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METABOLIC SYNDROME AND THYROID DYSFUNCTION IN PATIENTS WITH ACROMEGALY IN SULAIMANI
METABOLIC SYNDROME AND THYROID DYSFUNCTION IN PATIENTS WITH ACROMEGALY IN SULAIMANI
Shadan J. Abdullah a, Taha O. Mahwi b, and Zagros Ghaffor Rashid b
a Shar Hospital, Ministry of Health, Sulaimani city, Kurdistan Region, Iraq.
b College of Medicine, University of Sulaimani, Kurdistan Region, Iraq.
Submitted: 25/4/2021; Accepted: 20/7/2022; Published: 21/9/2022
DOI Link: https://doi.org/10.17656/jsmc.10368
ABSTRACT
Background
Acromegaly is a chronic endocrinology disorder caused by the over-production of growth hormone (GH) predominantly by a pituitary adenoma. Acromegaly is associated with metabolic changes and thyroid dysfunction (ThD) in the body. However, the frequency of metabolic syndrome (MtS) in acromegaly patients is unknown, and studies assessing the frequency of different ThD types in acromegaly cases were few.
Objectives
To analyze the frequencies of MtS and ThD in patients with acromegaly in comparison to controls in Sulaimani city, to find the frequencies of MtS and ThDs in active cases compared to inactive cases in acromegaly patients, and to assess the relationship between the cumulative exposure to Insulin-like Growth Factor 1 (IGF-1) with ThD and MtS in acromegaly.
Patients and Methods
In this case-control study, 82 subjects were enrolled, which included 22 patients with acromegaly who visited the Sulaimani endocrinology center from August 2021 to February 2022 and 60 control subjects. The mean age of cases was 47.55 [11.50] years, with 7 (31.8%) male and 15 (68.2%) female. Thyroid function test, clinical, and biochemical parameters of MtS were measured in both groups in addition to IGF1. Chi-square test, Student T-test, and ANOVA were used in data analysis. Correlation between quantitative variables determined by Pearson correlation, with a P-value ≤ 0.05, is significant
Results
Out of 22 patients with acromegaly, 68.2% were euthyroid, 9.1% had primary hypothyroidism, 18.2% had central hypothyroidism, and 4.5% had hyperthyroidism, which is significantly higher than the control group (p-value =0.002). MtS frequency is 68.18% in cases, significantly higher than control, p-value=0.011. Most MtS and ThD parameters were significantly higher in acromegaly patients than in controls, P-value < 0.001. No significant correlation between the last IGF1 and other parameters existed except free T3, which has a significant negative correlation with IGF1, P < 0.05.
Conclusion
In acromegaly, the frequency of MtS is high (68.18%), and the frequency of ThD is 31.8%. Both MtS and ThDs are more common in patients compared to controls. No significant relationship exists between disease activity and the presence of MtS or ThD. Because both MtS and ThDs increase the metabolic markers, consequently increasing cardiovascular disease (CVD) morbidity and mortality in cases.
KEYWORDS
Keywords: Metabolic syndrome, Acromegaly, Thyroid dysfunction, IGF1, Disease activity, Control.
References
1. Melmed S. Acromegaly. N Engl J Med. 1990;322:966-77.
2. Katznelson L; Atkinson JL; Cook DM; Ezzat SZ; Hamrahian AH; Miller KK. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Acromegaly--2011 update: executive summary. The USA. 2011.
3. Dekkers OM, Biermasz NR, Pereira AM, Romijn JA, Vandenbroucke JP. Mortality in acromegaly: A meta-analysis.Departments of Endocrinology and Metabolic Diseases (OMD, NRB, AMP, JAR) and Clinical Epidemiology (OMD, JPV), LeidenUniversity Medical Center, 2300 RC Leiden, The Netherlands. J Clin Endocrinol Metab. 2008;93(1):61–7.
4. Otto J, J L, Blum WF, Michael B, Christiansen JS. Binding Protein 3 in Growth hormone-deficient Patients and Age- and Sex-Matched Normal Subjects. Acta Endocrinol (Copenh. 1990;123:62.
5. Freda PU, Shen W, Heymsfield SB, Reyes-Vidal CM, Geer EB, Bruce JN, et al. Lower visceral and subcutaneous but higher intermuscular adipose tissue depots in patients with growth hormone and insulin-like growth factor I excess due to acromegaly. J Clin Endocrinol Metab. 2008;93(6):2334–43.
6. Clemmons DR. Roles of insulin-like growth factor-I and growth hormone mediate insulin resistance in acromegaly. Pituitary. 2002;5(3):181–3.
