 may receive corticosteroids along with131-I, or may be selected for surgical management.
The indications and contraindications for 131-I therapy are given in Table 5.
|Table 5. Iodine-131 Therapy for Graves’ Disease|
SELECTION OF 131-I Dosage
There are two basically different goals in 131-I dose selection. The traditional approach has been to attempt to give the thyroid 1)sufficient radiation to return the patient to euthyroidism, but not induce hypothyroidism.An alternative approach is to intend to 2) induce hypothyroidism, or euthyroidism and avoid any possible return of hyperthyroidism. Background–The dosage initially was worked out by a trial-and-error method and by successive approximations. By 1950, the standard dose was 160 uCi 131 I per gram of estimated thyroid weight. Of course, estimating the weight of the thyroid gland by examination of the neck is an inexact procedure, but can now be made more accurate by use of ultrasound. Also, marked variation in radiation sensitivity no doubt exists and cannot be estimated at all. It was gratifying that in practice this dosage scheme worked well enough.
In the early 1960s, it was recognized that a complication of RAI therapy was a high incidence of hypothyroidism. This reached 20 – 40% in the first year after therapy and increased about 2.5% per year, so that by 10 years 50 – 80% of patients had low function . In an effort to reduce the incidence of late hypothyroidism, Hagen and colleagues reduced the quantity of 131-I to 0.08 mCi per gram of estimated gland weight . No increase was reported in the number of patients requiring retreatment, and there was a substantial reduction in the incidence of hypothyroidism. Most of these patients were maintained on potassium iodide for several months after therapy, in order to ameliorate the thyrotoxicosis while the radioiodine had its effect [ 49, 50]. Patients previously treated with 131-I are sensitive to and generally easily controlled by KI. However KI often precipitates hypothyroidism in these patients, which may revert to hyperthyroidism when the KI is discontinued. Over the years some effort was made to refine the calculation. Account was taken of uptake, half-life of the radioisotope in the thyroid, concentration per gram, and so on, but it is evident that the result in a given instance depends on factors that cannot be estimated precisely [46, 47]. One factor must be the tendency of the thyroid to return to normal if a dose of radiation is given that is large enough to make the gland approach, for a time, a normal functional state.In many patients, “cure” is associated with partial or total thyroid ablation.
Although we, and many endocrinologists, attempt to scale the dose to the particular patient, some therapists believe it is futile, advocate giving up this attempt, and provide a standard dose giving up to 10000 rads to the thyroid(47.1). Leslie et al reported a comparison of fixed dose treatment and treatment adjusted for 24 hour RAIU, using low or high doses, and found no difference in outcome in either rate of control or induction of hypothyroidism on comparison of the methods. They favor the use of a fixed dose treatment with a single high or low dose (47.2). Many attempts have been made to improve the therapeutic program by giving the RAI in smaller doses. Reinwein et al . studied 334 patients several years after they had been treated with serial doses of less than 50 uCi 131-I per gram of estimated thyroid weight. One-third of these patients had increased levels of TSH, although they were clinically euthyroid. Only 3% were reported to be clinically hypothyroid.
Dosage adjustmentsmade to induce euthyroidism usually include a factor for gland size, a standard dose in microCuries per gram, and a correction to account for 131-I uptake .
A“Low Dose Protocol” was designed to compensate for the apparent radiosensitivity of small glands and resistance of larger glands . Using this approach, after one year, 10% of patients were hypothyroid, 60% are euthyroid, and 30% remained intrinsically toxic , although euthyroid by v