摘要
Consumptive hypothyroidism is often the clinical condition that results from neoplasms producing their own selenodionases that convert T4 needed to be converted to active T3 into an active form of thyroid hormone, rT3. This often requires treatment with high doses of IV T4, with or without doses of T3 as well, until the neoplasm is treated. This principle is demonstrated in the below case of a 65 y/o female with medical history significant for Ia Kappa multiple myeloma, complete heart block s/p AICD placement, and papillary thyroid cancer status post thyroidectomy in 2020, who had initially presented <span>with persistent bone pain, progressive encephalopathy and failure to thrive</span> with more than a 50 lb weight loss over a few months. Labs on presentation <span>were not remarkable for progression of her underlying multiple myeloma</span>, however<span style="font-family:;" "="">,</span><span style="font-family:;" "=""> she was found to have a new significantly elevated TSH. She underwent imaging with a CT chest, abdomen, and pelvis, which showed new hepatic lesions, subcutaneous nodules, and new pulmonary nodules with associated lymphadenopathy and a left-sided pleural effusion. CT-guided liver biopsy evinced a metastatic neuroendocrine carcinoma, further supported by an elevated calcitonin and chromogranin. She was treated with high dose IV T4 at 1.38 mcg/kg however continued to worsening thyroid function labs. She was then started on Liothyronine at 20 mcg and subsequently improved. This <span>patient’s case illustrates the importance of considering consumptive hypo</span>thy<span>roidism when thyroid profile abnormalities and symptoms of severe hypo</span>thyroidism are seen in the context of malignant neoplasms, and further illu<span>strates the important of considering T3 as part of the treatment regimen</span> when IV T4 is not resulting in improvement.</span>
Consumptive hypothyroidism is often the clinical condition that results from neoplasms producing their own selenodionases that convert T4 needed to be converted to active T3 into an active form of thyroid hormone, rT3. This often requires treatment with high doses of IV T4, with or without doses of T3 as well, until the neoplasm is treated. This principle is demonstrated in the below case of a 65 y/o female with medical history significant for Ia Kappa multiple myeloma, complete heart block s/p AICD placement, and papillary thyroid cancer status post thyroidectomy in 2020, who had initially presented <span>with persistent bone pain, progressive encephalopathy and failure to thrive</span> with more than a 50 lb weight loss over a few months. Labs on presentation <span>were not remarkable for progression of her underlying multiple myeloma</span>, however<span style="font-family:;" "="">,</span><span style="font-family:;" "=""> she was found to have a new significantly elevated TSH. She underwent imaging with a CT chest, abdomen, and pelvis, which showed new hepatic lesions, subcutaneous nodules, and new pulmonary nodules with associated lymphadenopathy and a left-sided pleural effusion. CT-guided liver biopsy evinced a metastatic neuroendocrine carcinoma, further supported by an elevated calcitonin and chromogranin. She was treated with high dose IV T4 at 1.38 mcg/kg however continued to worsening thyroid function labs. She was then started on Liothyronine at 20 mcg and subsequently improved. This <span>patient’s case illustrates the importance of considering consumptive hypo</span>thy<span>roidism when thyroid profile abnormalities and symptoms of severe hypo</span>thyroidism are seen in the context of malignant neoplasms, and further illu<span>strates the important of considering T3 as part of the treatment regimen</span> when IV T4 is not resulting in improvement.</span>
作者
Kevin Hess
Soraya Bascoy
James Lenhard
Kevin Hess;Soraya Bascoy;James Lenhard(Department of Internal Medicine, Christiana Care, Newark, USA;Department of Endocrinology, Christiana Care, Newark, USA)
