Abstract

IntroductionAplastic anemia is a rare disease caused by destruction of pluripotent stem cells in bone marrow. During pregnancy it could be life-threatening for both mother and child. The only causal therapy for aplastic anemia is bone marrow transplantation, which is contraindicated during pregnancy because of potential embryo toxicity. Treatment options are erythrocytes and platelet transfusions and immunosuppressive therapy. There is, however, no agreement about the optimal supportive care and treatment regime for this disorder during pregnancy.Case PresentationA 26-year-old nulliparous Asian woman with an uneventful medical history was admitted to the hospital at 14 weeks' gestation because of excessive vomiting. Routine laboratory tests showed pancytopenia (Hb 3.5 mmol/L, leukocytes 3.5 *109/L, platelets 45 *109L). A bone marrow biopsy confirmed aplastic anemia. Methylprednisolon, cyclosporine A, packed cells and platelet transfusions were initiated. At 33 weeks she developed neutropenia (0.1 *109/L) for which oral colistin and tobramycin were given prophylactically. At 35 weeks labor was induced, during which she developed a fever of 38.2°C. She gave birth spontaneously to a healthy son weighing 2415 grams, who had no signs of pancytopenia. After delivery the blood count of the patient did not recover and did not respond to medication. Eighteen weeks after delivery she died of sepsis complicated by cerebral bleeding and infarction due to severe thrombocytopenia and neutropenia, despite optimal supportive treatment.ConclusionThis potential life-threatening disease has a relatively good prognosis for both mother and child after optimal treatment. Transfusion during pregnancy is the first choice treatment with recommended hemoglobin levels of >5.5 mmol/L and platelet counts of >20 *109/L. Cyclosporine A seems a reasonable alternative therapy with a reported success rate in non-pregnant patients of 70% when combined with antithymocyte globuline. Our patient died 18 weeks postpartum from cerebral bleeding and infarction due to severe thrombocytopenia despite intensive supportive treatment, methylprednisolon and cyclosporine A.

Highlights

  • Aplastic anemia is a rare disease caused by destruction of pluripotent stem cells in bone marrow

  • Cyclosporine A seems a reasonable alternative therapy with a reported success rate in non-pregnant patients of 70% when combined with antithymocyte globuline

  • Aplastic anemia is a rare disease caused by destruction of pluripotent stem cells in bone marrow with an annual incidence of 2 to 6/1.000.000 [1]

Read more

Summary

Conclusion

Aplastic anemia is a serious condition which may manifest during pregnancy. The seriousness depends on the degree of bone marrow suppression. Our patient died 18 weeks postpartum from sepsis, cerebral bleeding and infarction due to severe thrombocytopenia despite intensive supportive treatment, methylprednisolon and CsA. This case shows that aplastic anemia during pregnancy is potentially a life-threatening condition despite the favorable prognosis for both mother and child. Author details 1Department of Obstetrics of Gynaecology, Erasmus University Medical Center, PO Box 2040, 3000 CA Rotterdam, The Netherlands. Authors’ contributions HW provided antenatal care to the patient during the pregnancy and delivery He supervised the writing and edited earlier drafts of the manuscript. Competing interests The authors declare that they have no competing interests

Introduction
Discussion
Findings
Young NS

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.