Evaluation of Caspase-8 Level in Serum of Patients with Autoimmune Thyroid Disorders
Article Sidebar
Main Article Content
Abstract
Autoimmune thyroid diseases (AITDs), including Graves' disease and Hashimoto's thyroiditis, are characterized by lymphocytic infiltration of the thyroid and the production of thyroid autoantibodies. While the etiology of AITDs is still not fully understood, a combination of genetic susceptibility and environmental triggers is believed to contribute to the breakdown in immune tolerance. This study aimed to evaluate the levels of thyroid hormones (T3, T4, TSH), Anti-thyroid peroxidase Abs (Anti-TPO Abs), Anti-Thyroglobulin Abs (Anti-TG(, and apoptosis marker (Caspase-8 ) in Iraqi patients with AITDs compared to healthy controls.
A total of 1000 patients participated in the study 820 were excluded from the study because it was non-immune thyroid disease, and 180 subjects were recruited, including 60 Graves’ disease patients, 60 HT patients, and 60 healthy controls. Serum levels of T3, T4, TSH, Anti-TPO Abs and Anti-TG, caspase 8, and inhibin were measured. T3 and T4 levels were significantly decreased in Hashimoto's thyroiditis patients and increased in Graves’ disease patients compared to controls. TSH was significantly elevated in Hashimoto's thyroiditis and reduced in Graves’ disease patients. Caspase-8 was significantly higher in Hashimoto's groups compared with the control group, and Significantly lower in Graves group compared with the control group.
In conclusion, an altered balance in thyroid hormones, Anti-TPO Abs, Anti-TG, and apoptosis markers occurs in AITDs. Elevated caspase-8 suggests that increased apoptosis may contribute to thyroid damage in AITDs. Further research is needed to clarify the roles of these mediators in AITD pathogenesis.
Article Details
This work is licensed under a Creative Commons Attribution 4.0 International License.
References
Ruggeri RM, Giuffrida G, Campennì A. Autoimmune endocrine diseases. Minerva Endocrinol.(2018) 43(3):305–22. doi: 10.23736/S0391-1977.17.02757-2. https://doi.org/10.23736/s0391-1977.17.02757-2
Mincer DL, Jialal I. Hashimoto Thyroiditis. StatPearls Publishing LLC: Treasure Island (FL). 2022. PMID: 29083758 Bookshelf ID: NBK459262
Antonelli, P. Fallahi, G. Elia, F. Ragusa, S.R. Paparo, I. Ruffilli, et al., Graves’ disease: clinical manifestations, immune pathogenesis (cytokines and chemokines) and therapy, Best Pract. Res. Clin. Endocrinol. Metabol. (2020) 101388.DOI: 10.1016/j.beem.2020.101388
Song, Y., Wang, X., Ma, W., Yang, Y., Yan, S., Sun, J., ... & Tang, Y. (2023). Graves’ disease as a driver of depression: a mechanistic insight. Frontiers in Endocrinology, 14, 1162445. https://doi.org/10.3389/fendo.2023.1162445
Ralli, M.; Angeletti, D.; Fiore, M.; D’Aguanno, V.; Lambiase, A.; Artico, M.; de Vincentiis, M.; Greco, A. Hashimoto’s thyroiditis: An update on pathogenic mechanisms, diagnostic protocols, therapeutic strategies, and potential malignant transformation.Autoimmun. Rev. 2020, 19, 102649. DOI: 10.1016/j.autrev.2020.102649
Hoang, T.D.; Stocker, D.J.; Chou, E.L.; Burch, H.B. 2022 Update on Clinical Management of Graves Disease and Thyroid Eye Disease. Endocrinol. Metab. Clin. North Am. 2022, 51, 287–304. doi: 10.1016/j.ecl.2021.12.004
Effraimidis G, Wiersinga Wm. Mechanisms In Endocrinology: Autoimmune Thyroid Disease: Old And New Players. Eur J Endocrinol 2014; 170: R241- 252.
Galluzzi, L.; Lopez-Soto, A.; Kumar, S.; Kroemer, G. Caspases Connect Cell-Death Signaling to Organismal Homeostasis. Immunity 2016, 44, 221–231. [CrossRef] [PubMed]
Elmore, S. Apoptosis: A Review of Programmed Cell Death. Toxicol. Pathol. 2007, 35, 495–516. [CrossRef]
Pop, C.; Fitzgerald, P.; Green, D.R.; Salvesen, G.S. Role of Proteolysis in Caspase-8 Activation and Stabilization. Biochemistry 2007, 46, 4398–4407. [CrossRef]
Salvesen, G.S.; Dixit, V.M. Caspase Activation: The Induced-Proximity Model. Proc. Natl. Acad. Sci. USA 1999, 96, 10964–10967.[CrossRef] [PubMed]
Chang, D.W.; Xing, Z.; Capacio, V.L.; Peter, M.E.; Yang, X. Interdimer Processing Mechanism of Procaspase-8 Activation. EMBO J.2003, 22, 4132–4142. [CrossRef]
-Ragusa F, Fallahi P, Elia G, Debora Gonnella, Sabrina Rosaria Paparo, Claudia Giusti, Leonid P. Churilov, Silvia Martina Ferrari, and Alessandro Antonelli,″Hashimotos' thyroiditis: epidemiology, pathogenesis, clinic, and therapy‶, Best Practice & Research Clinical Endocrinology & Metabolism. 2019;33(6):101367.DOI: 10.1016/j.beem.2019.101367
.Michael L LeFevre,″U.S. Preventive Services Task Force.Screening for Thyroid Disease: Recommendation Statement‶, Ann Intern Med. 2004; 140(2):125-7. DOI: 10.7326/M15-0483.
Bahn R, , Henry B Burch, David S Cooper, Jeffrey R Garber, M Carol Greenlee, Irwin Klein, Peter Laurberg, I Ross McDougall, Victor M Montori, Scott A Rivkees, Douglas S Ross, Julie Ann Sosa and Marius N Stan,″ Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American thyroid association and American association of clinical endocrinologists‶, Thyroid, 2010;21(6):593-646. DOI: 10.1089/thy.2010.0417
Mark F Prummel 1, Wilmar M Wiersinga.( 2005). Thyroid peroxidase autoantibodies in euthyroid subjects. Best Pract Res Clin Endocrinol Metab.2005 Mar;19(1):1-15. doi: 10.1016/j.beem.2004.11.003.
Hasanat M, Rumi M, Alam M, et al. Status of antithyroid antibodies inBangladesh. Postgrad Med J 2000;76:345-9.
AL-Naqdy A, Kutty I, AL-Harthi S, AL-Buloshi M , Masoud AL-Maskari. Anti-Thyroglobulin and Anti-Thyroid Microsomal Antibodies in Thyroid Disorders. Bahrain Medical Bulletin, Vol. 25, No. 3, September 2003.
Abdelgadir Elmugadam,Elshaikh A Elobied, Moawia H.Elebaid .Prevalence of Anti-thyroid Peroxidase, and Anti-thyroglobulin in Sudanese Patients with Thyroid Diseases. December 2010Egyptian Academic Journal of Biological Sciences C Physiology and Molecular Biology 2(2):93-97 DOI:10.21608/eajbsc.2010.16268
Su He Wang , James R Baker.(2007). The role of apoptosis in thyroid autoimmunity.Thyroid 2007 Oct;17(10):975-9. doi: 10.1089/thy.2007.0208.