Summary:Despite recent advances in understanding the biology of thrombopoiesis, autoimmune thrombocytopenia caused by inhibition of megakaryocytic precursors, remains a treatment dilemma. We report a case of a 43-year-old female who developed amegakaryocytic thrombocytopenia refractory to intravenous immunoglobulin (IVIG), prednisone, cytoxan and vincristine. She was subsequently treated with myeloablative chemotherapy (busulfan and cyclophosphamide) followed by allogeneic bone marrow transplant from a 6/6 HLA-matched sibling. The patient is currently more than 1 year after transplant with complete donor chimerism and restoration of normal thrombopoiesis. A review of the literature shows that the clinical syndrome known as amegakaryocytic thrombocytopenia represents a heterogeneous group of disorders, and clinical experience with immunosuppression varies. Appropriate initial treatment for these patients requires immunosuppressive agents, including antithymocyte globulin (ATG) for steroid refractory disease. However, in the case of symptomatic patients who have an appropriate sibling donor, early hematopoietic progenitor cell transplant, even before administration of ATG, may be necessary. Further studies are needed to better define the pathogenesis and mechanism of this heterogeneous disorder before more definitive treatment algorithms can be established. Keywords: amegakaryocytic thrombocytopenia; allogeneic BMT A 43-year-old female first noted the onset of a petechial rash in August 1996. Laboratory studies performed by her primary care physician revealed a marked thrombocytopenia with platelet count of 36 000/l, a WBC of 6.2 × 10 3 /l, hemoglobin (Hgb) of 11.4 gm/dl, serum B12 level of 328 pg/ml, serum folate of 2.9 ng/ml, and serum ferritin of 9 ng/ml. She was treated with oral iron therapy

Selective breeding to maintain specific physical and behavioral traits has made the modern dog one of the most physically diverse species on earth. One unfortunate consequence of the common breeding practices used to develop lines of dogs with the desired traits is amplification and propagation of genetic diseases within distinct breeds. To map disease loci we have constructed a first-generation framework map of the canine genome. We developed large numbers of highly polymorphic markers, constructed a panel of canine-rodent hybrid cell lines, and assigned those markers to chromosome groups using the hybrid cell lines. Finally, we determined the order and spacing of markers on individual canine chromosomes by linkage analysis using a reference panel of 17 outbred pedigrees. This article describes approaches and strategies to accomplish these goals.

High-dose chemotherapy and/or radiation followed by transplantation of allogeneic bone marrow (BM) or blood

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