THYROID DYSFUNCTION CAUSED BY SECOND-GENERATION TYROSINE KINASE INHIBITORS IN PHILADELPHIA CHROMOSOME-POSITIVE CHRONIC MYELOID LEUKEMIA
(Abstract release date: 05/19/16)
EHA Library. Tothova E. 06/09/16; 134730; PB1830
Prof. Dr. Elena Tothova
Contributions
Contributions
Abstract
Abstract: PB1830
Type: Publication Only
Background
Protein tyrosine kinase inhibitors (TKI) are currently an important drug class in the treatment of leukemia. They represent targeted cancer therapy and have become the treatment of choice in chronic myeloid leukemia (CML). Many studies clearly have demonstrated that they were able to induce thyroid abnormalities including hypothyroidism and less often hyperthyroidism. Increased awareness and monitoring of thyroid function tests are important in patients maintained on TKIs. Thyroid dysfunction is a well-known adverse effect of first-generation tyrosine kinase inhibitors (TKIs), like sunitinib.
Aims
The aim of this study was to investigate the effect of second-generation TKIs on thyroid function in chronic myeloid leukemia (CML) patients treated in 2 centres.
Methods
We retrospectively assessed the effect of the first-generation TKI imatinib and the second-generation TKI nilotinib and dasatinib on thyroid function tests in 73 Philadelphia chromosome-positive (Ph-positive) chronic myeloid leukemia patients.
Results
Overall, 11 of 73 (15% ) had one or more thyroid function test abnormalities during follow-up. Hypothyroidism or hyperthyroidism were found in 6 of 73 (8,2%) and 3 of 73 (4.1%) cases after a median of 6 and 22 weeks, respectively. In most patients thyroid dysfunction was transient without clinical symptoms. Therapy of hypo-/hyperthyroidism was required in three patients. Thyroid dysfunction never resulted in the discontinuation of TKI therapy. Under treatment with imatinib, nilotinib, and dasatinib, thyroid abnormalities were detected in 25%, 35%, and 40%, respectively. Three of 45 patients treated with nilotinib had evidence for an autoimmune thyroiditis (antibody positive in 2 of 3 patients) with an episode of hyperthyroidism preceding hypothyroidism.
Conclusion
Thyroid dysfunction is a common adverse event with second-generation TKI therapy in patients with Ph-positive chronic myeloid leukemia. Although the mechanism is still unclear, the higher frequency of thyroid abnormalities, including autoimmune thyroiditis, warrants regular and long-term monitoring of thyroid function in these patients.
Session topic: E-poster
Type: Publication Only
Background
Protein tyrosine kinase inhibitors (TKI) are currently an important drug class in the treatment of leukemia. They represent targeted cancer therapy and have become the treatment of choice in chronic myeloid leukemia (CML). Many studies clearly have demonstrated that they were able to induce thyroid abnormalities including hypothyroidism and less often hyperthyroidism. Increased awareness and monitoring of thyroid function tests are important in patients maintained on TKIs. Thyroid dysfunction is a well-known adverse effect of first-generation tyrosine kinase inhibitors (TKIs), like sunitinib.
Aims
The aim of this study was to investigate the effect of second-generation TKIs on thyroid function in chronic myeloid leukemia (CML) patients treated in 2 centres.
Methods
We retrospectively assessed the effect of the first-generation TKI imatinib and the second-generation TKI nilotinib and dasatinib on thyroid function tests in 73 Philadelphia chromosome-positive (Ph-positive) chronic myeloid leukemia patients.
Results
Overall, 11 of 73 (15% ) had one or more thyroid function test abnormalities during follow-up. Hypothyroidism or hyperthyroidism were found in 6 of 73 (8,2%) and 3 of 73 (4.1%) cases after a median of 6 and 22 weeks, respectively. In most patients thyroid dysfunction was transient without clinical symptoms. Therapy of hypo-/hyperthyroidism was required in three patients. Thyroid dysfunction never resulted in the discontinuation of TKI therapy. Under treatment with imatinib, nilotinib, and dasatinib, thyroid abnormalities were detected in 25%, 35%, and 40%, respectively. Three of 45 patients treated with nilotinib had evidence for an autoimmune thyroiditis (antibody positive in 2 of 3 patients) with an episode of hyperthyroidism preceding hypothyroidism.
