The comorbidity of systemic lupus erythematosus (SLE) and autoimmune thyroid disease (AITD) has become a significant area of research focus in the fields of rheumatology and immunology. This article reviews recent advances in epidemiology, immunopathological mechanisms, genetic background, and clinical management.

Relevant literature was searched in PubMed using Medical Subject Headings and title/abstract terms related to systemic lupus erythematosus, autoimmune thyroid disease, Hashimoto disease, Graves disease, and thyroid dysfunction. A total of 600 records were identified, and 136 studies were finally included after title and abstract screening as well as full-text review based on topic relevance.

SLE patients exhibit a significantly elevated risk of developing AITD, particularly Hashimoto's thyroiditis (HT) and Graves' disease (GD). The mechanisms underlying this comorbidity involve abnormal activation of the Th1/IFN-γ axis, overexpression of the type I interferon pathway, shared susceptibility genes (e.g., PTPN22, CTLA-4, HLA-DR3/DR15), and interactions between epigenetic and environmental factors. Clinically, SLE patients more commonly present with hypothyroidism, which correlates closely with disease activity, renal involvement, and anti-dsDNA antibody positivity. Additionally, SLE patients exhibit markedly elevated thyroid cancer risk, suggesting chronic inflammation and immune dysregulation may promote tumorigenesis. These findings further underscore the close interplay between systemic autoimmunity and thyroid-specific immune abnormalities and support greater clinical attention to early recognition and monitoring efforts in routine rheumatology clinical practice.

The article emphasizes the importance of establishing a screening system for thyroid function and antibodies in SLE patients, with a particular focus on high-risk groups, including females, younger individuals, antibody-positive patients, and those with concomitant Sjögren's syndrome. Therapeutic management must address both SLE and thyroid disease, with vigilance regarding glucocorticoid suppression of TSH. Dual-targeted therapeutic strategies targeting TYK2, JAK-STAT, and IFN pathways warrant exploration. Future research should focus on multi-omics integration and precision interventions to achieve personalized management and optimized outcomes for patients with comorbidities.