The Causes of Thyrotoxicosis, Clinical Features, and Treatment Strategies in a Former Iodine Deficient Area

Yıl 2024, Cilt: 45 Sayı: 2, 291 – 298, 30.06.2024

Osman Akıdan , Mustafa Koçak , Hülya Coşkun , Halil Önder Ersöz

https://doi.org/10.17776/csj.1465192

Öz

Thyrotoxicosis is a hypermetabolic condition caused by excess thyroid hormones in the circulation with/without increased production from the thyroid gland. In this prospective study, we aimed to investigate the causes of thyrotoxicosis, clinical features, and treatment strategies in a former iodine-deficient area. Thyroid function tests, antithyroid and antithyroid receptor antibodies, and routine thyroid ultrasonography was obtained, and a thyroid scintigraphy/radioactive iodine uptake test was performed on need. A statistically significant difference was found between toxic multinodular goiter (TMNG) and Graves’ disease (GD) groups when mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) values were analyzed. TSH levels were significantly lower in GD patients compared to those in TMNG and TNG patients, but free triiodothyronine (FT3) and free thyroxine (FT4) values were higher. A high level of TSH receptor antibody (TRAb) was observed in patients with normal antithyroid peroxidase (Anti-TPO). TRAb levels were found to be high. Anti-TPO and anti-thyroglobulin (Anti-Tg) levels were observed to be positively correlated with sT3 and sT4 levels. TMNG is the leading cause of thyrotoxicosis; despite sufficient iodide intake in our former iodine-deficient region, TMNG is characteristically seen in older patients with much lower thyroid hormone levels than GD. According to the study results, the diagnosis of patients with thyrotoxicosis, their clinical presentation, the treatment they will receive, early detection of postoperative complications were predicted

Anahtar Kelimeler

: Thyrotoxicosis, Toxic multinodular goiter, Graves’ disease, TSH

Etik Beyan

Ethical approval The study was performed according to the principles of the declaration of Helsinki as revised in 1983 and approval was obtained by the Ethics Committee of Karadeniz University Medical Faculty. The permission has been granted by Karadeniz University Medical Faculty of Ethics Committee via the resolution dated 18.11.2014 and no. 2014/81. All participants in the study obtained informed consent before entering the study.

