and high intact FGF23 level indicating FGF23-related hypophosphatemic rickets/osteomalacia. However, genetic analyses for hereditary FGF23-related hypophosphatemic rickets were negative. 111In-pentetreotide scintigraphy and 18F-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography (PET/CT) which were available at that time failed to find a tumor associated with tumor-induced rickets/osteomalacia. She was first treated with active vitamin D and phosphate salt followed by burosumab which alleviated her symptoms

Osteomalacia Osteomalacia - Symptoms, diagnosis and treatment | BMJ Best PracticeSkip to main contentSkip to search * About us * Help * Subscribe * Access through your institution * Log inBMJ Best Practice * Help * Getting started * FAQs * Contact us * Recent updates * Specialties * Calculators * Patient leaflets * Videos * Evidence * Drugs * Recent updates * Specialties replacement.DefinitionOsteomalacia is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults.In contrast, rickets is a metabolic bone disease characterised by defective mineralisation of the epiphyseal growth plate cartilage in children, resulting in skeletal deformities and growth retardation. Rickets and osteomalacia

A retrospective cohort of tumor-induced osteomalacia and case series of malignant disease. We aimed to describe the clinical characteristics of a large cohort of patients diagnosed with tumor-induced osteomalacia (TIO), with a focus on patients with non-localizing and malignant TIO. This is a retrospective cohort of TIO patients in an academic medical center, diagnosed between January 1998

Healthcare resource use associated with tumor-induced osteomalacia: a literature review. Tumor-induced osteomalacia (TIO) is an ultra-rare, paraneoplastic syndrome caused by tumors that secrete fibroblast growth factor 23 (FGF23). Initial signs and musculoskeletal symptoms can be non-specific and unrecognized, leading to long delays in diagnosis and treatment, which results in severe

Patterns of symptoms and insufficiency fractures in patients with tumour-induced osteomalacia. The aim of this study was to report the patterns of symptoms and insufficiency fractures in patients with tumour-induced osteomalacia (TIO) to allow the early diagnosis of this rare condition. The study included 33 patients with TIO who were treated between January 2000 and June 2022. The causative

Spinal phosphaturic mesenchymal tumors: a rare etiology causing tumor-induced osteomalacia-a review of experience at a UK tertiary referral center and literature review. This article aims to provide a comprehensive review of the management challenges associated with Spinal Phosphaturic Mesenchymal tumors (PMTs) and evaluates the surgical management outcomes for this rare entity linked to Tumor information, clinical presentation, radiological findings, surgical details, and follow-up outcomes. A total of three cases of Spinal PMTs causing Tumor-induced osteomalacia were identified. The diagnosis of Spinal PMTs presented challenges, with incidental detection often occurring during routine imaging. Surgical management was undertaken, resulting in successful symptom resolution and normalization

UPLC-MS based serum metabolomics for early diagnosis of refractory tumor-induced osteomalacia: a case-control study. Nearly 20% patients with Tumor-induced osteomalacia (TIO) experienced recurrence or nonrecovery after surgery. Serum FGF23 and phosphate concentrations are not capable for prognosis in such cases. Despite its importance for understanding of prognosis and underlying pathogenesis

Tumor-induced Osteomalacia: A Comprehensive Review. Tumor-induced osteomalacia (TIO) is an ultrarare paraneoplastic syndrome due to overproduction of fibroblast growth factor 23 (FGF23), with profound effects on patient morbidity. TIO is an underdiagnosed disease, whose awareness should be increased among physicians for timely and proper management of patients. Symptoms reported by patients

Burosumab improves patient-reported outcomes in adults with tumor-induced osteomalacia: mixed-methods analysis. Tumor-induced osteomalacia (TIO) is an ultra-rare disease caused by tumors that secrete fibroblast growth factor 23, leading to chronic hypophosphatemia, poor skeletal health and impaired physical function. In a phase 2 trial (UX023T-CL201; NCT02304367; n = 14), 48 weeks' burosumab

