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Calcinosis cutis dermatologic toxicity associated with fibroblast growth factor receptor inhibitor for the treatment of Wilms tumor
Author(s) -
Arudra Krishna,
Patel Ravi,
Tetzlaff Michael T.,
Hymes Sharon,
Subbiah Vivek,
MericBernstam Funda,
TorresCabala Carlos,
Aung Phyu P.,
Nagarajan Priyadharsini,
Diab Adi,
Prieto Victor G.,
Nelson Kelly,
Curry Jonathan L.
Publication year - 2018
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/cup.13319
Subject(s) - medicine , toxicity , calcinosis cutis , pathology , fibroblast growth factor 23 , dermatology , calcinosis , calcification , calcium , parathyroid hormone
Small‐molecule inhibitors ( nibs ) have revolutionized cancer therapy with the emergence of clinically efficacious treatment for advanced‐stage malignancies. Fibroblast growth factor receptor (FGFR) inhibitors have shown therapeutic efficacy in malignancies with molecular‐genetic alterations in the FGFR/fibroblast growth factor pathway. In a phase 1 clinical trial, erdafitinib, a pan FGFR inhibitor, was well tolerated with a manageable toxicity profile. Hyperphosphatemia was a frequent adverse event in patients treated with erdafitinib; however, no serious complications were observed with this therapy. Here, we report the development of calcinosis cutis dermatologic toxicity in a patient with hyperphosphatemia while treated with a novel selective FGFR inhibitor, INCB 54828‐101. Awareness of this form of dermatologic toxicity from an FGFR inhibitor will be important for close monitoring of serum levels of phosphate, FGF23, vitamin D, and calcitriol, the management of adverse serum chemistry with chelators, and treatment decisions to either reduce dose or withhold FGFR inhibitor.