Splenomegaly Case Summary
A 62 year old white male named Wayne D. had been healthy until recently, when he experienced significant discomfort in his abdomen that left him feeling full after eating less than usual and he felt tired all time. After consulting his physician, it was uncovered that Wayne D. had indeed lost weight, that he appeared pale, and that he had developed splenomegaly. The physician decided to order a complete blood count (CBC) with differential as well as the following chemistry tests: uric acid, lactate dehydrogenase (LD), and leukocyte alkaline phosphatase (LAP) score, to obtain a better understanding on his patient health status. The following abnormal results caught the physician’s attention:
On the CBC with differential:
a severely increased
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→ Calculation of the absolute values of the different leukocytes in the differential was accomplished via the following formula: (total WBC count x relative value in %)/100
On the chemistry tests: increased uric acid (8.4 with normal being 4-6 mg/dL) increased lactate dehydrogenase (LD) (692 with normal being 140-280
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Shet, Jahagirdar and Verfaillie (2002) explain that the Philadelphia chromosome is a shortened chromosome 22 due to a reciprocal translocation between the long arms of chromosomes 9 and 22 t(9; 22q34;q11). During the translocation, the ABL proto-oncogene is relocated from its normal position in chromosome 9 to a major breakpoint cluster region - the M-BCR region located on chromosome 22 - which causes the formation of a BCR-ABL fusion gene. This fusion gene, according to Shet, Jahagirdar and Verfaillie (2002), will produce an onco-protein (p210BCR/ABL) that not just results in more tyrosine kinase (TK) activity, rather than also in increased binding to the actin cytoskeleton; an unregulated growth factor; an accelerated proliferation of leukemic hematopoietic cells; as well as an increased resistance of progenitors/precursors to apoptosis. Moreover, particularly the constantly accelerated proliferation of leukemic hematopoietic cells will increase the chance of secondary genetic abnormalities that eventually can lead to a disease progression and/or a blast crisis (Shet, Jahagirdar and Verfaillie,
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