A recent report demonstrated that t(8;16) (p11;p13) may be linked to acute monocytic leukaemia (AMoL) of differentiated subtype (M5b) with active haemophagocytosis by leukaemic cells. Only two cases of neonatal AMoL with t(8;16) (p11;p13) have been reported; M5b with haemophogocytosis and M5a. We report a case of neonatal AMoL (M5b) with t(8;16)(p11;p13), but haemophagocytosis by the leukaemic cells was not detected.
811Acyclovir for 10 days. Despite this treatment, she was referred 3 weeks later to our intensive care unit with pyrexia, disseminated vesicular and petechial eruption, bleeding of the upper digestive tract, acute pulmonary oedema, and hepatitis. A severe thrombocytopenia was found (18 x 109/1 platelet), as well as anaemia (9.3 g/dl haemoglobin) low reticulocyte count and moderate neutropenia (3.7 • 109/1 WBC and 1.2 • 109/1 PMN). Disseminated intravascular coagulation was present and treated with an exchange transfusion. Meticillin, Netilmicin and Cefotaxim were prescribed. The patient's clinical status improved gradually, whereas pancytopenia persisted. On day 6, bone marrows smears exhibited a marked hypoplasia with reduction in granulocytic and erythroid lineages, and were devoid of megakaryocytes. Serological tests were positive for varicella-zoster virus with presence of IgM antibody and negative for EBV, hepatitis B, HIV and parvovirus infections. Direct Coombs test was positive and raised IgG platelet antibodies were found on days 6 and 14. During the following month, the persistence of severe thrombocytopenia led to digestive and urinary tract bleeding requiring 4 packed erythrocyte transfusions and daily platelet transfusions. The patient was also administered a commercial immunoglobulin preparation (Bio transfusion, Les Ulis, France; 400 mg/ kg per day) from day 7 to day 11. Neutropenia resolved during the following 10 days, thrombocytopenia and anaemia during the following month. Direct Coombs test was negative on day 35. Complete recovery persisted with a 6 month follow up.Varicella-related severe pneumonia, as well as encephalitis and hepatitis have been described during steroid therapy [2]. However, haematological complications are unusual, albeit some cases of immune thrombocytopenia [1,6] and disseminated intravascular coagulation [4] have been reported. Only two cases of varicella-associated hypoplastic anaemia have been observed in the absence of any previous steroid (or other) therapy; both patients recovered in a 6-week and 3-month period respectively [3,5]. In our case we assume that varicella was the cause of hypoplastic anaemia since: (1) pancytopenia completely resolved after the recovery from varicella; (2) serological tests for other viral infections known to be responsible for aplastic anaemia were negative; (3) Meticillin and Cefotaxim are not likely causative agents since pancytopenia appeared before initiation of this treatment. Hypoplastic anaemia was associated with auto-immune markers directed against platelets and erythrocytes, as described in other virus-related hypoplasias; therefore immunoglobulin therapy may have had a beneficial effect. This report suggests that varicella-zoster virus infection should be added to the list of possible viral causes of aplastic anaemia.
We report a child with relapsed acute lymphocytic leukaemia in whom cytoplasmic granules were present in the leukaemic cells of the cerebrospinal fluid (CSF) but not in those of the bone marrow (BM). The leukaemic cells of the BM were of B-cell lineage whereas those of the CSF had both B-cell and myeloid antigens.
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