What is the role of glucocorticoid therapy in the treatment of myxedema coma (crisis)?

Updated: Oct 10, 2018
  • Author: Mohsen S Eledrisi, MD, FACP, FACE; Chief Editor: George T Griffing, MD  more...
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Answer

Patients with primary hypothyroidism may have concomitant primary adrenal insufficiency while patients with secondary hypothyroidism may have associated hypopituitarism and secondary adrenal insufficiency. The other rationale for the treatment with corticosteroids is the potential risk of precipitating acute adrenal insufficiency caused by the accelerated metabolism of cortisol that follows T4 therapy. [2]

Stress doses of intravenous glucocorticoids should be administered until the possibility of adrenal insufficiency is excluded by a random serum cortisol, which is helpful only if very low, or, better, by an ACTH stimulation test.

Hydrocortisone at a dose of 50-100 mg every 8 hours is administered. An alternative is dexamethasone at a dose of 2-4 mg every 12 hours. Dexamethasone has the advantage of not affecting the serum cortisol concentration and can be used immediately without affecting the results of the ACTH stimulation test, which can be performed at any time. If the test is normal, corticosteroids can be stopped without tapering.

A study by Ren et al indicated that pretibial myxedema can be effectively treated with multipoint intralesional injections of compound betamethasone. The investigators found that after one treatment, 21.7% of patients achieved complete remission, while two, three, and four treatments were followed by complete remission in 34.8%, 17.4%, and 17.4% of patients, respectively. [32]


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