Severe thrombocytopenia in a patient with diffuse toxic goitre

Abstract

Abstract Introduction Diffuse toxic goitre is an autoimmune disorder with a marked prevalence in women. Thrombocytopenia may coexist with diffuse toxic goitre. Nevertheless, the mechanisms of decline in platelet count alongside with autoimmune thyroid disease have not been extensively investigated. Clinical Case A case of diffuse toxic goitre is reported in a 55-year-old man who has been receiving continuous treatment with methimazole for 7 years. The physical examination revealed an asthenic man, with an enlarged thyroid gland, inactive bilateral orbitopathy and multiple ecchymosis, but no lymphadenopathy or hepatosplenomegaly. Laboratory analysis revealed suppressed thyroid stimulating hormone (TSH) 0.01 mlU/ml, normal free T4 level 21.60 pmol/l, increased free T3 6.99 pmol/l and thyroid stimulating immunoglobulin (TSI) level of 23.60 IU/L. Complete blood count revealed severely decreased platelets 3×10^9 / l, decreased hemoglobin 110.00 g/l and hematocrit 21.90%, normal leucocytes 9.58×10^9/l, low prothrombin Index 11% and International normalized ratio (INR) 7.00. Additional serological investigations excluded HIV infection and C viral hepatitis. The bone marrow aspiration disclosed a rich cellular and polymorph marrow, an increased number of megakaryocytes suggesting that the thrombocytopenia is due to platelet destruction. The patient has recovered from viral pneumonia caused by SARS-COV-2, 1 month prior to the medical consultation. He received platelet transfusion and was started on 1 mg/kg oral prednisolone followed by a gradual taper and improvement of platelet count. Thrombocytopenia observed in diffuse toxic goitre may be mediated by both metabolic and immunological phenomena. In our case, the following causes may be considered: (1) an overlapping autoimmune process; (2) methimazole creating destructive antibodies; (3) COVID-19 disease. An autoimmune process is capable of triggering both conditions by activation of the reticuloendothelial system by thyroid hormones along with a cross-reaction between thyroid antibodies and platelet epitopes. Methimazole generates a drug-dependent immune response against platelets, involving platelet endothelial cell adhesion molecules and thus provoking thrombocytopenia. SARS-CoV-2 can induce thrombocytopenia by increasing the number of autoantibodies and immune complexes that destroy platelets. Lung damage by decreasing pulmonary capillary bed and platelet aggregation in the lungs indirectly leads to a reduced number of circulatory platelets. Conclusion Severe thrombocytopenia was detected in a patient with Grave's disease, in whom the number of platelets was 50 times below the lower limit of the reference range. Coexistence of thrombocytopenia may be explained by (1) an overlapping autoimmune process; (2) the effect of methimazole; (3) its occurrence or aggravation secondary to COVID-19.