Cernaro Valeria, Calimeri Sebastiano, Laudani Alfredo, Santoro Domenico
Unit of Nephrology and Dialysis, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Ther Clin Risk Manag. 2020 Sep 15;16:871-880. doi: 10.2147/TCRM.S196805. eCollection 2020.
Patients with progressive chronic kidney disease (CKD) commonly develop mineral and bone abnormalities and extraskeletal calcifications with following increased cardiovascular risk. A key pathophysiological role is played by hyperphosphatemia. Since diet and dialysis are often insufficient to control serum phosphorus levels, many patients require treatment with phosphate binders. Among them is lanthanum carbonate, an aluminum-free non-calcium-based compound. The present review summarizes the most recent literature data concerning the safety, efficacy and tolerability of lanthanum carbonate in patients with end-stage renal disease and hyperphosphatemia. The drug is taken orally as chewable tablets or powder with only minimal gastrointestinal absorption and resulting reduced risk of tissue deposition and systemic drug interactions. The dissociation of the drug in the acid environment of the upper gastrointestinal tract induces the release of lanthanum ions, which bind to dietary phosphate forming insoluble complexes then excreted in the feces. Even though there is no clear evidence that lowering serum phosphorus levels can improve patient-centered outcomes, a mortality benefit with all phosphate binders, especially non-calcium containing ones, is not excluded. Lanthanum carbonate has been suggested to decrease all-cause mortality but not cardiovascular event rate compared to other phosphate binders. It induces a lower suppression of bone turnover than calcium carbonate and calcium acetate and may improve systolic function and cardiac dimension compared to calcium carbonate. Moreover, the use of lanthanum carbonate has been associated with better nutritional status compared to other phosphate binders, lower risk for hypercalcemia than calcium-containing binders, and amelioration of mild metabolic acidosis contrary to sevelamer hydrochloride. Main adverse effects include nausea, alkaline gastric reflux, gastric deposition of lanthanum, gastrointestinal obstruction, subileus, ileus, perforation, fecal impaction, and reduction of gastrointestinal absorption of some drugs including statins, angiotensin-converting enzyme inhibitors and some antibiotics such as fluoroquinolones or tetracyclines.
进展性慢性肾脏病（CKD）患者通常会出现矿物质和骨异常以及骨骼外钙化，进而增加心血管疾病风险。高磷血症在其中起着关键的病理生理作用。由于饮食和透析往往不足以控制血清磷水平，许多患者需要使用磷结合剂进行治疗。碳酸镧就是其中一种，它是一种无铝的非钙基化合物。本综述总结了有关碳酸镧在终末期肾病和高磷血症患者中的安全性、有效性和耐受性的最新文献数据。该药物以咀嚼片或粉末形式口服，胃肠道吸收极少，从而降低了组织沉积和全身药物相互作用的风险。药物在上消化道酸性环境中解离，释放出镧离子，镧离子与饮食中的磷酸盐结合形成不溶性复合物，然后随粪便排出。尽管没有明确证据表明降低血清磷水平能改善以患者为中心的结局，但不排除所有磷结合剂，尤其是不含钙的磷结合剂具有降低死亡率的益处。与其他磷结合剂相比，碳酸镧已被证明可降低全因死亡率，但不会降低心血管事件发生率。与碳酸钙和醋酸钙相比，它对骨转换的抑制作用更低，与碳酸钙相比，可能改善收缩功能和心脏大小。此外，与其他磷结合剂相比，使用碳酸镧与更好的营养状况相关，与含钙结合剂相比，高钙血症风险更低，与盐酸司维拉姆相反，可改善轻度代谢性酸中毒。主要不良反应包括恶心、碱性胃反流、镧在胃内沉积、胃肠道梗阻、小肠梗阻、肠梗阻、穿孔、粪便嵌塞，以及降低某些药物（包括他汀类药物、血管紧张素转换酶抑制剂和一些抗生素，如氟喹诺酮类或四环素类）的胃肠道吸收。
