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[Gemcitabine-induced thrombotic microangiopathy].
L Teixeira1, P Debourdeau, C Zammit
1Département de clinique médicale, service de médecine interne, Hôpital d'Instruction des Armées Desgenettes, 108, bd Pinel, 69003 Lyon.
Presse Medicale (Paris, France : 1983)
|August 1, 2002
Summary
Gemcitabine chemotherapy can cause thrombotic microangiopathy (TMA), a serious condition. Early detection and gemcitabine withdrawal are key for favorable outcomes in patients with cancer.
Area of Science:
- Oncology
- Nephrology
- Hematology
Background:
- Thrombotic microangiopathy (TMA) encompasses hemolytic uremic syndrome (HUS) and thrombocytopenic thrombotic purpura (TTP).
- Cancer-associated TMA can manifest as TTP (secondary to cancer) or HUS (secondary to chemotherapy).
- Gemcitabine, a chemotherapy agent for various carcinomas, has been linked to TMA development.
Observation:
- A patient with metastatic urothelial carcinoma developed HUS after eight cycles of gemcitabine monotherapy.
- Symptomatic treatment and gemcitabine cessation led to the resolution of hematological abnormalities.
- Renal function returned to baseline levels following gemcitabine withdrawal.
Findings:
- Gemcitabine-induced TMA, primarily HUS, is a recently recognized complication with approximately twelve reported cases.
- TMA incidence in metastatic carcinomas is estimated at 5-6%.
- Gemcitabine-induced TMA typically presents with a delayed onset relative to treatment initiation.
Implications:
- Gemcitabine-induced HUS generally has a good prognosis, with renal abnormalities regressing upon drug withdrawal.
- Screening for TMA is recommended after more than ten cycles of gemcitabine treatment.
- This highlights the importance of monitoring for TMA in patients undergoing gemcitabine chemotherapy, particularly for urothelial carcinomas.