Abstract:
Introduction. Thrombocytopenia may coexist with Grave’s disease. However, the mechanisms of decrease
in platelet count alongside with autoimmune thyroid disease have not been comprehensively investigated.
Case presentation. A case of Grave’s disease is reported in a 55-year-old man who has been receiving
continuous treatment with synthetic antithyroid drugs for 7 years. Laboratory analysis showed 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) 23.60 IU/L. Complete blood test revealed severely
decreased platelets 3 x 10^9 / l, decreased hemoglobin 110.00 g/l, leucocytes 9.58 x 10^9/l, hematocrit
21.90%, Prothrombin Index 11%, International normalized ratio (INR) 7.00. The patient has recovered
from viral pneumonia caused by SARS-COV-2, 1 month prior to the medical consultation.
Discussion. Thrombocytopenia observed in hyperthyroidism may be mediated by both metabolic and
immunological phenomena. In our case, the following causes may be considered: (1) an overlapping
autoimmune process; (2) antithyroid drugs 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 [1,3].
Carbimazole generates a drug-dependent immune response against platelets, involving platelet endothelial
cell adhesion molecules and thus provoking thrombocytopenia [4]. SARS-CoV-2 can induce
thrombocytopenia by mass production of cytokines causing progenitor destruction in the bone marrow with
decreased primary platelet production. Infection increases the number of autoantibodies and immune
complexes that destroy platelets. Lung damage by decreasing pulmonary capillary bed and evoking the
fragmentation of megakaryocytes, leads to a reduced number of circulatory platelets [2].
Conclusion. A 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
carbimazole; (3) its occurrence or aggravation secondary to COVID-19.
