scholarly journals Ferric carboxymaltose (Ferinject®) associated hypophosphataemia: case report illustrating the need for increased awareness to minimise incidence and risk

2020 ◽  
Vol 19 (2) ◽  
pp. 102-105
Author(s):  
Stacey Fisher ◽  
◽  
Leon Jonker ◽  

Ferric carboxymaltose (Ferinject®) is an infusion administered for the treatment of iron deficiency anaemia. A number of previous case reports have shown the occurrence of hypophosphataemia after Ferinject® treatment, supposedly managed though high dose phosphate therapy. This case report highlights the risk associated with, and futility of, managing this adverse effect through high dose phosphate infusion. A review of the available literature suggests that if hypophosphataemia develops as a result of Ferinject®, through upregulation of the renal protein Fibroblast Growth Factor-23, it cannot be readily reversed and on average persists for circa 50 days. Acute medical units should be aware of this – likely underreported – adverse effect, and avoid treating these hypophosphataemic patients with high dose phosphate since it can compound symptoms.

2021 ◽  
Vol 22 (7) ◽  
pp. 3321
Author(s):  
Mark F. McCarty

Although well documented drug therapies are available for the management of ventricular hypertrophy (VH) and heart failure (HF), most patients nonetheless experience a downhill course, and further therapeutic measures are needed. Nutraceutical, dietary, and lifestyle measures may have particular merit in this regard, as they are currently available, relatively safe and inexpensive, and can lend themselves to primary prevention as well. A consideration of the pathogenic mechanisms underlying the VH/HF syndrome suggests that measures which control oxidative and endoplasmic reticulum (ER) stress, that support effective nitric oxide and hydrogen sulfide bioactivity, that prevent a reduction in cardiomyocyte pH, and that boost the production of protective hormones, such as fibroblast growth factor 21 (FGF21), while suppressing fibroblast growth factor 23 (FGF23) and marinobufagenin, may have utility for preventing and controlling this syndrome. Agents considered in this essay include phycocyanobilin, N-acetylcysteine, lipoic acid, ferulic acid, zinc, selenium, ubiquinol, astaxanthin, melatonin, tauroursodeoxycholic acid, berberine, citrulline, high-dose folate, cocoa flavanols, hawthorn extract, dietary nitrate, high-dose biotin, soy isoflavones, taurine, carnitine, magnesium orotate, EPA-rich fish oil, glycine, and copper. The potential advantages of whole-food plant-based diets, moderation in salt intake, avoidance of phosphate additives, and regular exercise training and sauna sessions are also discussed. There should be considerable scope for the development of functional foods and supplements which make it more convenient and affordable for patients to consume complementary combinations of the agents discussed here. Research Strategy: Key word searching of PubMed was employed to locate the research papers whose findings are cited in this essay.


2013 ◽  
Vol 98 (2) ◽  
pp. 550-556 ◽  
Author(s):  
C. Turner ◽  
N. Dalton ◽  
R. Inaoui ◽  
I. Fogelman ◽  
W. D. Fraser ◽  
...  

Abstract Context: Several trials have reported an increased risk of fractures and falls after intermittent high-dose vitamin D. Treatment with loading doses of vitamin D may increase 1,25(OH)2 vitamin D catabolism through changes in calcium/phosphate homeostasis and fibroblast growth factor-23 (FGF-23). Objective: The aim was to determine the effects of high-dose vitamin D on circulating concentrations of 1,25(OH)2 vitamin D and FGF-23 in patients with osteoporosis and vitamin D insufficiency. Design, Setting, Patients, and Intervention: We carried out a prospective study of 45 subjects with vitamin D deficiency/insufficiency treated with a bolus dose of 300 000 IU of vitamin D2 im. Blood samples were obtained at baseline and 1, 2, and 3 months after treatment. Outcome Measures: Changes in 1,25(OH)2-vitamin D and FGF-23 were measured. Results: Loading dose of vitamin D2 increased 1,25(OH)2-vitamin D2 at 3 months, with a mean [SD] of 41 [56] pmol/L at baseline and 162.3 [137.8] pmol/L at 3 months (P < .001). FGF-23 increased significantly at all time points with a peak at 3 months, with percent change from baseline (mean [SEM]) of 50% [48%] at 3 months (P < .01). There was a positive correlation between FGF-23 and serum phosphate (r = 0.36, P = .024) and calcium (r = 0.532, P < .001) and a negative correlation between total 1,25(OH)2-vitamin D and FGF-23 (r = −0.32, P = .036) at 3 months. Conclusions: High-dose vitamin D increases 1,25(OH)2-vitamin D and FGF-23 concentration. Further studies are required to determine whether adjusting vitamin D dose and frequency to minimize increases in FGF-23 may prevent the adverse outcomes associated with high-dose intermittent vitamin D supplementation.


