Calcium acetate 435mg / Magnesium carbonate heavy 235mg tablets

ObjectiveTo evaluate the efficacy and safety of 12 phosphorus-lowering drugs for hyperphosphatemia in chronic kidney disease 3-5 stages.Study design & methodsSystematic review and network meta-analysis of randomized controlled trials (RCTs). We searched 3 databases from inception through September 2023 for RCTs evaluating 12 phosphorus-lowering drugs. We performed frequentist random-effects network meta-analyses and present mean differences and 95% CIs. Subgroup analyses were performed between the dialysis and nondialysis patients to assess robustness, source of heterogeneity, and risk of bias using the Cochrane risk of bias assessment tool.ResultsWe included 121 trials (18,376 participants) and compared 13 drugs or placebo. In terms of efficacy, except for sodium ferrous citrate, all drugs lowered the level of serum phosphorus compared with placebo. Sucroferric oxyhydroxide (PA21), nicotinic acid, and tenapanor were most likely to be ranked the best, second best, or third best. Calcium/magnesium carbonate, nicotinic acid, and colestilan posed lower risks for hypercalcemia than calcium-based phosphorus binders. All phosphorus-lowering drugs significantly affect serum intact parathyroid hormone levels compared with placebo. Colestilan, tenapanor, and PA21 posed a higher risk for gastrointestinal discomfort. In addition, iron-containing drugs showed positive effects on iron parameters.LimitationsFew high-quality RCTs; unclear allocation concealment and blinding; low evidence quality reduced reliability.ConclusionsPA21 has the best phosphorus-lowering effect in hyperphosphatemic adults with chronic kidney disease; considering efficacy and safety, calcium carbonate shows evidence of being the most appropriate drug with or without dialysis.RegistrationRegistered at PROSPERO (CRD42024500243).

Abstract licence: CC BY-NC-ND

BACKGROUND: Phosphate binders are used to manage hyperphosphatemia in patients with chronic kidney disease-mineral and bone disorder (CKD-MBD) and may influence fibroblast growth factor 23 (FGF-23), a biomarker associated with disease progression and mortality. However, the comparative effects of calcium-based phosphate binders (CPBs) and non-calcium-based phosphate binders (NCPBs) on FGF-23 levels remain unclear. We conducted a meta-analysis of randomized controlled trials to compare the effects of NCPBs and CPBs on FGF-23 levels in patients with CKD-MBD with hyperphosphatemia. METHODS: A systematic search of PubMed, EMBASE, and the Cochrane Library was performed for studies published up to August 2024. Only randomized controlled trials were eligible; non-randomized controlled trials, studies with overlapping patient populations, pediatric or animal studies, and trials without quantitative FGF-23 outcomes were excluded. Language restrictions were not imposed. Data were synthesized as standardized mean differences using a random-effects model, and the risk of bias was assessed using the Cochrane Risk of Bias 2 tool. RESULTS: Eleven randomized controlled trials involving 791 patients were included. Overall, NCPBs were associated with a greater reduction in FGF-23 levels compared with CPBs (standardized mean difference −0.56, 95% confidence interval −0.95 to −0.17, p = 0.005). Subgroup analyses suggested consistent trends across binder types (sevelamer and lanthanum), dialysis status, and treatment duration. However, the subgroup differences were not statistically significant, and heterogeneity remained substantial in several subgroups, indicating that these findings should be interpreted with caution. CONCLUSIONS: In CKD-MBD patients with hyperphosphatemia, NCPBs were associated with greater reductions in FGF-23 levels compared with CPBs. The subgroup results suggested possible trends by binder type, CKD category, and treatment duration. However, given the heterogeneity and lack of statistically significant subgroup differences, these findings should be considered hypothesis-generating. Further well-designed trials are needed to confirm these results and clarify the underlying mechanisms and clinical implications.

