Endocrine Abstracts

A gentleman in his 70s with a background of atrial fibrillation, hypertension, and mesothelioma undergoing immunotherapy via Nivolumab and Ipilimumab, presented with general unwellness, fevers, confusion, and headaches. He had no prior endocrine history but was found to have significantly deranged thyroid function tests. He was treated for thyrotoxicosis and an impending thyroid storm with carbimazole. He remained treatment resistant for several days, with continuous delirium, fast atrial fibrillation, refractory hypotension, and persistent pyrexia. His treatment was therefore switched to PTU with addition of Lugol’s iodine, IV beta blockers, and IV hydrocortisone. The source of his thyrotoxicosis was hypothesised to be due to amiodarone, immunotherapy, or Jod Basedow effect post contrast. His TFTs started to improve after about 1 week of this treatment regimen. His medications were reduced to prevent hypothyroidism and he was discharged appropriately with a plan in place for urgent follow up. Days later, he was readmitted with hypotension; therefore, his carbimazole was reduced and prednisolone was added. The patient’s TFTs normalised while in hospital and he was discharged on a low dose of carbimazole and prednisolone with repeat bloods and endocrine follow up. The discussion revolves around the potential effect of immunotherapy on hormones, and distinguishing at what level the effect is taking place. At the level of the thyroid, the increased free T4 and T3 causes negative feedback on the pituitary gland to suppress TSH in an attempt to counteract this. Similarly, if the effect is on the pituitary itself, the TSH may be dually suppressed in this manner. To distinguish whether the pituitary was also being affected, it was necessary to observe the changes in TSH as the other thyroid hormones normalised. If TSH reverted to normal levels when free T4 and T3 were within range, it is unlikely that the pituitary gland was contributing to the suppressed TSH, and much more likely that it had been low as a result of negative feedback from the elevated levels of T4 and T3 that were being produced by the thyroid gland. Additionally, we tested the other pituitary hormones to look for other derangements in values. We found that once the patient’s T4 and T3 were within normal ranges, the TSH gradually also went back to normal. This suggests that the derangement occurred primarily at the level of the thyroid, as pituitary involvement would have continued to suppress TSH despite the correction on T4 and T3.