A. Gorchane, T. Ach, J. Sahli, S. Nouira, A. Ben Abdelkrim, Y. Hasni, M. Chadli Chaieb, K. Ach
{"title":"COVID-19对糖尿病酮症酸中毒患者甲状腺功能影响的比较研究","authors":"A. Gorchane, T. Ach, J. Sahli, S. Nouira, A. Ben Abdelkrim, Y. Hasni, M. Chadli Chaieb, K. Ach","doi":"10.1016/j.ando.2023.07.240","DOIUrl":null,"url":null,"abstract":"COVID-19 has been associated with thyroid dysfunction. Our objective was to compare thyroid function in patients presenting with new onset diabetic ketoacidosis (DKA) before and during the COVID-19 pandemic. We conducted a cross-sectional analytical study where we compared thyroid stimulating hormone (TSH), free thyroxine (FT4) and anti-thyroperoxydase (anti-TPO) of patients hospitalized with new onset DKA two years before and during COVID-19. The population was divided in two groups: G1: before COVID-19, G2: during COVID-19. Statistical analysis was made using SPSS software. TSH and FT4 levels were comparable between the two groups (1.88 [Q1–Q3 = 1.11–2.88] mUI/ml in G1 vs. 2.01 [1.19–2.91] mUI/ml in G2) (P = 0.615) and (12.10 [9.8–13.65] pmol/l in G1 vs. 12.20 [10.65–14.15] pmol/l in G2) (P = 0.567), respectively. Anti-TPO were significantly higher during COVID-19 (300 [145–772] IU/mL in G2 vs. 99 [2–214] in G1) IU/mL (P = 0.019). SARS-CoV-2 may trigger thyroid disorders directly via cytotoxic effect as COVID-19 has been shown to infect and replicate in thyroid cells via ACE2 receptors. COVID-19 can cause dysregulation of the immune system, resulting in an overactive immune response and increased inflammation throughout the body, leading to autoimmune reactions against the thyroid gland. The higher level of anti-TPO titers in our study may plead in favor of the latter mechanism.","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":"29 1","pages":"0"},"PeriodicalIF":2.9000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The impact of COVID-19 on thyroid function in patients with diabetic ketoacidosis: A comparative study\",\"authors\":\"A. Gorchane, T. Ach, J. Sahli, S. Nouira, A. Ben Abdelkrim, Y. Hasni, M. Chadli Chaieb, K. Ach\",\"doi\":\"10.1016/j.ando.2023.07.240\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"COVID-19 has been associated with thyroid dysfunction. Our objective was to compare thyroid function in patients presenting with new onset diabetic ketoacidosis (DKA) before and during the COVID-19 pandemic. We conducted a cross-sectional analytical study where we compared thyroid stimulating hormone (TSH), free thyroxine (FT4) and anti-thyroperoxydase (anti-TPO) of patients hospitalized with new onset DKA two years before and during COVID-19. The population was divided in two groups: G1: before COVID-19, G2: during COVID-19. Statistical analysis was made using SPSS software. TSH and FT4 levels were comparable between the two groups (1.88 [Q1–Q3 = 1.11–2.88] mUI/ml in G1 vs. 2.01 [1.19–2.91] mUI/ml in G2) (P = 0.615) and (12.10 [9.8–13.65] pmol/l in G1 vs. 12.20 [10.65–14.15] pmol/l in G2) (P = 0.567), respectively. Anti-TPO were significantly higher during COVID-19 (300 [145–772] IU/mL in G2 vs. 99 [2–214] in G1) IU/mL (P = 0.019). SARS-CoV-2 may trigger thyroid disorders directly via cytotoxic effect as COVID-19 has been shown to infect and replicate in thyroid cells via ACE2 receptors. COVID-19 can cause dysregulation of the immune system, resulting in an overactive immune response and increased inflammation throughout the body, leading to autoimmune reactions against the thyroid gland. The higher level of anti-TPO titers in our study may plead in favor of the latter mechanism.\",\"PeriodicalId\":93871,\"journal\":{\"name\":\"Annales d'endocrinologie\",\"volume\":\"29 1\",\"pages\":\"0\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2023-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annales d'endocrinologie\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1016/j.ando.2023.07.240\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annales d'endocrinologie","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.ando.2023.07.240","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The impact of COVID-19 on thyroid function in patients with diabetic ketoacidosis: A comparative study
COVID-19 has been associated with thyroid dysfunction. Our objective was to compare thyroid function in patients presenting with new onset diabetic ketoacidosis (DKA) before and during the COVID-19 pandemic. We conducted a cross-sectional analytical study where we compared thyroid stimulating hormone (TSH), free thyroxine (FT4) and anti-thyroperoxydase (anti-TPO) of patients hospitalized with new onset DKA two years before and during COVID-19. The population was divided in two groups: G1: before COVID-19, G2: during COVID-19. Statistical analysis was made using SPSS software. TSH and FT4 levels were comparable between the two groups (1.88 [Q1–Q3 = 1.11–2.88] mUI/ml in G1 vs. 2.01 [1.19–2.91] mUI/ml in G2) (P = 0.615) and (12.10 [9.8–13.65] pmol/l in G1 vs. 12.20 [10.65–14.15] pmol/l in G2) (P = 0.567), respectively. Anti-TPO were significantly higher during COVID-19 (300 [145–772] IU/mL in G2 vs. 99 [2–214] in G1) IU/mL (P = 0.019). SARS-CoV-2 may trigger thyroid disorders directly via cytotoxic effect as COVID-19 has been shown to infect and replicate in thyroid cells via ACE2 receptors. COVID-19 can cause dysregulation of the immune system, resulting in an overactive immune response and increased inflammation throughout the body, leading to autoimmune reactions against the thyroid gland. The higher level of anti-TPO titers in our study may plead in favor of the latter mechanism.