The Relationship Between Insulin Resistance And Thyroid Disorders

Yıl 2018, Cilt: 10 Sayı: 6, 13 - 17, 28.11.2018

Medine Şişman

Öz

Abstract

Aim: There are researches that the thyroid disorders effect carbonhydrate metabolizm and the insulin resistance causes impaired glucose tolerance, diabetes, dyslipidemia, obesity, metabolic syndrome and hypertension. The purpose ofthis study is; to investigate whether thyroid disorders are related to insulin resistance and to investigate what family physicians may do before complications develop.

Methods: After the approval of the ethics committee, 2000 patients (age 18-85 years) were evaluated retrospectively and 301 patients were included in the study. According to the diagnosis the patients were grouped as hypothyroid, hyperthyroid and euthyroid. TSH, fT3, fT4, insulin,FPG, HbA1c, anti-TG, anti-TPO were recorded. HOMA-IRs were calculated.

Results: Of the patients, 264 (87.7%) were female and37 (12.3%) were male. 45.8% of the patients were hypothy-roid, 19.6% were hyperthyroid and 34.6% were euthyroid.95.6% of hypothyroid ones and 93.2% of hyperthyroid oneswere receiving treatment. 29.6% of the patients’ FPG were between 100-126 mg/dl. HOMA-IR ≥ 2.5 in 49.6% of thepatients. In 34.9% of patients HBA1C was detected as bet-ween 5.7-6.4%. 48.6% of the hypothyroid group, 52.5% ofthe hyperthyroid group and 48.1% of the euthyroid group had HOMA-IR ≥ 2.5. There were no significant correlation and significant difference between insulin resistance andany of the hypothyroid, hyperthyroid and euthyroid patients.There was a significant difference for anti-TG and anti-TPO in the groups. There was a significant positive correlation between HOMA-IR and TSH, and a negative correlation bet-ween TSH and sT4.

Conclusion: Treatment of thyroid disorders may preventthe development of insulin resistance and / or progressionto diseases such as T2DM, obesity, metabolic syndrome. Monitoring metabolic parameters in thyroid disorders’  follow-up may be clinically important. In this way, a common etio-logical factor such as insulin resistance and many public health problems can be avoided, and / or the course can be slowed down.

Anahtar Kelimeler

Diabetes, Insulin Resistance, Metabolic Syndrome, Obesity, Thyroid Di-sorders

Tiroid Bozuklukları İle İnsülin Direnci Arasındaki İlişki

Öz

Öz

Amaç: Tiroid bozukluklarının glukoz metabolizmasını etkilediği; insülin direncinin,bozulmuş glukoz toleransı, diyabet, dislipidemi, obezite, metabolik sendrom ve hipertansiyona neden olduğu bilinmektedir. Bu çalışmanın amacı, tiroid bozukluklarının insülin direnci ile herhangi bir ilişkisinin olup olmadığını incelemek ve komplikasyonlar gelişmeden önce aile hekimlerinin neler yapabileceğini araştırmaktır.

Yöntem: Bakırköy Dr. Sadi Konuk SUAM etik kurul onayı alınarak, 2015-2017 yıl-ları arasinda takipli, tiroid hastalığı ön tanılı ve kilo verememe yakınması ile başvuran 2000 hasta retrospektif olarak tarandı, 301 hastanın kayıtları incelendi. Hastalar hipotiroid, hipertiroid, ötiroid olarak gruplandırıldı. Tiroid uyarıcı hormon (TSH), serbest triiyodotironin(sT3), serbest tiroksin (sT4), insülin, açlık plazma glukozu (APG), hemog-lobin A1c (HbA1c), anti tiroglobulin antikoru (anti-TG), anti tiroid peroksidaz antikoru (anti-TPO) değerlendirildi. Hastaların Homeostasis Model Assesment-Insulin Resistance (HOMA-IR) değerleri hesaplandı.

