Search Results (79)

Background/Objectives: Vitamin D deficiency remains common in UVB-constrained, pollution-exposed, sedentary, and ageing populations, yet recent guidelines discourage routine screening and empiric high-dose supplementation in generally healthy adults. This review clarifies the clinical distinction between untargeted population supplementation and monitored repletion of documented deficiency in high-risk individuals. Methods: We conducted a focused narrative review of PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library. The focused evidence search supporting the narrative synthesis was completed in June 2026. References published subsequently were included during manuscript preparation only when relevant for contextual purposes and were not incorporated retrospectively into the evidence-selection process underlying the review’s clinical conclusions. Evidence was interpreted according to baseline and achieved 25-hydroxyvitamin D [25(OH)D], dosing schedule, route, body composition, endpoint, and population risk. No formal risk-of-bias assessment, certainty grading, or systematic meta-analytic synthesis was performed. Key Findings: The strongest rationale for vitamin D repletion remains musculoskeletal, particularly for osteomalacia, muscle function, osteoporosis care, and fracture-related vulnerability in deficient or high-risk patients. Management should separate generally healthy adults from patients with an indication for testing or treatment. Historical and regional expert frameworks describe time-limited higher-dose repletion for documented deficiency, but these regimens should not be interpreted as a current universal Endocrine Society treatment standard. Short-term trials using moderate cumulative oral doses suggest broadly comparable biochemical repletion with daily, weekly, or monthly schedules; equivalence has not been established for long-term clinical outcomes, frail populations, or large intermittent doses. Extra-skeletal associations remain less trial-supported. Conclusions: Vitamin D deficiency should be managed using clinically indicated assessment, explicit repletion and maintenance regimens, and selective biochemical reassessment. Targets above conventional skeletal adequacy thresholds remain investigational and should not be applied as universal treatment goals. Full article

Background and Clinical Significance: Tenofovir disoproxil fumarate (TDF) is a widely prescribed nucleotide reverse transcriptase inhibitor (NtRTI) for HIV-1 infection. Though generally well-tolerated, proximal renal tubulopathy resulting in full-blown Fanconi syndrome remains a rare but severe complication (<0.1%). Case Presentation: We present the case of a 52-year-old female living with HIV-1 (diagnosed in 1999, CDC stage A3) who had been treated with a TDF-based antiretroviral regimen for 12 years. Upon admission, she complained of progressive bone pain and polyuria over the preceding six months. Laboratory investigations revealed profound hypokalemia, severe hypophosphatemia, hypouricemia, elevated alkaline phosphatase (ALP) and a decline in renal function (creatinine 1.3 mg/dL from a baseline of 0.7 mg/dL). Arterial blood gas (ABG) analysis showed a normal anion gap hyperchloremic metabolic acidosis alongside respiratory acidosis. Urinalysis demonstrated profound glycosuria in the setting of normal blood glucose levels, coupled with increased 24 h urinary excretion of potassium and phosphorus. A bone scintigraphy demonstrated a “super scan” pattern of metabolic etiology, establishing secondary osteomalacia driven by renal phosphate wasting. Secondary hyperparathyroidism and severe vitamin D3 deficiency were also recorded. The diagnosis of TDF-induced Fanconi syndrome was established. TDF was discontinued, and her antiretroviral regimen was modified to tenofovir alafenamide fumarate (TAF), emtricitabine (FTC), darunavir, and ritonavir, combined with vitamin D supplementation. Over a 6-month follow-up period, renal function normalized, electrolyte wasting resolved, and metabolic acidosis completely reversed. Conclusions: This case highlights that TDF-induced proximal tubulopathy can manifest even after a decade of uneventful therapy, particularly when co-administered with a boosted protease inhibitor. Full article

