View clinical trials related to Hypophosphatemia.
Filter by:Iron deficiency anemia (IDA) is a very common health problem during pregnancy and intravenous (IV) iron substitution has become part of routine management. Recent studies have raised concerns about association of IV iron infusion and development of secondary transitory hypophosphatemia (HP) in adults including pregnant women. The study aimed to evaluate the impact of IV iron administration during pregnancy on newborn's phosphatemia. The investigators conducted a prospective, single-center, observational study in the Geneva University Hospitals (HUG), from September 2022 to March 2023. Pregnant women treated either with IV iron or with oral iron during pregnancy were included. At delivery, a maternal blood sample to assess hemoglobin, hematocrit, ferritin, phosphate and calcium and an umbilical cord blood sample to assess levels of phosphate and calcium were collected. Difference in demographics and clinical characteristics between the two groups were explored using univariate analyses. Multivariate analyses were performed to test the contribution of IV iron substitution on cord blood phosphatemia and calcemia, considering potential confounding factors. Neonatal HP was defined as a phosphate level lower than 1.3 mmol/L.
This study aimed to characterize foot pathologies using X-rays and clinical examination and assess related outcome scores in adolescents and adults with X-linked Hypophophatemia
This is a confirmatory trial to establish superior serum phosphate stability associated with use of Phoscap® compared with placebo as a supplement for treatment of iron deficiency or iron deficiency anemia with Ferinject® before elective surgery.
The discovery of FGF23, the missing link in the long researched and finally found phosphate metabolism, marked a turning point in the understanding and physiopathology of specific hypophosphatemia. By inhibiting the renal reabsorption of phosphate and the production of calcitriol, FGF23 behaves like a hypophosphatemia hormone. Hypersecretion of FGF23 can occur in the case of genetic abnormalities (X-linked hypophosphatemic vitamin-resistant rickets, recessive or dominant hypophosphatemic rickets, McCune-Albright syndrome ...) or acquired abnormalities (oncogenic osteomalacia). Oncogenic osteomalacia can be induced by hyperproduction of FGF23 by benign tumours of mesenchymal origin. But more recently, several cases of malignant tumours secreting FGF23 have also been described (prostate, colon, breast, ovarian and lung cancers, pulmonary carcinoma, etc.)
This study aims to provide Health-related Quality of Life (HRQoL) data from children and adolescents with growing skeletons in the United Kingdom (UK), including those treated with burosumab or alternative XLH treatment, as part of an updated submission to the SMC in early 2023. This study will utilise data from a subset of UK sites already within the XLH Registry (including participating Scottish sites) and collect additional HRQoL data within these sites (that are otherwise not included in the wider XLH Registry protocol). The HRQoL data will enable the calculation of HRQoL to derive the HRQoL utility estimates in children and adolescents with growing skeletons for the RSS health states, hence addressing an area of uncertainty.
X-linked hypophosphatemia (XLH) rare genetic disorder due by inactivating mutations in the PHEX gene leading to increased levels in FGF-23. Elevated FGF-23 reduces renal phosphate reabsorbtion and and limits 1-alpha hydroxylase driven Vitamin D activation, eventually leading to phosphate wasting, defective bone mineralization and additional health issues. Burosumab is a recombinant fully human IgG1 monoclonal antibody developed to treat XLH by binding FGF23, thereby restoring normal phosphate homeostasis. BUR03 is a Phase 3b open-label, single-arm, single-center study to confirm the efficacy and safety of Burosumab treatment in adult (age ≥18 years) XLH patients without upper age limit and irrespective of baseline pain level and to further evaluate the efficacy in this cohort and the assocaited effect of treatment on physical functioning, mobility and activity. The study aims at enrolling and treating 34 subjects with a confirmed diagnosis of XLH with q4w s.c. injection of Burosumab 1mg/kg body weight over 48 weeks. Primary objective is to attiain normal serum phosphorus levels, secondary objectives include key parameters of physical function and activity, mobility and mineral homeostasis.
Patients with severe sepsis/septic shock complicated by hypophosphatemia are at high risk of developing morbidities other than that underlying sepsis and more vulnerable to higher mortality rate. Thus, the current study hypothesized that diagnosis and management of hypophosphatemia may be advantageous for reduction of morbidity and mortality rates of septic patients admitted to ICU
Hereditary hypophosphatemia (XLH) is a rare, inherited disease. Loss-of-function mutation in the phosphate regulating gene with homologies to endopeptidases on the X-chromosome (PHEX) results in excess fibroblast growth factor 23 (FGF23) production and manifests as rickets in children and osteomalacia in adults. This study aims to characterize and measure pain, quality of life, muscle function, body composition, arterial stiffness, bone mineral density, geometry and microarchitecture in patients with XLH compared to age and gender-matched controls.
The point prevalence survey aims at defining the until now unknown real prevalence of hypophosphatemia (defined as blood phosphate value < 0.8 mmol/l) in international critical care settings
Patients with X-linked hypophosphatemia (XLH) often report symptoms of fatigue and weakness particularly after exertion, in addition to their skeletal complaints. In previous trials using KRN23 (same drug as burosumab/Crysvita®), patients report these symptoms improve. The investigators wish to test this hypothesis directly by measuring muscle energy when patients begin treatment with Crysvita® for the first time.