Does thyroid dysfunction happen in CML patients receiving Imatinib for treatment?

ABSTRACT

Subarachnoid hemorrhage is one of the most important and dangerous neurologic emergencies worldwide. It is characterized by a sudden and severe headache caused most commonly by the rupture of intracranial aneurysm. Cerebral vasospasm is the Chronic myelogenous leukemia is a myeloproliferative disorder presenting with anemia, elevated blood granulocytosis and the presence of immature granulocytes, basophilia, frequently thrombocytosis and spleen enlargement. The diagnosis is stabilized by hematopoietic stem cell expressing a fusion gene [BCR/ABL] resulted from translocation of 9 and 22 chromosomes. The products of this gene play a central role in developing chronic myelogenous leukemia including maintenance of chronicity and/or progress to accelerated phase and or blastic crisis. Imatinib is the first generated tyrosine kinase Inhibitor, which prevents ATP binding to a specific situation of tyrosine kinase molecules that are involved in phosphorylation of membranous proteins and activation of the pathways that are necessary for tumor cell survey and proliferation. Therefore, tyrosine kinase inhibitor inhibits signaling proteins, which are responsible for tumor growth, invasion, angiogenesis and even metastasis. Although tyrosine kinase inhibitor are specific targeted-designed compounds, every agent interacts with many kinds of tyrosine kinases and produces many unwanted effects. One of the undesirable adverse effects is thyroid dysfunction. The first reported article about tyrosine kinase inhibitor-induced thyroid dysfunction published in 2005 and since then few studies have demonstrated thyroid disturbances ranging from subclinical thyroid dysfunctions to overt clinically thyroid disorders during tyrosine kinase inhibitor therapy. This review attends to summarize only imatinib-induced thyroid disturbances in CML patients with positive Philadelphia chromosome in recent years