探讨毒性弥漫性甲状腺肿(GD)合并桥本甲状腺炎，并在病程中叠加甲巯咪唑致粒细胞缺乏、甲状腺危象及药物性狼疮(DILE)的临床特征与干预策略。

回顾性分析2024年12月1日郑州大学第五附属医院内分泌科收治的1例33岁甲亢危象并严重粒细胞缺乏合并药物性狼疮女性患者的临床表现、实验室检查及治疗经过。

患者33岁，初诊时甲状腺功能显著亢进，游离三碘甲状腺原氨酸(16.23 pmol/L)、游离甲状腺素(45.38 pmol/L)水平升高，促甲状腺激素水平低下(0.006 U/L)，促甲状腺激素受体抗体及甲状腺过氧化物酶抗体阳性，甲状腺摄碘率增高(2 h 49.40%，6 h 80.90%，24 h 94.10%)。超声提示甲状腺轻度肿大、实质回声弥漫性减低不均且血流稍丰富，符合GD病合并桥本甲状腺炎表现，且伴粒细胞减少。予以甲巯咪唑治疗后，患者出现骨髓抑制(表现为粒细胞缺乏、红细胞及血小板减少)，继发急性化脓性扁桃体炎，并诱发甲亢危象(BWPS评分45分)。骨髓活检提示造血组织增生低下，关键免疫学检查发现抗核抗体(≥1∶160)及抗Sm抗体阳性，考虑DILE所致血液系统损害。停用甲巯咪唑，经积极抗感染，应用重组人粒细胞刺激因子、糖皮质激素、免疫抑制剂及后续碘-131治疗后，患者感染控制，血常规逐渐恢复正常。甲状腺功能于碘-131治疗后转为亚临床甲减，补充左甲状腺素钠片后恢复正常。患者DILE相关指标(抗核抗体滴度)下降，糖皮质激素及免疫抑制剂用量减少，病情稳定。

抗甲状腺药物(如甲巯咪唑)可能引发包括DILE在内的自身免疫反应，临床在诊治甲亢合并血细胞异常时，应及时筛查继发性免疫异常，以实现早期识别与干预。

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.