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Divalent cations such as calcium and ferrous sulfate interfere with the absorption of levothyroxine due to complexing. To our knowledge, the effects of magnesium on levothyroxine absorption have never been studied. The open-label cross-over pharmacokinetic study was conducted in 15 healthy, euthyroid adults. 1 mg of levothyroxine was administered in tablet form alone or co-administered with either magnesium aspartate or magnesium citrate. Participants received all three treatments, separated by a washout period, but were randomly allocated 1:1:1 to one of three treatment sequences. We measured thyroxine (T4) over a 6-h period after ingestion. The primary endpoint was the area under the curve (AUC) of thyroxine; secondary endpoints were Cmax and Tmax. Coadministration of magnesium aspartate significantly reduced thyroxine AUC by 12% (geometric mean ratio, GMR = 0.88, 95% CI 0.81-0.95, p = 0.002) and coadministration of magnesium citrate reduced thyroxine AUC non-significantly by 7% compared with levothyroxine alone (GMR = 0.93, 95% CI 0.86-1.01, p = 0.076). Cmax was significantly reduced by 7% and Tmax was significantly increased by 17% when magnesium aspartate was co-administered. The changes in Cmax and Tmax were smaller when magnesium citrate was co-administered. In conclusion, magnesium reduces the absorption of levothyroxine. However, we found smaller effects compared to those already described for other divalent cations, possibly due to the liquid formulation. Hypothyroid patients should nonetheless take levothyroxine separated from magnesium-containing formulations, especially if TSH levels are desired to be within a narrow range. If taken together, magnesium citrate may be a better option than magnesium aspartate.

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Electrolyte disorders are pivotal determinants of morbidity and mortality in neurocritical care and exacerbated by acute brain injury, neuroendocrine dysfunction, and therapeutic interventions. This narrative review synthesized contemporary evidence on the pathophysiology, diagnosis, and management of hydroelectrolytic disturbances in neuroanesthesia and neurocritical populations. Dysnatremias (hyponatremia and hypernatremia) are prevalent with emerging data challenging historical correction paradigms: Rapid sodium normalization may reduce mortality without increasing complications. Distinct strategies are required for syndromes of inappropriate antidiuretic hormone secretion (fluid restriction, vaptans) vs cerebral salt wasting (volume resuscitation). Chloride dysregulation, driven by cation-chloride cotransporter imbalances, exacerbates cytotoxic edema and seizures, warranting trials of bumetanide and balanced crystalloids. Hypokalemia, prevalent in traumatic brain injury, demands proactive surveillance to prevent arrhythmias while hyperkalemia management prioritizes membrane stabilization and renal clearance. Hypocalcemia correlates with adverse outcomes in subarachnoid hemorrhage, necessitating timely replacement. Magnesium disorders lack consistent prognostic associations in neurocritical cohorts, contrasting with general critical care. Current evidence underscores the need for individualized, pathophysiology-driven correction, integrating endocrine and neurological principles. Innovations such as point-of-care testing and targeted therapies (e.g., acetate-buffered hypertonic saline) show promise, yet reliance on observational data and preclinical models highlights the urgency for randomized controlled trials. This review advocated for protocolized monitoring, dynamic assessments, and research to define optimal correction thresholds and validate emerging interventions in this high-risk population.

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BackgroundSanjad-Sakati syndrome (SSS) is a rare autosomal recessive disorder characterized by congenital hypoparathyroidism, persistent hypocalcemia, growth retardation, and distinctive craniofacial dysmorphism. Despite its rarity, SSS is more prevalent in the Middle East due to high consanguinity rates. Its multisystem involvement-including endocrine, neurologic, respiratory, renal, dental, and immunologic systems-poses significant challenges in pediatric emergency care and long-term management.ObjectiveThis review aims to provide a comprehensive, clinically focused overview and expert opinion on the emergency management, diagnostic evaluation, and acute and long-term treatment strategies for SSS, with an emphasis on high-risk manifestations such as hypocalcemic crises, airway instability, immune vulnerability, and difficult vascular access.FindingsChildren with SSS often present with hypocalcemia, seizures, tetany, apnea, or laryngospasm, necessitating urgent calcium correction and airway stabilization. Microtubule dysfunction due to tubulin-specific chaperone E gene mutations contributes to endocrine and structural abnormalities, leading to neurodevelopmental impairment, sleep-disordered breathing, nephrocalcinosis, dental anomalies, and heightened susceptibility to infections associated with immune deficiency. Emergency care is complicated by abnormal airway anatomy, challenging intravenous access, susceptibility to sepsis, and metabolic instability. Early identification of biochemical abnormalities remains the cornerstone of diagnosis and timely stabilization. Long-term care requires lifelong calcium and vitamin D supplementation, regular metabolic monitoring, renal assessment, psychosocial support, and caregiver education.ConclusionSSS demands clinical vigilance due to its multisystem involvement and potential for life-threatening metabolic and respiratory events. Early biochemical correction, cautious airway management, infection prevention, and coordinated multidisciplinary follow-up are critical to improving outcomes and reducing morbidity and mortality. Implementing standardized emergency protocols, family-directed action plans, and genetic counseling in high-risk populations can significantly enhance long-term prognosis for affected children.

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