Bulgular: Hastaların %87.7’si (264 hasta) kadın, %12.3’ü (37 hasta) ise erkekti. %4.,8’sihipotiroid, %19.6’sı hipertiroid, %34.6’sı ötiroid idi. Hipotiroidlerin %95.6’sı, hipertiroidlerin %93.2’si tedavi almaktaydı. Hastaların %29.6’sında APG 100-126 mg/dl arasında, %49.6’sında HOMA-IR yüksek, %34.9’unda HbA1c %5.7-6.4 olarak saptandı. Hipotiroid grubun %48.6’sında, hipertiroid grubun %52.5’inde, ötirod grubun ise %48.1’in-de HOMA-IR yüksekti. Hasta gruplarının hiçbiriyle HOMA-IR arasında anlamlı ilişkive anlamlı fark saptanmadı. Hasta gruplarında anti-TG ve anti-TPO için ise anlamlı farksaptandı, anlamlı ilişki saptanmadı. HOMA-IR ile TSH arasında pozitif anlamlı ilişki,sT4 ile negatif anlamlı ilişki saptandı.

Sonuç: Tiroid bozukluklarında tedavi, insülin direncinin gelişmesini ve/veya T2DM,obezite, metabolik sendrom gibi hastalıklara ilerlemesini önleyebilir. Tiroid hastalığı olanlar ötiroid halde tutulsalar bile, takiplerinde metabolik parametrelerin izlenmesi klinikaçıdan önemli olabilir.  Bu şekilde insülin direncinin ortak etiyolojik faktör olduğu vehalk sağlığı sorununa dönüşen tip2 diyabet, obezite, metabolik sendrom gibi patolojilerin önüne geçilebilir ve/veya seyri yavaşlatılabilir.

