Clinical Nutrition by Marinos Elia

Author:Marinos Elia
Language: eng
Format: epub
Publisher: Wiley
Published: 2013-03-06T16:00:00+00:00

A transient reduction of energy expenditure may be induced by chemotherapy. However, fever, immunosuppression, and consequent opportunistic infections may again increase metabolic rate and protein wasting, particularly in the neutropaenic period.

Chronic myeloid leukaemia

CML is a clonal myeloproliferative disorder of a pluripotent stem cell with a specific cytogenetic abnormality, the Philadelphia (Ph) chromosome, which is responsible for the generation of a pathologic fusion protein (p210) with tyrosine-kinase activity. The proein induces a dysregulation in the control mechanisms of white blood cell proliferation and death. The first phase of the disease, the chronic phase, terminates in a second, more acute or abrupt course, called the blast phase. Symptoms and signs usually develop insidiously and include fatigue, anaemia, progressive splenomegaly, and leukocytosis. In the chronic phase, the myeloid cells in the peripheral blood show all stages of differentiation, but the myelocyte predominates. The therapeutic approach of CML has radically changed in the last 10 years. Until 2000, the best therapeutic options for young CML patients were recombinant interferon-gamma (rIFN-γ) and allogeneic stem-cell transplant; but since then the first treatment choice has become the use of tyrosine-kinase inhibitors (TKIs) (imatinib, dasatinib, nilotinib). These compounds, orally administered, target the pathologic fusion protein responsible for the proliferation and apoptosis impairment, and are capable of inducing cytogenetic remissions in a high proportion of patients. Currently the indication for stem-cell transplant in CML is limited to those patients not responding to TKI and to those in accelerated/blastic phase.

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