Hypophosphataemia due to FGF-23 producing B cell non-Hodgkin's lymphoma

Elderman, Jan H; Wabbijn, Marike; Jongh, Felix de

doi:10.1136/bcr-2015-213954

Cited by 16 publications

(13 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…PMTs are usually small, benign and characterised by low grade and mitotic index, requiring PET imaging to be detected [3]. However, it has also been linked with malignant haematological and solid tumours such as leukaemia [14], head and neck cancer [15], B cell non-Hodgkin's lymphoma [16], sarcoma [17], anaplastic thyroid carcinoma [18], small cell lung cancer [19], prostate cancer [20] and adenocarcinoma of the colon [21].…”

Section: Discussionmentioning

confidence: 99%

Oncogenic osteomalacia and metastatic breast cancer: a case report and review of the literature

Savva

Adhikaree

Madhusudan

et al. 2019

J Diabetes Metab Disord

View full text Add to dashboard Cite

Objectives Oncogenic osteomalacia is a rare paraneoplastic metabolic syndrome that is characterised by severe hypophosphataemia, hyperphosphaturia and osteomalacia secondary to renal loss of phosphate. It is commonly caused by overproduction of fibroblast growth factor-23 (FGF23) from benign tumours of mesenchymal origin. Currently, there is no clear evidence on the management of oncogenic osteomalacia in patients with metastatic solid tumours. Methods We report a case of breast cancer-induced oncogenic osteomalacia and discuss its diagnosis and management. Results A 71-year-old woman with advanced breast cancer developed symptomatic oncogenic osteomalacia with raised FGF23, severe hypophosphataemia and hypocalcaemia. The electrolytic disturbances were exacerbated after the administration of bisphosphonates in the context of her oncological treatment. Systemic chemotherapy and maintenance endocrine treatment along with phosphate and calcium supplementation reduced the activity of oncogenic osteomalacia and resolved the electrolytic imbalances. Conclusions To our knowledge, this is the first reported case of oncogenic osteomalacia in a patient with breast cancer. Oncogenic osteomalacia constitutes a diagnostic and therapeutic challenge. Pre-clinical and clinical evidence suggest that a possible underlying mechanism is the presence of molecular alterations in the FGF/FGFR signalling pathway leading to overexpression of FGF23. In metastatic setting, anticancer treatment can potentially lead to the normalisation of the electrolytic disturbances and reduction of the activity of oncogenic osteomalacia. The use of antiresorptive therapy in patients with bone metastases can potentially trigger FGF23 overexpression. Its use should be guided by the patients' risk of skeletal-related events and electrolytic disturbances as well as the degree of activity of oncogenic osteomalacia.

show abstract

Section: Discussionmentioning

confidence: 99%

Oncogenic osteomalacia and metastatic breast cancer: a case report and review of the literature

Savva

Adhikaree

Madhusudan

et al. 2019

J Diabetes Metab Disord

View full text Add to dashboard Cite

show abstract

“…At a cellular level, dendritic cells and macrophages express FGF23 and increase their production during inflammation (55) and macrophage polarization (30). FGF23 production has also been shown to occur in clonal lymphocytes and plasma cells in patients with B cell neoplasms, including plasma cell dyscrasias (81) and B cell non-Hodgkin's lymphoma (22). In this context, cFGF23 is elevated in circulation, although iFGF23 remains in the normal range in the majority of cases.…”

Section: Fgf23 As a Proinflammatory And Immune-modulatory Hormonementioning

confidence: 99%

Ironing out the cross talk between FGF23 and inflammation

David

Francis

Babitt

2017

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

The bone-secreted hormone fibroblast growth factor 23 (FGF23) has an essential role in phosphate homeostasis by regulating expression of the kidney proximal tubule sodium-phosphate cotransporters as well as parathyroid hormone levels. Induction of FGF23 early in chronic kidney disease (CKD) helps to maintain normal phosphorous levels. However, high FGF23 levels become pathological as kidney disease progresses and are associated with an increased risk of CKD progression, cardiovascular events, and death. The factors responsible for increasing FGF23 levels early in CKD are unknown, but recent work has proposed a role for inflammation and disordered iron homeostasis. Notably, FGF23 has recently been shown to elicit an inflammatory response and to display immunomodulatory properties. Here, we will review emerging evidence on the cross talk between inflammation, iron, FGF23, and bone and mineral metabolism and discuss the relevance for CKD patients.

show abstract

“…TIO is an uncommon paraneoplastic syndrome characterized by phosphate wasting attributed to increased circulating FGF23. The syndrome is classically associated with benign mesenchymal tumors; however, recent case reports have associated this syndrome with malignancies, including anaplastic thyroid, colon, and lung carcinomas and diffuse large B cell non-Hodgkin lymphoma [ 11 , 12 ]. One study evaluated FGF23 concentrations in various plasma cell dyscrasias after finding elevated circulating FGF23 in one patient with chronic lymphocytic leukemia and hypophosphatemia, but the authors paradoxically found a weakly positive correlation of FGF23 with serum phosphate in their cohort [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor 23–Induced Hypophosphatemia in Acute Leukemia

Reinert

Bixby

Koenig

2018

Journal of the Endocrine Society

View full text Add to dashboard Cite

Fibroblast growth factor 23 (FGF23)–induced hypophosphatemia is a rare paraneoplastic syndrome of phosphate wasting that, if unrecognized, may cause tumor-induced osteomalacia. It is classically associated with benign mesenchymal tumors but occasionally has been found in patients with other malignancies. Hypophosphatemia has been associated with acute leukemia but has not previously been reported to be due to inappropriate FGF23 secretion. Here, we describe FGF23-induced severe hypophosphatemia and renal phosphate wasting associated with a mixed-phenotype Philadelphia chromosome-like acute leukemia in a previously healthy 22-year-old man. He was found to have low serum 1,25-dihydroxyvitamin D and extremely high FGF23 levels, as well as inappropriate urinary phosphorus excretion. The hypophosphatemia improved with calcitriol and oral phosphate treatment but normalized only during chemotherapy-induced ablation of the blasts. FGF23 levels declined with a reduction in peripheral blast counts. Using real-time reverse transcription polymerase chain reaction, we found that the leukemia cells were the source of FGF23. To our knowledge, this is the first description of FGF23-induced hypophosphatemia associated with acute leukemia. We recommend that the FGF23 paraneoplastic syndrome be considered as a possible etiology of hypophosphatemia in patients with acute leukemia.

show abstract

Hypophosphataemia due to FGF-23 producing B cell non-Hodgkin's lymphoma

Cited by 16 publications

References 8 publications

Oncogenic osteomalacia and metastatic breast cancer: a case report and review of the literature

Oncogenic osteomalacia and metastatic breast cancer: a case report and review of the literature

Ironing out the cross talk between FGF23 and inflammation

Fibroblast Growth Factor 23–Induced Hypophosphatemia in Acute Leukemia

Contact Info

Product

Resources

About