Intravenous Iron and Low Phosphate: The Ferric Carboxymaltose Effect

Table of Contents

1. How an Iron Infusion Lowers Phosphate
2. The PHOSPHARE-IDA Trials
3. Trials in Inflammatory Bowel Disease
4. Other Head-to-Head Comparisons
5. What the Pooled Analyses Found
6. Symptoms and Fatigue
7. Bone Softening and Fractures After Repeated Infusions
8. Risk Factors Reported in Studies
9. What the FDA Labels Say
10. Monitoring as Labels and Reviews Describe It
11. What Is Not Known
12. Key Research Papers
13. Connections
14. Featured Videos

How an Iron Infusion Lowers Phosphate

Phosphate in the blood is held steady largely by the kidneys, which decide how much to keep and how much to pass into the urine. One of the signals that tells them to let phosphate go is a hormone made by bone cells called fibroblast growth factor 23 (FGF23). When this hormone rises, the kidney spills phosphate into the urine and makes less of the active form of vitamin D (1,25-dihydroxyvitamin D), which in turn means less phosphate and calcium absorbed from food. Rare inherited diseases and rare tumors that overproduce the same hormone cause the same pattern; the Bone Pain and Softening page describes those conditions.

A 2013 randomized study in 55 women with iron-deficiency anemia after heavy uterine bleeding measured the hormone in two forms. Iron deficiency itself was linked with very high levels of the broken-down (C-terminal) fragment but normal levels of the intact, active hormone. Within 24 hours of an infusion, the fragment fell by about 80% with both products tested. The intact, active hormone, however, rose briefly only in the women given ferric carboxymaltose, and 10 of them then developed a short-lived, symptom-free fall in phosphate below 2.0 mg/dL, against none of the women given iron dextran. The fall came with more phosphate in the urine, lower active vitamin D and higher parathyroid hormone. The authors proposed, as a hypothesis, that the sugar (carbohydrate) shell of certain iron products may block the normal breakdown of the hormone inside bone cells, so more of the active form reaches the blood (Wolf 2013).

Later trials measured the same chain of events. In a small randomized trial of 26 women, those given ferric carboxymaltose had higher intact hormone levels and lower active vitamin D within 24 hours than those given ferric derisomaltose, and more phosphate left in the urine at about day 7 (Emrich 2020). A comprehensive 2022 review describes the typical pattern as phosphate wasting into the urine driven by the hormone, causing low active vitamin D, low calcium and a secondary rise in parathyroid hormone (Schaefer 2022, Bone). The parathyroid response is covered on the Secondary Hyperparathyroidism page.

The PHOSPHARE-IDA Trials

The clearest head-to-head data come from two identically designed, open-label randomized trials, published together in 2020 and known as PHOSPHARE-IDA. Between October 2017 and June 2018 they enrolled 245 adults with iron-deficiency anemia (hemoglobin 11 g/dL or less, ferritin 100 ng/mL or less) who had not tolerated or not responded to at least a month of iron tablets, at 30 outpatient sites in the United States. People with reduced kidney function were excluded. Most participants were women (95.9% in trial A, 94.1% in trial B), with an average age in the early to mid 40s.

The trials gave either ferric derisomaltose (then called iron isomaltoside) 1,000 mg once, or ferric carboxymaltose 750 mg on day 0 and again on day 7. Blood phosphate and 12 other markers of mineral and bone balance were measured on days 0, 1, 7, 8, 14, 21 and 35.

Both differences were statistically significant (P < .001). Read the other way, roughly three in four people given ferric carboxymaltose developed low phosphate within five weeks, against roughly one in twelve given ferric derisomaltose. Apart from low phosphate and a rise in parathyroid hormone, the most common drug reactions were nausea (1 of 125 with ferric derisomaltose, 8 of 117 with ferric carboxymaltose) and headache (4 of 125 and 5 of 117). The authors concluded that ferric derisomaltose caused less low phosphate over 35 days, and wrote that further research is needed to determine how much this difference matters clinically (Wolf 2020). As the paper discloses, one author was an employee of the maker of ferric derisomaltose and most of the others reported fees from that maker during the study.

