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Hyperphosphatemic Tumoral Calcinosis With Pemigatinib Use
Akshan Puar1, Diane Donegan1, Paul Helft2
1Division of Endocrinology Diabetes and Metabolism, Indiana University School of Medicine, Indianapolis, Indiana.
AACE Clinical Case Reports
|October 3, 2022
Summary
Pemigatinib, an FGFR inhibitor, can cause tumoral calcinosis with soft tissue calcifications, a rare side effect. Discontinuation of pemigatinib led to regression of calcifications in a cholangiocarcinoma patient.
Area of Science:
- Oncology
- Pharmacology
- Nephrology
Background:
- Pemigatinib is an FGFR 1-3 inhibitor used for cholangiocarcinoma with FGFR fusions.
- Hyperphosphatemia is a known side effect, but tumoral calcinosis is less recognized.
- This case highlights a rare complication of pemigatinib therapy.
Observation:
- A patient with metastatic cholangiocarcinoma developed subcutaneous nodules after starting pemigatinib.
- Biopsies confirmed deep dermal and subcutaneous calcifications.
- Elevated serum phosphorus and FGF23 levels were noted.
Findings:
- Pemigatinib inhibits FGFR, potentially leading to FGF23 pathway disruption.
- This disruption caused hyperphosphatemia and tumoral calcinosis in the patient.
- Serum phosphorus normalized with dietary changes and phosphate binders.
Implications:
- Tumoral calcinosis is a potential adverse event associated with FGFR inhibitors like pemigatinib.
- Management involves lowering phosphate levels and potentially discontinuing the drug.
- Increased awareness is crucial as FGFR inhibitor use expands.
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