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Pharmaceutical-technological and physico-chemical examinations have been performed of the model for development of procedure for production of potassium-iodine preparations for peroral use in the forms of solutions, capsules and tablets for protection of the thyroid in radioactive iodine (I131) contamination.
This study investigated 1) the relationship between thyroid volume and thyroid function in radioactive iodine (RAI) treatment for Graves' disease, and 2) the activity of thyroid-related Ig in serum on the responsiveness of thyroid tissue to RAI. The changes in thyroid volume per megabecquerel (MBq) of 131I retained in thyroid tissue was calculated by ultrasonography as a quantitative indicator of the effect of RAI on thyroid volume. Of the 52 patients treated with 131I (3.7 MBq retained/g thyroid tissue), 26 patients showed thyrotoxicosis, 20 patients became euthyroid, and 6 patients developed hypothyroidism 6 months after therapy. The change in thyroid volume per MBq 131I was lower (P < 0.01) in the hyperthyroid patients than in the euthyroid or hypothyroid patients. The activity of thyroid-stimulating antibody in serum immediately before the therapy was greater (P < 0.01) in the hyperthyroid patients than in the euthyroid patients and was greater (P < 0.05) in the euthyroid patients than in the hypothyroid patients; it was inversely correlated with the changes in thyroid volume per MBq 131I (r = -0.667; P < 0.01). Accurate measurement of changes in thyroid volume during the course of RAI treatment provides evidence of the responsiveness of Graves' disease thyroid tissue to RAI, which is related to the outcome of thyroid function. Thyroid-stimulating antibody determination may be useful in deciding the appropriate dose of RAI to obtain euthyroidism instead of hyperthyroidism.
A 7.5-yr-old boy with Graves' disease, difficult to control with antithyroid medication and radioactive iodine (RAI) therapy, developed thyroid storm encephalopathy on day 13 after withdrawal of methimazole therapy, 4 days after iodine-131 treatment. We attributed his thyroid storm to withdrawal of antithyroid medication as opposed to RAI therapy. We interpret this case as indicating that there may be a need to reevaluate the duration of antithyroid medication withdrawal before RAI therapy for hyperthyroid children at increased risk for thyroid storm.
OBJECTIVES: To assess the prognostic factors and the role of radioactive iodine (RAI) and external beam radiotherapy (RT) in patients with differentiated thyroid cancer. DESIGN: A retrospective review of 729 patients treated between 1958 and 1998. The median follow-up was 11.3 years (range 0.3-39.8 years). Primary outcomes included time to cause-specific survival and time to local-regional relapse. Baseline and treatment variables were assessed for statistical significance using the Cox proportional hazards model. RESULTS: The 10-year cause-specific survival (CSS) was 87.3% and the 10-year local-regional relapse-free rate (LRFR) was 84.9%. In multivariate analysis there was no statistically significant improvement in CSS with more aggressive treatment (i.e. more extensive surgery, the administration of RAI and/or RT). By multivariate analysis the use of RAI resulted in a statistically significant improvement in LRFR (hazard ratio 0.5; 95% confidence interval 0.3-0.8; P = 0.007). In low-risk patients at AJCC stage I < or = 45 years, there was no apparent benefit from RAI. For patients over 60, with extrathyroid extension but no gross residual disease (n = 70), adjuvant external RT resulted in statistically significantly higher CSS (10-year CSS 81.0%vs. 64.6%, P = 0.04) and LRFR (10-year LRFR 86.4%vs. 65.7%, P = 0.01). CONCLUSIONS: The use of RAI was associated with improved LRFR but not in low-risk patients. External beam RT improved LRFR and CSS in high-risk patients.