Tumor-induced osteomalacia characterized by "painful knee joint with difficulty in moving": a case report. Tumor-related osteomalacia (TIO) is a rare paraneoplastic syndrome characterized by severe hypophosphatemia and osteomalacia. The diagnosis of TIO can be very difficult because of its nonspecific nature of clinical manifestations. Here we reported a case of young TIO patient with "painful phosphate level rapidly recovered and symptoms significantly improved. TIO should be considered in patients with chronically hypophosphorus osteomalacia in the setting of no family history. Early removal of the responsible tumors is clinically essential for the treatment, and imaging examination is of great significance for tumor localization.

A rare combination of tumor-induced osteomalacia caused by sinonasal glomangiopericytoma and coexisting parathyroid adenoma: case report and literature review. Tumor-induced osteomalacia (TIO) is a rare, acquired disease of renal phosphate wasting and disturbed vitamin D homeostasis as a result of the action of a phosphaturic protein - FGF-23, produced by a neoplasm. Although the clinical and biochemical profile of the syndrome is characteristic, it remains underreported and unrecognized by clinicians. Hyperparathyroidism is rarely associated with oncogenic osteomalacia, but it should be considered because of potentially life-threatening hypophosphatemia caused by both conditions. We report a case of a 42-year-old woman admitted to the Department of Otolaryngology of the Military Institute

Lambda light chain-induced monoclonal gammopathy of renal significance, manifesting with Fanconi Syndrome and osteomalacia. Monoclonal gammopathy of renal significance (MGRS) encompasses a heterogeneous group of kidney diseases in which a monoclonal immunoglobulin secreted by a clone of B cells or plasma cells causes kidney damage without meeting the hematological criteria for malignancy. Among and osteomalacia. The diagnosis of MGRS is not always easy, it requires knowledge of the clinical characteristics, diagnostic criteria and prognosis of each case. Therefore, all possible efforts should be made for multidisciplinary diagnosis.

Clinical Challenges in Diagnosis, Tumor Localization and Treatment of Tumor-Induced Osteomalacia: Outcome of a Retrospective Surveillance. Tumor-induced osteomalacia (TIO) is an acquired fibroblast growth factor 23 (FGF23)-related hypophosphatemic osteomalacia caused by phosphaturic mesenchymal tumors (PMTs) developed in the bone or soft tissue. Diagnostic delay should be addressed, and ideal

Bone Impairment in a Large Cohort of Chinese Patients With Tumor-Induced Osteomalacia Assessed by HR-pQCT and TBS. Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by excessive production of fibroblast growth factor 23 (FGF23) by a tumor. Previous studies have revealed generalized mineralization defects and low areal bone mineral density (aBMD) in TIO. However, data

Low Levels of Serum Sclerostin in Adult Patients With Tumor-Induced Osteomalacia Compared With X-linked Hypophosphatemia. Sclerostin inhibits Wnt-β-catenin signaling, regulating bone formation. Circulating sclerostin was reported to be elevated in X-linked hypophosphatemia (XLH) patients, and sclerostin antibody (Scl-Ab) increased bone mass and normalized circulating phosphate in Hyp mice . However, circulating sclerostin levels in patients with acquired hypophosphatemia due to tumor-induced osteomalacia (TIO) are rarely reported. This study was designed to evaluate serum sclerostin levels in TIO patients compared with age- and sex-matched healthy controls and XLH patients to analyze correlations with bone mineral density (BMD) and laboratory parameters. This cross-sectional study

Hyperparathyroidism in a Large Cohort of Chinese Patients with Tumor-Induced Osteomalacia. Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by excessive production of fibroblast growth factor 23 (FGF23) by a tumor. Hyperparathyroidism (HPT) including secondary HPT (SHPT) and tertiary HPT (THPT) in TIO patients, which is considered to associate with phosphate