Summary
A search of the medical records at the Hospital for Sick Children, Great Ormond Street and Chelsea Hospital for Women, London, revealed 51 cases of vaginal bleeding in children under the age of 10 occurring in the years 1962 through 1977. The bleeding was caused by some form of precocious puberty in 37 patients (73 per cent). Eight of these patients had cyclical vaginal bleeding in the absence of secondary sexual development or advanced bone age. Fourteen patients (27 per cent) bled because of a local lesion and six of these had a malignant neoplasm of the genital tract.
Iron deficiency reduces T cell counts; however, iron sufficiency is difficult to maintain during pregnancy and to reestablish in the early postpartum period. This cross-sectional study examined relations among postpartum maternal iron status, parity, lactation, supplement use, and maternal blood T cell populations. Sixty lactating and 41 nonlactating postpartum (NLPP) women at 1-2 wk and 1, 2, 4, or 8 mo postpartum and 13 nulliparous women were studied. Among multiparous women, multiple linear regression showed that relative percentages and absolute numbers of CD3+CD8+ cells were correlated positively with maternal serum transferrin saturation. In a separate multiple linear regression model, multiparous NLPP women who did not use multivitamin and mineral supplements had lower CD3+CD4+ cell percentages in the first month postpartum than did nulliparous control women. Lactating women who used supplements, however, had reduced CD3+CD4+ percentages 4-8 mo postpartum compared with control women. CD3+CD4+ percentages did not differ among control women, NLPP women who used supplements, or lactating women who did not use them. These results suggest that nutritional factors such as maternal iron status and use of dietary supplements play a role in a mother's postpartum immune status.
A 69-year-old woman with a previous history of type 2 diabetes mellitus presented with a 2-week history of worsening abdominal pain, reduced oral intake, and lethargy. She was pyrexial (39 C) with a sinus tachycardia. Her full blood count showed: hemoglobin concentration 119 g/l, white cell count 151.5 3 10 9 /l, and platelet count 33 3 10 9 /l. The blood film showed many circulating blast cells. These were of medium size with a high nucleocytoplasmic ratio. Many of them had an indentation in the nucleus, producing a cup-like shape when viewed in profile; when viewed from above, the invagination sometimes simulated a giant nucleolus (images). Nuclear indentations were apparent also in smear cells. Cytoplasmic basophilia varied from moderate to strong. A minority of basophilic blast cells had cytoplasmic blebs. Some blast cells contained Auer rods, usually one but up to three per cell, these often being related to the nuclear indentation. The cytological features were considered strongly suggestive of acute myeloid leukemia (AML) with NPM1 mutation and further investigations were arranged.A bone marrow aspirate showed 89% blast cells with similar cytological features to those in the peripheral blood. Flow cytometry gated on the blast population showed expression of CD33, CD117 and CD123 with partial expression of HLA-DR and myeloperoxidase. CD34 was not expressed. Blast cells were also negative for CD13, CD11b, CD14, CD64, CD56, and CD7. Standard cytogenetic analysis yielded no metaphases but molecular analysis showed both a 4 bp insertion in NPM1 and a FLT3-internal tandem duplication (ITD) of 24 bp.The patient responded to broad-spectrum antibiotics without a focus of infection being identified, and entered complete remission following the initial course of cytarabine and daunorubicin.Cup-shaped blast cells are associated with NPM1 mutation, particularly when there is coexisting FLT3-ITD.[1,2] They can also occur with AML associated with FLT3-ITD without NPM1 mutation. The nuclear pockets are shown on ultrastructural examination to be occupied by a collection of mitochondria, lysosomes and endoplasmic reticulum.[1,2] The light microscopy features of NPM1-mutated AML are sufficiently distinctive to suggest this diagnosis. The CD34-negativity, often with HLA-DR also being negative, could lead to confusion with the variant form of acute promyelocytic leukemia but the nuclear shape differs. High frequency of NPM1 mutations in acute myeloid leukemia with prominent nuclear invaginations ("cup-like" nuclei).
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