|
The question is whether or not it matters for the eyes if the patient is
not euthyroid. The answer seems to be yes, it does matter. In patients
with both Graves' hyperthyroidism and GO the ophthalmopathy was more severe
in those who had still an abnormal thyroid function despite antithyroid
treatment (Prummel et al. 1990). Subsequent normalization of thyroid function
was associated with a slight amelioration of eye signs, especially in classes
2 and 4 of the NO SPECS system (Prummel et al. 1989). Meticulous control
of thyroid function in GO is thus important.
Next one may ask whether or not it matters for the eyes how the patient is made euthyroid, by antithyroid drugs, by surgery, or by radioactive iodine. This topic is the subject of much controversy (Gorman 1995). An often quoted large retrospective study found similar outcomes for all three treatment modalities (Sridama and DeGroot 1989). However, the study is biased in several ways: the groups differ in age, sex and severity of the eye disease, the prevalence of class 4 eye signs is surprisingly low, and the long time interval between thyroid treatment and outcome of the eyes suggests that the natural history of the eye disease rather than any specific effect of thyroid treatment has been studied. Data from prospective, preferably randomized trials provide in general more conclusive evidence. In a Swedish study Graves' hyperthyroid patients were randomized to receive antithyroid drugs, subtotal thyroidectomy, or 131I (Tallstedt et al. 1992). Worsening or development of GO was observed in 12.3% of patients treated with methimazole, in 14% after surgery, and in 33% after 131I. The authors conclude that a pretreatment serum T3 value of greater that 5nmol/l or 131I treatment are both risk factors for GO. The study has been criticized because the patients receiving 131I (in half of them more than one treatment was required!) were allowed to develop hypothyroidism before thyroxine was given, whereas thyroxine was administered routinely to the surgical and medical groups. Subsequent studies indeed have shown that prevention of the rise of TSH has a beneficial effect in this respect (Kung et al 1994; Tallstedt et al. 1994). The appealing explanation for the development of GO after 131I therapy is release of shared thyroid-orbit antigens from the radiation-damaged thyroid; in support of this hypothesis are the sustained elevations of TSH-R stimulating antibodies after radioiodine but not after surgery or during antithyroid drug treatment. A recent Italian study (reported so far only in abstract form) randomized Graves' hyperthyroid patients to receive 131I, 131I + prednisone, or anti-thyroid drugs (Bartalena et al. 1995). Developing or worsening of GO was observed in 15.3%, 0% and 2.7% respectively. The results again imply 131I as a risk factor for GO. It should be realized that the eye changes after radioiodine are usually mild (and limited to class 2 and 4) and transient in nature. The findings should thus not be construed as an argument against 131I therpy in patients without eye changes. In patients with active GO it seems, however, prudent to refrain from 131I therapy, or to administer 131I in combination with a short course of steroids. Our own policy is to continue antithyroid drugs preferably in combination with thyroxine until the eye treatment has been completed. Very recently there has been a renewed surge of interest in performing total thyroidectomy in Graves' hyperthyroidism in order to get rid of all thyroid antigens and thereby hopefully to prevent the development of GO (Winsa et al. 1995). Its claimed superiority has to be validated in future prospective trials, both in terms of efficacy and safety. |
