Calcium phosphate
Sources réglementaires consultées
Indications approuvées
- États de carence en calcium et situations nécessitant un apport supplémentaire de ce minéral.
Contre-indications
Absolues
- Affections ou situations entraînant une hypercalcémie ou une hypercalciurie
- Néphrolithiase
- Hypersensibilité au phosphate de calcium ou à l’un des excipients
Mises en garde cliniques
- Mise en garde majeure · En cas d'insuffisance rénale, administrer uniquement sous surveillance de l'hyperphosphatémie ; il existe un risque potentiel d'hyperphosphatémie, de néphrolithiase et de néphrocalcinose. À fortes doses, en particulier avec la vitamine D concomitante, surveiller la calcémie et la fonction rénale. Le benzoate de sodium peut augmenter l'ictère néonatal et favoriser un ictère nucléaire chez les nouveau-nés jusqu'à 4 semaines. — AEMPS CIMA ficha técnica, registro 17337
Interactions médicamenteuses
- ModéréeDiurétiques thiazidiques
Mécanisme: Les thiazidiques réduisent l’excrétion urinaire de calcium et augmentent le risque d’hypercalcémie.
Recommandation: Surveiller régulièrement la calcémie lors de l’utilisation concomitante.
AEMPS CIMA ficha técnica, registro 17337
- ModéréeCorticostéroïdes systémiques
Mécanisme: Les corticostéroïdes systémiques réduisent l’absorption du calcium.
Recommandation: Une dose plus élevée de phosphate de calcium peut être nécessaire lors de l’utilisation concomitante.
AEMPS CIMA ficha técnica, registro 17337
- ModéréeTétracyclines
Mécanisme: Le phosphate tricalcique peut interférer avec l’absorption des tétracyclines.
Recommandation: Administrer les tétracyclines au moins 2 heures avant ou 4–6 heures après le calcium oral.
AEMPS CIMA ficha técnica, registro 17337
- ModéréeGlycosides cardiaques
Mécanisme: L’hypercalcémie peut augmenter la toxicité des glycosides cardiaques.
Recommandation: Surveiller l’ECG et la calcémie pendant le traitement concomitant.
AEMPS CIMA ficha técnica, registro 17337
- ModéréeBisphosphonates ou fluorure de sodium
Mécanisme: Le calcium peut réduire l’absorption gastro-intestinale des bisphosphonates ou du fluorure de sodium.
Recommandation: Administrer le bisphosphonate ou le fluorure de sodium au moins 3 heures avant le phosphate de calcium.
AEMPS CIMA ficha técnica, registro 17337
- ModéréeAliments riches en acide oxalique ou en acide phytique
Mécanisme: L’acide oxalique et l’acide phytique peuvent inhiber l’absorption du calcium en formant des composés insolubles.
Recommandation: Ne pas prendre de produits contenant du calcium pendant les 2 heures suivant ces aliments.
AEMPS CIMA ficha técnica, registro 17337
Effets indésirables
Communs (≥1%)
Peu fréquents : hypercalcémie et hypercalciurie · Rares : constipation, flatulences, nausées, douleur abdominale et diarrhée · Rares : prurit, éruption cutanée et urticaire
Grossesse et allaitement
Peut être utilisé pendant la grossesse en cas de carence en calcium. L’apport total de calcium provenant des aliments et des compléments ne doit pas dépasser 1500 mg/jour pendant la grossesse.
Bibliographie récente (PubMed)
Tumor lysis syndrome (TLS) is an oncologic emergency due to massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation. Clinical presentation is characterized by hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Acute kidney injury due to tumor lysis is potentiated by the precipitation of uric acid and calcium phosphate as well as renal vasoconstriction. Early recognition of tumor lysis can help prevent cardiac arrhythmias, seizures, and death. Management includes intravenous hydration to maintain urine flow, medications targeting hyperuricemia including rasburicase and allopurinol and in severe cases renal replacement therapy may be required.
