RESUMEN
Bone is the second most common site of metastasis for differentiated thyroid carcinoma (DTC). Bone metastasis (BMs) occur in about 10% of patients with DTC and is observed more often in follicular thyroid carcinoma (FTC) (7-28%) than papillary thyroid carcinoma (PTC) (1-7%). Bone metastasis is associated with unfavorable clinical outcomes mainly including skeletal-related events (SREs), such as pathologic fractures, bone pain, spinal cord compressions, and hypercalcemia, which negatively impact the quality of life of patients and reduce their life expectancy. Patients with BMs from DTC require comprehensive and multimodal treatment approaches, including radioiodine (RAI) therapy, palliative care, surgery, external beam radiotherapy, and targeted drug therapy. RAI therapy is the first-line treatment, despite being rather ineffective, especially in large BMs. The response to RAI therapy, either alone or in combination with BM focal treatment depends on iodine avidity. This study reports a rare case of metachronous skull bone metastasis from FTC in a 72-year-old female patient 15 years after initial treatment. The patient had an excellent response to RAI therapy, which resulted in the abnormal uptake disappearing. Following treatment, the patient has been disease-free for six years. This case confirms that a complete response to RAI treatment for BM depends on the degree of dedifferentiation of cancer cells, which highlights the need for long-term follow-up, especially for FTC patients.
RESUMEN
Resistance to thyroid hormone (RTH) is a rare autosomal dominant disease characterized by an alteration of thyroid hormone negative feedback, usually as a consequence of a mutation in the thyroid hormone receptor-b gene (THRß). It is characterized by high variability of clinical manifestations, ranging from isolated abnormal thyroid function tests without symptoms to severe and impaired clinical conditions. Here we report the case of a woman who was diagnosed with RTHß when she was 35 years old and was treated with 3,5,3-triiodiothyroacetic acid (TRIAC) because of the onset of clinical symptoms of hyperthyroidism. This therapy has been effective in controlling thyrotoxicosis for 5 years. After this time the patient developed an autoimmune hyperthyroidism, with TSH receptor autoantibodies appearance, which caused a loss of efficacy of the drug in controlling the disease. The development of different pathophysiological mechanisms of thyrotoxicosis, as in this case, could be the reason for both variability of disease manifestations and of loss of response to drug therapy.