Posted by Lilly from ? (184.108.40.206) on Thursday, November 14, 2002 at 7:18PM :
Site that gives more info on what platelets do. It's good for anyone to read. Please excuse the baby language. I forgot to say this, but bruises are caused when red blood cells leak out of a site of vascular injury into the tissue under the skin - hence the reddish color you see at the beginning of the bruise. I'm guessing that Lina is in the process of regenerating her blood cells (now derived from the transplanted bone marrow cells), which includes platelets, b/c her bone marrow, which was producing the cancerous/defective white blood cells in her body, was killed off by the chemo. Since her platelet count was low, it means that more red blood cells are able to leak out into the tissue under the skin whenever a vessel breaks b/c it takes longer for the platelet plug to form at the site of injury.
from Goldman: Cecil Textbook of Medicine, 21st ed., Copyright © 2000
CHRONIC MYELOGENOUS LEUKEMIA (CHRONIC MYELOID LEUKEMIA, CHRONIC MYELOCYTIC LEUKEMIA, CHRONIC GRANULOCYTIC LEUKEMIA)
Chronic myelogenous leukemia (CML) is a disease characterized by overproduction of cells of the granulocytic, especially the neutrophilic, series and occasionally the monocytic series, leading to marked splenomegaly and very high white blood cell (WBC) counts. Basophilia and thrombocytosis are common. A characteristic cytogenetic abnormality, the Philadelphia (Ph1 ) chromosome, is present in the bone marrow cells in more than 95% of cases. The granulocytes usually appear relatively normal, although those of many patients exhibit dysplastic changes, including Pelger-Huet anomalies. Neutrophil functions, such as phagocytosis and bactericidal activity, are largely preserved. Before effective treatment was available, patients survived, on the average, approximately 2 years after diagnosis.
Usually no etiologic agent can be incriminated in CML. Exposure to ionizing radiation increases the risk of subsequent CML. Survivors of the atomic bomb explosions in Japan in 1945 have had an increased incidence of CML, with a peak occurring 5 to 12 years after exposure and seeming to be dose related. The relative risk has been falling since that time but is still above the expected rate for Japan. Radiation treatment of ankylosing spondylitis and cervical cancer has increased the incidence of CML. No increase in the risk of CML has been demonstrated in individuals working in the nuclear industry. Radiologists working without adequate protection before 1940 were more likely to develop myeloid leukemia, but no such association has been found in recent studies. Benzene exposure increases the risk of acute myelogenous leukemia (AML) but not of CML. Patients with CML have an increased frequency of the Cw3 and Cw4 human leukocyte antigens (HLAs). CML is not a frequent secondary leukemia following the treatment of other cancers with radiation and/or alkylating agents.
from Hoffman: Hematology: Basic Principles and Practice, 3rd ed., Copyright © 2000
PATHOGENESIS OF CML
The cytogenetic hallmark of CML, a reciprocal translocation between chromosomes 9 and 22 (t(9;22)(q34;q11)), results in the juxtaposition of the c-abl oncogene on chromosome 9 with the bcr region of chromosome 22 and the resulting formation of a chimeric bcr/abl gene. In most cases of CML, this chimeric gene expresses an 8.5-kb hybrid mRNA transcript giving rise to a 210-kd fusion protein (p210bcr/abl) with transforming activity for hematopoietic cells and the ability to cause CML-like myelopoiesis in mice.
Also, Stella, please check your email...
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