Tumour lysis syndrome (TLS) represents a critical oncological emergency characterized by extensive tumour cell breakdown, leading to the swift release of intracellular contents into the systemic circulation, outpacing homeostatic mechanisms. This process results in hyperuricaemia (a by-product of intracellular DNA release), hyperkalaemia, hyperphosphataemia, hypocalcaemia and the accumulation of xanthine. These electrolyte and metabolic imbalances pose a significant risk of acute kidney injury, cardiac arrhythmias, seizures, multiorgan failure and, rarely, death. While TLS can occur spontaneously, it usually arises shortly after the initiation of effective treatment, particularly in patients with a large cancer cell mass (defined as ≥500 g or ≥300 g/m2 of body surface area in children). To prevent TLS, close monitoring and hydration to improve renal perfusion and urine output and to minimize uric acid or calcium phosphate precipitation in renal tubules are essential. Intervention is based on the risk of a patient of having TLS and can include rasburicase and allopurinol. Xanthine, typically enzymatically converted to uric acid, can accumulate when xanthine oxidases, such as allopurinol, are administered during TLS management. Whether measurement of xanthine is clinically useful to optimize the use of allopurinol or rasburicase remains to be determined.
Mitochondria calcium is a double-edged sword. While low levels of calcium are essential to maintain optimal rates of ATP production, extreme levels of calcium overcoming the mitochondrial calcium retention capacity leads to loss of mitochondrial function. In moderate amounts, however, ATP synthesis rates are inhibited in a calcium-titratable manner. While the consequences of extreme calcium overload are well-known, the effects on mitochondrial function in the moderately loaded range remain enigmatic. These observations are associated with changes in the mitochondria ultrastructure and cristae network. The present mini review/perspective follows up on previous studies using well-established cryo-electron microscopy and poses an explanation for the observable depressed ATP synthesis rates in mitochondria during calcium-overloaded states. The results presented herein suggest that the inhibition of oxidative phosphorylation is not caused by a direct decoupling of energy metabolism via the opening of a calcium-sensitive, proteinaceous pore but rather a separate but related calcium-dependent phenomenon. Such inhibition during calcium-overloaded states points towards mitochondrial ultrastructural modifications, enzyme activity changes, or an interplay between both events.
Kidney stone disease (KSD) is one of the most common urological diseases. The incidence of kidney stones has increased dramatically in the last few decades. Kidney stones are mineral deposits in the calyces or the pelvis, free or attached to the renal papillae. They contain crystals and organic components, and they are made when urine is supersaturated with minerals. Calcium-containing stones are the most common, with calcium oxalate as the main component of most stones. However, many of these form on a calcium phosphate matrix called Randall's plaque, which is found on the surface of the kidney papilla. The etiology is multifactorial, and the recurrence rate is as high as 50% within 5 years after the first stone onset. There is a great need for recurrence prevention that requires a better understanding of the mechanisms involved in stone formation to facilitate the development of more effective drugs. This review aims to understand the pathophysiology and the main molecular mechanisms known to date to prevent recurrences, which requires behavioral and nutritional interventions, as well as pharmacological treatments that are specific to the type of stone.
Medial arterial calcification (MAC) is a chronic systemic vascular disorder distinct from atherosclerosis that is frequently but not always associated with diabetes mellitus, chronic kidney disease, and aging. MAC is also a part of more complex phenotypes in numerous less common diseases. The hallmarks of MAC include disseminated and progressive precipitation of calcium phosphate within the medial layer, a prolonged and clinically silent course, and compromise of hemodynamics associated with chronic limb-threatening ischemia. MAC increases the risk of complications during vascular interventions and mitigates their outcomes. With the exception of rare monogenetic defects affecting adenosine triphosphate metabolism, MAC pathogenesis remains unknown, and causal therapy is not available. Implementation of genetics and omics-based approaches in research recognizing the critical importance of calcium phosphate thermodynamics holds promise to unravel MAC molecular pathogenesis and to provide guidance for therapy. The current state of knowledge concerning MAC is reviewed, and future perspectives are outlined.