Sodium phosphate
Sources réglementaires consultées
Indications approuvées
- Évacuation intestinale lorsque nécessaire avant ou après des procédures et en cas d'impaction fécale, conformément à la notice locale.
Contre-indications
Absolues
- Hypersensibilité aux principes actifs ou aux excipients ; insuffisance rénale modérée ou sévère ; insuffisance cardiaque symptomatique ; déshydratation ; hypertension artérielle non contrôlée ; saignement rectal non diagnostiqué ; symptômes compatibles avec une appendicite, une perforation intestinale ou une maladie inflammatoire intestinale active ; occlusion, mégacôlon, anus imperforé, iléostomie, iléus paralytique, maladie de Hirschsprung ou sténose anorectale ; et âge inférieur à 2 ans.
Mises en garde cliniques
- Mise en garde majeure · Les phosphates rectaux peuvent provoquer des troubles hydro-électrolytiques graves, surtout chez les personnes vulnérables; une sélection et une utilisation prudentes sont nécessaires. — CIMA AEMPS
- Mise en garde majeure · L'évacuation survient généralement environ 5 minutes après l'administration et une rétention supérieure à 5 minutes n'est pas recommandée. En l'absence d'évacuation ou si la rétention dépasse 10 minutes, une évaluation clinique et un bilan électrolytique sont nécessaires afin de réduire le risque d'hyperphosphatémie sévère. — CIMA AEMPS
Interactions médicamenteuses
- SévèreIEC, ARA, AINS, inhibiteurs calciques, diurétiques, lithium et autres médicaments modifiant les électrolytes
Mécanisme: Les IEC, ARA, AINS et diurétiques peuvent augmenter le risque de déshydratation et d'atteinte rénale ; ces traitements et d'autres peuvent aggraver les troubles du calcium, du phosphate, du sodium et du potassium ou l'acidose. L'hypernatrémie peut également réduire les concentrations de lithium et son efficacité.
Recommandation: L'équipe soignante doit revoir l'association, l'hydratation et les électrolytes et surveiller les concentrations de lithium le cas échéant.
CIMA AEMPS
- SévèreAutres préparations de phosphate de sodium
Mécanisme: L'exposition cumulée augmente le risque de troubles hydro-électrolytiques graves.
Recommandation: Ne pas utiliser en même temps que des solutions orales, des comprimés ou d'autres préparations de phosphate de sodium.
CIMA AEMPS
Effets indésirables
Rares mais graves
Troubles hydro-électrolytiques graves
Bibliographie récente (PubMed)
Inflammatory arthritis is a major cause of disability in the elderly. This condition causes joint pain, loss of function, and deterioration of quality of life, mainly due to osteoarthritis (OA) and rheumatoid arthritis (RA). Currently, available treatment options for inflammatory arthritis include anti-inflammatory medications administered via oral, topical, or intra-articular routes, surgery, and physical rehabilitation. Novel alternative approaches to managing inflammatory arthritis, so far, remain the grand challenge owing to catastrophic financial burden and insignificant therapeutic benefit. In the view of non-targeted systemic cytotoxicity and limited bioavailability of drug therapies, a major concern is to establish stimuli-responsive drug delivery systems using nanomaterials with on-off switching potential for biomedical applications. This review summarizes the advanced applications of triggerable nanomaterials dependent on various internal stimuli (including reduction-oxidation (redox), pH, and enzymes) and external stimuli (including temperature, ultrasound (US), magnetic, photo, voltage, and mechanical friction). The review also explores the progress and challenges with the use of stimuli-responsive nanomaterials to manage inflammatory arthritis based on pathological changes, including cartilage degeneration, synovitis, and subchondral bone destruction. Exposure to appropriate stimuli induced by such histopathological alterations can trigger the release of therapeutic medications, imperative in the joint-targeted treatment of inflammatory arthritis.
The bone-derived hormone fibroblast growth factor 23 (FGF23) functions in concert with parathyroid hormone (PTH) and the active vitamin D metabolite, 1,25(OH)2 vitamin D (1,25D), to control phosphate and calcium homeostasis. A rise in circulating levels of phosphate and 1,25D leads to FGF23 production in bone. Circulating FGF23 acts on the kidney by binding to FGF receptors and the co-receptor α-Klotho to promote phosphaturia and reduce circulating 1,25D levels. Various other biomolecules that are produced by the kidney, including lipocalin-2, glycerol 3-phosphate, 1-acyl lysophosphatidic acid and erythropoietin, are involved in the regulation of mineral metabolism via effects on FGF23 synthesis in bone. Understanding of the molecular mechanisms that control FGF23 synthesis in the bone and its bioactivity in the kidney has led to the identification of potential targets for novel interventions. Emerging approaches to target aberrant phosphate metabolism include small molecule inhibitors that directly bind FGF23 and prevent its interactions with FGF receptors and α-Klotho, FGF23 peptide fragments that act as competitive inhibitors of intact FGF23 and small molecule inhibitors of kidney sodium-phosphate cotransporters.
