Systematic lupus erythematosus (SLE) is a common autoimmune disease involving multiple organs and systems in clinic. The incidence of SLE in China is 8.37–8.77/100 000 people/year, ranking as the fourth highest globally, following the United States, Poland and Barbados.1 The pathological manifestation of SLE involve excessive activation, abnormal differentiation of T cells, acquired immune abnormalities caused by enhanced differentiation of B cells, and innate immune abnormalities characterized of immune complexes composed of autoantibodies.2 Genetic susceptibility and environmental factors contribute to the production of various autoantibodies, which in turn contribute to the occurrence and development of other diseases.

Thyroid hormones play a crucial role in regulating cell growth, affecting neural development, and maintaining body homeostasis. Thyroid hormone secretion disorder can manifest as hypothyroidism or hyperthyroidism, altering the body's metabolic state, and potentially leading to severe conditions, such as myxedema, coma, and thyroid crisis.3 Studies have found that SLE patients are often complicated with other autoimmune diseases such as Sjogren's syndrome (SS), rheumatoid arthritis (RA), and thyroid disease, which have been defined multiple autoimmune syndrome (MAS).4,5 Timely detection and treatment of thyroid diseases in SLE patients can reduce the risk of critical symptoms and improve disease prognosis.

Thus, this retrospective study aims to analyze the clinical and laboratory indicators of SLE patients, explore the potential pathogenic association between thyroid function and SLE based on a single medical center.