Kaynakça

• [1] Sharma A., Stan M.N., Thyrotoxicosis: Diagnosis and Management, Mayo Clin. Proc., 94(6) (2019) 1048-1064.
• [2] Brent G.A., Clinical practice. Graves' disease, N Engl J Med, 358 (2008) 2594-2605.
• [3] Golden S.H., Robinson K.A., Saldanha I., Anton B., Ladenson P.W., Prevalence and incidence of endocrine and metabolic disorders in the United States: a comprehensive review, J. Clin. Endocrinol. Metab., 94(6) (2009) 1853-1878.
• [4] Laurberg P., Pedersen I. B., Knudse, N., Ovesen, L., Andersen S., Environmental iodine intake affects the type of nonmalignant thyroid disease, Thyroid, 11(5) (2001) 457-469.
• [5] Schwartz F., Bergmann N., Zerahn B., Faber J., Incidence rate of symptomatic painless thyroiditis presenting with thyrotoxicosis in Denmark as evaluated by consecutive thyroid scintigraphies, Scand J. Clin. Lab. Invest.., 73(3) (2013) 240-244.
• [6] Weetman A.P., Graves’ disease, N Engl J Med, 343 (2000) 1236-1248.
• [7] Morshed S.A., Davies T.F., Graves' Disease Mechanisms: The Role of Stimulating, Blocking, and Cleavage Region TSH Receptor Antibodies,. Horm. Metab. Res., 47(10) (2015) 727-734.
• [8] Tonacchera M., Agretti P., Chiovato L., Rosellini V., Ceccarini G., Perri A., et al., Activating thyrotropin receptor mutations are present in nonadenomatous hyperfunctioning nodules of toxic or autonomous multinodular goiter, J. Clin. Endocrinol. Metab., 85(6) (2000) 2270-2274.
• [9] Davies T. F. and Larsen, P.R., Thyrotoxicosis. Williams Textbook of Endocrinology, 10th edition, Saunders, Philadelphia, (2003) 374-422.
• [10] Boelaert K., Torlinska B., Holder R. L., Franklyn J. A. Older subjects with hyperthyroidism present with a paucity of symptoms and signs: a large cross-sectional study, J. Clin. Endocrinol. Metab., 95(6) (2010) 2715-2726.
• [11] Vaidya B., Pearce S.H., Diagnosis and management of thyrotoxicosis, BMJ, 349 (2014).
• [12] Schneider D. F., Sonderman P. E., Jones M. F., Ojomo K. A., Chen H., Jaume J. C., et al., Failure of radioactive iodine in the treatment of hyperthyroidism, Ann. Surg. Oncol., 21 (2014). 4174-4180.
• [13] Kologlu S., Kologlu B., Su ve gıda maddeleri ile vücuda giren günlük iyod miktarı (Daily iodide intake by water and nutrients). AU Tip Fak. Mec., 19(3) (1966) 372.
• [14] Urgancıoglu I., Hatemi H., Türkiye’de Endemik Guatr (Endemic goiter in Turkey), İstanbul: Cerrahpaşa Tıp Fak. Nükleer Tıp ABD Yayın, (1989) 14.
• [15] Erdogan G., Erdoğan M. F., Delange F., Sav H., Güllü S., Kamel N., Moderate to severe iodine deficiency in three endemic goitre areas from the Black Sea region and the capital of Turkey, Eur. J. Epidemiol,16 (2000). 1131-1134.
• [16] World Health Organization. Assessment of iodine deficiency disorders and monitoring their elimination A Guide For Program Managers. 2007. Available at: https://www.who.int/publications/i/item/9789241595827.
• [17] Erdogan G., Erdoğan M. F., Emral R., Baştemir M., Sav H., Haznedaroğlu D.,et al., Iodine status and goiter prevalence in Turkey before mandatory iodization, J. Endocrinol Invest., 25 (2002) 224-228.
• [18] Erdoğan M. F., Ağbaht K., Altunsu T., Özbaş S., Yücesan F., Tezel B., et al., Current iodine status in Turkey, J. Endocrinol. Invest., 32 (2009) 617-622.
• [19] Kocak M., Erem C., Deger O., Topbas M., Ersoz H. O., Can E., Current prevalence of goiter determined by ultrasonography and associated risk factors in a formerly iodine-deficient area of Turkey, Endocrine, 47 (2014) 290-298.
• [20] Atmiş V., Bulbul B., Bahsi R., Gumussoy M., Yalçin A., Dogan Z., et al., Iodine concentration and prevalence of thyroid disease in older people after salt iodization in Turkey, East Mediterr. Health J., 27(2) (2021) 151-158.
