Treatment of multiple myeloma with radioactive iodine and radioactive iodinated serum albumin.
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Radioactive iodine (131I) is an important therapeutic option for the treatment of metastatic thyroid carcinoma. Survival in patients with metastases that concentrate radioiodine is better than those whose metastatic lesions do not take up radioiodine. Survival is markedly reduced in patients who have metastatic lesions that concentrate 18F-fluorodeoxyglucose (FDG) on positron emission tomography (PET). In this retrospective study, we evaluated the ability of 131I to destroy FDG-avid metastatic lesions in thyroid cancer patients. Twenty-five patients with positive FDG-PET scans received at least one dose of 131I treatment before a second FDG-PET was performed. The average interval between the two PET scans was 12.9 months. The average interval between the 131I treatment and the follow-up FDG-PET was 10.1 months. We measured posttherapy changes in lesional volume, in standard uptake values (SUV) of FDG, and in serum thyroglobulin (Tg) levels. The total volume of FDG-avid metastases rose significantly (p = 0.036) from a mean of 159 mL to 235 mL after 131I therapy, the maximum SUV rose from 9.3 to 11.9, the median Tg at the time of the second PET scan was 132% of that at baseline. Statistical analyses demonstrated no significant changes in maximum SUV, or serum Tg levels after 131I in the FDG-PET-positive group. In a control group of FDG-PET-negative patients, the serum Tg decreased to 38% of baseline after 131I therapy (p < 0.001). We conclude that high-dose 131I therapy appears to have little or no effect on the viability of metastatic FDG-avid thyroid cancer lesions.
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Radioactive iodine is used extensively for the treatment of thyrotoxicosis and thyroid carcinoma. Iodine is actively taken up by the salivary glands and, following its use, salivary dysfunction may result as a consequence of radiation damage. The literature is reviewed and a case is reported in which a patient presented with a significant increase in caries rate attributed to salivary dysfunction following radioactive iodine therapy for a thyroid carcinoma.
Although literature has offered methods to predict 24-hour radioactive iodine uptake values from early (4- to 6-hour) measurements, the resultant dosage errors have not been examined. Potential errors include underdosage, overdosage, and a failure to recognize rapid turnover patients (early-to-late uptake ratios > or = 1) who are at high risk for treatment failure and full-body radiation exposure. We developed and tested a novel method for minimizing error involved in using a single early uptake measurement to derive late uptake. From a retrospective analysis of 203 Graves' disease patients, receiver operating characteristic (ROC) curve analysis enabled us to identify patients likely to experience rapid turnover and therefore should receive 24-hour studies. Twenty-four-hour uptake measurements are necessary with 77% or more 4-hour uptake values and 80% or more 6-hour values. After eliminating these patients, we developed linear regression equations to predict the 24-hour uptake from 4-hour (n = 61) and 6-hour (n = 22) rule groups, testing their efficacy on separate 4-hour (n = 61) and 6-hour (n = 21) patient groups. We also used our test population to measure error in four early-to-late uptake conversion formulas presented in the literature. Error involved in these predictions ranged from a 10.6% overestimate for 4-hour calculations to a 5.9% underestimate for 6-hour calculations. When applied to two dosage formulas incorporating gland size, absorbed dose, and 24-hour uptake, average dosage error was 7%. In comparison to the other sources of error radioactive iodine (131I) dosimetry, potential error in predicting 24-hour uptake from 4- or 6-hour uptake values is low.
Uptake and loss of radioactive iodine by marine organisms were studied in the artificial seawater in which the concentration as well as chemical forms of both stable and radioactive iodine were controlled. The concentration factors of radioactive iodine by these organisms were clearly dependent upon the concentration of stable iodide ion in the culture media while the concentration of stable iodate ion did not affect the uptake and loss of radioactive iodine. It was observed that the higher the concentration of iodide ion was in the culture media the shorter the biological half-life of radioactive iodine became, and thus the lower the concentration factor resulted in.
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Ingestion of potassium iodide (KI) offers effective protection against irradiation of the thyroid after accidental exposure to radioactive iodine. This prophylaxis aims at rapidly obtaining maximal thyroid protection without adverse effects. This article reviews studies on iodine kinetics in humans and on the efficacy of KI in protecting the thyroid. In adults with normal thyroid function, ingestion of 100 mg of iodide just before exposure to radioactive iodine blocks at least 95% of the thyroid dose. If exposure persists after iodide ingestion (100 mg), the percentage of averted dose may decrease significantly. Daily ingestion of a dose of 15 mg of KI would then maintain the thyroid blockade at a level above 90%. The efficacy of iodide and the occurrence of antithyroid effects also depend on external and individual factors such as dietary iodine intake, thyroid function, and age. The KI dosage regimen should be adjusted for age at exposure. For the fetus, the newborn, children, and adolescents, the risk of radiation-induced thyroid cancer in case of accidental exposure to radioactive iodine justifies KI prophylaxis, despite the risk of hypothyroidism, especially in newborns. For the elderly, the benefits of KI may be lower than the risk of iodine-induced hyperthyroidism.
Older reports have suggested that the use of antithyroid drugs with radioactive iodine-131 (RAI) results in higher rates of persistent hyperthyroidism than treatment with RAI alone. Our objective was to determine if propylthiouracil (PTU) given prior to RAI would be associated with a higher single dose RAI failure rate than treatment with RAI alone. Patients were considered treatment failures if a second dose of RAI was required to produce euthyroidism or hypothyroidism. All study patients stopped PTU at least 4 days before RAI therapy and did not receive PTU after RAI. The overall failure rate of one course of treatment in the 86 study patients was 17% (15/86). Persistent hyperthyroidism was seen in 4% of patients (2/48) treated with only RAI and in 34% of patients (13/38) receiving RAI after pretreatment with PTU (p = 0.003). Patients were treated with PTU for a mean of 151 +/- 32 days. There were no significant differences in race, gender, thyroid size, RAI dose, or days of follow-up between patients receiving RAI alone and those receiving PTU before RAI therapy. These data suggest that pretreatment with PTU leads to a higher failure rate even if PTU is discontinued at least 4 days before RAI therapy and not restarted after RAI dosing. Consideration should be given to increasing the dose of RAI in patients pretreated with PTU to ensure adequate treatment of Graves' disease.
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