A follow-up analysis of the same 245 patients looked for risk factors. Ferric carboxymaltose was the only consistent one: compared with ferric derisomaltose, the odds of low phosphate were about 38 times higher (odds ratio 38.37). Only people given ferric carboxymaltose developed severe low phosphate below 1.0 mg/dL (11.3%, 13 of 115) or low phosphate still present at the end of the study (40.0%, 46 of 115). The deeper the fall in phosphate, the greater the rise in the hormone, parathyroid hormone and alkaline phosphatase (a bone-building enzyme), and the greater the fall in active vitamin D and ionized calcium. Changes in bone markers continued after phosphate had returned to normal, which the authors suggest may help explain the link between ferric carboxymaltose and bone softening and fractures (Schaefer 2022, J Clin Endocrinol Metab).

Trials in Inflammatory Bowel Disease

Iron deficiency is common in inflammatory bowel disease (IBD), the group that includes Crohn’s disease and ulcerative colitis, because of blood loss and poor absorption, so people with inflammatory bowel disease often receive intravenous iron.

PHOSPHARE-IBD was a double-blind randomized trial at 20 hospital clinics in Austria, Denmark, Germany, Sweden and the United Kingdom. Adults with inflammatory bowel disease and iron-deficiency anemia received either product at the start and again at day 35, dosed by hemoglobin and body weight in the same way for both groups. Ninety-seven patients were treated. Low phosphate at any time up to day 35 occurred in 8.3% (4 of 48) given ferric derisomaltose and 51.0% (25 of 49) given ferric carboxymaltose, an adjusted difference of 42.8 percentage points. Both products corrected the anemia. Fatigue scores improved in both groups, but more slowly and to a smaller extent with ferric carboxymaltose, and slower improvement in fatigue went along with a larger fall in phosphate (Zoller 2023). The abstract’s enrolment line lists 49 patients on ferric derisomaltose and 48 on ferric carboxymaltose, while its result fractions use 48 and 49; the percentages above are the ones the abstract reports.

An earlier prospective observational study in Norway followed 106 people with inflammatory bowel disease (per-protocol) given 1,000 mg of either product. Moderate-to-severe low phosphate at week 2 occurred in 56.9% given ferric carboxymaltose against 5.7% given iron isomaltoside (the former name of ferric derisomaltose). Any low phosphate was found in 72.5% against 11.3% at week 2 and in 21.6% against 3.7% at week 6. The authors described the persistence of moderate-to-severe low phosphate beyond six weeks as a clinical concern needing further study (Detlie 2019). Because patients were not randomized, differences between the groups other than the product may have played a part.

Other Head-to-Head Comparisons

Several other randomized trials compared ferric carboxymaltose with a different intravenous iron and counted low phosphate:

• Against ferric derisomaltose, single high dose. In the HOMe aFers trial, 26 women with iron-deficiency anemia received one infusion of 20 mg per kg of body weight (maximum 1,000 mg) of either product. Low phosphate occurred in 9 of 12 (75%) given ferric carboxymaltose and 1 of 13 (8%) given ferric derisomaltose. The trial found no differences in heart or skeletal markers, which the authors attribute possibly to its small size (Emrich 2020).
• Against ferumoxytol. A large double-blind trial in 1,997 adults, designed mainly to compare allergic reactions, gave ferumoxytol (1.02 g total) or ferric carboxymaltose (1.50 g total) in two infusions about a week apart. Low phosphate occurred in 0.4% given ferumoxytol and 38.7% given ferric carboxymaltose. Serious allergic reactions or low blood pressure were rare and similar in both groups (0.6% and 0.7%), with no anaphylaxis reported (Adkinson 2018).
• Against iron dextran. In the 2013 study of women with heavy uterine bleeding described above, 10 women given ferric carboxymaltose and none given iron dextran developed low phosphate (Wolf 2013).

Studies comparing ferric carboxymaltose with iron sucrose appear in the pooled analyses below.

What the Pooled Analyses Found

Ferric carboxymaltose against ferric derisomaltose. A 2021 systematic review and meta-analysis pooled 42 prospective clinical trials. Low phosphate occurred in 47% of people given ferric carboxymaltose (95% confidence interval 36–58%) and 4% of people given ferric derisomaltose (2–5%). The average fall in blood phosphate was 0.40 mmol/L against 0.06 mmol/L. In up to 45% of people given ferric carboxymaltose, low phosphate was still present at the end of the study periods, which lasted at most 3 months (Schaefer 2021).

