Q J Med 2003; 96: 949-950
© Association of Physicians 2003; all rights reserved.
Correspondence |
Men are at increased risk of amiodarone-associated thyrotoxicosis in the UK
Sir,Amiodarone is associated with both thyrotoxicosis and hypothyroidism.1 Previous estimates of the frequency of thyroid problems in amiodarone users have been based on small numbers of patients or hospital clinic populations. They range from 1% to 23% for thyrotoxicosis and from 1% to 32% for hypothyroidism.2 Amiodarone-associated thyrotoxicosis (AAT) seems commoner in men.3,4 This could reflect a bias toward greater use of amiodarone by males, who are at increased risk of cardiovascular disease.
In South Worcestershire, all chronic prescribing of amiodarone is done in primary care. The BNF guideline of 6-monthly thyroid function testing in such patients is recommended. We estimated the frequency of amiodarone-associated thyroid disease by examining the occurrence of both AAT and amiodarone-associated hypothyroidism (AAH) in a general practice population.
All general practitioners in Worcester and Droitwich (West Midlands, UK) participated. Patients who had taken amiodarone between January 1995 and October 2000 were identified from computer-held prescription records of the 12 practices. Patient records were examined by JS. Demographic details, dose, duration of drug treatment and thyroid function test results were recorded.
Thyroid hormone levels were analysed at Worcester Royal Infirmary. AAT was defined as suppression of TSH (laboratory reference range 0.5–4.5 mIU/l) in combination with elevation of both free T3 (3.7–7 pmol/l) and free T4 (10–26 pmol/l). AAH was defined as elevation of TSH > 10 mIU/l with a low fT4 and/or a record of thyroxine being commenced while taking amiodarone. The frequencies of both AAT and AAH were compared in men and women. Local ethics committee approval was obtained.
The combined list size of the 12 practices was 122 600. Overall, 216 patients (142 men, 74 women) had been prescribed amiodarone; 59 (27.3%) had no thyroid function tests recorded. The patient details are shown in Table 1. The mean daily maintenance dose of amiodarone did not differ significantly between males (181 mg) and females (177.4 mg). AAT was commoner in men (8.5%) than in women (0%, p < 0.02). The frequencies of AAH did not differ significantly between men (7.7%) and women (5.4%).
|
Amiodarone-associated thyroid dysfunction was common, with an overall incidence of 12.5% during the 5.5 years studied. AAT occurred significantly more often in males, but AAH was not significantly different in frequency between sexes. The explanation for this is unknown. In general, thyroid disease affects women more frequently.5 AAT comprises two types: type 1, a triggering of underlying thyroid disease by the iodine load of amiodarone; and type 2, a destructive thyroiditis. Our retrospective data do not indicate what proportion of AAT in our population was type 1. It seems, however, that AAT may be different from other thyroid diseases, in that males are more strongly predisposed than females.
Our study may underestimate the incidence of thyroid dysfunction, since no thyroid function tests were available for 59 individuals. It is possible (although intuitively improbable) that the apparent excess of AAT among men could be caused by selective failure to detect biochemical thyrotoxicosis among the women rather than the men who did not have thyroid function tests recorded. The prevalence of AAT in our population lies within the range of previously reported estimates,2 but significant underestimation of the overall level of thyrotoxicosis cannot be excluded. The high prevalence of thyroid dysfunction identified argues for rigorous adherence to the recommendation of 6-monthly thyroid function testing in such patients. General practitioners and cardiologists need to establish robust programmes of regular thyroid function screening in users of amiodarone.
-->
Worcestershire Royal Hospital Worcester UK e-mail: david.jenkins{at}worcsacute.wmids.nhs.uk
Acknowledgments
We thank all the staff of the practices involved for their enthusiastic support of this study. We are grateful to Professor Jayne Franklyn for helpful comments on the manuscript.
References
1. Nademanee K, Piwonka RW, Singh BN, Hershman JM. Amiodarone and thyroid function. Prog Cardiovasc Dis 1989; 31:427–37.[CrossRef][Medline]
2. Trip MD, Wiersinga W, Plomp TA. Incidence, predictability and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism. Am J Med 1991; 91:507–11.[CrossRef][Web of Science][Medline]
3. Lombardi A, Martino E, Braverman LE. Amiodarone and the thyroid. Thyroid Today 1990; 13:1–7.
4. Vanderpump MPJ, Tunbridge WMG. The epidemiology of thyroid diseases. In: Braverman LE, Utiger RD, eds. Werner and Ingbar's The Thyroid, 7th ed. Philadelphia, New York, Lippincott-Raven, 1997:474–82.
5. Daniels GH. Amiodarone-induced thyrotoxicosis. J Clin Endocrinol Metab 2001; 86:3–8.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  K.-H. Yiu, M.-H. Jim, C.-W. Siu, C.-H. Lee, M. Yuen, M. Mok, Y.-F. Shea, K. Fan, H.-F. Tse, and W.-H. Chow Amiodarone-Induced Thyrotoxicosis Is a Predictor of Adverse Cardiovascular Outcome J. Clin. Endocrinol. Metab., January 1, 2009; 94(1): 109 - 114. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||