Summary
  Medications can precipitate true thyroid disease, modify the therapeutic response in hypothyroidism or thyrotoxicosis, or produce assay results which falsely suggest thyroid dysfunction. A detailed knowledge of various drug effects may increase therapeutic options, for example in unusual or complicated cases of thyrotoxicosis, where there may be a place for agents such as lithium, cholestyramine, cholecystographic contrast agents, iodide or glucocorticoids as second-line therapy.

Some important drug influences on thyroid function can be summarized as follows:
  1. in patients taking medications that increase the serum concentration of TBG, serum total T4 will often be elevated, but free T4 estimates will be normal;


  2. during treatment with dopaminergics or glucocorticoids, serum TSH will be abnormally low in relation to the serum free T4 level;


  3. when a medication that displaces T4 and T3 from TBG binding is present in the serum sample, the measured concentration of free T4, generally performed after dilution of the serum sample, is likely to be falsely low in relation to its true in vivo concentration;


  4. when rapidly cleared competitors for T4 binding to TBG are used, free T4 estimates may be influenced by the time interval between dosage and sampling;


  5. in heparin-treated patients, the free T4 concentration can be spuriously high because of in vitro generation during sample storage and incubation, of non-esterified fatty acids (NEFA) that displace T4 from TBG; this artefact is method-dependent;


  6. drug-induced impairment of absorption, and accelerated clearance and metabolism impair the therapeutic response to ingested T4 in hypothyroid subjects and may exacerbate diminished thyroid reserve;


  7. during longterm treatment with phenytoin, serum free T4 and TSH may be similar to the findings in secondary hypothyroidism;


  8. amiodarone can cause diverse changes in thyroid function, the most difficult being thyrotoxicosis due to a unique form of persistent thyroiditis, that presents with atypical clinical features and may respond poorly to medical therapy.

The phenomena that occur in the so-called "sick euthyroid syndrome" are often attributable to medications. No study of thyroid function in critical illness is convincing without meticulous documentation of medications such as dopaminergics, glucocorticoids, radiologic contrast agents, beta blockers, furosemide and heparin - agents that are frequently used during critical illness.