Conclusion
Thyroid dysfunction is a common adverse event with second-generation TKI therapy in patients with Ph-positive chronic myeloid leukemia. Although the mechanism is still unclear, the higher frequency of thyroid abnormalities, including autoimmune thyroiditis, warrants regular and long-term monitoring of thyroid function in these patients.
Session topic: E-poster
Abstract: PB1830
Type: Publication Only
Background
Protein tyrosine kinase inhibitors (TKI) are currently an important drug class in the treatment of leukemia. They represent targeted cancer therapy and have become the treatment of choice in chronic myeloid leukemia (CML). Many studies clearly have demonstrated that they were able to induce thyroid abnormalities including hypothyroidism and less often hyperthyroidism. Increased awareness and monitoring of thyroid function tests are important in patients maintained on TKIs. Thyroid dysfunction is a well-known adverse effect of first-generation tyrosine kinase inhibitors (TKIs), like sunitinib.
Aims
The aim of this study was to investigate the effect of second-generation TKIs on thyroid function in chronic myeloid leukemia (CML) patients treated in 2 centres.
Methods
We retrospectively assessed the effect of the first-generation TKI imatinib and the second-generation TKI nilotinib and dasatinib on thyroid function tests in 73 Philadelphia chromosome-positive (Ph-positive) chronic myeloid leukemia patients.
Results
Overall, 11 of 73 (15% ) had one or more thyroid function test abnormalities during follow-up. Hypothyroidism or hyperthyroidism were found in 6 of 73 (8,2%) and 3 of 73 (4.1%) cases after a median of 6 and 22 weeks, respectively. In most patients thyroid dysfunction was transient without clinical symptoms. Therapy of hypo-/hyperthyroidism was required in three patients. Thyroid dysfunction never resulted in the discontinuation of TKI therapy. Under treatment with imatinib, nilotinib, and dasatinib, thyroid abnormalities were detected in 25%, 35%, and 40%, respectively. Three of 45 patients treated with nilotinib had evidence for an autoimmune thyroiditis (antibody positive in 2 of 3 patients) with an episode of hyperthyroidism preceding hypothyroidism.
Conclusion
Thyroid dysfunction is a common adverse event with second-generation TKI therapy in patients with Ph-positive chronic myeloid leukemia. Although the mechanism is still unclear, the higher frequency of thyroid abnormalities, including autoimmune thyroiditis, warrants regular and long-term monitoring of thyroid function in these patients.
Session topic: E-poster
Type: Publication Only
Background
Protein tyrosine kinase inhibitors (TKI) are currently an important drug class in the treatment of leukemia. They represent targeted cancer therapy and have become the treatment of choice in chronic myeloid leukemia (CML). Many studies clearly have demonstrated that they were able to induce thyroid abnormalities including hypothyroidism and less often hyperthyroidism. Increased awareness and monitoring of thyroid function tests are important in patients maintained on TKIs. Thyroid dysfunction is a well-known adverse effect of first-generation tyrosine kinase inhibitors (TKIs), like sunitinib.
Aims
The aim of this study was to investigate the effect of second-generation TKIs on thyroid function in chronic myeloid leukemia (CML) patients treated in 2 centres.
Methods
We retrospectively assessed the effect of the first-generation TKI imatinib and the second-generation TKI nilotinib and dasatinib on thyroid function tests in 73 Philadelphia chromosome-positive (Ph-positive) chronic myeloid leukemia patients.
Results
Overall, 11 of 73 (15% ) had one or more thyroid function test abnormalities during follow-up. Hypothyroidism or hyperthyroidism were found in 6 of 73 (8,2%) and 3 of 73 (4.1%) cases after a median of 6 and 22 weeks, respectively. In most patients thyroid dysfunction was transient without clinical symptoms. Therapy of hypo-/hyperthyroidism was required in three patients. Thyroid dysfunction never resulted in the discontinuation of TKI therapy. Under treatment with imatinib, nilotinib, and dasatinib, thyroid abnormalities were detected in 25%, 35%, and 40%, respectively. Three of 45 patients treated with nilotinib had evidence for an autoimmune thyroiditis (antibody positive in 2 of 3 patients) with an episode of hyperthyroidism preceding hypothyroidism.
Conclusion
Thyroid dysfunction is a common adverse event with second-generation TKI therapy in patients with Ph-positive chronic myeloid leukemia. Although the mechanism is still unclear, the higher frequency of thyroid abnormalities, including autoimmune thyroiditis, warrants regular and long-term monitoring of thyroid function in these patients.
Session topic: E-poster
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