Hashimoto’s thyroiditis (HT) is the most common autoimmune thyroid disease and papillary thyroid carcinoma (PTC) is the most common malignant tumor of the thyroid gland. HT, also known as chronic lymphocytic thyroiditis (CLT), was first described by Japanese scholar Hakaru Hashimoto in 1912 and is characterized by diffuse lymphocytic infiltration, fibrosis and parenchymal atrophy in the thyroid gland. Ninety percent of patients with HT have increased titers of antithyroid peroxidase antibodies (TPOAb) and antithyroglobulin antibodies (TgAb). Ultrasonography shows hypoechoic and heterogeneous thyroid gland with abundant vascularity, which may be accompanied by microscopic hypoechoic nodules with clear margins. Clinical evaluation plus antibody testing is the initial basis for diagnosis. The incidence of HT is about 0.3 to 1.5%. The incidence of HT is about 0.3 to 1.5%, and the incidence in women is about 5 to 20 times higher than that in men. In recent years, the incidence of thyroid cancer, especially papillary thyroid cancer, has been increasing, and PTC accounts for more than 90% of thyroid cancer. Pathologically, PTC is characterized by well-differentiated columnar epithelium with papillary protrusions, clear nuclei with eosinophilic cytoplasm, and often calcium deposits. The prognosis is good, and the survival period after surgery is more than 10-20 years. Secondly, we understand the relationship between Hashimoto’s thyroiditis and papillary thyroid cancer. For this issue, two aspects of the mutuality are discussed. One is the risk of concomitant papillary thyroid cancer in patients with Hashimoto’s thyroiditis. in 1955, Dailey raised the question about the association between Hashimoto’s thyroiditis and papillary thyroid cancer. Most of the early studies were retrospective analyses of surgical specimens. In eight studies of surgically resected thyroid specimens (9,431 cases), the prevalence of PTC in the HT population ranged from 9.46% to 36.60%, with a mean of 27.56%. Fine needle aspiration cytology (FNAC) has been used more often in the last 10 years. In eight studies of FNAC specimens (18,023 cases), the prevalence of PTC in patients with HT ranged from 0% to 2.95%, with a mean of 1.20%. These were all eight studies with large samples, but the conclusions reached were significantly different. The reasons for the different conclusions are firstly thought to be due to the different methods of sampling, while factors such as race, geographical location and gender differences in the study population are also relevant. Another important reason is that most patients with HT do not require surgery, and those who take surgical treatment are already at high risk for malignancy, so selection bias and related confounding factors occur. Although FNAC is an accepted method for diagnosing patients with HT for concomitant PTC, its sensitivity is >90%. However, false positives (HT-associated follicular cell changes mistaken for thyroid tumors) and false negatives (insufficient cell counts on biopsy and missed diagnosis) may occur. The second is the risk of concomitant Hashimoto’s thyroiditis in patients with papillary thyroid cancer. On this issue, three different researchers from the East and West, Yoon, Singh, Lee et al, had similar results in their respective studies, i.e., patients with PTC with I-IT were higher than other benign and malignant thyroid lesions with I-IT. They were 28.7%; 15% and 23.2% (2471/10648), respectively. Compared to patients with PTC alone, those with PTC with HT are characterized by being more common in women, often multiple lesions, no extrathyroidal invasion, no lymph node metastasis, and a low rate of postoperative tumor recurrence. Finally, we look at the current basic research on the links related to the pathogenesis of both. There are two hypotheses for the pathogenesis of Hashimoto’s thyroiditis and papillary thyroid carcinoma. The inflammatory response hypothesis and the elevated TSH hypothesis. The most discussed hypothesis is the inflammatory response hypothesis. In the inflammatory response firstly, reactive oxygen radicals cause DNA damage, leading to DNA mutation, and secondly, multiple factors (chemokines, cytokines, growth factors, etc.) cause stromal cell damage, leading to reactive stromal changes and tumor formation. However, studies have also found that lymphocyte infiltration on the other hand, as an immune response, can stunt further tumor growth and development. In clinical practice, PTC complicated by HT is therefore seen mostly in young women, with low tumor aggressiveness, small tumor size, low peritumor infiltration and lymphatic metastasis, and relatively good prognosis; and these patients have a low recurrence rate and higher survival rate. elevated TSH hypothesis suggests that elevated TSH in HT patients stimulates follicular epithelial cell proliferation, which in turn promotes PTC formation. Therefore, the clinical use of suppressive therapy for HT patients can reduce TSH levels. and reduce the incidence of clinical PTC. In addition to the inflammatory response hypothesis and TSH hypothesis. There are also studies and controversies about whether HT and PTC share a common molecular pathway alteration. Some investigators believe that there are common pathway alterations. They have studied P13K/Akt, CD98, RET/PTC gene rearrangement, p63, and hOGGl. Their study concluded that the expression of HT and PTC on these molecular pathways is consistent and significantly different from benign and malignant thyroid disorders that are not both diseases. But there are also different views. Researchers at Johns Hopkins Hospital have suggested that the association between Hashimoto’s thyroiditis and papillary thyroid cancer in the last 20 years is responsible for the great increase in the number of surgical cases of Hashimoto’s thyroiditis. Whether it is the routine use of ultrasonography that is responsible for the coincidence of two relatively common diseases or whether there is a true causal relationship is not known. If there is a true causal relationship, it is unclear whether the cancer appeared first or whether the autoimmunity appeared first. In the authors’ analysis, papillary thyroid carcinoma is an initiating injury that then induces a lymphocytic infiltrate that can progress to fully characterized Hashimoto’s thyroiditis in some patients, while in others it is maintained at the stage of chronic nonspecific thyroiditis, where it is a “mild form” of lymphocytic infiltration. Thus lymphocytic infiltration of the thyroid appears to be the result of neoplastic transformation of the thyroid rather than part of the same pathway. Chen Guofang Liu Chao, Hashimoto’s thyroiditis with papillary thyroid carcinoma: cause and effect or chance? [J] Chinese Journal of Endocrinology and Metabolism 2013, 29(12):1006-1009Patrizio Caturegli et al. Hashimoto’s thyroiditis: A century of surgical pathology at Johns Hopkins Hospital in retrospect [J] Thyroid 2013(2):23:65-74