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Subclinical Thyroid Disease: “Grading” the Risk of Atrial Fibrillation According to Thyrotropin Concentration Is Not Justified
LETTER
Subclinical Thyroid Disease: “Grading” the Risk of Atrial Fibrillation According to Thyrotropin Concentration Is Not Justified To the Editor: We read with interest the Update in Office Management on subclinical thyroid disease.1 As the authors stated, management of subclinical hyperthyroidism is based on experts’ recommendations because there are no published clinical trials demonstrating the benefits of treating subclinical hyperthyroidism, in particular on its main complication, atrial fibrillation. We would like to comment on the distinction made by Jones et al1 and by many other experts between patients with a thyroid-stimulating hormone level less than 0.1 mU/L and patients with a thyroid-stimulating hormone level between 0.1 and 0.4 mU/L. Three independent studies have demonstrated that subclinical hyperthyroidism is associated with an increased risk of atrial fibrillation with a relative risk of approximately 2 to 3 compared with euthyroid subjects.2-4 Four other studies have studied the relationships between subclinical hyperthyroidism and mortality, and showed inconsistent results.5-8 The only study that has distinguished the 2 levels of thyroid-stimulating hormone was that of Sawin et al.2 Subjects with a thyroid-stimulating hormone level less than 0.1 mU/L (n ⫽ 61) had a relative risk of developing atrial fibrillation of 3 compared with subjects with a thyroid-stimulating hormone level between 0.4 and 5 mU/L. The relative risk was only 1.6 for subjects with a thyroid-stimulating hormone level between 0.1 and 0.4 mU/L (n ⫽ 187), but it was statistically significant (P ⫽ .05). No direct statistical comparisons of both relative risks were given in the article. All the other studies (concerning atrial fibrillation or mortality) used a thyroid-stimulating hormone threshold between 0.3 and 0.5 mU/L. We think the data that could justify “grading” the levels of subclinical hyperthyroidism are too limited to propose distinct recommendations. From a theoretic point of view, if one can reasonably assume that the relationship between thyroidstimulating hormone and atrial fibrillation risk is linear, clinicians must keep in mind that this assumption has never Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this letter.
0002-9343/$ -see front matter © 2012 Elsevier Inc. All rights reserved.
been demonstrated. The question of “normality” of thyroidstimulating hormone, that is, the threshold under which therapeutic intervention could be needed, is already complex enough9 without introducing subtleties that do not rely on scientific data. The risk of atrial fibrillation in subclinical hyperthyroidism has been convincingly demonstrated for a thyroid-stimulating hormone level less than 0.4 mU/L. If a therapeutic intervention is discussed in a given patient, age and associated heart disease, which are well-known risk factors of atrial fibrillation, should be taken into account. The degree of decrease of thyroid-stimulating hormone should not. Expert opinions are useful when no evidence-based recommendations are available. However, these opinions must not give an appearance of science when and where there is none. Bernard Goichot, MD, PhD Stéphane Vinzio, MD Service de Médecine Interne Endocrinologie et Nutrition Hôpital de Hautepierre Hôpitaux Universitaires de Strasbourg Faculté de Médecine Strasbourg Cedex, France
doi:10.1016/j.amjmed.2010.07.033
References 1. Jones DA, May KE, Geraci SA. Subclinical thyroid disease. Am J Med. 2010;123:502-504. 2. Sawin CT, Geller A, Wolf PA, et al. Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons. N Engl J Med. 1994;331:1249-1252. 3. Auer J, Scheibner P, Mische T, et al. Subclinical hyperthyroidism as a risk factor for atrial fibrillation. Am Heart J. 2001;142:838-842. 4. Cappola AR, Fried LP, Arnold AM, et al. Thyroid status, cardiovascular risk, and mortality in older adults. JAMA. 2006; 295:1033-1041. 5. Parle JV, Maisonneuve P, Sheppard MC, et al. Prediction of all-cause and cardiovascular mortality in elderly people from one low serum thyrotropin result: a 10-year cohort study. Lancet. 2001;358:861-865. 6. Gussekloo J, van Exel E, de Craen AJ, et al. Thyroid status, disability and cognitive function, and survival in old age. JAMA. 2004;292:25912599. 7. Van den Beld AW, Visser TJ, Feelders RA, et al. Thyroid hormone concentrations, disease, physical function, and mortality in elderly men. J Clin Endocrinol Metab. 2005;90:6403-6409. 8. Walsh JP, Bremner AP, Bulsara MK, et al. Subclinical thyroid dysfunction as a risk factor for cardiovascular disease. Arch Intern Med. 2005; 165:2467-2472. 9. Goichot B, Sapin R, Schlienger JL. Subclinical hyperthyroidism: considerations in defining the lower limit of the thyrotropin reference interval. Clin Chem. 2009;55:420-424.