• [21] 5Gozu H. I., Bircan R., Krohn K., Müller S., Vural S., Gezen C.,et al.,Similar prevalence of somatic TSH receptor and Gsα mutations in toxic thyroid nodules in geographical regions with different iodine supply in Turkey, Eur. J. Endocrinol.,155(4) (2006) 535-545.
• [22] Esen I., Bayramoğlu E., Yıldız M., Aydın M., Özturhan E. K., Aycan Z., et al., Management of thyrotoxicosis in children and adolescents: a Turkish multi-center experience, J. Clin. Res. Pediatr. Endocrinol., 11(2) (2019) 164-172.
• [23] Burch H.B., Wartofsky L., Graves’ ophthalmopathy: current concepts regarding pathogenesis and management, Endocr. Rev., 14(6) (1993) 747-793.
• [24] Bartley G. B., Fatourechi V., Kadrmas E. F., Jacobsen S. J., Ilstrup D. M., Garrity J. A., Gorman C. A., Clinical features of Graves' ophthalmopathy in an incidence cohort, Am. J. Ophthalmol., 121(3) (1996) 284-290.
• [25] Paunkovic N., Paunkovic J., The diagnostic criteria of graves diseas and especially the thyrotropin reseptör antibody, our own experience, Hell J. Nucl. Med., 10(2) (2007) 89-94.
• [26] Costagliola S., Morgenthaler N. G., Hoermann R., Badenhoop K., Struck J., Freitag D., et al., Second generation assay for thyrotropin receptor antibodies has superior diagnostic sensitivity for Graves’ disease, J. Clin. Endocrinol. Metab., 84(1) (1999) 90-97.
• [27] Zingrillo M., D'Aloiso L., Ghiggi M. R., Di Cerbo A., Chiodini I., Torlontano M., Liuzzi A. Thyroid hypoechogenicity after methimazole withdrawal in Graves' disease: a useful index for predicting recurrence?, Clin. Endocrinol., 45(2) (1996) 201-206.
• [28] Gauna A., Segura G., Sartorio G., Soto, R., Segal-Eiras A., Immunological aspects of Graves’ disease patients in different clinical stages, J. Endocrinol. Invest., 12 (1989) 671-677.
• [29] Myint K. S., Andappa G. S., MacFarlane I., Gurnell M., Wood D., Chatterjee K., et al., Use of anti thyroid hormone receptor antibody (TRAB) in Graves’ Disease, Endocrine, 13 (2007) 81.
• [30] Mariotti S., Caturegli P., Piccolo P., Barbesino G., Pinchera A., Antithyroid peroxidase autoantibodies in thyroid diseases, J. Clin. Endocrinol. Metab., 71(3) (1990) 661-669.
• [31] Fong T.L., McHutchison J.G., Reynolds T.B., Hyperthyroidism and hepatic dysfunction. A case series analysis, J. Clin. Gastroenterol., 14(3) (1992) 240-244.
• [32] Huang M.J., Li K.L., Wei J.S., Wu S.S., Fan K.D., Liaw Y.F., Sequential liver and bone biochemical changes in hyperthyroidism: prospective controlled follow- up study, Am J. Gastroenterol., 89(7) (1994) 1071-1076.
• [33] Ford H.C, Carter J.M., The haematology of hyperthyroidism: abnormalities of erythrocytes, leucocytes, thrombocytes and haemostasis, Postgrad Med. J., 64(756) (1988) 735-742.
• [34] Omar S., Kanoun F., Hammami M. B., Kamoun S., Romdhane B., Feki M., et al., Erythrocyte abnormalities in thyroid dysfunction. La Tunis Med., 88(11) (2010) 783-788.
• [35] Hambsch K, Fischer H, Langpeter D, Müller P, Hyperthyroidism and anemia. Zeitschrift fur die Gesamte Innere Medizin und Ihre Grenzgebiete 36(6) (1981) 203-208.
• [36] Franklyn J.A., Boelaert K., Thyrotoxicosis, Lancet, 379 (2012) 1155-1166.
• [37] Gilbert J., Thyrotoxicosis – investigation and management, Clin. Med. (Lond), 17(3) (2017) 274–277.
• [38] Dokmetas H.S., Erselcan T., Yüksel I., Ataseven H., Dogan, D., Koyuncu A., Yönem Ö., Hipertiroidizmi Olan Hastalarımızda Radyoaktif İyot Tedavisinin Sonuçları (Results of radio active iodine treatment in patients with hyperthyroidism), Cerrahpaşa Üniv. Tıp Fak. Derg., 23(3) (2001) 121-125.
• [39] Farrar J.J., Toft A.D., Iodine-131 treatment of hyperthyroidism: current issues, Clin. Endocrinol., 35(3) (1991) 207-212.
• [40] Ghadban W. K., Zirie M. A., Al-Khateeb D. A., Jayyousi A. A., Mobayedh H. M., Ahmed S., Radioiodine treatment of hyperthyroidism, Saudi Med. J., 24(4) (2003) 347-351.

