i've just read an article about thyroid issues with tki. they said most of people did not need treatment for that and that's transitory. there are some medications for hyperthyroidism maybe you should give a chance to them and have another test in a month, but it's up to you. you had a great result with tasigna and will do well long term. thanks for the support. hope i can maintain my thyroid and solve this issue
Thyroid dysfunction is a well-known adverse effect of ﬁrst-generation TKI therapy (1-3). Athyroid patients with CML (31,32) or metastatic medullary thyroid carcinoma (33)
simultaneously being treated with thyroid hormones and imatinib seem to need a signiﬁcant increase of the levothyroxine replacement dose. Increased nondeiodination clearance through enzyme induction has been proposed as a potential mechanism (32). However, there was no thyroid dysfunction in patients with the thyroid in situ (34). Here, we analyzed thyroid function through serial monitoring of TFTs in patients being treated with imatinib, nilotinib, and dasatinib. To avoid the potential inﬂuence of comorbidities as well as the inﬂuence of CML cells and intensive treatment regimens on thyroid function, only patients with CML in chronic or early accelerated phase and one patient with hypereosinophilic syndrome were included in the present study Thyroid abnormalities were very common with only about a third of the population being strictly euthyroid during follow-up. Both hypothyroidism and hyperthyroidism were each found in about a quarter of patients. However, these changes were mostly subclinical and transient and, according to the American Thyroid Association guidelines (30), rarely needed any treatment. Due to the transient nature of druginduced hypo-orhyperthyroidism, aswellasthemildclinical course with lack of symptoms in all but two patients, no speciﬁc treatment was initiated. The therapeutic relevance of early diagnosis of hypothyroidism or hyperthyroidism is therefore unclear. Due to the retrospective nature of this study, more detailed analyses of mechanisms were not possible. However, 4 of 18 patients (22%) with hypothyroidism and 4 of 55 patients (7%) being treated with nilotinib had evidence for an autoimmune thyroiditis, which, however, did not lead to persistent hypothyroidism. Only one of these four patients, who did not have autoantibodies, had previously been treated with interferon arguing against cytokine-induced generation of autoantibodies as a major factor. In conclusion, we found thyroid dysfunction to be common in patients with Ph-positive CML under treatment with imatinib and the second-generation TKIs, nilotinib and dasatinib. However, these abnormalities rarely implied a change in clinical management or required treatment, and never led to discontinuation of the TKI. Due to the inherent limitations of a retrospective, uncontrolled study and the sample size of our cohort no direct comparisons between different drug therapies is possible. Nevertheless, the frequency of thyroid abnormalities and occurrence of cases with evidence for thyroiditis indicates that these patients should be monitored regularly. Despite their reported kinase speciﬁcity, TKIs share still elusive off-target effects that frequently result in abnormal TFTs, including autoimmune thyroiditis. We therefore suggest careful monitoring of TFTs in second-generation TKI-treated patients".