磷是所有生物体的必需元素，参与了多种生物途径。严重的低磷血症可以导致严重的并发症（急性心脏或呼吸衰竭，横纹肌溶解，溶血...），并增加处于风险中的患者的死亡率。众所周知，各种药物通过不同机制引起低磷血症。本研究的目的是通过描述性分析和病例对照分析，利用法国药物监测网络报告的药物诱发低磷血症病例，突出显示与低磷血症相关的主要药物，并推断其潜在机制。本研究共纳入368例低磷血症病例。患者的平均年龄为52±18岁。其中191例（52%）为严重病例，包括131例（36%）住院。血清磷水平的中位数为0.54mmol/L [0.40-0.66]（n=309）。这368例病例对应了185种不同的疑似物质，其中最常见的药物是替诺福韦二丙胺（n=175，48％）、羟乙酸铁羧基麦芽糊精（n=29，8％）、骨抑素（n=16，4％）、佐莱隆酸（n=14，4％）和氯噻嗪（n=10，3％）。对于这五种药物，发现了明显的不均衡性。替诺福韦二丙胺相关的低磷血症在其上市一年多后发生，共有44例报道了肾小管病变（范科尼综合征）。与羟乙酸铁羧基麦芽糊精相关的低磷血症在注射后中位数20天内发生，且多数严重。其中的机制包括可测量的纤维母细胞生长因子23，以确定药物来源。关于抗骨质疏松治疗，低磷血症可能可以通过它们的作用机制（由低钙血症引起的甲旁素急剧增加）来解释，但患者的病史（恶性病变状态）是主要的偏倚因素。对于氯噻嗪，低磷血症常常是中度的，与其他电解质紊乱有关，并在长期治疗过程中发生。医疗保健专业人员的意识对于及早发现与这些药物有关的低磷血症及其并发症至关重要。版权所有©2023 Société française de pharmacologie et de thérapeutique。由Elsevier Masson SAS出版。保留所有权利。

Phosphorus is an essential element for all living organisms and is involved in various biological pathways. A severe hypophosphatemia can lead to serious complications (acute heart or respiratory failure, rhabdomyolysis, hemolysis…) and increases mortality in patients at risk. Various drugs are known to induce hypophosphatemia through various mechanisms. The aim of this study was to highlight the main drugs associated with hypophosphatemia and to deduce the underlying mechanisms based on a descriptive analysis and a case/non-case analysis using the cases of drug-induced hypophosphatemia reported to the French Pharmacovigilance Network. A total of 368 cases of hypophosphatemia were included in the study. Patients' mean age was 52±18 years. One hundred and ninety-one cases (52%) were serious including 131 (36%) hospitalizations. The median value of serum phosphorus level was 0.54mmol/L [0.40-0.66] (n=309). Those 368 cases corresponded to 185 different suspected substances among which the most frequent drugs were tenofovir disoproxil (n=175; 48%), ferric carboxymaltose (n=29; 8%), denosumab (n=16; 4%), zoledronic acid (n=14; 4%) and hydrochlorothiazide (n=10; 3%). For these five drugs, a significant disproportionality was found. Tenofovir-disoproxil related hypophosphatemia occurred more than one year after its introduction, and a renal tubulopathy (Fanconi's syndrome) was reported in 44 cases (25%). Hypophosphatemia related to iron carboxymaltose occurred within a median of 20 days after injection and was mostly severe. Mechanism included the fibroblast growth factor 23 which can be measured to confirm drug origin. Concerning anti-osteoporosis treatments, hypophosphatemia could be explained by their mechanism of action (abrupt increase of parathormone induced by hypocalcemia) but the patient history (malignancy condition) was a major bias. For hydrochlorothiazide, hyphosphatemia was often moderate, associated with other electrolytic disturbances and occurred during a long-term treatment. Awareness of healthcare professionals is essential to detect as soon as possible hypophosphatemia and its complications related to these drugs.Copyright © 2023 Société française de pharmacologie et de thérapeutique. Published by Elsevier Masson SAS. All rights reserved.