Most intervention studies investigating the effects of ergogenic aids (EAs) on sports performance have been carried out in the male population. Thus, the aim of this systematic review and meta-analysis was to summarize the effects in the existing literature of EAs used by female athletes on performance. A literature research was conducted, and a descriptive analysis of the articles included in the systematic review was carried out. Meta-analyses could be performed on 32 of the included articles, evaluating performance in strength, sprint, and cardiovascular capacity. A random-effects model and the standardized mean differences (SMD) ± 95% confidence intervals (CI) were reported. The results showed that caffeine helped to improve jumping performance, isometric strength values, and the number of repetitions until failure. Caffeine and sodium phosphate helped to improve sprint performance. Aerobic tests could be improved with the use of taurine, caffeine, and beta-alanine. No conclusive effects of beetroot juice, polyphenols, or creatine in improving aerobic performance were shown. In terms of anaerobic variables, both caffeine and sodium phosphate could help to improve repeated sprint ability. More studies are needed in female athletes that measure the effects of different EAs on sports performance, such as beetroot juice, beta-alanine or sodium phosphate, as the studies to date are scarce and there are many types of EA that need to be further considered in this population, such as creatine and taurine.
Intracellular phosphate is critical for cellular processes such as signaling, nucleic acid synthesis, and membrane function. Extracellular phosphate (Pi) is an important component of the skeleton. Normal levels of serum phosphate are maintained by the coordinated actions of 1,25-dihydroxyvitamin D3, parathyroid hormone and fibroblast growth factor-23, which intersect in the proximal tubule to control the reabsorption of phosphate via the sodium-phosphate cotransporters Npt2a and Npt2c. Furthermore, 1,25-dihydroxyvitamin D3 participates in the regulation of dietary phosphate absorption in the small intestine. Clinical manifestations associated with abnormal serum phosphate levels are common and occur as a result of genetic or acquired conditions affecting phosphate homeostasis. For example, chronic hypophosphatemia leads to osteomalacia in adults and rickets in children. Acute severe hypophosphatemia can affect multiple organs leading to rhabdomyolysis, respiratory dysfunction, and hemolysis. Patients with impaired kidney function, such as those with advanced CKD, have high prevalence of hyperphosphatemia, with approximately two-thirds of patients on chronic hemodialysis in the United States having serum phosphate levels above the recommended goal of 5.5 mg/dL, a cutoff associated with excess risk of cardiovascular complications. Furthermore, patients with advanced kidney disease and hyperphosphatemia (>6.5 mg/dL) have almost one-third excess risk of death than those with phosphate levels between 2.4 and 6.5 mg/dL. Given the complex mechanisms that regulate phosphate levels, the interventions to treat the various diseases associated with hypophosphatemia or hyperphosphatemia rely on the understanding of the underlying pathobiological mechanisms governing each patient condition.
The purpose of this review is to highlight the publications from the prior 12-18 months that have contributed significant advances in the field of renal phosphate handling. The discoveries include new mechanisms for the trafficking and expression of the sodium phosphate cotransporters; direct link between phosphate uptake and intracellular metabolic pathways; interdependence between proximal tubule transporters; and the persistent renal expression of phosphate transporters in chronic kidney disease. Discovery of new mechanisms for trafficking and regulation of expression of phosphate transporters suggest new targets for the therapy of disorders of phosphate homeostasis. Demonstration of stimulation of glycolysis by phosphate transported into a proximal tubule cell expands the scope of function for the type IIa sodium phosphate transporter from merely a mechanism to reclaim filtered phosphate to a regulator of cell metabolism. This observation opens the door to new therapies for preserving kidney function through alteration in transport. The evidence for persistence of active renal phosphate transport even with chronic kidney disease upends our assumptions of how expression of these transporters is regulated, suggests the possibility of alternative functions for the transporters, and raises the possibility of new therapies for phosphate retention.