Endocrine Abstracts

Introduction: The coexistence of myasthenia gravis (MG) and autoimmune thyroid disease (AITD) is well recognised, with 5-10% of MG patients also having an AITD^1-2. Among AITD, hyperthyroidism association with MG is the most common³. Conversely, MG has a relatively low incidence of around 0.2% in individuals with hyperthyroidism^{2, 4}. This implies a potential immunological cross-reactivity between the neuromuscular junction and thyroid components in certain cases of MG and hyperthyroidism³. Nevertheless, the precise pathogenic link between these two autoimmune diseases remains uncertain. There are reports of ocular MG in conjunction with hyperthyroidism^5-8. There are limited reports of ocular MG in association with sub-clinical hyperthyroidism¹⁰.

Case summary: A 60-year-old man with a history of prostate cancer underwent various treatments. In April 2023, he presented with right ptosis for three months with no associated symptoms. Initial thyroid tests in June revealed sub-clinical hyperthyroidism, suggesting thyroid-associated orbitopathy. Despite starting carbimazole, his ocular motility worsened, and he developed double vision when looking to each side. Positive acetylcholine receptor antibodies led to an ocular myasthenia gravis diagnosis in August 2023. A pyridostigmine trial showed inconsistent improvement, so prednisolone was initiated in September. A CT thorax and neck ruled out significant abnormalities, and thyroid function tests returned to normal. Ongoing carbimazole treatment was recommended after an October endocrinology review.

Discussion: The exact cause of this is unclear; immunological cross-reactivity and a genetic link have been postulated. For instance, an increase in thyroid antibodies has been found in patients with ocular MG^5-6. Human leukocyte antigen (HLA) specificity (B8, DR3 and BW46) has also been reported between MG and thyroid disease^{6, 11}. More recently, the TNF- α-863 polymorphism and HLA DQ-3 have both been linked with MG and Graves’ disease¹². However, our understanding of the underlying mechanism behind MG and hyperthyroidism’s association remains limited. Both hyperthyroidism and MG can present with ocular manifestations⁹. Thus, the initial presentation in this case was thought to be thyroid-associated orbitopathy. The patient’s symptoms initially worsened until ocular MG was diagnosed; this highlights the importance of early diagnosis as about half of patients who present with ocular myasthenia develop generalised weakness within 6 months¹³. Previous case reports have also demonstrated thyrotoxicosis delaying the diagnosis of MG¹⁴. The patient in this case initially presented with unilateral ptosis. Ptosis is uncommon in thyroid-associated orbitopathy and suggests coexistence of MG^{9-10, 15}. He then developed orbicularis oculi weakness and a positive Cogan lid twitch sign which strongly indicated MG^{10, 15}.