Yıl 2024, Cilt: 45 Sayı: 2, 291 – 298, 30.06.2024

Osman Akıdan , Mustafa Koçak , Hülya Coşkun , Halil Önder Ersöz

https://doi.org/10.17776/csj.1465192

Öz

Kaynakça

• [1] Sharma A., Stan M.N., Thyrotoxicosis: Diagnosis and Management, Mayo Clin. Proc., 94(6) (2019) 1048-1064.
• [2] Brent G.A., Clinical practice. Graves' disease, N Engl J Med, 358 (2008) 2594-2605.
• [3] Golden S.H., Robinson K.A., Saldanha I., Anton B., Ladenson P.W., Prevalence and incidence of endocrine and metabolic disorders in the United States: a comprehensive review, J. Clin. Endocrinol. Metab., 94(6) (2009) 1853-1878.
• [4] Laurberg P., Pedersen I. B., Knudse, N., Ovesen, L., Andersen S., Environmental iodine intake affects the type of nonmalignant thyroid disease, Thyroid, 11(5) (2001) 457-469.
• [5] Schwartz F., Bergmann N., Zerahn B., Faber J., Incidence rate of symptomatic painless thyroiditis presenting with thyrotoxicosis in Denmark as evaluated by consecutive thyroid scintigraphies, Scand J. Clin. Lab. Invest.., 73(3) (2013) 240-244.
• [6] Weetman A.P., Graves’ disease, N Engl J Med, 343 (2000) 1236-1248.
• [7] Morshed S.A., Davies T.F., Graves' Disease Mechanisms: The Role of Stimulating, Blocking, and Cleavage Region TSH Receptor Antibodies,. Horm. Metab. Res., 47(10) (2015) 727-734.
• [8] Tonacchera M., Agretti P., Chiovato L., Rosellini V., Ceccarini G., Perri A., et al., Activating thyrotropin receptor mutations are present in nonadenomatous hyperfunctioning nodules of toxic or autonomous multinodular goiter, J. Clin. Endocrinol. Metab., 85(6) (2000) 2270-2274.
• [9] Davies T. F. and Larsen, P.R., Thyrotoxicosis. Williams Textbook of Endocrinology, 10th edition, Saunders, Philadelphia, (2003) 374-422.
• [10] Boelaert K., Torlinska B., Holder R. L., Franklyn J. A. Older subjects with hyperthyroidism present with a paucity of symptoms and signs: a large cross-sectional study, J. Clin. Endocrinol. Metab., 95(6) (2010) 2715-2726.
• [11] Vaidya B., Pearce S.H., Diagnosis and management of thyrotoxicosis, BMJ, 349 (2014).
• [12] Schneider D. F., Sonderman P. E., Jones M. F., Ojomo K. A., Chen H., Jaume J. C., et al., Failure of radioactive iodine in the treatment of hyperthyroidism, Ann. Surg. Oncol., 21 (2014). 4174-4180.
• [13] Kologlu S., Kologlu B., Su ve gıda maddeleri ile vücuda giren günlük iyod miktarı (Daily iodide intake by water and nutrients). AU Tip Fak. Mec., 19(3) (1966) 372.
• [14] Urgancıoglu I., Hatemi H., Türkiye’de Endemik Guatr (Endemic goiter in Turkey), İstanbul: Cerrahpaşa Tıp Fak. Nükleer Tıp ABD Yayın, (1989) 14.
• [15] Erdogan G., Erdoğan M. F., Delange F., Sav H., Güllü S., Kamel N., Moderate to severe iodine deficiency in three endemic goitre areas from the Black Sea region and the capital of Turkey, Eur. J. Epidemiol,16 (2000). 1131-1134.
• [16] World Health Organization. Assessment of iodine deficiency disorders and monitoring their elimination A Guide For Program Managers. 2007. Available at: https://www.who.int/publications/i/item/9789241595827.
• [17] Erdogan G., Erdoğan M. F., Emral R., Baştemir M., Sav H., Haznedaroğlu D.,et al., Iodine status and goiter prevalence in Turkey before mandatory iodization, J. Endocrinol Invest., 25 (2002) 224-228.
• [18] Erdoğan M. F., Ağbaht K., Altunsu T., Özbaş S., Yücesan F., Tezel B., et al., Current iodine status in Turkey, J. Endocrinol. Invest., 32 (2009) 617-622.
• [19] Kocak M., Erem C., Deger O., Topbas M., Ersoz H. O., Can E., Current prevalence of goiter determined by ultrasonography and associated risk factors in a formerly iodine-deficient area of Turkey, Endocrine, 47 (2014) 290-298.
• [20] Atmiş V., Bulbul B., Bahsi R., Gumussoy M., Yalçin A., Dogan Z., et al., Iodine concentration and prevalence of thyroid disease in older people after salt iodization in Turkey, East Mediterr. Health J., 27(2) (2021) 151-158.
