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Multiple sclerosis, interferon beta and clinical thyroid dysfunction
Author(s) -
Kreisler A.,
De Seze J.,
Stojkovic T.,
Delisse B.,
Combelles M.,
Vérier A.,
Hautecoeur P.,
Vermersch P.
Publication year - 2003
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1034/j.1600-0404.2003.02009.x
Subject(s) - carbimazole , medicine , multiple sclerosis , thyroid , interferon beta 1a , thyroid dysfunction , hormone , interferon beta , gastroenterology , endocrinology , graves' disease , immunology
The objective of this study was to investigate frequency and presentation of clinical thyroid dysfunction in patients treated with interferon beta (IFN‐β). We have collected the cases of clinical thyroid dysfunction in 700 consecutive patients receiving IFN‐β for multiple sclerosis (MS). Five patients (four women, one man) treated with IFN‐β1b developed hyperthyroidism. Three of them have secondary progressive MS, and two have relapsing–remitting MS. It was necessary to stop IFN‐β in three cases; these patients still require carbimazole after several months. In the two other cases, hyperthyroidism disappeared spontaneously. Two patients (one man and one woman) treated with IFN‐β1a developed hypothyroidism. One of them required l ‐thyroxine. Lastly, an increased thyroid volume without modification of thyroid hormones plasma levels was discovered in a patient receiving IFN‐β1a. Among patients treated with IFN‐β, clinical thyroid dysfunction is much rarer than laboratory thyroid dysfunction. However, this side‐effect is sometimes severe.