An investigation of the pattern and mechanism of co-morbidity in patients with Hashimoto's thyroiditis

Caihong Zhao¹Haodong Xiong²Lingfei Zhu¹Azijiang • Adali¹Weijie Yu³Simiao Tan¹Shuying Wang¹Cheng-Bowen Zhao¹Yan Lin^1*Zinan Wei¹He Huang¹Xinyu Peng¹

• ¹Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China
• ²School of Life Sciences, Beijing University of Chinese Medicine, Beijing, Beijing, China
• ³College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, Beijing, China

Objective: This study aims to investigate the co-morbidity patterns and pathogenesis in patients with Hashimoto's thyroiditis (HT).Methods: Patients with HT who visited the outpatient clinic of the Thyroid Department at Dongzhimen Hospital, Beijing University of Chinese Medicine, between June 2021 and December 2024 were included in the study. Association rule analysis and logistic regression analysis were performed using SPSS 25.0 and SPSS Modeler 18.0 to identify co-morbidity patterns in patients with HT. Disease targets were screened using the GeneCard database, and protein interaction networks for the intersecting targets were constructed using STRING and Cytoscape. Metascape was employed to perform GO function and KEGG pathway enrichment analysis, uncovering relevant targets and potential pathways associated with co-morbidities in patients with HT.Results: Of the 429 patients with HT, 348 had co-morbidities, resulting in a co-morbidity prevalence of 81.19%. Association rule analysis identified thyroid nodules (TN) as the central factor in binary co-morbidities, while the combination of TN and hyperplasia of the mammary gland (HMG) was central to ternary co-morbidities, and the trio of TN, HMG, and uterine leiomyomas (UL) characterized quaternary co-morbidities. Female gender and advancing age were associated with an increased likelihood of co-morbidities, whereas levothyroxine sodium (L-T4) therapy was linked to a reduced likelihood. Core targets for predicting co-morbidities in HT included AKT1, TP53, EGFR, INS, and TNF, with potential pathways including the cancer pathway and PI3K-Akt signaling pathway.The high co-morbidity prevalence in patients with HT warrants considerable attention within the medical community.