Induction Therapy is the initial phase of chemotherapy where an antibiotic is combined with cytarabine to prevent DNA production of leukemia cells. The therapy stops their growth and kills them by getting rid of blood and marrow with detected leukemia blast cells. Successful chemotherapy can lead to severe shortage of red blood cells and platelets and transfusion may be required. With normal cell count the patient residual leukemic cells are said to be inactive since they do not interfere with the development of the cell but additional therapy is needed to prevent re-growth.
For acute lymphocytic leukemia which is a frequent problem, the leukemic blast cells invade the spinal cord lining or brain so the therapy is given into the spinal canal or radiation therapy is used to treat accumulated leukemia cells in a troublesome site. (Leukemia and Lymhoma Society, 2001) Pathophysiology diagnosis review The pathophysiology of acute myelogenous leukemia (AML) involves a block of myeloid maturation, which is a desirable therapeutic strategy that induces leukemic cell maturation to increase the efficacy especially in children diagnosis and avoid the side effects of chemotherapy.
6-benzylthioinosine (6BT) is a promising inducing agent for screening. It induces differentiation and is a subset of AML cell lines and makes them to undergo 6BT-mediated cell death. Despite inducing cell death in some leukemic cells, it exhibits extremely low toxicity on several nonmalignant cells such as bone marrow. (Yarbro, Goodman and Frogge, 2005). In contrast, it most likely enters at least some leukemic cell lines as required by Pathophysiology diagnosis and is able to synergize with currently used myeloid differentiation agents.
According to Yarbro, Goodman and Frogge, on diagnosis in 2005, resent research indicate that the mechanism of action of this compound may lead to growth inhibition and subsequent differentiation besides showing the ability to impair tumor growths. This inducing agent is promising on new discovery of better differentiation agents that will be perceptible with leukemic cell–specific activity. Patient’s History: P. M was originally diagnosed on July 24, 2008 with AML.
He is in remission on chemotherapy according to children cancer group protocol (AAML 0531), and just completed ara-c and etoposide. During my shift on October 14, 2008 he was complaining of severe headache and had feelings of nausea and vomiting. We also had problem regulating his temperature and the lowest it got was 102. 9 Fahrenheit which was still too hot for him, and as a result we weren’t able to administer his platelets and red cell transfusion as it was contradicting with his body temperature until later that night when his temperature dropped.
The following day he got discharge from children hospital, and less than 24 hours later he was complaining about vomiting, diarrhea, and stomach ache to the point that he was readmitted. Little about his background, P. M is attending high school but for the moment remains on home instruction. He continues to have severe Pancytopenia and is also always worried about his health. He has visual changes related to bilateral severe retinal hemorrhages that he had the month prior to this one. His vision on right is still poorer than the vision on left.