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Niraparib-induced pure red cell aplasia. | LitMetric

AI Article Synopsis

  • Niraparib, a PARP inhibitor, is effective for maintaining progression-free survival in ovarian cancer but can cause grade 3-4 anemia in about 25% of patients, with no previous reports of pure red cell aplasia (PRCA) linked to its use.
  • A case study highlights a 65-year-old woman with stage 3 ovarian cancer who developed severe anemia after three months of niraparib treatment and required red blood cell transfusions.
  • After confirming PRCA through a bone marrow biopsy, treatment with steroids normalized her hemoglobin levels, suggesting that PRCA should be considered in cases of refractory anemia from niraparib.

Article Abstract

Introduction: Niraparib, a strong poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, contributed significantly to progression-free survival as a maintenance therapy in the platinum-sensitive period in both first-line and recurrent ovarian cancer, regardless of the BRCA mutation. Grade 3-4 anemia, which has a manageable side effect profile, especially hematological, is seen in almost 1 out of every 4 patients. To the best of our knowledge, there has been no reported case of pure red cell aplasia (PRCA) induced by niraparib treatment.

Case Report: A 65-year-old woman diagnosed with stage 3 serous carcinoma of the tuba received niraparib front-line maintenance treatment had grade 4 anemia after 3 months of niraparib treatment. She underwent bone marrow aspiration and biopsy because of refractory anemia, which needs red blood cell (RBC) transfusions despite interruption of treatment.

Management And Outcome: The patient was treated with 1 mg/kg methyl prednisolone, after histopathological assessment was consistent with PRCA. The hemoglobin count returned to the normal range with steroid treatment.

Discussion: In daily practice, it should be kept in mind that in the case of refractory anemia induced by niraparib, the underlying cause might be PRCA and can be improved with steroid administration.

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Source
http://dx.doi.org/10.1177/10781552231197808DOI Listing

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