Endocrine Abstracts

Case history: Carbimazole, a widely used medication to treat hyperthyroidism, is associated with several well-established side effects. Carbimazole-induced lymphopenia is however rarely reported in the literature. This case focuses on a 57-year-old lady diagnosed with Graves’ Disease (GD) in 2015. She was started on Carbimazole which eventually stabilised her thyroid function; her severe thyroid eye disease precluded definitive treatment with radioiodine however she was reluctant to consider thyroidectomy as definitive therapy due to personal reasons and opted for ongoing medical thyroid management. Soon after commencing Carbimazole treatment, she developed a resistant lymphopenia which could not be explained by other haematological or immune disorders.

Investigations: Initial Thyroid function tests confirmed significant hyperthyroidism (TSH <0.014 [0.35-4.94 miu/l], T3 41.2 [2.9-4.9 pmol/l], Free T4 >100 [9-19 pmol/l]) with positive Anti-TSH receptor antibody (44.05 IU/l [0-2 IU/l]). Both the history and examination were consistent with Graves thyrotoxicosis. She was monitored regularly with blood tests including thyroid function and full blood count.

Results: Upon confirming a diagnosis of GD, the patient was started on Carbimazole with the usual precautions taken against agranulocytosis. One year after initiating Carbimazole treatment, she had developed lymphopenia which did not recover after a brief period of discontinuation of Carbimazole while the rest of the haematological indices were all normal. Patient did not receive any treatment for lymphopenia since she was asymptomatic.

Discussion: Neutropenia is a rare but well-known side effect of Carbimazole, on the other hand, lymphopenia is not an often-associated feature consequently there is very limited relevant literature. It is not unusual for thyrotoxicosis to be associated with neutropenia; it frequently precedes Carbimazole initiation and mostly settles after treatment. The mechanism behind Carbimazole-induced lymphopenia has not been confirmed; however, the literature suggests that Carbimazole can lead to the production of antibodies and autoantibodies which can lead to cell lineage-specific cytopenia. In conclusion, we present the case of a patient with GD where lymphopenia appears to have a temporal relationship with commencement of Carbimazole. The cause of this rare phenomenon in this context is probably due to a combination of Carbimazole effects and the condition itself, however the effect of this combination cannot be precisely established. We present this case to raise awareness among clinicians and to attract comments from our specialist colleagues based on their extensive collective clinical and research experience.