Cases reported "Anemia"

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1/4. Favourable effect of chemotherapy on clinical symptoms and human herpesvirus-8 dna load in a patient with Kaposi's sarcoma presenting with fever and anemia.

    The case of a patient infected with human immunodeficiency virus type 1 (hiv-1) with Kaposi's sarcoma who presented with fever of unknown origin, severe anemia, thrombocytopenia and hypoalbuminemia but only limited involvement of the skin is presented. Chemotherapy directed at Kaposi's sarcoma resulted in resolution of these clinical signs and symptoms and was associated with a significant reduction in human herpesvirus-8 dna load in serum, despite continued hiv-1 replication. Such a decreasing human herpesvirus-8 load following Kaposi's sarcoma-directed chemotherapy has not been reported previously. These findings suggest that Kaposi's sarcoma was indeed responsible for the clinical syndrome and that this neoplasm is a source of human herpesvirus-8 virus particle production, which can be inhibited by chemotherapy-induced reduction in tumor burden.
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2/4. A case of 'smouldering' mastocytosis with high mast cell burden, monoclonal myeloid cells, and C-KIT mutation Asp-816-Val.

    mastocytosis is a term used for a group of disorders characterized by abnormal growth and accumulation of tissue mast cells (MC) in one or more organ systems. In patients with systemic mastocytosis (SM) the clinical course may be indolent or aggressive or even complicated by leukemic progression or an associated clonal hematologic non mast cell lineage disease (AHNMD). However, at first presentation (diagnosis) it may be difficult to define the category of disease and the prognosis. We report on a 48-year-old female patient with SM with urticaria pigmentosa-like skin lesions and mediator-related symptoms. She was found to have splenomegaly, a high infiltration grade (MC) in bone marrow biopsies (>30%), mild anemia, and a high serum tryptase level (>500 ng/ml). In addition, she exhibited discrete histologic signs of myeloproliferation in the 'non-affected' marrow and monoclonal blood cells established by C-KIT 2468A-->T mutation (Asp-816-Val) -analysis and HUMARA assay. Despite these findings, however, the clinical course was stable over years and no AHNMD or organ impairment developed. Because of the 'intermediate' clinical signs and absence of progression to aggressive disease, we proposed the term 'smouldering mastocytosis'.
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3/4. Geophagic lead nephropathy: case report.

    An adult presenting with anemia and seizures was found to have lead poisoning. chelation therapy undertaken before the source of exposure was known was accompanied by clinical improvement. recurrence of an excessive body lead burden despite chelation led to the discovery of pica for lead-contaminated garden soil. Lead nephropathy progressed when the geophagia was resumed.
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4/4. Bullets, lead poisoning and thyrotoxicosis.

    A patient with a retained bullet developed lead poisoning in association with thyrotoxicosis. The clinical and laboratory data suggest that lead was mobilized from an increased mobile bone pool during the hypermetabolic period with resultant poisoning. The findings give factual support to earlier concepts that lead poisoning may occur during periods of metabolic change in an individual with an increased body lead burden.
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