Abstract
Background: Treatment options for metastases of differentiated thyroid carcinoma with absent uptake of radioiodine (RaI) are limited. Broad spectrum tyrosine kinase inhibitors may offer new perspectives. Clinical case A 54-year old woman with a metastasized T4N1M0 H?rthle cell follicular thyroid carcinoma was referred to the Leiden University Medical Center for experimental treatment with Sorafenib. Initial treatment consisted of irradical total thyroidectomy and a modified radical neck dissection (18 /42 lymph nodes positive). She was subsequently treated with 5550 MBq RaI. At that time the stimulated thyroglobulin (Tg) level was 28 µg/l (n<0.5 µg/l). RaI therapy was repeated once, without uptake on whole body scanning. The unstimulated Tg increased to 7.7 µg/l and a CT scan showed multiple pulmonary and lymph node metastases. Hereafter the Tg was regularly measured, without further treatment. At referral her unstimulated Tg was 1664 µg/l. A Thyrogen stimulated 185 MBq RaI whole body scan showed no uptake and Tg was 4154 µg/l. CT scanning showed progression of the extensive pulmonary metastases. She started Sorafenib 400 mg bid. After 4 weeks Sorafenib therapy, her unstimulated Tg increased to 5440 μg/l. She suffered from adverse side effects including: grade II mucositis; hypocalcaemia; grade II hand-foot-reaction. Unexpectedly, 8 weeks after start of therapy, unstimulated Tg rose to 99.900 μg/l with an increased lactate dehydrogenase (LDH) of 725 U/l (n 200-450 U/l).She was dyspnoeic and had pleural chest pain. A chest CT revealed an impressive decrease in number, size and density of all metastases. Surprisingly, a spontaneous pneumothorax in both lungs was present.
Conclusion: In this case we demonstrated an impressive regression of metastases of a H?rthle cell carcinoma after Sorafenib treatment. The immense rise in Tg and LDH can be attributed to tumorlysis. Furthermore, the decline in tumorload apparently induced visceral pleura defects, leading to a double pneumothorax.