7. Zimmet PZ, McCarty DJ, De Courten MP. global epidemiology of non-insulin-dependent diabetes mellitus and the metabolic syndrome. USA Newyork. J diabetes its Complications [Internet]. 1997 Mar [cited 2022 Feb 17];11(2):60–8. Available from: https://pubmed.ncbi.nlm.nih.gov/9101389/
8. Marchesini G, Brizi M, Blanchi G, Tomassetti S, Bugianesi E, Lenzi M, et al. Non-alcoholic fatty liver disease: a feature of the metabolic syndrome.Italy. Diabetes [Internet]. 2001 [cited 2022 Feb 17];50(8):1844–50. Available from: https://pubmed.ncbi.nlm.nih.gov/11473047/
9. Kreze A, Kreze-Spirova E, Mikulecky M. Risk factors for glucose intolerance in active acromegaly. Brazilian J Med Biol Res. 2001;34(11):1429–33.
10. Neely RDG, Rooney DP, Bell PM, Bell NP, Sheridan B, Atkinson AB, et al. Influence of growth hormone on glucose-glucose 6-phosphate cycle and insulin action in normal humans. Am J Physiol - Endocrinol Metab. 1992;263(5 26-5).
11. Alexopoulou O, Bex M, Kamenicky P, Mvoula AB, Chanson P, Maiter D. Prevalence and risk factors of impaired glucose tolerance and diabetes mellitus at diagnosis of acromegaly: A study in 148 patients. Pituitary. 2014;17(1):81–9.
12. Pivonello R, Auriemma RS, Grasso LFS, Pivonello C, Simeoli C, Patalano R, et al. Complications of acromegaly: cardiovascular, respiratory and metabolic comorbidities. Pituitary. 2017;20(1):46–62.
13. Colao A, Ferone D, Marzullo P, Lombardi G. Systemic Complications of Acromegaly: Epidemiology, Pathogenesis, and Management. Endocr Rev. 2004 Feb;25(1):102–52.
14. Mercado M, Gonzalez B, Vargas G, Ramirez C, Espinosa De Los Monteros AL, Sosa E, et al. Successful mortality reduction and control of comorbidities in patients with acromegaly followed at a highly specialized multidisciplinary clinic. J Clin Endocrinol Metab. 2014;99(12):4438–46.
15. elmed S, Casanueva FF, Klibanski • A, Bronstein • M D, Chanson • P, Lamberts • S W, et al. A consensus on the diagnosis and treatment of acromegaly complications. 2012;
16. Mariotti Stefano. PHYSIOLOGY OF THE HYPOTHALAMIC-PITUITARY-THYROID AXIS - Thyroid Disease ManagerThyroid Disease Manager [Internet]. Available from: https://www.thyroidmanager.org/chapter/physiology-of-the-hypothalamic-pituitary-thyroid-axis/
17. Hollenberg AN. The role of the thyrotropin-releasing hormone (TRH) neuron as a metabolic sensor. Thyroid. 2008 Feb 1;18(2):131–9.
18. Lechan RM, Fekete C. Chapter 12: The TRH neuron: a hypothalamic integrator of energy metabolism. Prog Brain Res. 2006;153:209–35.
19. Kalsbeek A, Fliers E, Franke AN, Wortel J, Buijs RM. Functional connections between the suprachiasmatic nucleus and the thyroid gland as revealed by lesioning and viral tracing techniques in the rat. Endocrinology. 2000;141(10):3832–41.
20. Sakane N, Yoshida T, Shimatsu A, Umekawa T, Kondo M. Octreotide and Bromocriptine bevels and Thyroid Nodule in Nontoxic Autonomous Goiter Suppress Thyroid Hormone an Acromegalic Patient with. Vol. 44, Endocrine Journal.Japan. 1997.
21. KÖBBERLING J, DARRAGH A, POZO E DEL. CHRONIC DOPAMINE RECEPTOR STIMULATION USING BROMOCRIPTINE: FAILURE TO MODIFY THYROID FUNCTION. Clin Endocrinol (Oxf). 1979;11(4):367–70.
22. Barkan AL, Kelch RP, Hopwood NJ, Beitins IZ. Treatment of acromegaly with the long-acting somatostatin analogue SMS 201-995. J Clin Endocrinol Metab. 1988;66(1):16–23.
23. Ho KY, Weissberger AJ, Marbach P, Lazarus L. Therapeutic efficacy of the somatostatin analogue SMS 201-995 (octreotide) in acromegaly. Effects of dose and frequency and long-term safety. Ann Intern Med. 1990;112(3):173–81.
24. Inada M, Sterling K. Thyroxine turnover and transport in active acromegaly. J Clin Endocrinol Metab. 1967;27(7):1019–27.