Intravenous (IV) iron is used to replenish iron stores in patients with iron-deficiency anemia (IDA) who do not benefit from oral iron supplementation. Hypophosphatemia is an increasingly recognized adverse event associated with certain IV iron formulations. Mild/moderate hypophosphatemia may be asymptomatic or present with symptoms similar to those seen in patients with IDA, including fatigue, malaise, and muscle weakness. Persistent hypophosphatemia can cause osteomalacia due to reduced bone mineralization, leading to bone pain and pseudofractures. Ferric carboxymaltose (FCM) can impact phosphate homeostasis through an increase in fibroblast growth factor 23, leading to increased urinary phosphate excretion and hypophosphatemia. In clinical trials, rates of hypophosphatemia were significantly higher in patients receiving FCM compared with other IV iron formulations, such as ferric derisomaltose and ferumoxytol. Treatment guidelines recommend monitoring serum phosphate levels in patients receiving FCM who are at risk for low phosphate or who require repeat infusions, and alternative iron formulations should be considered in at-risk patients. This narrative review summarizes current evidence regarding IV iron-induced hypophosphatemia in individuals with IDA and examines the underlying pathophysiology and clinical evidence for IV iron-induced hypophosphatemia, particularly with FCM, the populations most at risk, and the clinical consequences of persistent hypophosphatemia. Full article

Background: Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by fibroblast growth factor 23 (FGF-23)-secreting tumors, typically of mesenchymal origin, leading to renal phosphate wasting and severe bone demineralization and fragility fractures. Diagnosing TIO remains a significant clinical challenge, particularly when coexisting mineral metabolism disorders, such as hypercalcemic hyperparathyroidism, are masking its clinical presentation. Case Presentation: A 74-year-old woman with fragility fractures, generalized bone pain, and nephrolithiasis was initially diagnosed with primary hyperparathyroidism due to concomitant hypercalcemia, hypophosphatemia, and elevated parathyroid hormone (PTH). Despite a successful parathyroidectomy, which normalized calcium levels, severe hypophosphatemia persisted due to renal phosphate wasting. High FGF-23 levels and subsequent functional imaging indicating a somatostatin receptor-positive lesion in the left popliteal fossa led to the diagnosis of TIO. Surgical resection immediately normalized FGF-23 levels, leading to a slower rise in phosphorus during follow-up. Histopathology revealed a tophaceous-like giant cell granulomatous reaction, recalling the earlier report by Prader. Conclusions: This case highlights that parathyroid disorders can coexist with TIO, and they may delay its diagnosis. In this circumstance, a high index of clinical suspicion is represented by the persistence of hypophosphatemia post-parathyroidectomy. Full article

Vitamin D, a fat-soluble vitamin functioning as a hormone via the vitamin D receptor (VDR), is critical for calcium homeostasis and bone health. Vitamin D deficiency is linked to nutritional rickets, osteomalacia, and increased risk of non-communicable diseases such as cancer and diabetes. While serum 25(OH)D₃ is used to assess vitamin D status, its active form, 1α,25(OH)₂D₃, exerts context-dependent effects on calcium metabolism. Nonetheless, the therapeutic utility of native vitamin D is limited in certain pathologies. In chronic kidney disease (CKD), the renal conversion of 25(OH)D₃ to active 1α,25(OH)₂D₃ is compromised, necessitating the use of active synthetic analogs to bypass this metabolic defect. Furthermore, for dermatological and oncological disorders requiring supraphysiological dosing, synthetic analogs have been designed to dissociate beneficial anti-proliferative effects from the severe hypercalcemia induced by high-dose 1α,25(OH)₂D₃. VDR mediates transcriptional responses, modulated by co-regulators and chromatin remodeling complexes. Recent discoveries include non-genomic VDR pathways and SCAP (SREBP cleavage-activating protein)-dependent signaling that modulate lipid metabolism. Despite promising preclinical results, most synthetic VDR agonists fail to show efficacy in cancer therapy due to calcemic toxicity. However, compounds like eldecalcitol are effective in osteoporosis, especially in low-calcium-intake populations. Selective VDR modulators, akin to SERMs, exhibit tissue-specific effects. Moreover, novel VDR antagonists such as ZK168281 demonstrate potential to suppress hypercalcemia and vitamin D toxicity by inhibiting transcriptional activity and altering VDR localization. These agents may enable anti-inflammatory or anti-proliferative actions without calcemic risks. Understanding the nuanced biology of vitamin D and its analogs offers new avenues for therapeutic intervention beyond bone metabolism, including managing hyperparathyroidism, granulomatous diseases, and inflammation-associated disorders. Full article