Two patients with persistent lymphocytic thyroiditis and thyrotoxicosis were studied. Both patients presented with severe hyperthyroidism of nine months' duration and had nontender, small thyroid glands. Uptake of radioactive iodine (131I) was consistently low. Serum thyroxine and triiodothyronine levels remained elevated without remission until thyroidectomy. The serum thyroglobulin level was normal, but testing for microsomal antibody gave weakly positive results in one case. Thyroglobulin and thyroid stimulatory antibodies were not found. The ratio of helper to suppressor T cells was elevated in one case. Neither patient showed response to propranolol, prednisone, or iodine. Light microscopic and immunohistologic studies showed severe lymphocytic thyroiditis with formation of secondary lymphoid follicles. Lymphocytes were predominately T cells (OKT11-positive), primarily helper/inducer T cells (OKT4-positive). Hyperplastic nodules contained high immunoreactive thyroglobulin and thyroxine levels. Aberrant thymus was seen within the thyroid. These studies suggest the possibility of intrathyroidal stimulation and hydrolysis of thyroglobulin within thyroid cells and also support the hypothesis that T and B cell immunoregulatory defects are important in the pathogenesis of this disease.
Testicular damage was evaluated in twelve men by determination of sperm counts, serum FSH, LH, and testosterone up to 3 1/2 years after treatment with radioactive iodine (131I) therapy for thyroid cancer. Dose-dependent spermatogenic damage with elevation of serum FSH was evident. Full recovery in one and partial recovery in another patient was documented during 2 1/2 years of follow-up. Serial study in two patients documented a small but significant effect of 50 mCi 131I on serum FSH levels and clinically important effects appear to be restricted to men having multiple doses totalling over 100 mCi.
Seven cats with thyroid carcinomas that had previously undergone surgical removal of neoplastic tissue were treated with 30 mCi of radioactive iodine (131I). Six of the cats had clinical signs of hyperthyroidism; 1 did not. There were no complications associated with 131I treatment, and clinical signs resolved in all cats. Technetium scans of 4 cats made after treatment did not have evidence of isotope uptake. In the remaining 3 cats, small areas of isotope uptake, the intensity of which was equal to or less than the intensity of uptake in the salivary glands, were seen. All 7 cats became hypothyroid after treatment; 4 required L-thyroxine supplementation. One cat was alive 33 months after treatment. The other 6 cats were euthanatized because of unrelated diseases 10 to 41 months after treatment.
Recombinant human TSH (rhTSH), usually given as 0.9-mg doses im on 2 successive days, increases serum thyroglobulin (Tg) and radioactive iodine uptake (RAIU) in residual thyroid tissue in patients with thyroid cancer. We previously reported that a single, relatively low dose of rhTSH (0.1 mg im) is a potent stimulator of T(4), T(3), and Tg secretion in normal subjects. The present study describes the effects of higher doses of rhTSH on thyroid hormone and Tg secretion. Six normal subjects for each dose group, having no evidence of thyroid disease, received either 0.3 or 0.9 mg rhTSH by im injection. Serum TSH, T(4), T(3), and Tg concentrations were measured at 2, 4, and 8 h and 1, 2, 3, 4, and 7 days after rhTSH administration. The peak serum TSH concentrations were 82 +/- 18 and 277 +/- 89 mU/L, respectively, for the 0.3- and 0.9-mg doses of rhTSH. Serum T(4), T(3), and Tg concentrations increased significantly in subjects receiving 0.3 and 0.9 mg rhTSH, with significant increases in T(4) and T(3) being observed before significant increases in serum TG: Peak concentrations of serum T(4), T(3), and Tg, after 0.3 mg rhTSH administration, were 100 +/- 19, 131 +/- 14, and 1035 +/- 724% above individual baselines, respectively. Similarly, peak concentrations of serum T(4), T(3), and Tg, after 0.9 mg rhTSH administration, were 102 +/- 16, 134 +/- 7, and 1890 +/- 768% above individual baselines, respectively. These data, compared with previously reported data for the responses to 0.1 mg rhTSH, indicated that 0.1, 0.3, and 0.9 mg rhTSH had similar quantitative stimulatory effects on thyroid hormone and Tg secretion, except that the T(4) response was greater in groups receiving 0.3 and 0.9 mg rhTSH than in the group receiving 0.1 mg rhTSH. We also studied the effect of rhTSH on the thyroid RAIU in the group that received 0.9 mg rhTSH. The 6- and 24-h RAIU values were significantly higher after rhTSH (pre-rhTSH, 6-h value = 12.5 +/- 1.8%; 24 h value = 23 +/- 2.7%; post-rhTSH, 6 h value = 27 +/- 4.8%; 24-h value = 41 +/- 4.2%). The stimulating effects of 0.9 mg rhTSH on the 6- and 24-h RAIUs were similar. rhTSH is a potent stimulator of T(4), T(3), and Tg secretion and the RAIU in normal subjects. Single doses greater than 0.1--0.3 mg do not seem to further enhance thyroid hormone or Tg secretion.
