TO THE EDITOR: Treatment of amiodarone-induced thyrotoxicosis has been recognized as a disturbing medical problem because the response to conventional medical therapy is frequently disappointing [1]. Nevertheless, it seems that incomplete knowledge of the pathogenesis of amiodarone-induced thyrotoxicosis may have contributed to inadequate treatment schedules and the varied responses reported. Two mechanisms are actually accepted [2, 3]. In type I, exposure of a latent autonomously functioning thyroid to iodide (nodular goiter, Graves disease) results in increased hormone synthesis. Patients present with underlying thyroid abnormalities on physical and echographic examination; diminished, normal, or increased radioactive iodine uptake; and slightly elevated serum interleukin-6 levels. The high iodine content in the thyroid results in a poor response to thionamides, but patients benefit from perchlorate (1 g/d for no more than 40 days because of possible serious dose-dependent side effects). Hyperthyroidism can be exacerbated when perchlorate therapy is discontinued. In type II, thyrotoxicosis results from presynthesized hormone release caused by amiodarone-induced thyroiditis [4] and therefore has acute onset in the absence of premonitory hormonal changes. Patients with this condition have normal results on thyroid examination, decreased radioactive iodine uptake, and markedly elevated serum interleukin-6 levels. Given the pathogenesis, no benefit from thionamide or perchlorate treatment is seen, but a prompt response to glucocorticoids occurs (prednisone, 40 mg/d or equivalent, slowly tapered over 2 to 3 months), mainly because of the membrane-stabilizing actions of these agents. If thyrotoxicosis is exacerbated during tapering, the glucocorticoid dose should temporarily be increased. Patients may subsequently develop self-limited spontaneous or iodine-induced hypothyroidism, and occasional cases of persistent subclinical hypothyroidism have been described [5]. There are probably mixed forms of amiodarone-induced thyrotoxicosis, both from the beginning and during follow-up. Other pathogenic mechanisms may play a role in certain cases. Recognition of the precise mechanism acting in a given patient will aid in management because thyrotoxicosis due to the type I mechanism will respond to thionamide plus perchlorate treatment and because thyrotoxicosis due to the type II mechanism will respond to glucocorticoids. Mixed forms should be managed with a combination of thionamide, perchlorate, and glucocorticoids. The general practice is to withdraw amiodarone if possible, although worsening of thyrotoxicosis with this practice has been described (probably because of loss of amiodarone antiadrenergic and 5 deiodinase inhibitory actions) and amiodarone-induced thyrotoxicosis has occasionally been controlled with conventional treatment despite amiodarone maintenance.
[1]
S. Friis,et al.
Prostate cancer in Denmark: a 50-year population-based study.
,
1998,
Urology.
[2]
H. Yamanaka,et al.
Familial Prostate Cancer in Japan
,
1998,
International journal of urology : official journal of the Japanese Urological Association.
[3]
A Pacult,et al.
The magnitude of the problem.
,
1994,
Journal of the South Carolina Medical Association.
[4]
E. Greenberg,et al.
Changes in prostate cancer incidence and treatment in USA
,
1994,
The Lancet.
[5]
J. Oesterling,et al.
Prostate-specific antigen, digital rectal examination, and transrectal ultrasonography: their roles in diagnosing early prostate cancer.
,
1993,
Mayo Clinic proceedings.
[6]
P. Walsh,et al.
Evaluation of transrectal ultrasound in the early detection of prostate cancer.
,
1989,
The Journal of urology.
[7]
H. J. Jewett.
Radical perineal prostatectomy for palpable, clinically localized, non-obstructive cancer: experience at the Johns Hopkins Hospital 1909-1963.
,
1980,
The Journal of urology.
[8]
G. Murphy,et al.
A prostate antigen in sera of prostatic cancer patients.
,
1980,
Cancer research.
[9]
R. Stephenson,et al.
Monitoring percent free PSA in serial specimens: Improvement of test specificity, early detection, and identification of occult tumors
,
1998,
Journal of clinical laboratory analysis.
[10]
Curtis Mettlin,et al.
Defining and updating the american cancer society guidelines for the cancer‐related checkup: Prostate and endometrial cancers
,
1993,
CA: a cancer journal for clinicians.