Anahtar Kelimeler

Diyabet, İnsülin Direnci, Metabolik Sendrom, Obezite, Tiroid bozuklukları

Kaynakça

• Kaynaklar 1. Vanderpump MPJ. The epidemiology of thyroid diseases. In:Braverman LE, Utiger RD (eds), Werner and Ingbar’s, thethyroid. A fundamental and clinical text, ed 9, Lippincott, Wil-liams & Wilkins, Philadelphia 2005, pp 398–406. 2. Yen PM: Genomic and nongenomic actions of thyroid hormothe thyroid. A fundamental and clinical text, ed 9, Lippincott,Williams & Wilkins, Philadelphia 2005, pp 135–150. 3. Wesołowski P, Wańkowicz Z. Insulinooporność — metody roz-poznawania i następstwa kliniczne. Nephrol Dial Pol 2011;15: 243–246. 4. Sesti g: pathophysiology of insulin resistance, best pract res clinendocrinol metab 20(4):665–679, 2006) 5. Hollenbeck C, Reaven GM. Variations in insulin stimulated glu-cose uptake in healthy individuals with normal glucose tole-rance. J Clin Endocrinol Metab 1987;64(6):1169-73. ) 6. Scott M, Grundy MD, James I, et al. Diagnosis and manage-ment of the metabolic syndrome. Circulation2005;112(17):2735-52. 7. Yenigün M (Editör). İnsülin direnci ve ölçüm metodları. In: Al-tuntaş Y. Her yönüyle diabetes mellitus. 2nci Baskı, İstanbul:Nobel Tıp Kitapevi, 2001:839-52. 8. Handisurya A, Pacini G, Tura A et al. Effects of T4 replacementtherapy on glucose metabolism in subjects with subclinical (SH)and overt hy¬pothyroidism (OH). Clin Endocrinol 2008; 69:963–969. 9. Chubb SA, Davis WA, Inman Z et al. Prevalence and progres-sion of sub¬clinical hypothyroidism in women with type 2 dia-betes: the Fremantle Diabetes Study. Clin Endocrinol 2005;62: 480–486 10. Donckier JE: Endocrine diseases and diabetes. W: Pickup J.C.,Williams G. (red.). Textbook of diabetes. Blackwell Publishing2003: 27.1–27.15. 11. Brenta G. Why can insulin resistance be a natural consequen-ce of thyroid dysfunction? J Thyroid Res 2011; 7: 1–9. 12. Rochon C, Tauveron I, Dejax C et al. Response of glucose dis-posal to hyperinsulinaemia in human hypothyroidism andhyperthyroidism. Clin Sci 2003; 104: 7–15. 13. Tamer G, Mert M, Tamer I et al. Effects of thyroid autoimmunity on abdominal obesity and hyperlipidaemia. Endokry-nol Pol 2011; 62: 421–428. 14. Maratou E, Hadjidakis DJ, Kollias A et al. Studies of insulinresistance in patients with clinical and subclinical hypothy-roidism. Eur J Endocrinol 2009; 160: 785–79 15. Türkiye Endokrinoloji Ve Metabolizma Derneği. Metabolik Sen-drom Kılavuzu. Tuna Matbaacılık, Ankara 2009. 16. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, TreacherDF, Turner RC. Homeostasis model assessment: Insulin resis-tance and beta-cell function from fasting plasma glucose andinsulin concentrations in man. Diabetologia. 1985;28:412–9. 17. Maratou E, Hadjidakis DJ, Tsegka K, et al. Studies of insu-lin resistance in patients with clinical and subclinicalhyperthyroidism. Eur J Endocrinol 2009;160(5):785-790 18. Yavoz DG, Yuksel M, Deyneli O et al. Association of serumparaoxonase activity with insulin sensitivity and oxidative stressin hyperthyroid and TSH-suppressed nodular goitre patients.Clin Endocrinol 2004; 61: 515–521. 19. Yavuz DG, Yazici D, Toprak A et al. Exogenous subclinicalhyperthyroid¬ism impairs endothelial function in nodular goi-ter patient. Thyroid 2008; 18: 395–400. 20. Roos A, Bakker SJ, Links TP et al. Thyroid function is asso-ciated with components of the metabolic syndrome in euthy-roid subjects. J Clin Endocr Metab 2007; 92: 491–496. 21. Yücel H, Çelebi A, Avlağı G ve ark. Metabolik Sendromlu Has-talarda Tiroid Hormonları Fonksiyon Bozuklukları (ThyroidHormones Disfunctions in the Metabolic Syndrome Patients).JAREM 2014; 4:102-7. 22. Chugh K, Goyal S, Shankar V, Chugh SN. Thyroid functiontests in metabolic syndrome. Indian J Endocrinol Metab2012;16(6): 958–96. 23. Handisurya A, Pacini G, Tura A, Gessl A, Kautzky-Willer A.Effects of T4 replacement therapy on glucose metabolism insubjects with subclinical (SH) and overt hypothyroidism(OH). Clinical endocrinology 2008;69(6):963-969. 24. Khan SH, Fazal N, Ejaz A, et al. Insulin Resistance and Glu-cose Levels in Subjects with Subclinical Hypothyroidism. Jo-urnal of the College of Physicians and Surgeons--Pakistan:JCPSP, 2017, 27.6: 329. 25. Ferrannini E, Iervasi G, Cobb J, Ndreu R, Nannipieri M. Ame-rican Journal of Physiology-Endocrinology and Metabolism2017;312(5): E429-E436 26. Dimitriadis G, Mitrou P, Lambadiari V et al. Insulin actionin adipose tissue and muscle in hypothyroidism. J Clin Endoc-rinol and Metab 2006; 91: 4930–4937. 27. Owecki M, Nikisch E, Sowiński J. Hypothyroidism has no im-pact on insulin sensitivity assessed with HOMA-IR in totallythyroidectomized patients. Acta Clin Belg 2006; 61: 69–73. 28. Altunoğlu E, Ülgen E, Müderrisoğlu C, Erdenen F, Boz M. Obe-zite ve Tiroid Fonksiyonları. Istanbul Tıp Dergisi 2011;12(2):69-71. 29. Türker T. 2005. Tiroid Hastalıkları ve Metabolik Sendrom (ya-yınlamamış doktora tezi), Haseki Eğitim ve Araştırma Has-tanesi 4. İc Hastalıkları Kliniği. İstanbul. 30. Chu CH, Lam HC, Lee JK, et al. Hyperthyroidism-Associa-ted Insulin Resistance Is Not Mediated by Adiponectin Levels.Journal of thyroid research, 2011.