• [21] 5Gozu H. I., Bircan R., Krohn K., Müller S., Vural S., Gezen C.,et al.,Similar prevalence of somatic TSH receptor and Gsα mutations in toxic thyroid nodules in geographical regions with different iodine supply in Turkey, Eur. J. Endocrinol.,155(4) (2006) 535-545.
• [22] Esen I., Bayramoğlu E., Yıldız M., Aydın M., Özturhan E. K., Aycan Z., et al., Management of thyrotoxicosis in children and adolescents: a Turkish multi-center experience, J. Clin. Res. Pediatr. Endocrinol., 11(2) (2019) 164-172.
• [23] Burch H.B., Wartofsky L., Graves’ ophthalmopathy: current concepts regarding pathogenesis and management, Endocr. Rev., 14(6) (1993) 747-793.
• [24] Bartley G. B., Fatourechi V., Kadrmas E. F., Jacobsen S. J., Ilstrup D. M., Garrity J. A., Gorman C. A., Clinical features of Graves' ophthalmopathy in an incidence cohort, Am. J. Ophthalmol., 121(3) (1996) 284-290.
• [25] Paunkovic N., Paunkovic J., The diagnostic criteria of graves diseas and especially the thyrotropin reseptör antibody, our own experience, Hell J. Nucl. Med., 10(2) (2007) 89-94.
• [26] Costagliola S., Morgenthaler N. G., Hoermann R., Badenhoop K., Struck J., Freitag D., et al., Second generation assay for thyrotropin receptor antibodies has superior diagnostic sensitivity for Graves’ disease, J. Clin. Endocrinol. Metab., 84(1) (1999) 90-97.
• [27] Zingrillo M., D'Aloiso L., Ghiggi M. R., Di Cerbo A., Chiodini I., Torlontano M., Liuzzi A. Thyroid hypoechogenicity after methimazole withdrawal in Graves' disease: a useful index for predicting recurrence?, Clin. Endocrinol., 45(2) (1996) 201-206.
• [28] Gauna A., Segura G., Sartorio G., Soto, R., Segal-Eiras A., Immunological aspects of Graves’ disease patients in different clinical stages, J. Endocrinol. Invest., 12 (1989) 671-677.
• [29] Myint K. S., Andappa G. S., MacFarlane I., Gurnell M., Wood D., Chatterjee K., et al., Use of anti thyroid hormone receptor antibody (TRAB) in Graves’ Disease, Endocrine, 13 (2007) 81.
• [30] Mariotti S., Caturegli P., Piccolo P., Barbesino G., Pinchera A., Antithyroid peroxidase autoantibodies in thyroid diseases, J. Clin. Endocrinol. Metab., 71(3) (1990) 661-669.
• [31] Fong T.L., McHutchison J.G., Reynolds T.B., Hyperthyroidism and hepatic dysfunction. A case series analysis, J. Clin. Gastroenterol., 14(3) (1992) 240-244.
• [32] Huang M.J., Li K.L., Wei J.S., Wu S.S., Fan K.D., Liaw Y.F., Sequential liver and bone biochemical changes in hyperthyroidism: prospective controlled follow- up study, Am J. Gastroenterol., 89(7) (1994) 1071-1076.
• [33] Ford H.C, Carter J.M., The haematology of hyperthyroidism: abnormalities of erythrocytes, leucocytes, thrombocytes and haemostasis, Postgrad Med. J., 64(756) (1988) 735-742.
• [34] Omar S., Kanoun F., Hammami M. B., Kamoun S., Romdhane B., Feki M., et al., Erythrocyte abnormalities in thyroid dysfunction. La Tunis Med., 88(11) (2010) 783-788.
• [35] Hambsch K, Fischer H, Langpeter D, Müller P, Hyperthyroidism and anemia. Zeitschrift fur die Gesamte Innere Medizin und Ihre Grenzgebiete 36(6) (1981) 203-208.
• [36] Franklyn J.A., Boelaert K., Thyrotoxicosis, Lancet, 379 (2012) 1155-1166.
• [37] Gilbert J., Thyrotoxicosis – investigation and management, Clin. Med. (Lond), 17(3) (2017) 274–277.
• [38] Dokmetas H.S., Erselcan T., Yüksel I., Ataseven H., Dogan, D., Koyuncu A., Yönem Ö., Hipertiroidizmi Olan Hastalarımızda Radyoaktif İyot Tedavisinin Sonuçları (Results of radio active iodine treatment in patients with hyperthyroidism), Cerrahpaşa Üniv. Tıp Fak. Derg., 23(3) (2001) 121-125.
• [39] Farrar J.J., Toft A.D., Iodine-131 treatment of hyperthyroidism: current issues, Clin. Endocrinol., 35(3) (1991) 207-212.
• [40] Ghadban W. K., Zirie M. A., Al-Khateeb D. A., Jayyousi A. A., Mobayedh H. M., Ahmed S., Radioiodine treatment of hyperthyroidism, Saudi Med. J., 24(4) (2003) 347-351.

Toplam 40 adet kaynakça vardır.

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