To explore the clinical characteristics and management strategies of Graves disease (GD) complicated with concurrent Hashimoto′s thyroiditis, and the occurrence of agranulocytosis, thyroid storm, and drug-induced lupus erythematosus (DILE) during the course of treatment with methimazole.

A retrospective analysis was conducted on a 33-year-old woman admitted to the Department of Endocrinology, the Fifth Affiliated Hospital of Zhengzhou University with a thyroid storm complicated by severe granulocytopenia and DILE. Her comprehensive clinical presentation, laboratory evaluations, and therapeutic management were reviewed.

The patient, a 33-year-old woman, presented with significant hyperthyroidism at initial diagnosis, characterized by elevated levels of free triiodothyronine (FT3) (16.23 pmol/L) and free thyroxine (FT4) (45.38 pmol/L), decreased thyroid-stimulating hormone (TSH) levels (0.006 U/L), positive thyrotropin receptor antibody (TRAb) and thyroid peroxidase antibody (TPOAb), and increased thyroid iodine uptake (2 h 49.40%, 6 h 80.90%, 24 h 94.10%). Ultrasonography revealed a mildly enlarged thyroid with diffuse heterogeneous hypoechogenicity and slightly increased vascularity, consistent with the clinical presentation of GD complicated by HT, accompanied by granulocytopenia. Methimazole therapy induced myelosuppression (characterized by agranulocytosis, anemia, and thrombocytopenia), leading to secondary acute suppurative tonsillitis and triggering a thyroid storm (BWPS score 45). A bone marrow biopsy revealed hypoplasia of hematopoietic tissue. Key immunological tests were positive for antinuclear antibodies (≥1∶160) and anti-Sm antibodies, suggesting hematologic damage caused by DILE. After discontinuation of methimazole, aggressive antimicrobial therapy, administration of recombinant human granulocyte colony-stimulating factor (G-CSF), glucocorticoids, immunosuppressants, and subsequent I¹³¹ therapy, the patient′s infection was controlled. Complete blood count parameters gradually normalized. Thyroid function converted to subclinical hypothyroidism after I¹³¹ therapy and normalized with levothyroxine supplementation. DILE-related markers (antinuclear antibody titers) decreased, allowing for a reduction in glucocorticoid and immunosuppressive doses, and the patient′s condition remained stable.

Antithyroid drugs (e.g., methimazole) may trigger autoimmune responses, including DILE. In clinical practice, secondary immune abnormalities should be promptly screened during the diagnosis and treatment of hyperthyroidism with hematologic abnormalities to achieve early identification and intervention.