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University Hospital S-751 85 Uppsala, Sweden
The management of Graves’ disease in childhood is often difficult for both patients and their parents, and places a great deal of responsibility on physicians for appropriate treatment guidelines. Glaser and Styne (1) recently presented a retrospective investigation of 191 patients aged 1–19 yr treated for Graves’ disease at 5 pediatric hospitals in California from 1976–1996. They found that among patients with BMI scores above -0.5 SD and small goiters, 86% responded favorably to pharmacological treatment (remission, defined as normal T4 or fT4 concentrations when off medication for 6 months within 2 yr after initiation of therapy). In a group with lower BMI and larger goiters, remission was seen in only 13%. Despite the large number of patients the authors were unable to identify other predictive factors, possibly because several parameters were missing in the records reviewed. A total of 85/191 patients were excluded from the analyses. These patients had been subjected to radio-iodine or surgical treatment, failed to achieve remission or were lost to follow-up. This seems to imply that the true number of patients who failed to achieve remission was larger than that of the final comparison between 27 remitters and 79 nonremitters. Moreover, the 6 month follow-up period was remarkably short, contributing additional bias to the study.
In their report, Glaser and Styne subscribe to previous claims that 25% of children with Graves’ disease enter remission every 2 yr on pharmacological treatment (2). We disagree, and we object to this frequently cited and oversimplified figure. In our experience, comprising 31 carefully monitored cases subjected to a long-term thyrostatic-thyroxine regimen, only 19% entered remission after a median of 6.5 yr (range 4.5–8 yr) (3). The mean age at diagnosis was 11 yr, and the majority of the patients were girls. Although our material was smaller, it was population-based, and all the patients were followed into adulthood. We argue strongly that a proper evaluation of therapeutic response must be based on long-term follow-up.
In our view, the majority of children with Graves’ disease are notoriously difficult to cure with pharmacotherapy, and even during long-term therapy only a small fraction will enter permanent remission. We therefore recommend a limited period of thyrostatic drug treatment. If the disease activity is not readily reduced (as reflected by the dose of thyrostatics required and the level of TSH receptor antibodies), extensive thyroid surgery is advised. We believe that this active strategy reduces the risk of exposing children with Graves’ disease (and their families) to extended periods of unsuccessful thyrostatic drug treatment and the potential impairment of school performance and development.
Another point we would like to emphasize is that children with Down’s syndrome are at high risk of developing autoimmune thyroid disease; in our material 13% had Down’s syndrome. This connection was not mentioned by Glaser and Styne, and we wonder if this may reflect differences in the care of children with Down’s syndrome or if such patients were excluded from the analyses.
Footnotes
Address correspondence to: Professor F. Anders Karlsson, Section of Endocrinology and Diabetes, Department of Medicine, University Hospital, S-751 85 Uppsala, Sweden.
Received November 13, 1997.
References
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