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[Severe pancytopenia in old age after 12-month ACE inhibitor therapy]
G Schratzlseer1, T Lipp, G Riess
1I. Medizinische Abteilung, Krankenhauses Bogenhausen, München.
Insights
A 79-year-old woman developed pancytopenia, a severe blood disorder, while on ACE inhibitor therapy. Treatment with steroids and growth factors led to partial recovery, suggesting a link between ACE inhibitors and aplastic anemia.
Area of Science:
- Hematology
- Pharmacology
- Internal Medicine
Background:
- Angiotensin-converting enzyme (ACE) inhibitors are widely prescribed for hypertension.
- Indapamide and lisinopril are common antihypertensive medications.
Observation:
- A 79-year-old woman presented with pancytopenia after 12 months of treatment with indapamide and lisinopril.
- Bone marrow biopsy revealed severe hypoplasia of all three cell lines with reactive plasmocytosis, excluding malignancy.
Findings:
- The patient received transfusions and supportive care, including high-dose steroids and filgrastim.
- Hematologic parameters showed incomplete recovery after several weeks, with bone marrow showing signs of regeneration.
Implications:
- This case suggests a potential link between ACE inhibitor therapy and secondary aplastic anemia.
- Further investigation into drug-induced bone marrow suppression is warranted.
Abstract:
A sprightly 79-year-old woman was treated for high blood pressure with indapamide (2.5 mg/day) and the angiotensin converting enzyme (ACE) inhibitor lisinopril (5 mg/day). About 12 months after starting treatment a blood count carried out because of a syncopal attack revealed pancytopenia (haemoglobin 3.3 g/dl, erythrocytes 1.0 x 10(6)/microliters, leucocytes 1100/microliters, platelets 8000/microliters). Until then the blood count had been unremarkable. The bone marrow showed severe hypoplasia of all three cell lines with reactive plasmocytosis. Malignant cells were not present. The patient received a total of nine units of erythrocytes and seven units of platelets. Her care included reverse barrier nursing and antibiotic treatment. She was also given high dose steroid therapy (methylprednisone up to 150 mg/day) and granulocyte colony stimulating factor (filgrastim 300 micrograms/day subcutaneously for 25 days), and after a latent period of several weeks juvenile myeloid precursors reappeared in the blood. Before discharge from hospital the results rose to subnormal levels without further transfusions (haemoglobin 8.5/dl, erythrocytes 3.1 x 10(6)/microliters, leucocytes 3900/microliters, platelets 21.000/microliters). In the bone marrow, all three cell lines were beginning to recover. The final diagnosis was incompletely reversible pancytopenia resulting from secondary aplastic anaemia during ACE inhibitor therapy.