TSH Suppression after Differentiated Thyroid Cancer Surgery and Osteoporosis

Kyoung Sik Park

doi:10.16956/kjes.2016.16.1.1

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Park: TSH Suppression after Differentiated Thyroid Cancer Surgery and Osteoporosis

Review Article

Korean Journal of Endocrine Surgery 2016; 16(1): 1-5.

Published online: 15 March 2016

DOI: https://doi.org/10.16956/kjes.2016.16.1.1

TSH Suppression after Differentiated Thyroid Cancer Surgery and Osteoporosis

Kyoung Sik Park

Department of Surgery, Konkuk University School of Medicine, Seoul, Korea.

Correspondence: Kyoung Sik Park. Department of Surgery, Konkuk University School of Medicine, 120 Neung dong-ro, Gwangjin-gu, Seoul 05029, Korea. Tel: +82-2-2030-7697, Fax: +82-2-2030-8270, ks2002p@hanmail.net

Received 2 January 2016 Revised 3 February 2016 Accepted 10 February 2016

(open-access):

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Thyroid stimulating hormone (TSH) suppression therapy has been known to play an important role in lowering the risk of recurrence after surgery for differentiated thyroid carcinoma. Osteoporosis is a major complication of TSH suppression. The purpose of this study is to review the current thyroid stimulating hormone suppression therapy and osteoporosis risk and examine the proper TSH suppression after surgery for patients with differentiated thyroid cancer. Previous studies and current guidelines on TSH suppression and osteoporosis were collected from databases in Korea and other countries and reviewed. According to the recommendations of the Korean Thyroid Association in 2010, initial TSH suppression to below 0.1 mU/L is recommended for high-risk and intermediate-risk thyroid cancer patients, while TSH level at or slightly below the lower limit of normal (0.1~0.5 mU/L) is appropriate for low-risk patients. During follow-up, in patients with persistent disease, the serum TSH should be maintained below 0.1 mU/L indefinitely in the absence of specific contraindications, while in patients free of disease, especially those at low risk for recurrence, the serum TSH may be kept within the low normal range (0.3~2 mU/L). In 2015, the American Thyroid Association recommended revised guidelines considering the initial ATA risk classification, Tg level, Tg trend over time, and risk of TSH suppression during the long term follow-up period. Appropriate recommendations considering the risk stratification of thyroid cancer and adverse effects of TSH suppression are required to improve the survival of differentiated thyroid cancer patients and minimize the adverse effects of long-term therapy.

Keywords: Thyroid cancer, Hormone, Osteoporosis, Risk

Figures and Tables

Table 1

TSH suppression range goal of Korean Thyroid Association Guideline

Risk group	Initial TSH level	Risk group reassesed every 6~12 month	Follow-up TSH level
Low risk	0.1~0.5 mU/L	Low risk	0.3~2 mU/L
Intermediate risk	<0.1 mU/L	High risk-disease free	0.1~0.5 mU/L
High risk	<0.1 mU/L	High risk-persistent	<0.1 mU/L

Source: Adapted from Korean Thyroid Association (ATA) Guidelines 2010.

Table 2

TSH suppression range goal of American Thyroid Association Guideline

Risk group	Initial TSH level	Risk group reassesed every 6~12 month	Follow-up TSH level
Low risk	0.1~0.5 mU/L (0.5~2 mU/L)^*	Low risk	0.5~2 mU/L
Intermediate risk	0.1~0.5 mU/L	High risk-disease free	0.1~0.5 mU/L
High risk	<0.1 mU/L	High risk-persistent	<0.1 mU/L (0.1~0.5 mU/L)^†

Source: Adapted from American Thyroid Association (ATA) Guidelines 2015. ^*For low-risk patients who have undergone remnant ablation and have undetectable serum Tg levels or for low-risk patients who have undergone lobectomy. ^†Taking into account the initial ATA risk classification, Tg level, Tg trend over time, and risk of TSH suppression.

