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A prospective study of the effects of lithium on thyroid function and on the prevalence of antithyroid antibodies

Published online by Cambridge University Press:  09 July 2009

D. H. Myers*
Affiliation:
Royal Shrewsbury Hospital, Shrewsbury, and Hollymoor Hospital, Birmingham
R. A. Carter
Affiliation:
Royal Shrewsbury Hospital, Shrewsbury, and Hollymoor Hospital, Birmingham
B. H. Burns
Affiliation:
Royal Shrewsbury Hospital, Shrewsbury, and Hollymoor Hospital, Birmingham
A. Armond
Affiliation:
Royal Shrewsbury Hospital, Shrewsbury, and Hollymoor Hospital, Birmingham
S. B. Hussain
Affiliation:
Royal Shrewsbury Hospital, Shrewsbury, and Hollymoor Hospital, Birmingham
Vinnie K. Chengapa
Affiliation:
Royal Shrewsbury Hospital, Shrewsbury, and Hollymoor Hospital, Birmingham
*
1 Address for correspondence: Dr D. H. Myers, Royal Shrewsbury Hospital, Shelton, Shrewsbury SY3 8DN.

Synopsis

Tests of thyroid function and pathology were carried out on 133 patients before they were treated with lithium (Li+). Of the 12 patients who subsequently became hypothyroid during treatment with lithium 9 had, before the commencement of treatment, thyroid autoantibodies and/or an exaggerated thyroid stimulating hormone (TSH) response to thyrotropin releasing hormone (TRH), whereas 3 patients had neither of these indicators. Lithium administration was accompanied by a rise in thyroid antibody titre in 20 patients but a fall in only 5, a statistically significant difference. Evidence that it may be an immunostimulant is discussed. Li+-induced thyroid failure cannot be accurately predicted, and may occur suddenly. The best minimum safeguard, therefore, is serial thyroxine (T4) (or free T4) estimation, supplemented if equivocal by a free thyroxine index (FTI), a basal TSH and, if doubt remains, by a TRH test.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1985

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