Cadmium (Cd) is a ubiquitous environmental pollutant that enters the circulation from the lungs and gastrointestinal tract. For most people, staple foods form the main route of Cd exposure. Current evidence suggests that Cd may increase the prevalence of iron deficiency and anemia in environmentally exposed people. Concerningly, intravenous iron administration to treat iron deficiency anemia has resulted in adverse bone outcomes at a higher-than-expected frequency, for which reasons remain unclear. The bone-derived hormone fibroblast growth factor 23 (FGF23), the regulator of vitamin D and phosphate homeostasis, has been speculated to be implicated, given that anemia, iron deficiency and inflammatory conditions are all known to increase FGF23 expression levels in osteoblasts. Additionally, early studies have demonstrated that Cd increases FGF23 expression by osteoblast-like cells and suppresses FGF23 cleavage, leading to an abrupt rise in serum FGF23, which, in turn, mediates an effect of Cd on tubular phosphate reabsorption. In this review, experimental breakthrough studies showing Cd-induced iron deficiency and a reduction in iron absorption by Cd are summarized, together with intestinal absorption of Cd and an increment in Cd uptake and Cd body burden in those with low body iron stores. Potential contributions of Cd, anemia and iron deficiency in the context of hypophosphatemic osteomalacia development after intravenous iron supplementation are discussed. The molecular basis of Cd-induced ferroptosis in pathogenesis of osteoporosis, emphasizing heme oxygenase-1 (HO-1)/bilirubin axis and zinc deficiency, is presented. Full article

Vitamin D is well established for its skeletal effects, being a cornerstone of several endocrine disorders. In recent years, it has come under investigation as a potential disease-modifying drug in several endocrine disorders through its immune modulatory and anti-tumorigenic action, particularly in thyroid disease, gynecologic disorders, and general fertility. Vitamin D supplementation is well established in the treatment of osteoporosis, osteomalacia, hypoparathyroidism, and primary hyperparathyroidism. In autoimmune thyroid disease, there is a negative correlation between 25(OH)D3 levels and prevalence. Currently available data are inconclusive on supplementation as a disease-modifying treatment. In Hashimoto’s thyroiditis, while some found improved thyroid function, a decline in progression, and antibody titers, these findings were not consistent, and some found no improvements. Painless postpartum thyroiditis severely lacks evidence. Interventional studies failed to demonstrate benefits in Graves’ disease. The literature consistently reports lower vitamin D levels in infertility, polycystic ovarian syndrome (PCOS), and endometriosis. In PCOS, data suggest that vitamin D supplementation is beneficial; however, results in exact benefits vary and there is no consensus on dosing. Current guidelines support supplementation as part of preconception nutritional care. In general, for female infertility and endometriosis, the results are conflicting, with a lack of high-quality evidence. The literature suggests there is a possible benefit regarding sperm motility, but not in testosterone levels for males. In conclusion, while in vitro studies and animal models are promising, the available evidence is often contradictory, with high heterogeneity in study designs and populations. Our paper highlights the need for further high-quality research to resolve current controversies. Full article

Hypophosphatasia (HPP) is an exceptional genetic bone disorder of metabolic character caused by a deficit of the tissue-nonspecific alkaline phosphatase isoenzyme (TNSALP). This protein is encoded by the ALPL (alkaline phosphatase liver/bone/kidney) gene. In the medical literature, HPP is also known as Rathbun’s syndrome, named after the Canadian physician who first identified this disorder. Patients exhibit persistently low serum alkaline phosphatase (ALP) levels. In fact, ALP renders this measure a reliable indicator of the condition. Adult HPP is varied, with some patients exhibiting only moderate, non-pathognomonic symptoms. They include arthropathy, arthrodynia, chondrocalcinosis, osteopenia, osteomalacia, and generic musculoskeletal discomfort. Healthcare may require coordinating several services to manage a patient with HPP. This comprehensive review will highlight the genetic knowledge, pathology data, and patient management approaches, including Medicare’s coverage. In addition, this paper aims to address specific themes related to HPP, including its significance, current challenges, and controversies. Full article