Notes

This study was supported by Konkuk University School of Medicine in 2016.

References

1. Yi KH, Park YJ, Koong SS, Kim JH, Na DG, Ryu JS, et al. Revised Korean thyroid association management guidelines for patients with thyroid nodules and thyroid cancer. Korean J Otorhinolaryngol-Head Neck Surg. 2011; 54:8–36.

2. American Thyroid Association (ATA) Guidelines Taskforce on Thyroid Nodules and Differentiated Thyroid Cancer. Cooper DS, Doherty GM, Haugen BR, Kloos RT, Lee SL, et al. Revised American Thyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid. 2009; 19:1167–1214.

3. Haugen BR, Alexander EK, Bible KC, Doherty GM, Mandel SJ, Nikiforov YE, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid. 2016; 26:1–133.

4. Cooper DS, Specker B, Ho M, Sperling M, Ladenson PW, Ross DS, et al. Thyrotropin suppression and disease progression in patients with differentiated thyroid cancer: results from the National Thyroid Cancer Treatment Cooperative Registry. Thyroid. 1998; 8:737–744.

5. McGriff NJ, Csako G, Gourgiotis L, Lori CG, Pucino F, Sarlis NJ. Effects of thyroid hormone suppression therapy on adverse clinical outcomes in thyroid cancer. Ann Med. 2002; 34:554–564.

6. Pujol P, Daures JP, Nsakala N, Baldet L, Bringer J, Jaffiol C. Degree of thyrotropin suppression as a prognostic determinant in differentiated thyroid cancer. J Clin Endocrinol Metab. 1996; 81:4318–4323.

7. Toft AD. Clinical practice. Subclinical hyperthyroidism. N Engl J Med. 2001; 345:512–516.

8. Vestergaard P, Rejnmark L, Weeke J, Mosekilde L. Fracture risk in patients treated for hyperthyroidism. Thyroid. 2000; 10:341–348.

9. Kalra S, Williams A, Whitaker R, Hossain M, Curtis G, Giles M, et al. Subclinical thyroid dysfunction does not affect one-year mortality in elderly patients after hip fracture: a prospective longitudinal study. Injury. 2010; 41:385–387.

10. Heijckmann AC, Huijberts MS, Geusens P, de Vries J, Menheere PP, Wolffenbuttel BH. Hip bone mineral density, bone turnover and risk of fracture in patients on long-term suppressive L-thyroxine therapy for differentiated thyroid carcinoma. Eur J Endocrinol. 2005; 153:23–29.

11. Franklyn JA, Maisonneuve P, Sheppard MC, Betteridge J, Boyle P. Mortality after the treatment of hyperthyroidism with radioactive iodine. N Engl J Med. 1998; 338:712–718.

12. Ross DS. Hyperthyroidism, thyroid hormone therapy, and bone. Thyroid. 1994; 4:319–326.

13. Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990; 19:35–63.

14. Solomon BL, Wartofsky L, Burman KD. Prevalence of fractures in postmenopausal women with thyroid disease. Thyroid. 1993; 3:17–23.

15. Ongphiphadhanakul B, Alex S, Braverman LE, Baran DT. Excessive L-thyroxine therapy decreases femoral bone mineral densities in the male rat: effect of hypogonadism and calcitonin. J Bone Miner Res. 1992; 7:1227–1231.

16. Abe E, Marians RC, Yu W, Wu XB, Ando T, Li Y, et al. TSH is a negative regulator of skeletal remodeling. Cell. 2003; 115:151–162.

17. Bassett JH, O'Shea PJ, Sriskantharajah S, Rabier B, Boyde A, Howell PG, et al. Thyroid hormone excess rather than thyrotropin deficiency induces osteoporosis in hyperthyroidism. Mol Endocrinol. 2007; 21:1095–1107.