All intravenous iron products. A 2020 network meta-analysis of 8 randomized trials with 5,989 patients ranked ferric carboxymaltose as having the highest risk of low phosphate of the products studied. Compared with it, the risk ratio favored iron isomaltoside (7.9 times lower), iron sucrose (9.4 times lower), iron dextran (6.6 times lower) and ferumoxytol (24 times lower). The other four products did not differ significantly from one another. The authors called for large randomized trials to measure the risk of symptomatic and long-lasting low phosphate (Bellos 2020).

Products sold in the United States. A 2020 systematic review of 40 publications found reported rates of low phosphate ranging from 0.0% to 92.1% for ferric carboxymaltose, 0.0% to 40.0% for iron sucrose, 0.4% for ferumoxytol and 0.0% for low-molecular-weight iron dextran. Most studies did not describe how phosphate was monitored or give a definition of low phosphate, and randomized trials described the low phosphate as “asymptomatic” or did not report what followed. The reviewers concluded that the trials may underestimate how common the problem is (Glaspy 2020). Several authors of this review were employed by the maker of a competing product, as the paper discloses.

A 2025 systematic review drew on FDA adverse-event reports, case reports, case series, observational databases, trials, meta-analyses and the labels. In trials comparing ferric carboxymaltose with other intravenous iron products, low phosphate rates were 50% to 92% with ferric carboxymaltose against 2% to 8% with the others (Magagnoli 2025). These authors declared no conflicts of interest.

Symptoms and Fatigue

Many people with low phosphate after an infusion notice nothing, and the large trials often recorded it only as a blood result. When symptoms occur, the sources describe a consistent set:

• The ferric carboxymaltose label lists fatigue, muscle weakness or pain, bone and joint pain, and bone fractures as signs and symptoms of low phosphate.
• The 2025 systematic review found the most common reported features to be general weakness, fatigue, bone pain, muscle pain, bone softening (osteomalacia) and fractures (Magagnoli 2025).
• In the 2020 systematic review, case reports of short-term low phosphate described mainly severe fatigue, while people given repeated doses of ferric carboxymaltose developed long-lasting low phosphate with bone softening and bone deformities (Glaspy 2020).

Fatigue matters here because it is also the main symptom of iron-deficiency anemia itself, so a person may not be able to tell whether tiredness after an infusion comes from the anemia that has not yet recovered or from the new phosphate drop. The PHOSPHARE-IBD trial is the one randomized trial in this list that measured fatigue directly: fatigue improved more slowly with ferric carboxymaltose, and the slower improvement tracked with the size of the phosphate fall (Zoller 2023). The Phosphorus Deficiency and Fatigue page explains why cells low in phosphate run short of energy.

Bone Softening and Fractures After Repeated Infusions

A single course of treatment usually lowers phosphate for weeks. The serious bone problems described in the literature come mostly from people who received many infusions over months or years. This evidence comes from case reports and case series, which describe what happened to individual patients but cannot give a rate and tend to report the most severe cases.

A systematic review of case reports (2022). The review found 28 published reports describing 30 adults aged 28 to 80. Eighteen had received ferric carboxymaltose, 8 saccharated ferric oxide and 3 iron polymaltose. All but 2 had received more than five infusions (range 2 to 198, median 17). The lowest phosphate levels ranged from 0.16 to 0.77 mmol/L. The intact hormone was high whenever it was measured; alkaline phosphatase was high in 18 of 22. Bone or muscle pain was reported in 28 of 30 patients. Twenty had pseudofractures (incomplete stress lines typical of bone softening), 9 had fractures, and 6 had both. The authors identified bone softening as a potential complication of repeated iron infusion, especially in people with gastrointestinal disorders receiving long-term therapy, and found that stopping or switching the iron product worked in most cases. They noted that case reports favor severe cases, so reporting bias is possible (Vilaca 2022).

A case series of 13 patients (2024). A German bone clinic described 13 people with infusion-related bone softening; all had received ferric carboxymaltose and all had low phosphate. After the infusions were stopped and phosphate, calcium and vitamin D were given, average phosphate rose from 0.50 to 0.93 mmol/L, pain scores fell from 7.3 to 2.7 on a 10-point scale, and bone density improved. One patient who needed to keep receiving infusions was also given burosumab, an antibody that blocks the phosphate-wasting hormone, and the authors report additional benefit in that single case (von Brackel 2024).

A single case with a bone biopsy (2018). A person with Crohn’s disease and long-term gastrointestinal bleeding, receiving regular iron infusions, developed persistent low phosphate and insufficiency fractures. A bone biopsy from the hip bone showed typical bone softening, with a greatly increased amount of unmineralized bone and reduced bone formation. The patient had previously received vitamin D and the bone drug zoledronic acid (Bartko 2018).