Subclinical Thyroid Disease: “Grading” the Risk of Atrial Fibrillation According to Thyrotropin Concentration Is Not Justified To the Editor: We read with interest the Update in Office Management on subclinical thyroid disease.1 As the authors stated, management of subclinical hyperthyroidism is based on experts’ recommendations because there are no published clinical trials demonstrating the benefits of treating subclinical hyperthyroidism, in particular on its main complication, atrial fibrillation. We would like to comment on the distinction made by Jones et al1 and by many other experts between patients with a thyroid-stimulating hormone level less than 0.1 mU/L and patients with a thyroid-stimulating hormone level between 0.1 and 0.4 mU/L. Three independent studies have demonstrated that subclinical hyperthyroidism is associated with an increased risk of atrial fibrillation with a relative risk of approximately 2 to 3 compared with euthyroid subjects.2-4 Four other studies have studied the relationships between subclinical hyperthyroidism and mortality, and showed inconsistent results.5-8 The only study that has distinguished the 2 levels of thyroid-stimulating hormone was that of Sawin et al.2 Subjects with a thyroid-stimulating hormone level less than 0.1 mU/L (n ⫽ 61) had a relative risk of developing atrial fibrillation of 3 compared with subjects with a thyroid-stimulating hormone level between 0.4 and 5 mU/L. The relative risk was only 1.6 for subjects with a thyroid-stimulating hormone level between 0.1 and 0.4 mU/L (n ⫽ 187), but it was statistically significant (P ⫽ .05). No direct statistical comparisons of both relative risks were given in the article. All the other studies (concerning atrial fibrillation or mortality) used a thyroid-stimulating hormone threshold between 0.3 and 0.5 mU/L. We think the data that could justify “grading” the levels of subclinical hyperthyroidism are too limited to propose distinct recommendations. From a theoretic point of view, if one can reasonably assume that the relationship between thyroidstimulating hormone and atrial fibrillation risk is linear, clinicians must keep in mind that this assumption has never Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this letter.
0002-9343/$ -see front matter © 2012 Elsevier Inc. All rights reserved.
been demonstrated. The question of “normality” of thyroidstimulating hormone, that is, the threshold under which therapeutic intervention could be needed, is already complex enough9 without introducing subtleties that do not rely on scientific data. The risk of atrial fibrillation in subclinical hyperthyroidism has been convincingly demonstrated for a thyroid-stimulating hormone level less than 0.4 mU/L. If a therapeutic intervention is discussed in a given patient, age and associated heart disease, which are well-known risk factors of atrial fibrillation, should be taken into account. The degree of decrease of thyroid-stimulating hormone should not. Expert opinions are useful when no evidence-based recommendations are available. However, these opinions must not give an appearance of science when and where there is none. Bernard Goichot, MD, PhD Stéphane Vinzio, MD Service de Médecine Interne Endocrinologie et Nutrition Hôpital de Hautepierre Hôpitaux Universitaires de Strasbourg Faculté de Médecine Strasbourg Cedex, France
doi:10.1016/j.amjmed.2010.07.033
References 1. Jones DA, May KE, Geraci SA. Subclinical thyroid disease. Am J Med. 2010;123:502-504. 2. Sawin CT, Geller A, Wolf PA, et al. Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons. N Engl J Med. 1994;331:1249-1252. 3. Auer J, Scheibner P, Mische T, et al. Subclinical hyperthyroidism as a risk factor for atrial fibrillation. Am Heart J. 2001;142:838-842. 4. Cappola AR, Fried LP, Arnold AM, et al. Thyroid status, cardiovascular risk, and mortality in older adults. JAMA. 2006; 295:1033-1041. 5. Parle JV, Maisonneuve P, Sheppard MC, et al. Prediction of all-cause and cardiovascular mortality in elderly people from one low serum thyrotropin result: a 10-year cohort study. Lancet. 2001;358:861-865. 6. Gussekloo J, van Exel E, de Craen AJ, et al. Thyroid status, disability and cognitive function, and survival in old age. JAMA. 2004;292:25912599. 7. Van den Beld AW, Visser TJ, Feelders RA, et al. Thyroid hormone concentrations, disease, physical function, and mortality in elderly men. J Clin Endocrinol Metab. 2005;90:6403-6409. 8. Walsh JP, Bremner AP, Bulsara MK, et al. Subclinical thyroid dysfunction as a risk factor for cardiovascular disease. Arch Intern Med. 2005; 165:2467-2472. 9. Goichot B, Sapin R, Schlienger JL. Subclinical hyperthyroidism: considerations in defining the lower limit of the thyrotropin reference interval. Clin Chem. 2009;55:420-424.