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hypothyroidism/l tyrosin

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Hypothyroidism in patients with metastatic renal cell carcinoma (mRCC) during treatment with the tyrosine kinase inhibitors (TKIs) sunitinib and sorafenib is a well-established side effect. Furthermore, the potential role of hypothyroidism as predictive marker of outcome has been studied but with
BACKGROUND Hypothyroidism is a common adverse effect of vascular endothelial growth factor receptor tyrosine kinase inhibitor (VEGFR-TKI) therapy in patients with metastatic renal cell carcinoma (mRCC). Some studies have shown an association with improved survival. However, hypothyroidism severity

Hypothyroidism during treatment with tyrosine kinase inhibitors.

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Tyrosine kinase inhibitors are relatively new targeted therapy drugs used for the treatment of metastatic clear cell kidney carcinoma, gastrointestinal stromal tumours, thyroid carcinoma and pancreatic neuroendocrine tumours during the progression of the disease. Hypothyroidism or thyroid

[Side effect management of tyrosine kinase inhibitors in urology : Fatigue and hypothyroidism].

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Not only has the use of tyrosine kinase inhibitors (TKI) for the treatment of metastatic renal cell carcinomas (mRCC) changed the therapeutic options for this disease significantly, but with the occurrence of typical side effects this therapy also poses a challenge for the treating physician.
Tyrosine kinase inhibitor (TKI)-induced thyroid dysfunction has been identified as an important but manageable adverse effect of targeted therapy. Several studies have suggested that patients who develop hypothyroidism respond better to TKIs, but this relationship is not well elucidated. We
BACKGROUND It has been established that hypothyroidism protects rats against renal ischemia and reperfusion (IR) oxidative damage. However, it is not clear if hypothyroidism is able to prevent protein tyrosine nitration, an index of nitrosative stress, induced by IR or if antioxidant enzymes have
The ontogenic development of the transsynaptic induction of adrenal tyrosine hydroxylase (TH), evoked by reserpine and nicotine was studied in control and hypothyroid young rats, aged 3-52 days. The enzymatic induction was measured as an increase in the enzyme activity, since this increase was shown

A novel tyrosine-kinase selective inhibitor, sunitinib, induces transient hypothyroidism by blocking iodine uptake.

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BACKGROUND Sunitinib (sunitinib malate; SU11248; Sutent; Pfizer Inc., New York, NY) is a multitarget inhibitor of tyrosine kinases for the treatment of some human cancers. A myxedematous coma in a patient treated with sunitinib for a gastrointestinal stromal tumor was unexpectedly

Risk Factors for New Hypothyroidism During Tyrosine Kinase Inhibitor Therapy in Advanced Nonthyroidal Cancer Patients.

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Thyroid dysfunction during tyrosine kinase inhibitor (TKI) cancer treatment is common, but predisposing risk factors have not been determined. Recommendations for monitoring patients treated with one or multiple TKI and in conjunction with other relevant cancer therapies could be improved. The study
Tyrosine kinase inhibitor (TKI)-induced thyroid dysfunction is recognized as a common adverse effect of treatment, but the importance of incident hypothyroidism during TKI therapy remains unclear. This study analyzed the prognostic significance of hypothyroidism during TKI therapy in cancer

Hypothyroidism related to tyrosine kinase inhibitors: an emerging toxic effect of targeted therapy.

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Despite their inherent selectivity, targeted therapies such as tyrosine kinase inhibitors (TKIs) can cause unusual adverse effects. Sunitinib and sorafenib are multitargeted TKIs that have been demonstrated to induce hypothyroidism and thyroid dysfunction. Retrospective studies indicate that

Tyrosine kinase inhibitor-induced hypothyroidism: incidence, etiology, and management.

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In recent years, tyrosine kinase inhibitors (TKIs) have emerged as a new class of anti-cancer therapy with proven efficacy in several types of carcinoma. Although generally considered less toxic than cytotoxic chemotherapy, TKIs do have significant side effects including fatigue and hypertension. In

Influence of neonatal hypothyroidism on adrenal tyrosine hydroxylase activation in the young rat.

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1. Adrenal TH activation was elicited in young rats (aged 4, 6 and 14 days) by insulin hypoglycaemia. In the control rats, TH activation varied between 125 and 147% above basal values. 2. Neonatal hypothyroidism induced by PTU treatment impaired TH activation. Compensatory treatment with T3 to the

[Congenital hypothyroidism caused by iodo-tyrosine-desiodase deficiency. Clinical, biological and therapeutic study].

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[Measurement of tyrosine serum levels used as a control of substitution therapy in hypothyroidism].

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