The ferric carboxymaltose label itself states that severe cases with bone softening and fractures needing medical treatment have occurred after marketing, and its post-marketing list includes joint pain, back pain and low-phosphate bone softening. The broader causes and treatment of phosphate-related bone softening are covered on the Bone Pain and Softening page.

Risk Factors Reported in Studies

The product given is the largest single factor in every comparison above. Beyond that, the studies and the label report the following:

• Repeated infusions. In the case-report review, all but 2 of 30 patients with bone softening had received more than five infusions, with a median of 17 (Vilaca 2022). A 2022 review describes long-lasting low phosphate with repeated dosing as the setting for muscle disease, bone softening and fractures (Schaefer 2022, Bone).
• Normal kidney function. In the 2021 meta-analysis, normal kidney function predicted low phosphate (Schaefer 2021). The PHOSPHARE-IDA trials excluded people with reduced kidney function, and still found low phosphate in three of four given ferric carboxymaltose (Wolf 2020).
• More severe iron deficiency. Low ferritin and low transferrin saturation at the start predicted low phosphate in the 2021 meta-analysis (Schaefer 2021). In the follow-up analysis of PHOSPHARE-IDA, however, the product was the only consistent risk factor (Schaefer 2022, J Clin Endocrinol Metab).
• Inflammatory bowel disease and other gut disorders. The two inflammatory bowel disease studies found high rates with ferric carboxymaltose (Detlie 2019; Zoller 2023), and the case-report review singled out people with gastrointestinal disorders on long-term therapy (Vilaca 2022).
• Previous weight-loss (bariatric) surgery. In a prospective study of 52 people after gastric bypass (50) or sleeve gastrectomy (2), 29% developed new low phosphate one week after ferric carboxymaltose, and 21% were given phosphate by mouth, for a median of 14 days. Phosphate fell together with a 56% rise in urinary phosphate loss, a 30% rise in the intact hormone and a 37.6% fall in active vitamin D. The authors note this group often already has raised parathyroid hormone. The study had no comparison product (Schoeb 2020). Other nutrient losses after this surgery are covered on the Weight-Loss Drugs, Surgery and Vitamin B1 page.
• Factors listed on the ferric carboxymaltose label. Gastrointestinal disorders with poor absorption of fat-soluble vitamins or phosphate, inflammatory bowel disease, current or past use of medicines that affect the kidney’s proximal tubule, raised parathyroid hormone, vitamin D deficiency, malnutrition, and hereditary hemorrhagic telangiectasia (an inherited bleeding-vessel disorder; see Hereditary Hemorrhagic Telangiectasia). The label adds that people with none of these risk factors have also developed symptomatic low phosphate.

What the FDA Labels Say

The labels below were read in the FDA’s openFDA label database in November 2026. Products are named here by their generic names only.

Ferric carboxymaltose. The label carries a boxed warning, the FDA’s strongest, titled “Symptomatic Hypophosphatemia.” It states that the drug “can cause severe, prolonged hypophosphatemia associated with serious outcomes, including hospitalization, osteomalacia and fractures requiring clinical intervention,” and that low phosphate “has occurred in patients with normal baseline phosphate levels and without apparent risk factors.” The warnings section adds that “in most cases, hypophosphatemia resolved within three months,” and lists permanent stopping of the drug as an option for severe symptomatic or persistent low phosphate. The 2025 systematic review notes that this wording was updated in 2023 (Magagnoli 2025).

The same label’s table of adverse reactions in its two main adult trials lists hypophosphatemia in 2.1% of 1,775 patients, against 0.1% with the pooled comparison treatments. That figure counts low phosphate reported as an adverse reaction; the trials above measured phosphate in every participant on fixed days and found rates of 38.7% to 75%. In a children’s trial on the same label, hypophosphatemia was reported in 13% of 40 children, against 0% of 38 given iron by mouth.

Ferric derisomaltose. The label read carries no boxed warning and no warning section on phosphate. Its adverse-reaction section states that low phosphate (below 2.0 mg/dL) was reported in 3.5% of patients treated in its two main trials, which compared it with iron sucrose in 2,008 treated patients, including people with chronic kidney disease. The warnings section covers allergic reactions and iron overload.

Iron sucrose. The iron sucrose labels read (versions dated 2025 and 2026) contain no mention of low phosphate or bone softening.

