Acta Clin Croat, Vol. 48, No. 3, 2009 67 Acta Clin Croat 2010; 49:67-71 Case Report MYASTHENIC CRISIS AS A SIDE EFFECT OF METHIMAZOLE THERAPY: CASE REPORT Maja Baretić 1 , Stjepan Balić 2 and Goran Gudelj 3 1 Department of Endocrinology, University Department of Medicine, Zagreb University Hospital Center; 2 Department of Endocrinology and Metabolic Diseases; 3 Department of ENT and Head and Neck Surgery, Sveti Duh University Hospital, Zagreb, Croatia SUMMARY – Myasthenia gravis and Graves’ disease are two autoimmune diseases with a similar mechanism, both having circulating organ autoantibodies and cell specific autoantibodies. It is not unusual for these diseases to occur together. Tere is a large body of data proving that antithyroid drugs such as methimazole and propylthiouracil have an immunomodulatory effect in addition to their thyrosuppressant action. Tis case report describes a 34-year-old woman hospitali- zed for just diagnosed myasthenic crisis (Osserman IV). She had a prior history of hyperthyroidism and treatment with methimazole was initiated. However, improvement in thyroid disease led to the burst of myasthenia. Te phenomenon described as worsening of one disease while improving the other, the so-called ‘see-saw’ relationship, occurred in this case. Te question is whether antithyroid drugs improve hyperthyroidism while unveiling or worsening myasthenia. Is the ‘see-saw’ relation- ship actually a therapeutic side effect of antithyroid drug? Te proposed mechanism of methimazole action is intracellular: it lowers the level of proliferating cell nuclear antigen (PCNA). PCNA pro- motes selective apoptosis in some T lymphocyte clones. In this way, CD4 + CD25 + regulatory T cells might ‘skip’ immune self-tolerance and autoantibodies against acetylcholine receptor may occur. Do antithyroid drugs actually create an immune ‘thymic surrounding’? Key words: Hiperhyroidism – complications; Hiperhyroidism – drug therapy; Myasthenia gravis – complications; Myasthenia gravis – drug therapy; Methimazole – adverse effects Correspondence to: Maja Baretić, MD, MS, Ulica grada Vukovara 254, HR-10000 Zagreb, Croatia E-mail: maja.simek@zg.t-com.hr Received March 4, 2009, accepted in revised form January 18, 2010 Introduction Tyroid gland is the organ with perhaps most com- mon autoimmune pathology. Having one autoimmune disease in the body increases the chance of developing another one 1 . Tere also are syndromes that include more autoimmune features connecting thyroid gland and myasthenia gravis, e.g., polyglandular syndrome type II (Schmidt’s syndrome) 2 . Schmidt’s syndrome is characterized by the presence of two or more autoim- mune diseases, usually affecting thyroid gland, adre- nal glands and endocrine pancreas. It is not unusual that other diseases like myasthenia, hypogonadism, pernicious anemia, Parkinson’s disease and celiac dis- ease occur. Polyglandular syndrome type II is linked with HLA DR3 and HLA DR4 locus, inherited in the autosomal dominant mode with variable expres- sivity 3 . Tere are a number of reports describing the same incidence of myasthenia gravis and thyroid disease, with or without polyglandular syndrome, so that statistically as many as 5%-10% of patients suf- fering from myasthenia have some kind of thyroid autoimmunity 4,5 . Te prevalence of myasthenia gravis in Graves’ disease is 0.14% 6 . Although there are known HLA typing points to the possible HLA DQ3 asso- ciation in patients with myasthenia and hyperthyroid- ism, the exact relationship between these two diseases Book Acta 1-2010.indb 67 Book Acta 1-2010.indb 67 14.6.2010 9:23:04 14.6.2010 9:23:04