A Down's syndrome patient was hospitalized for evaluation of vomiting, abdominal pain, and a history of weight loss. A subsequent workup revealed that she had hyperthyroidism. The treatment of choice was radioactive iodine therapy. The patient had a history of consistent nausea and incontinence for urine and feces. Special problems posed by the patient and radiation safety are discussed.
During a three and a half year period, 367 patients were referred from various areas of Sierra Leone for further evaluation of thyroid function. Thyroid hormone assays with commercial kits and radioactive iodine (131I) uptake confirmed the diagnosis of thyrotoxicosis in 17 patients. Thus, the relative rarity of thyrotoxicosis in black Africans, previously described by several authors, was demonstrated also in this study. Eleven of the 17 patients were treated with 131I and 10 of them are alive, well and euthyroid five to eight years after the initial dose of 131I. The only death occurred in a patient who was also suffering from disseminated thyroid carcinoma. Therapy for thyrotoxicosis in developing African countries appears limited to surgery and antithyroid drugs at present. However, this report indicates that radioiodine is probably the most suitable and effective form of treatment for thyrotoxicosis in developing countries in Africa.
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BACKGROUND: The aim of this study was to analyze the value of continuous leakage monitoring with radioactive iodine-131-labeled human serum albumin (RISA) in patients treated with hyperthermic isolated limb perfusion with tumor necrosis factor-alpha (TNF alpha) and melphalan. METHODS: Forty-eight patients with melanoma (n = 14) or soft tissue sarcoma (n = 34) of an extremity underwent 51 perfusions. Perfusion was performed at the iliac level in 22 cases, at the popliteal level in 16 cases, at the femoral level in 7 cases, and at the axillary level in 6 cases. Leakage rates and perfusion circuit and systemic levels of TNF alpha, interleukin-6, and C-reactive protein were determined, as were systemic hematological and metabolic profiles and tumor response. RESULTS: The mean isotopically measured leakage was 2.9%. Systemic leakage was < or = 2% in 28 perfusions and >2% in 23 perfusions. The correlation between the maximal monitored leakage and maximal systemic TNF alpha levels was.7114. The area under the curve for TNF alpha in the perfusion circuit, indicating the exposure of the perfused limb to TNF alpha, was 18.7% lower in the >2% leakage group. No significant differences in tumor response were found between groups. The area under the curve for systemic TNF alpha, indicating the exposure of the patient to TNF alpha, was 18.1 times higher in the >2% leakage group, resulting in a significant decrease in leukocyte and platelet count, hyperbilirubinemia, hypocholesterolemia, and proteinemia. No beneficial effect of the systemically leaked TNF and melphalan was seen on the occurrence of distant metastasis during follow-up. There was a significant difference between perfusions performed at the iliac and femoral levels compared with leakage values at the popliteal level. CONCLUSIONS: A good correlation between RISA leakage measurement and TNF alpha exposure during and after hyperthermic isolated limb perfusion with TNF alpha and melphalan was demonstrated. RISA leakage measurement serves as a good guide for the effectiveness of isolation during perfusion. If leakage exceeds the 2% limit during perfusion, less exposure of the tumor-bearing limb to TNF alpha, increased exposure of the patient systemic circulation to TNF alpha, and more systemic side effects can be expected.
