■ 学会名
The ENDO2025

■ 発表日
2025/07/12-15

■ 筆頭演者
Kuniaki Ozaki¹
1) Nara Medical University

■ 共同演者
Yuichi Nishioka¹,², Hiroki Nakajima¹, Fumika Kamitani¹, Yukako Kurematsu¹, Sadanori Okada¹, Tomoya Myojin², Tatsuya Noda², Tomoaki Imamura2, Yutaka Takahashi¹
1) Nara Medical University, Dept of Diabetes and Endocrinology, Kashihara, Japan
2) Nara Medical University, Dept of Public Health, Health Management and Policy, Kashihara, Japan

■ 発表形態
Poster

■ 要旨
Background: Virus infection including COVID-19 causes inflammation and sometimes cytokine storm, resulting in a disturbance of immune system and increased possibility of autoimmune diseases. Conflicting results have been reported regarding the development of thyroid diseases after COVID-19 and influenza infection in the previous studies. SARS-CoV-2 infects target cells through ACE2 as the virus receptor.
Purpose: The aim of this study is to clarify the incidence rates and characteristics of thyroid diseases following COVID-19 and influenza infection.
Methods: We used the DeSC database, an insurance claims database comprising 14.5 million individuals, targeting adults diagnosed with COVID-19 or influenza infection between 2015 and 2023. COVID-19 was defined by ICD-10 codes. Influenza infection was defined by ICD-10 codes and antiviral drug codes. Graves disease (GD) development was defined by the disease name and prescriptions for antithyroid drugs and hypothyroidism development was defined by prescriptions for levothyroxine, within 1-year post-infection.
Results: During the observation period, 486,979 COVID-19 cases and 530,772 influenza cases were diagnosed. Compared with the age- and sex-matched control group, the incidence of GD significantly increased in the COVID-19 group (RR 1.42, P < 0.01), while no significant difference was observed in the influenza group (RR 1.01, P = 0.93). In contrast, the incidence of hypothyroidism increased in both groups as compared with the control group (COVID-19: RR 1.70, P < 0.01; influenza: RR 1.57, P < 0.01). In multivariate analysis, the use of angiotensin II receptor blockers and mineralocorticoid receptor antagonists were associated with an increased risk of GD in men in the COVID-19 group (OR 2.67, P = 0.04; OR 3.56, P = 0.05, respectively), but no association was found in the influenza group (OR 0.63, P = 0.09; OR 1.445, P = 0.48, respectively). Discussion: In this study, we demonstrated the impact of COVID-19 and influenza infection on the risk of thyroid diseases by using a large cohort of the insurance claims database. The incidence of GD was increased specifically after COVID-19, while no increase was observed after influenza infection. In contrast, the risk of hypothyroidism increased in both groups. It has been suggested that viral infections may increase the risk of developing hypothyroidism, possibly through activation of the innate immune system, by increasing the expression of Toll-like receptor 3 and this may be common between COVID-19 and influenza. Interestingly, the development of GD was associated with the use of renin-angiotensin system inhibitors (RASi) in men after COVID-19, but not after influenza, suggesting distinct pathophysiological mechanisms for each infection. RASi reportedly increased ACE2 expression in several organs, which may explain such difference.