| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Letters to the Editor |
University of Vienna, Vienna, Austria
Dr. Marinó and coworkers report in their interesting article, recently published in JCEM (1) and presented some years earlier at the European Thyroid Association meeting in Vienna (2), that patients with myasthenia gravis (MG) and concomitant autoimmune thyroid disease (AITD) present with a relatively mild clinical form of MG. Based on their observation, they even suggest the existence of two separate disease entities within MG: one mild form with associated autoimmune thyroid disease (with frequent ocular involvement and rare thymic disease or acetylcholine antibodies) and one clinically more aggressive form without AITD.
The data presented by the authors are very convincing. There is, however, one—in my view, crucial—point that should be clarified: how do the authors explain the very high occurrence (77/129 = 60%) of thyroid disease in their patients with MG?
In their introduction they quote two "epidemiological" studies showing that AITD occur in approximately 5–10% of MG patients. In fact one of these studies (3) is a case report. The other study (4) investigated 46 patients with MG: two (4%) had Graves’ disease, five (12%) were euthyroid with autonomously functioning thyroid tissue, the remaining 39 patients had no thyroid disease. One year earlier the same first author (5) reported a somewhat higher incidence of thyroid disease in a larger series (n = 104) of MG patients (6% with thyrotoxicosis, 2% with hypothyroidism; 12% had antithyroglobulin antibodies and 28% had antimicrosomal antibodies). Interestingly enough, last and very recent issues of famous textbooks like Werner and Ingbar’s The Thyroid (6) also quote from Kiessling’s study (4), an "epidemiological" paper (7), which is in fact a case report, or do not offer any reference for statements such as "thyrotoxicosis occurs in 3% of patients with MG" like De Groot’s The Thyroid and Its Diseases (8).
In a hitherto unpublished study of 55 consecutive patients with MG, we found no patient with thyroid dysfunction; the frequency of thyroid autoantibodies was, however, relatively increased (thyroglobulin antibodies were found in 5%, antimicrosomal antibodies in 16%, TSH-receptor antibodies were normal).
In view of our data and the sparse data available in the literature, we actually challenged the dogma, that Graves’ disease is a frequent phenomenon in MG. The extremely high frequency of autoimmune thyroid disease in the series of Marinó et al. (1) contradicts our experience. We would therefore, be very interested in whether they can offer an explanation for the differences between the occurrence of thyroid disease in MG in Vienna and in Tuscany (both being areas of mild iodine deficiency).
Footnotes
1 Address correspondence to:
Michael Weissel, MD, 3rd Medical University Clinic, University of
Vienna, Waehringer Guertel 18-20, Vienna, Austria A-1090. 
Received April 3, 1997.
References
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
