[Acquired amegacaryocytic thrombocytopenic purpura hiding acute myeloid leukemia].

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Abstract

Acquired amegakaryocytic thrombocytopenic purpura is a very rare condition characterized by severe thrombocytopenia linked to the reduction or disappearance of megakaryocytes in the bone marrow. It may be primary idiopathic or secondary to many pathological conditions including hematologic disorders. We report the case of a 24-year-old patient admitted for haemorrhagic syndrome caused by immunological thrombocytopenic purpura. The diagnosis was acquired amegakaryocytosis after the failure of corticotherapy and the performance of myelography. The patient was treated with ciclosporin with rapid progression to acute myeloblastic leukemia. The progression of acquired amegakaryocytosis to acute leukemia is reported but it is generally not so rapid and above all it is preceded by myelodysplastic syndrome or medullary aplasia. This study highlights the importance of a close follow-up of these pathologies with a benign-like appearance.

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Acquired amegakaryocytic thrombocytopenia and pure red cell aplasia associated with an occult large granular lymphocyte leukemia.

Dominic Lai, Thomas Loughran, Jaroslaw Maciejewski … (2008)

Acquired amegakaryocytic thrombocytopenia and pure red cell aplasia rarely occur concurrently. We report a case in which these disorders were associated with an occult large granular lymphocyte leukemia. The peripheral blood cytopenias improved after glucocorticoids and intravenous immunoglobulin were administered, and response was maintained with cyclosporine. Large granular lymphocyte leukemia should be suspected in the setting of unexplained bone marrow failure.

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Rapid progression of acquired amegakaryocytic thrombocytopenia to myelodysplastic syndrome: case report.

Mehmet Erkurt, Emin Kaya, Murat Baran … (2005)

Acquired amegakaryocytic thrombocytopenia (AAT) is a rare disease characterized by severe thrombocytopenia due to selective reduction or absence of megakaryocytes in the bone marrow. More commonly, patients with AAT have additional hematologic abnormalities such as macrocytosis or dyserythropoiesis, abnormalities which may predict progression to aplastic anemia or myelodysplasia. A 52-year-old female was admitted to hospital with mucosal and gingival bleeding. Megakaryocytes were not seen on the bone marrow aspiration and biopsy. AAT was diagnosed. Although she was treated with immunosuppressive therapy including prednisolone and cyclosporine, her disease progressed to myelodysplastic syndrome. She died at the third month of diagnosis because of cerebral bleeding.