Vitamin D (VD), due to its hormonal action, plays a crucial role in calcium homeostasis and bone metabolism, and its deficiency has been associated with musculoskeletal disorders such as osteoporosis, fractures, and osteomalacia, as well as a growing attention of chronic conditions and certain cancers. Despite its physiological relevance and widespread prevalence, particularly among older individuals, patients with chronic diseases, institutionalized populations and pregnant or lactating women, clinical approaches to diagnosing and managing vitamin D deficiency (VDD) remain heterogeneous across guidelines and healthcare settings. This reflects a lack of consensus regarding the benefits and limitations of universal versus selective screening, the definition of adequate serum concentrations, and the clinical indications for supplementation across different patient profiles. This narrative review explores key controversies in the clinical management of VDD, including current perspectives on screening strategies and target populations, indications for empirical supplementation, criteria for biochemical monitoring, and therapeutic goals in bone-related outcomes. In particular, the review discusses the rationale for adopting a 30 ng/mL (75 nmol/L) threshold for adequate serum 25(OH) concentrations in skeletal health, the role of vitamin D and calcium in osteoporosis treatment, and the pharmacological advantages of cholecalciferol compared to other vitamin D compounds. Through a synthesis of available evidence and expert consensus, the review aims to support clinical decision-making in the prevention and treatment of VDD and to identify areas that require further clarification or research. This review aims to support evidence-based clinical decision-making. Full article

Background/Objectives: Tumor-induced osteomalacia (TIO) is a rare acquired paraneoplastic syndrome caused by phosphaturic mesenchymal tumors (PMTs). FGF23, which is overproduced by PMTs, causes hypophosphatemia and osteomalacia, ultimately leading to multiple insufficiency fractures, which are the cause of TIO symptoms. Therefore, recovery from TIO symptoms often takes several months. Due to its paracrine effects, even minuscule amounts of residual PMT can cause treatment to fail. To further compound this, the most confident methods for residual PMTs, serum FGF23 level and ⁶⁸Ga DOTA-based PET/CT, are not readily available. For these reasons, there is currently no established method for early prediction of TIO treatment outcomes after surgery. This study focuses on mineral metabolism and bone turnover markers to identify a clinically practical and readily available biomarker that can predict TIO treatment outcomes. Methods: During treatment, we analyzed repeated measurements during treatment of mineral metabolism and bone turnover markers for 19 cases of TIO—Ca, inorganic phosphate (Pi), parathyroid hormone (PTH), 25-hydroxyvitamin D, alkaline phosphatase, Procollagen 1 N-terminal Polypeptide, and β-CrossLaps—in relation to treatment outcomes. We selected predictive marker candidates from among these markers by analyzing their patterns of change during treatment based on three viewpoints—association with (1) cure status, (2) time after treatment, and (3) the interaction effects between (1) and (2) using Linear Mixed Model analysis. We also validated the predictive performance of the selected candidates. Results: In long-term follow-up, only serum Pi and PTH levels were significantly associated with all three metrics mentioned above, suggesting that their patterns of change reflect the clinical course and results of TIO treatment. Pi was the only marker that displayed the same associations during short-term follow-up (two weeks and six weeks after treatment), suggesting that it is a rapidly responsive marker. The serum Pi level two weeks after treatment (Odds Ratio = 7.314, p = 0.028, AUC value of 0.907) and the normalization of Pi at two weeks post-treatment (Relative Risk = 9.975, p = 0.010; sensitivity = 100.0% [95% Confidence Interval (CI) 0.860 to 1.000], specificity = 60.0% [95% CI, 0.208 to 0.600]) were both significantly associated with a complete cure. Conclusions: Serum Pi is a fast, simple, and highly sensitive marker that can replace serum FGF23 and ⁶⁸Ga DOTA-based PET/CT in clinical practice for predicting a complete cure of TIO within two weeks of surgery. Full article