2019 ◽  
Vol 12 (6) ◽  
pp. e229113 ◽  
Author(s):  
Clare Margaret Crowley ◽  
Gabriela McMahon ◽  
Joanna Desmond ◽  
Mendinaro Imcha

This report describes the case of a 36-year-old woman, gravida 3, para 2, at 11 weeks' gestation, who received a ferric carboxymaltose infusion for iron deficiency anaemia after medical management of a miscarriage. The following morning, light brown skin staining was noted at the infusion site, and the staining was present 2 months later at follow-up. Skin staining following intravenous iron infusion is a rare but important side effect. The skin staining is potentially permanent but may fade in time. Such an adverse effect may have cosmetic consequences for the patient.


2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Salema Khalid ◽  
Kassim Javaid ◽  
Neil Buchanan

Abstract Case report - Introduction Tumor-induced osteomalacia is a rare acquired metabolic bone disorder characterised by isolated renal phosphate wasting due to abnormal tumour production of fibroblast growth factor 23 (FGF23). Bloods show hypophosphatemia. However, given the lack of awareness of this disease, and the non-specific nature of the presenting symptoms, diagnosis is often delayed for years or even missed. With this case report, we want to shed light on this rare bone disorder and highlight the importance of not ignoring a low phosphate level. Case report - Case description We report the case of a 63-year-old gentleman who presented to us with a history of progressive bone pain, marked muscle weakness and fatigue. He had a persistently raised parathyroid hormone and very high alkaline phosphatase. Calcium was low normal, but vitamin D was normal. Phosphate was noted to be low and had been so since 6 years prior to being referred. X-ray pelvis showed sclerotic-looking iliac bones, but an isotope bone scan showed no evidence of metastatic disease. We referred him to our endocrinology colleagues to investigate for possible primary hyperparathyroidism.  However, ultrasound scan of neck showed no abnormal parathyroid gland. PET and CT scan of the chest, abdomen and pelvis did not show any significant pathology.   MIBI scan of parathyroid glands showed diffuse thyroid uptake. The SPECT-CT images showed a well-defined focal area of increased activity, posterior to the mid/lower pole of the right thyroid lobe, possibly indicative of hyperfunctioning parathyroid tissue. The radiologist questioned the possibility of renal osteodystrophy and resultant secondary hyperparathyroidism. However, there was no evidence for renal dysfunction with a creatinine of 80 umol/L. We referred this gentleman to the Oxfordshire Osteoporosis and Metabolic Bone Service. Bloods showed a raised P1NP. This was felt to be consistent with tumour-induced osteomalacia. Oversecretion of FGF23 was confirmed and DOTATATE scan revealed two areas of uptake: one in the right hip and one in the skull. Meanwhile, the patient had been started on Sandoz Phosphate and alfacalcidol, and his bone aches improved on this combination therapy. He had radio-ablation of the hip lesion this year and has now stopped all his medication. His fatigue and muscle strength has improved dramatically. The skull lesion is being monitored for now with yearly imaging and follow-up in the metabolic bone clinic. Case report - Discussion Tumour-induced or oncogenic osteomalacia is extremely rare. Symptoms include chronic muscle and bone pain, weakness, and fatigue and can result in fragility fractures due to osteomalacia. Lack of awareness of these clinical manifestations and relevance of low phosphate levels often leads to a diagnostic delay or misdiagnosis. As seen in our case, it took multiple investigations and almost 2 years before this gentleman had a confirmation of his diagnosis. The pathogenesis of tumour-induced osteomalacia involves tumour expression of fibroblast growth factor 23. This hormone inhibits reabsorption of phosphate in the proximal renal tubule and down-regulates renal conversion of 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D. Replacing phosphate on its own paradoxically increases PTH levels. The metabolic abnormalities may be partially or completely corrected with phosphate supplementation and calcitriol. In our patient, his PTH levels remained elevated, but alkaline phosphatase improved, as did calcium and phosphate levels. Unlike many other causes of osteomalacia, tumour-induced osteomalacia is curable by resection of the offending tumour. However, finding the responsible FGF23-secreting tumour can be incredibly challenging. There is ongoing research into medical treatment for this condition, especially if the tumour is not found or is unresectable, or the patient is not a surgical candidate. Case report - Key learning points Low phosphate levels can be easily overseen, with significant consequences. This case emphasises the need to recognise hypophosphatemia and to look for its cause.  Conversely, it also illustrates the need to investigate all patients with persistent musculoskeletal symptoms for hypophosphatemia. Our case underscores the importance of being aware of the rare condition of tumour-induced osteomalacia. This will enable early recognition and treatment of the metabolic abnormality, before the development of any deleterious effects of osteomalacia on the skeleton.


2015 ◽  
Vol 167 (10) ◽  
pp. 2430-2434
Author(s):  
Takeshi Sato ◽  
Koji Muroya ◽  
Yumi Asakura ◽  
Akihiro Yachie ◽  
Gen Nishimura ◽  
...  

2017 ◽  
Author(s):  
Elisa Holmlund-Suila ◽  
Maria Enlund-Cerullo ◽  
Saara Valkama ◽  
Helena Hauta-alus ◽  
Jenni Rosendahl ◽  
...  

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