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Usually such patients are on what is presumed to be appropriate T4 replacement therapy. Tigas et al note that such weight gain is less common after ablative therapy for thyroid cancer, in which case larger doses of thyroxine are generally prescribed. Permanent replacement therapy regardless of the degree of thyroid destruction for children who receive I has a better theoretical basis. In these cases, it is advisable to prevent TSH stimulation of the thyroid and so mitigate any possible tendency toward carcinoma formation.

Exacerbation of thyrotoxicosis -During the period immediately after therapy, there may be a transient elevation of the T4 or T3 level [70], but usually the T4 level falls progressively toward normal. These patients may have cardiac problems such as worsening angina pectoris, congestive heart failure, or disturbances of rhythm such as atrial fibrillation or even ventricular tachycardia. Radiation-induced thyroid storm and even death have unfortunately been reported [ 73]. These untoward events argue for pretreatment of selected patients who have other serious illness, especially cardiac disease, with antithyroid drugs prior to I therapy.

The immediate side effects of I therapy are typically minimal. As noted above, transient exacerbation of thyrotoxicosis can occur, and apparent thyroid storm has been induced within a day or days after I therapy. A few patients develop mild pain and tenderness over the thyroid and, rarely, dysphagia.

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Some patients develop temporary hair loss , but this condition occurs two to three months after therapy rather than at two to three weeks, as occurs after ordinary radiation epilation. Hair loss also occurs after surgical therapy, so that it is a metabolic rather than a radiation effect. If the loss of hair is due to the change in metabolic status, it generally recovers in a few weeks or months. In this situation the prognosis for recovery is less certain, and occasionally some other therapy for the hair loss such as steroids is indicated.

Permanent hypoparathyroidism has been reported very rarely as a complication of RAI therapy for heart disease and thyrotoxicosis[ 76]. This is reported to cause no significant changes in FSH. Long term studies of patients after RAI treatment by Franklyn et al Coincident with this condition, exophthalmos may be worsened [79]. This change is most likely an immunologic reaction to discharged thyroid antigens. The relationship of radiation therapy to exacerbation of exophthalmos has beem questioned], but much recent data indicates that there is a definite correlation[ 79, 80, Many therapists consider "bad eyes" to be a relative contraindication to RAI.

Induction of hypothyroidism, with elevation of TSH, may contribute to worsening of ophthalmopathy. This offers support for early induction of T4 replacement Pretreatment with antithyroid drugs has been used empirically in an attempt to prevent this complication. Its benefit, if any, may be related to an immunosuppressive effect of PTU, described below. Treatment with methimazole before and for three months after I therapy has been shown to help prevent the treatment-induced rise in TSH-R antibodies which is otherwise seen[81]. Prophylaxis with prednisone after I helps prevent exacerbation of exophthalmos, and this approach is now the standard approach in patients who have significant exophthalmos at the time of treatment [82, Of course prednisone or other measures can be instituted at the time of any worsening of ophthalmopathy.

While treatment with prednisone helps prevent eye problems, it does not appear to reduce the effectiveness of RAI in controlling the hyperthyroidism Thyroidectomy , with total removal of the gland, should be considered for patients with serious active eye disease. Operative removal of the thyroid is followed by gradual diminution is TSH-R antibodies. Several studies document better outcomes of ophthalmopathy in patients with GD who have total thyroidectomy vs those treated by other means Failure of I to cure thyrotoxicosis occurs occasionally even after 2 or 3 treatments, and rarely 4 or 5 therapies are given.

The reason for this failure is usually not clear. The radiation effect may occur slowly.

A large store of hormone in a large gland may be one cause of a slow response. Occasional glands having an extremely rapid turnover of I requiring such high doses of the isotope that surgery is preferable to continued I therapy and its attendant whole body radiation. If a patient fails to respond to one or two doses of I, it is important to consider that rapid turnover may reduce the effective radiation dose.

Turnover can easily be estimated by measuring RAIU at 4, 12, 24, and 48 hours, or longer. The usual combined physical and biological half-time of I retention is about 6 days. This may be reduced to 1 or 2 days in some cases, especially in patients who have had prior therapy or subtotal thyroidectomy. If this rapid release of I is found, and I therapy is desired, the total dose given must be increased to compensate for rapid release. A rough guide to this increment is as follows:.

Most successfully treated glands return to a normal or cosmetically satisfactory size. Some large glands remain large, and in that sense may constitute a treatment failure. In such a situation secondary thyroidectomy could be done, but it is rarely required in practice. Long term care- Patients who have been treated with RAI should continue under the care of a physician who is interested in their thyroid problem for the remainder of their lives.