Background: Phosphaturic mesenchymal tumours secreting fibroblast growth factor 23 (hereinafter referred to as FGF23+ PMT) are rare neoplasms that can cause hypophosphataemic osteomalacia, owing to excessive FGF23 production. Mast cells (MCs) play a key role in tumour biology by modulating proliferative activity of atypical cells, resistance to innate and acquired immunity, angiogenesis, and metastatic behaviour. However, MCs associated with FGF23+ PMT have not previously been investigated. This study, to our knowledge, is the first to characterise features of the tumour microenvironment through spatial phenotyping of the immune and stromal landscape, together with histotopographic mapping of intercellular MC interactions with other subcellular populations in FGF23+ PMT. Methods: Histochemical staining (haematoxylin and eosin, toluidine blue, Giemsa solution, picro-Mallory protocol, silver impregnation), as well as monoplex and multiplex immunohistochemical staining with spatial phenotyping, were performed to detect atypical FGF23-secreting cells, immune cells (CD3, CD4, CD8, CD14, CD20, CD38, CD68, or CD163), stromal components (CD31, α-SMA, or vimentin), and specific MC proteases (tryptase, chymase, or carboxypeptidase A3). Bioinformatics analysis using artificial intelligence technologies was applied for spatial profiling of MC interactions with tumour, immunocompetent, and stromal cells in the tumour microenvironment. Results: Bioinformatic analysis of the entire tumour histological section, comprising over 70,000 cells stained using monoplex and multiplex immunohistochemical protocols, enabled identification of more than half of the cell population. The most abundant were CD14+ (30.7%), CD163+ (23.2%), and CD31+ (17.9%) cells. Tumour-associated MCs accounted for 0.7% of the total pool of immunopositive cells and included both mucosal and connective tissue subpopulations, predominantly of the tryptase + chymase-CPA3-specific protease phenotype. This pattern reflected combined multidirectional morphogenetic processes in the patient’s FGF23+ PMT. More than 50% of MCs were colocalized with neighbouring cells of the tumour microenvironment within 20 μm, most frequently with monocytes (CD14+CD68+), M2 macrophages (CD68+CD163+), and endothelial cells (CD31+). In contrast, colocalization with atypical FGF23-secreting cells was rare, indicating minimal direct effects on tumour cell activity. Interaction with T lymphocytes, including CD8+, was also infrequent, excluding their activation and the development of antitumour effects. Mapping of MC histotopography validated the hypothesis of their inductive role in monocyte differentiation into M2 macrophages and probable polarisation of macrophages from M1 into M2, thereby contributing to slow tumour growth. MCs were further involved in extracellular matrix remodelling and participated in the formation of pro-osteogenic niches within the FGF23+ PMT microenvironment, leading to pathological osteoid development. Conclusions: This study demonstrated active MC participation in the evolution of the FGF23+ PMT microenvironment. The findings may be applied in translational medicine to develop novel algorithms for personalised therapy in patients with FGF23-secreting tumours, offering an alternative when surgical removal of the tumour is not feasible. Full article

Hypophosphatemia is a rare ion disorder in children, but it carries the risk of serious clinical sequelae in tissues and organs with high energy requirements, such as bone tissue. This article discusses the metabolism of phosphate in the body, the clinical manifestations of hypophosphatemia, and the diagnostic tests necessary in patients with this disorder. Extra-renal causes are analyzed, and renal forms of hypophosphatemia are discussed in detail. Renal hypophosphatemia, depending on the mechanism, is divided into PTH-dependent (e.g., primary hyperparathyroidism), FGF23-dependent (e.g., X-linked hypophosphatemia), and intrinsic renal hypophosphatemia (e.g., Fanconi syndrome). The treatment of hypophosphatemia involves compensating for phosphate deficiency, often simultaneously with the supply of an active form of vitamin D. Always seek causal treatment, such as parathyroidectomy in primary hyperparathyroidism. In the FGF-23-dependent forms of X-linked hypophosphatemia and tumor-induced osteomalacia, burosumab has proven to be an effective and safe drug. Conclusions: a child with hypophosphatemia requires a multidisciplinary approach and determination of the mechanism of phosphate deficiency in the body. Full article

Cadmium (Cd), a pervasive environmental and industrial toxicant, bioaccumulates and exerts severe detrimental effects on skeletal integrity across diverse animal species. Cd-induced bone injury manifests as osteoporosis, osteomalacia, and increased fracture risk, posing significant health and welfare concerns for wildlife and livestock inhabiting contaminated ecosystems. The pathogenesis hinges critically on the disruption of bone remodeling, a tightly regulated process orchestrated by osteoclasts (OCs) responsible for bone resorption and osteoblasts (OBs) responsible for bone formation. This comprehensive review synthesizes the latest mechanistic insights into how Cd disturbs OC and OB function and their intricate crosstalk, leading to net bone loss. Cd directly impairs OB proliferation, differentiation, and mineralization capacity through multiple pathways, including the inhibition of Wnt/β-catenin signaling, induction of oxidative stress and mitochondrial dysfunction, promotion of apoptosis and senescence, and disruption of extracellular matrix protein synthesis. Simultaneously, Cd potently stimulates excessive OC formation and activity. It achieves this by upregulating the RANKL/OPG axis, enhancing reactive oxygen species (ROS) production which activates key OC transcription factors, modulating key signaling pathways, and promoting pro-osteoclastogenic inflammatory cytokine release from bone marrow and immune cells. Critically, Cd disrupts the vital communication between OBs and OCs, perturbing the coupling signals essential for balanced remodeling. Emerging evidence highlights roles for Cd-induced epigenetic modifications and autophagy/mitophagy flux alterations. This narrative review integrates the findings from in vivo animal models and in vitro cellular studies, providing potential therapeutic interventions and mitigation strategies for Cd-induced bone toxicity. Understanding these complex and interacting mechanisms provides a foundation for identifying potential therapeutic targets to mitigate Cd bone toxicity in animals and informs ecological risk assessment and management strategies in contaminated environments. Full article