Monitoring as Labels and Reviews Describe It

The ferric carboxymaltose label states:

• Serum phosphate is to be checked before a repeat course in people at risk of low phosphate, and in anyone receiving a repeat course within three months of the previous one.
• Low phosphate already present is to be corrected before the drug is given.
• Phosphate is to be monitored in people at risk of long-lasting low phosphate.
• Patients are to be told about the risk and to report signs and symptoms such as fatigue, muscle weakness or pain, bone and joint pain, and fractures.

Some researchers argue for more than the label asks. The 2025 systematic review states that the label does not reflect the case reports, observational data, trials and meta-analyses now available, and its authors call for phosphate to be checked before the first dose and before every later dose in all patients, and for wider use of intravenous iron products with lower rates of low phosphate (Magagnoli 2025). The 2022 review by researchers who ran several of the trials calls for awareness of low phosphate as a common complication and for monitoring of phosphate in people receiving repeated doses of the specific products involved (Schaefer 2022, Bone). The authors of the 13-patient case series also stress phosphate monitoring with ferric carboxymaltose (von Brackel 2024).

Because the ferric derisomaltose and iron sucrose labels read here carry no phosphate warning, they give no phosphate monitoring schedule.

What Is Not Known

• How much a short drop matters. The authors of both PHOSPHARE trials wrote that the longer-term clinical consequences of the difference between products are not yet established (Wolf 2020; Zoller 2023). The trials followed patients for about five weeks and were not designed to count fractures.
• How often the serious outcomes happen. Bone softening and fractures are known mainly from case reports, which cannot give a rate and tend to describe severe cases (Vilaca 2022). The network meta-analysis authors called for large trials to measure symptomatic and persistent low phosphate (Bellos 2020), and the 2020 review found that trials did not assess it adequately (Glaspy 2020).
• The exact mechanism. The idea that the carbohydrate shell of certain products blocks the breakdown of the phosphate-wasting hormone was put forward as a proposal in 2013 (Wolf 2013); why products differ so much is still being studied.
• Long-term bone effects. Bone markers stayed abnormal after phosphate had recovered in PHOSPHARE-IDA, which the authors suggest points to ongoing effects on bone (Schaefer 2022, J Clin Endocrinol Metab); what this means years later has not been measured.
• Inconsistent definitions. Studies used different cut-offs and testing schedules, and many did not state them, so rates from different studies are hard to compare directly (Glaspy 2020).