18. Lee MY, Park JH, Bae KS, Jee YG, Ko AN, Han YJ, et al. Bone mineral density and bone turnover markers in patients on long-term suppressive levothyroxine therapy for differentiated thyroid cancer. Ann Surg Treat Res. 2014; 86:55–60.

19. Larijani B, Gharibdoost F, Pajouhi M, Sadjadi A, Aghakhani S, Eshraghian R, et al. Effects of levothyroxine suppressive therapy on bone mineral density in premenopausal women. J Clin Pharm Ther. 2004; 29:1–5.

20. Reverter JL, Holgado S, Alonso N, Salinas I, Granada ML, Sanmartí A. Lack of deleterious effect on bone mineral density of long-term thyroxine suppressive therapy for differentiated thyroid carcinoma. Endocr Relat Cancer. 2005; 12:973–981.

21. Marcocci C, Golia F, Bruno-Bossio G, Vignali E, Pinchera A. Carefully monitored levothyroxine suppressive therapy is not associated with bone loss in premenopausal women. J Clin Endocrinol Metab. 1994; 78:818–823.

22. Jódar E, Begoña López M, García L, Rigopoulou D, Martínez G, Hawkins F. Bone changes in pre- and postmenopausal women with thyroid cancer on levothyroxine therapy: evolution of axial and appendicular bone mass. Osteoporos Int. 1998; 8:311–316.

23. Kung AW, Yeung SS. Prevention of bone loss induced by thyroxine suppressive therapy in postmenopausal women: the effect of calcium and calcitonin. J Clin Endocrinol Metab. 1996; 81:1232–1236.

24. Kim MK, Yun KJ, Kim MH, Lim DJ, Kwon HS, Song KH, et al. The effects of thyrotropin-suppressing therapy on bone metabolism in patients with well-differentiated thyroid carcinoma. Bone. 2015; 71:101–105.

25. Mazokopakis EE, Starakis IK, Papadomanolaki MG, Batistakis AG, Papadakis JA. Changes of bone mineral density in pre-menopausal women with differentiated thyroid cancer receiving L-thyroxine suppressive therapy. Curr Med Res Opin. 2006; 22:1369–1373.

26. Mohammadi B, Haghpanah V, Tavangar SM, Larijani B. Modeling the effect of levothyroxine therapy on bone mass density in postmenopausal women: a different approach leads to new inference. Theor Biol Med Model. 2007; 4:23.

27. Kim CW, Hong S, Oh SH, Lee JJ, Han JY, Hong S, et al. Change of bone mineral density and biochemical markers of bone turnover in patients on suppressive levothyroxine therapy for differentiated thyroid carcinoma. J Bone Metab. 2015; 22:135–141.

28. Heemstra KA, Hamdy NA, Romijn JA, Smit JW. The effects of thyrotropin-suppressive therapy on bone metabolism in patients with well-differentiated thyroid carcinoma. Thyroid. 2006; 16:583–591.

29. Flynn RW, Bonellie SR, Jung RT, MacDonald TM, Morris AD, Leese GP. Serum thyroid-stimulating hormone concentration and morbidity from cardiovascular disease and fractures in patients on long-term thyroxine therapy. J Clin Endocrinol Metab. 2010; 95:186–193.

30. Bauer DC, Ettinger B, Nevitt MC, Stone KL. Study of Osteoporotic Fractures Research Group. Risk for fracture in women with low serum levels of thyroid-stimulating hormone. Ann Intern Med. 2001; 134:561–568.

31. Ko YJ, Kim JY, Lee J, Song HJ, Kim JY, Choi NK, et al. Levothyroxine dose and fracture risk according to the osteoporosis status in elderly women. J Prev Med Public Health. 2014; 47:36–46.

32. Biondi B, Cooper DS. Benefits of thyrotropin suppression versus the risks of adverse effects in differentiated thyroid cancer. Thyroid. 2010; 20:135–146.

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