Paraneoplastic syndromes (PNSs) are pathologic conditions produced by neoplasms not attributable to tumor invasion or metastasis. The clinical manifestations of PNSs can precede the diagnosis; these symptoms may serve as early indicators of underlying malignancy. Standard imaging modalities, such as computed tomography (CT) and magnetic resonance imaging (MRI), have limited sensitivity in detecting small or early-stage PNS-associated tumors. FDG PET/CT identifies hypermetabolic lesions suggestive of malignancy and, therefore, facilitates early diagnosis, refined treatment planning, and potentially prolonged patient survival. This review evaluates the diagnostic accuracy, clinical utility, and emerging role of FDG PET/CT in detecting occult malignancies. Syndrome-targeted applications discussed include limbic encephalitis, cerebellar degeneration, Lambert-Eaton myasthenic syndrome, Cushing’s syndrome, hypercalcemia of malignancy, dermatomyositis, and tumor-induced osteomalacia. In addition, the limitations of FDG PET/CT, including false-positive or false-negative findings, are reviewed, while newer PET tracers, like ⁶⁸Ga-DOTATATE, are also highlighted. Ultimately, FDG PET/CT has transformed clinical decision-making, enabling more timely interventions and improved patient management in the context of PNSs. Future directions in imaging, including PET/MRI and ongoing refinements in tracer design, promise to further enhance diagnostic precision, and therapeutic outcomes are also discussed. Full article

Background/Objectives: The development of hypophosphatemia has been associated with intravenous iron products, with the rate of hypophosphatemia found to be higher with ferric carboxymaltose. This consensus statement provides clinical guidance on the risk of hypophosphatemia development with ferric carboxymaltose and the approaches for management. To develop consensus recommendations regarding the clinical implications of hypophosphatemia after the administration of ferric carboxymaltose, the assessment of patient risk profile, and recommended approaches for risk reduction. Methods: Consensus statements were developed from an in-person meeting of specialists with expertise in iron pathophysiology and iron therapy and further supplemented with literature review. The multidisciplinary expert panel comprised global iron specialists spanning anesthesiology, cardiology, gastroenterology, obstetrics/gynecology, hematology, nephrology, and iron molecular biology. Structured discussions were held in an in-person meeting to gather expert opinion on the evidence base regarding intravenous iron and hypophosphatemia. Consolidated summary opinions underwent further iterations of panel review to form consensus recommendation statements. Results: The expert panel developed the following consensus statements: (1) Routine serum phosphate level measurement is not recommended for low-risk patients before or after treatment with ferric carboxymaltose, as most cases of hypophosphatemia that occur following the administration of ferric carboxymaltose are asymptomatic and transient; (2) patients receiving ferric carboxymaltose should be assessed for the degree of risk for developing symptomatic or severe hypophosphatemia prior to administration; (3) monitoring serum phosphate is recommended for patients at an increased risk for developing low serum phosphate or who require repeated courses of ferric carboxymaltose treatment at higher doses; (4) prophylactic oral phosphorus after ferric carboxymaltose is unlikely to effectively elevate phosphate and is not recommended for routine clinical practice; and (5) hypophosphatemic osteomalacia is rare and the risk of development after the administration of ferric carboxymaltose, in particular single infusion, is low. Conclusions: Hypophosphatemia following ferric carboxymaltose is predominantly asymptomatic and transient. Individuals at higher risk for developing hypophosphatemia with ferric carboxymaltose treatment include those who receive multiple infusions, higher cumulative doses, or long-term iron treatment or who have underlying clinical risk factors. These consensus statements provide structured guidance on the risk of hypophosphatemia with ferric carboxymaltose and the approaches to clinical management. Full article