25. Sato T, Suzuki Y, Taketani T, Ishiguro K, Masuyama T, Takata I, et al. Enhanced peripheral conversion of thyroxine to triiodothyronine during HGH therapy in GH deficient children. J Clin Endocrinol Metab. 1977;45(2):324–9.
26. Grunfeld C, Sherman BM, Cavalieri RR. The Acute Effects of Human Growth Hormone Administration on Thyroid Function in Normal Men. J Clin Endocrinol Metab. 1988;67(5):1111–4.
27. Ain KB, Taylor KD. Somatostatin analogues affect the proliferation of human thyroid carcinoma cell lines in vitro. J Clin Endocrinol Metab. 1994;78(5):1097–102.
28. Roelfsema F, Biermasz NR, Frolich M, Keenan DM, Veldhuis JD, Romijn JA. Diminished and irregular thyrotropin secretion with preserved diurnal rhythm in patients with active acromegaly. J Clin Endocrinol Metab. 2009;94(6):1945–50.
29. LJ H, SW L. Somatostatin receptors in pituitary function, diagnosis and therapy.Netherland. Front Horm Res [Internet]. 2004 [cited 2021 Jul 17];32:235–52. Available from: https://pubmed.ncbi.nlm.nih.gov/15281350/
30. Giustina A, Veldhuis JD. Pathophysiology of the neuroregulation of Growth Hormone Secretion in Experimental Animals and the Human*. Endocr Rev. 1998 Dec 1;19(6):717–97.
31. Looij BJ, Roelfsema F, Frolich M, Nieuwenhuijzen Kruseman AC. The interaction of GHRH with TRH in acromegaly: A controlled study. Acta Endocrinol (Copenh). 1991;125(4):337–41.
32. Geelhoed-Duijvestijn PHLM, Roelfsema F, Schroder-Van Der Elst JP, Van Doorn J, Van Der Heide D. Effect of growth hormone administration on plasma and intracellular levels of thyroxine and tri-iodothyronine in thyroidectomized thyroxine-treated rats. J Endocrinol. 1992;133(1):45–9.
33. MR D, NR F, V H-B, S M. Pituitary tumour registry: a novel clinical resource. J Clin Endocrinol Metab [Internet]. 2000 Jan [cited 2021 Jul 18];85(1):168–74. Available from: https://pubmed.ncbi.nlm.nih.gov/10634382/
34. L K, D K, ML V, S S, KJ P, DA S, et al. Hypogonadism in patients with acromegaly: data from the multi-centre acromegaly registry pilot study. Clin Endocrinol (Oxf) [Internet]. 2001 [cited 2021 Jul 18];54(2):183–8. Available from: https://pubmed.ncbi.nlm.nih.gov/11207632/
35. Chapter 2: Selecting target groups and Chapter 5: Selecting appropriate indicators: Biochemical indicators. In: Indicators for Assessing Iodine Deficiency Disorder and their Control Through Salt Iodination. Geneva: World Health Organization; 1994. WHO/UNI.
36. H Z, B M, P E, AR M, JJ S. Estimation of tissue hypothyroidism by a new clinical score: evaluation of patients with various grades of hypothyroidism and controls. J Clin Endocrinol Metab [Internet]. 1997 Mar 1 [cited 2021 Jul 28];82(3):771–6. Available from: https://pubmed.ncbi.nlm.nih.gov/9062480/
37. Crooks J, Murray IPC, Wayne EJ. Statistical methods are applied to the clinical diagnosis of thyrotoxicosis. QJM. 1959;28(2):211–34.
38. rundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and Management of the Metabolic Syndrome An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement Underlying Risk Factors and Metabolic Syndrome. 2005 [cited 2022 Apr 19]; Available from: http://www.circulationaha.org
39. Surks MI, Hollowell JG. Age-specific distribution of serum thyrotropin and antithyroid antibodies in the US population: implications for the prevalence of subclinical hypothyroidism. J Clin Endocrinol Metab [Internet]. 2007 [cited 2022 Apr 19];92(12):4575–82. Available from: https://pubmed.ncbi.nlm.nih.gov/17911171/
40. Beck-Peccoz P, Amr S, Menezes-Ferreira MM, Faglia G, Weintraub BD. It decreased receptor binding of biologically inactive thyrotropin in central hypothyroidism. Effect of treatment with a thyrotropin-releasing hormone. N Engl J Med [Internet]. 1985 Apr 25 [cited 2022 Apr 19];312(17):1085–90. Available from: https://pubmed.ncbi.nlm.nih.gov/2984564/
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