zaki
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A 65-year old man is admitted to the hospital with anginal chest pain. His general health has been excellent, although he has had a multinodular goiter for many years. He had a series of thyroid function tests 4 weeks before admission, and the results are shown below.
Laboratory studies:
Serum T4 8.0 µg/dL
Free T4 index 8.0
Serum T3 152 ng/dL
Serum thyrotropin (TSH) 0.7 µU/mL
A myocardial infarction is ruled out, but chest pain continues. A coronary arteriogram shows a 90% stenosis of the left main coronary artery. A coronary artery bypass graft is done. The patient has an uneventful postoperative course and is discharged on the seventh postoperative day. One month later, he is readmitted in atrial fibrillation with a rapid ventricular response. Repeat thyroid function testing shows the following:
Serum T4 15.0 µg/dL
Free T4 index 15.8
Serum T3 220 ng/dL
Serum TSH <0.01 µU/mL
What is the most likely diagnosis?
A) Graves’ disease
B) Stress-induced hyperthyroidism
C) Iodine-induced hyperthyroidism
D) Silent thyroiditis
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Maverick
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| helpful
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hum! I will pick
B) Stress-induced hyperthyroidism
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| gballarino
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I think it´s C: iodine induced: he has a history of Multinodular Goiter which seems to have been nontoxic, and a history of an imaging procedure that use iodide-containing contrasts. Nontoxic multinodular goiters tend to produce a Jod-Basedow effect when exposed to iodide. (isn´t a month too late, though?).
About stress... the only clinical picture I can think of that involves hyperthyroidism in response to stress (such as in surgery) is the "sick euthyroid syndrome", which consists of lab derangements with no clinical picture of thyrotoxicosis.
There´s no reason to think about Grave´s disease. The goiter is multinodular not difuse, and it doesn´t say anything about other clinical findings of grave´s disease (pretibial myxedema, exophtalmos, bruits, difuse goiter).
Silent tyroiditis it´s frequent among pregnant or postpartum woman.
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Guillermo Ballarino
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| zaki
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Answer: C
Educational Objective: Know the dangers of iodine exposure in a patient with a multinodular goiter.
The natural history of multinodular goiters is slow growth and gradual decrease in thyrotropin (TSH), reflecting increasing thyroid hormone production. This progression occurs over years to decades, however. Many patients with multinodular goiters have autonomous areas within their thyroid. This patient had normal thyroid function 1 month before admission. However, his serum TSH level was near the lower limits of normal, suggesting the possibility of autonomous thyroid function.
When patients with multinodular goiters are exposed to excess iodine, severe hyperthyroidism may occur. This is known as iodine-induced hyperthyroidism or the Jod-Basedow phenomenon. When iodine supplementation is introduced into areas of iodine deficiency, iodine-induced hyperthyroidism may occur in patients with multinodular goiters. Iodine-induced hyperthyroidism may occur in nonendemic goiter areas as well, often with devastating consequences.
The high iodine content of the dye used for the cardiac catheterization undoubtedly precipitated the hyperthyroidism in this patient. The onset of hyperthyroidism may be delayed for several weeks to months after the iodide exposure.
Although other causes of hyperthyroidism are possible, none is as likely as this scenario. When patients with multinodular goiter must be exposed to excess iodine (for example, during cardiac catheterization, computed tomographic [CT] scan with contrast medium, or amiodarone therapy), premedication with antithyroid drugs (methimazole or propylthiouracil) should be considered.
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| Cedrick
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| AAAAA
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Jod-Basedow phenomenon (yd-)
n.
Induction of thyrotoxicosis in a previously normal individual as a result of exposure to large quantities of iodine. Also called iodine-induced hyperthyroidism.
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| AAAAA
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Excellent question and some background history on this question.
Sorry to post 'HISTORY OF MEDICINE". Without knowing the past, how can we understand the future !!!!!!
The earliest report on thyrotoxicosis induced by administration of iodine is probably that of JF Coindet in the Ann Chim Phys (Paris) (16;252,1821), cited by Orgiazzi and Mornex (81). In 1859 Röser, cited elsewhere (82), noted that treating goiter with iodine could result in hyperthyroidism. He used the term "goiter cachexia" for this condition. Later the term Jod-Basedow was applied, although it should be realized that, in most instances, iodide induced hyperthyroidism does not involve patients with incipient Basedow-Graves' disease. Multinodular goiter may be rendered thyrotoxic by the administration of stable iodine. In their review on iodide-induced thyrotoxicosis Fradkin and Wolff (83) speculate that a decreased sensitivity to the Wolff-Chaikoff effect under conditions of moderate iodide excess would lead to iodide induced thyrotoxicosis (IIT). The Wolff-Chaikoff effect involves blockade of iodide organification and hormone synthesis by high intrathyroidal iodide. To date, there is no biochemical or pathological basis for the hypothetical difference in iodide sensitivity or autoregulation of thyroidal iodide metabolism in IIT. It may even be that the mechanism is heterogeneous in different patients with pre-existing thyroid disorders. IIT may be subdivided into different groups: 1. patients from endemic goiter areas; 2. patients with previous non-endemic goiter; 3. patients with previous or with actual Graves' disease and 4. patients without apparent previous thyroid disease (83). Sources of iodide in patients with IIT are listed in Table 13-6.
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