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We have examined the combined usefulness of TSH-receptor antibody detection and HLA status on the therapeutic response to standard doses of radioactive iodine (RAI) in forty-three hyperthyroid Graves' patients. Twenty-three patients had detectable TSH-receptor antibodies as measured by 125I-TSH binding-inhibition (TBI) prior to administration of 7 mCi RAI. Eighteen (78%) of these patients were rendered euthyroid within 3 months. In contrast, twenty patients were TBI negative prior to RAI and sixteen (80%) of these individuals remained hyperthyroid at 3 months and required two, or more, doses of RAI to control their thyroid function. DR3 status alone was not strongly associated with resistance to RAI. However, of sixteen patients without detectable TBI activity and who required two or more doses of RAI, ten patients were DR3 positive (62%) compared with 25% in a control population. Only one patient who was both TBI and DR3 negative required more than one dose of RAI. These data indicate that TBI may be an accurate predictor of the therapeutic response to RAI in patients with hyperthyroid Graves' disease. Investigation of HLA status alone was of limited value, although it appeared that the combination of TBI and DR3 may be of additional help in developing an overall strategy for the treatment of hyperthyroid Graves' disease.
Exposure to ionizing radiation causes radiolysis of water in tissues leading to generation of reactive oxygen species (ROS), which are known to affect the antioxidant defense systems and induce lipid peroxidation (LP). Use of radioactive iodine (131I) for diagnosis and therapy of thyroid disorders may also generate ROS in the thyroid. Early (24 and 48 hours) and late (18 days) effects of subablation doses of 131I (370/555/1110 kBq) on the antioxidant defense and LP in the thyroid tissues have been studied. LP was elevated in all 131I treated groups by 10% to 41%. Although there was no change in catalase (CAT), the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities showed evidence of change from 48 hours onwards--SOD decreased by 32% to 56% and GPx increased by 15% to 43%. Nonprotein thiols (reduced glutathione, GSH) showed an elevation of 16% at 24 hours, but later declined by 15% by day 18 after 370 KBq of 131I. Thus, the increase in LP observed may be due to beta irradiation induced ROS by 131I. The parallel decrease in SOD could be due to inactivation by ROS. The increase in GPx may be a consequence of induction due to elevated LP and/or ROS, which may be inadequate to lower the LP. In spite of elevated LP, the thyroid function appears to be normal.
CONTEXT: Hashimoto's thyroiditis is an autoimmune disease that can produce marked clinical symptoms when patients have large diffuse goiters. DESIGN: This retrospective cohort study was designed to evaluate whether radioactive iodine (RAI) is effective for Hashimoto's thyroiditis with a large goiter. Starting in November 1999, 13 Hashimoto's patients with large goiters, whose thyroiditis was refractory to TSH suppression therapy with thyroid hormone administration [two men and 11 women with a mean age of 61.2 +/- 8.9 yr (50-79 yr)], were recruited for the present study. The duration of symptomatic goiter before undergoing RAI was 12.0 +/- 7.9 yr (4-33 yr). Thirteen millicuries of 131I was administered two to six times, at an interval of 1-6 months on an outpatient basis. Thyroid weight was measured ultrasonographically, or by computed tomography if ultrasound was not possible due to the large size of the goiter. RESULTS: RAI was administered an average of 4.7 +/- 1.4 times (two to six times), with a total dose of 59.8 +/- 17.3 mCi (25.0-78.0 mCi). The observation period was 47.9 +/- 13.4 months (26-66 months) after the first RAI. The average weight of the thyroid gland was 125.3 +/- 57.7 g (42.9-269.4 g) before the first RAI, decreasing significantly to 49.7 +/- 25.8 g (18.3-93.3 g) after the last RAI (P < 0.001, paired Student's t test). The percent reduction from baseline was 58.7 +/- 14.2% (35.7-84.0%). None of the patients showed an increase in goiter size or complained of a pressure sensation after any of the RAI treatments. CONCLUSION: RAI is effective in Hashimoto's thyroiditis with a large goiter.
A patient with previously diagnosed Graves' hyperthyroidism had a transient episode of thyrotoxicosis three months postpartum. This was associated with a diffusely enlarged thyroid gland, a rise in antithyroid microsomal antibody titer, a 24-hour radioactive iodine uptake (RAIU) of 1%, and an aspiration biopsy specimen suggestive of chronic lymphocytic thyroiditis. An alternative cause for the depressed RAIU was not discovered. This case would suggest that patients with previously diagnosed Graves' disease can have thyrotoxicosis without an enhanced RAIU and that the postpartum thyrotoxic syndrome may involve an immunologic injury causing a release of performed thyroid hormone.