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The first follow-up visit should be made six to eight weeks after therapy. By this time, it will often be found that the patient has already experienced considerable improvement and has begun to gain weight. The frequency of subsequent visits will depend on the progress of the patient. Symptoms of hypothyroidism, if they develop, are usually not encountered until after two to four months, but one of the unfortunate facts of RAI therapy is that hypothyroidism may occur almost any time after the initial response.

This age limit was gradually lowered, and some clinics, after experience extending over nearly 40 years, have now abandoned most age limitation. The major fear has been concern for induction of neoplasia, as well as the possibility that I might induce undesirable mutations in the germ cells that would appear in later generations. Radiation is known to induce tumor formation in many kinds of tissues and to potentiate the carcinogenic properties of many chemical substances.

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Radiation therapy to the thymus or nasopharyngeal structures plays an etiologic role in thyroid carcinoma both in children and in adults[ 85]. Cancer of the thyroid has appeared more frequently in survivors of the atomic explosions at Hiroshima and Nagasaki than in control populations [87]. Thyroid nodules, some malignant, have appeared in the natives of Rongelap Island as the result of fallout after a nuclear test explosion in which the radiation cloud unexpectedly passed over the island [88].

The experience at 26 medical centers with thyroid carcinoma after I therapy was collected in a comprehensive study of the problem. A total of 34, patients treated in various ways were included. Beginning more than one year after I therapy, 19 malignant neoplasms were found; this result did not differ significantly from the frequency after subtotal thyroidectomy.

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Thyroid adenomas occurred with increased frequency in the I treated group, and the frequency was greatest when the patients were treated in the first two decades of life [39]. Holm et al [41] have thoroughly examined the history of a large cohort of I-treated patients in Sweden and similarly found no evidence for an increased incidence of thyroid carcinoma or other tumors.

This may be because the treatment has largely been given to adults with glands less sensitive to radiation, because damage from Itherapy is so severe that the irradiated cells are unable to undergo malignant transformations, or because all cells are destroyed, or possibly because of the slow rate at which the dose is delivered [89]. In up to one-half of patients followed for years, there may be no viable thyroid cells remaining.

We note that two studies reported above extend through an average follow-up period of 15 years. As described above [ However it remains uncertain that this is related to hyperthyroidism per se, or radioiodine therapy. While these data are reassuring in regard to I use in adults, Chernoby made it clear that its use in children can not be considered safe.

Children in the area surrounding Chernobyl have developed a hugely increased incidence of thyroid carcinoma predominately due to ingestion of iodine [ The latency has been about 5 years, and younger children are most affected. Risk is probably linearly related to dose. It is apparent that low doses, possibly down to 20 rads, produce malignant change in children Risk of carcinogenesis decreases with increasing age at exposure, and is much less common after age However some data indicates that an increased incidence of thyroid carcinoma is seen even among adults exposed at Chernobyl.

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This problem was also studied by the consortium of 26 hospitals [91]. The incidence of leukemia in this group was slightly lower than in a control group treated surgically, but slightly higher in the latter surgical group than in the general population. In the group of RAI-treated patients, there has been no evidence of genetic damage, although, as will shortly be seen, this problem cannot be disregarded. In the United States, about x 10 6 children will be born to a population of over x 10 6 persons.

Of these, about one-half will be genetically determined or ultimately mutational, and represent the effects of the baseline mutation rate in the human species.

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These mutations are attributed in part to naturally occurring radiation. All penetrating radiation, from whatever sources, produces mutations. The effects may vary with rate of application, age of the subject, and no doubt many other factors, and are partially cumulative. Almost all are minor changes, and those produced by experimental radiation are the same as those produced by natural radiation. Whether or not mutations are bad is in essence a philosophic question. Most of us would agree that the cumulative effect of mutations over past eras brought the human race to its present stage of development.

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However, most mutations, at least those that are observable, are detrimental to individual human adaptation to the present environment. In terms of the human population as a whole, detrimental mutant genes must be eliminated by the death of the carrier. We can agree that an increase in mutation rate is not desirable. It is hardly worth considering the pros and cons of the already considerable spontaneous mutation rate.

In mice, the occurrence of visible genetic mutations in any population group is probably doubled by acute exposure of each member of the group over many generations to about 30 - 40 rads, or by chronic exposure to - rads [92]. This radiation dosage is referred to as the doubling dose. Ten percent of this increase in mutations might be expressed in the first-generation offspring of radiated parents, the remainder gradually appearing over succeeding generations. The change in mutation rate in Drosophila is in proportion to the dosage in the range above 5 rads.

Data from studies of mice indicate that at low exposures from 0. Linearity, although surmised, has not been demonstrated at lower doses. Roughly half of this dose is from natural sources and half from medical and, to a lesser extent, industrial exposure. The National Research Council has recommended a maximum exposure rate for the general population of less than 10 rad above background before age The present level may therefore approach this limit.