Key Research Papers

1. Wolf M, Rubin J, Achebe M, Econs MJ, Peacock M, Imel EA, Thomsen LL, Carpenter TO, Weber T, Brandenburg V, Zoller H. Effects of Iron Isomaltoside vs Ferric Carboxymaltose on Hypophosphatemia in Iron-Deficiency Anemia: Two Randomized Clinical Trials. JAMA. 2020;323(5):432-443. PubMed PMID: 32016310
2. Schaefer B, Zoller H, Wolf M. Risk Factors for and Effects of Persistent and Severe Hypophosphatemia Following Ferric Carboxymaltose. J Clin Endocrinol Metab. 2022;107(4):1009-1019. PubMed PMID: 34850000
3. Zoller H, Wolf M, Blumenstein I, Primas C, Lindgren S, Thomsen LL, Reinisch W, Iqbal T. Hypophosphataemia following ferric derisomaltose and ferric carboxymaltose in patients with iron deficiency anaemia due to inflammatory bowel disease (PHOSPHARE-IBD): a randomised clinical trial. Gut. 2023;72(4):644-653. PubMed PMID: 36343979
4. Detlie TE, Lindstrøm JC, Jahnsen ME, Finnes E, Zoller H, Moum B, Jahnsen J. Incidence of hypophosphatemia in patients with inflammatory bowel disease treated with ferric carboxymaltose or iron isomaltoside. Aliment Pharmacol Ther. 2019;50(4):397-406. PubMed PMID: 31264261
5. Emrich IE, Lizzi F, Siegel JD, Seiler-Mussler S, Ukena C, Kaddu-Mulindwa D, D'Amelio R, Wagenpfeil S, Brandenburg VM, Böhm M, Fliser D, Heine GH. Hypophosphatemia after high-dose iron repletion with ferric carboxymaltose and ferric derisomaltose-the randomized controlled HOMe aFers study. BMC Med. 2020;18(1):178. PubMed PMID: 32654663
6. Adkinson NF, Strauss WE, Macdougall IC, Bernard KE, Auerbach M, Kaper RF, Chertow GM, Krop JS. Comparative safety of intravenous ferumoxytol versus ferric carboxymaltose in iron deficiency anemia: A randomized trial. Am J Hematol. 2018;93(5):683-690. PubMed PMID: 29417614
7. Wolf M, Koch TA, Bregman DB. Effects of iron deficiency anemia and its treatment on fibroblast growth factor 23 and phosphate homeostasis in women. J Bone Miner Res. 2013;28(8):1793-803. PubMed PMID: 23505057
8. Schaefer B, Tobiasch M, Viveiros A, Tilg H, Kennedy NA, Wolf M, Zoller H. Hypophosphataemia after treatment of iron deficiency with intravenous ferric carboxymaltose or iron isomaltoside-a systematic review and meta-analysis. Br J Clin Pharmacol. 2021;87(5):2256-2273. PubMed PMID: 33188534
9. Bellos I, Frountzas M, Pergialiotis V. Comparative Risk of Hypophosphatemia Following the Administration of Intravenous Iron Formulations: A Network Meta-Analysis. Transfus Med Rev. 2020;34(3):188-194. PubMed PMID: 32819760
10. Glaspy JA, Lim-Watson MZ, Libre MA, Karkare SS, Hadker N, Bajic-Lucas A, Strauss WE, Dahl NV. Hypophosphatemia Associated with Intravenous Iron Therapies for Iron Deficiency Anemia: A Systematic Literature Review. Ther Clin Risk Manag. 2020;16:245-259. PubMed PMID: 32308402
11. Magagnoli J, Knopf K, Hrushesky WJ, Carson KR, Bennett CL. Ferric Carboxymaltose (FCM)-Associated Hypophosphatemia (HPP): A Systematic Review. Am J Hematol. 2025;100(5):840-846. PubMed PMID: 39935027
12. Vilaca T, Velmurugan N, Smith C, Abrahamsen B, Eastell R. Osteomalacia as a Complication of Intravenous Iron Infusion: A Systematic Review of Case Reports. J Bone Miner Res. 2022;37(6):1188-1199. PubMed PMID: 35426179
13. von Brackel FN, Grambeck J, Barvencik F, Amling M, Oheim R. In-depth clinical characterization of intravenous iron infusion-induced hypophosphatemic osteomalacia and its resolution. JBMR Plus. 2024;8(12):ziae139. PubMed PMID: 39659775
14. Bartko J, Roschger P, Zandieh S, Brehm A, Zwerina J, Klaushofer K. Hypophosphatemia, Severe Bone Pain, Gait Disturbance, and Fatigue Fractures After Iron Substitution in Inflammatory Bowel Disease: A Case Report. J Bone Miner Res. 2018;33(3):534-539. PubMed PMID: 29068481
15. Schoeb M, Räss A, Frei N, Aczél S, Brändle M, Bilz S. High Risk of Hypophosphatemia in Patients with Previous Bariatric Surgery Receiving Ferric Carboxymaltose: A Prospective Cohort Study. Obes Surg. 2020;30(7):2659-2666. PubMed PMID: 32221822
16. Schaefer B, Tobiasch M, Wagner S, Glodny B, Tilg H, Wolf M, Zoller H. Hypophosphatemia after intravenous iron therapy: Comprehensive review of clinical findings and recommendations for management. Bone. 2022;154:116202. PubMed PMID: 34534708

PubMed Topic Searches

1. PubMed: Ferric carboxymaltose and hypophosphatemia
2. PubMed: Intravenous iron, FGF23 and phosphate
3. PubMed: Intravenous iron and osteomalacia
4. PubMed: Ferric derisomaltose and hypophosphatemia

Connections

• Iron-Deficiency Anemia — the parent page: causes, tests and the full range of treatments
• Phosphorus Deficiency — every cause of low phosphate, intravenous iron among them
• Bone Pain and Softening — how low phosphate softens bone, and other hormone-driven causes
• Phosphorus Deficiency and Fatigue — why low phosphate drains energy
• Iron Deficiency — the same deficiency from the nutrition side
• Inflammatory Bowel Disease — a group with high rates in the trials
• Secondary Hyperparathyroidism — the parathyroid response that follows the phosphate drop
• Hereditary Hemorrhagic Telangiectasia — a risk factor named on the label

Featured Videos