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Impact of cervical lymph node dissection on serum TG and the course of disease in TG-positive, radioactive iodine whole body scan-negative recurrent/persistent papillary thyroid cancer.
In the management of papillary thyroid cancer (PTC), surgery is indicated for locoregional recurrent/persistent disease. In this study, we examined the effect of such surgery on serum TG and the course of the disease in 21 patients with PTC (mean age 38.5 yr), who after the initial surgery and radioactive iodine (RAI) ablation developed high TG (>10 ng/ml) and negative 123I whole body scan (DxWBS). All patients had neck persistent/recurrent PTC that was confirmed by ultrasound-guided fine needle aspiration. Prior to neck re-exploration, radiological studies (chest X-rays, CT scan of the chest, and fluoro-18-deoxyglucose positron emission tomography [FDG-PET]) showed no evidence of distant metastases. TG autoantibodies were negative in 19 patients. Second surgery consisted of unilateral (13 patients) or bilateral (8 patients) modified neck dissection. The mean+/-SE TG prior to neck re-exploration was 184.8+/-79.0 ng/ml and declined after surgery to 127.5+/-59.0 ng/ml (p=0.25). The corresponding TSH values were 150.6+/-23.0 and 143.4+/-20.0 mU/l, respectively (p=0.34). After a mean follow-up of 20.7+/-3 months, TG increased to 168+/-68.0 ng/ml. This increase, however, was NS (p=0.67). The corresponding TSH values were 143.4+/-20.0 and 132.0+/-22.0 mU/l (p=0.27). Following second surgery, only 4 patients achieved remission, the other 17 patients received one or more of the following therapies; RAI (10 patients), third surgery (5 patients), and/or external radiation (7 patients). Thirteen patients continued to have persistent disease and 4 patients showed progressive course of their disease (distant metastases or grossly palpable neck disease). In conclusion, second surgery for recurrent/persistent PTC leads to remission in only a minority of cases but the course of the disease tends to be stable in most cases.
Dosimetry-guided radioactive iodine treatment in patients with metastatic differentiated thyroid cancer: largest safe dose using a risk-adapted approach.
UNLABELLED: This study is a retrospective analysis of 124 differentiated thyroid cancer patients who underwent dosimetric evaluation using MIRD methodology over a period of 15 y. The objectives of the study were to demonstrate the clinical use of dosimetry-guided radioactive iodine ([RAI] (131)I) treatment and the safe and effective application of a 3-Gy bone marrow (BM) dose in patients with differentiated thyroid cancer. METHODS: Tumor and BM dose estimates were obtained. The administered activity that would deliver a maximum safe dose to the organ at risk (red BM or lungs) was determined as well as the resulting doses to the metastases. The clinical benefit of an individual RAI treatment was predicted on the basis of the dose estimates and the expected therapeutic response. Each patient's response to treatment was assessed clinically and by monitoring the hematologic profile. RESULTS: One hundred twenty-four patients underwent 187 dosimetric evaluations. One hundred four RAI treatments were performed. A complete response at metastatic deposits was attained with absorbed doses of >100 Gy. No permanent BM suppression was observed in patients who received absorbed doses of <3 Gy to BM. The maximum administered dose was 38.5 GBq (1,040 mCi) with the BM dose limitation. CONCLUSION: Dosimetry-guided RAI treatment allows administration of the maximum possible RAI dose to achieve the maximum therapeutic benefit. Estimation of tumor dose rates helps to determine the curative versus the palliative intent of the therapy.
[Management of hyperthyroidism with radioactive iodine in end-stage renal disease patients undergoing dialysis].
Although, the abnormal thyroid hormone production and metabolism are relatively common, hyperthyroidism is a very unusual condition. The diagnosis may be difficult because of similar signs and symptoms as in uremia. To our knowledge till now only 18 well documented cases have been reported, 8 of them successfully treated with radioactive iodine. We report here the results of radioiodine treatment, performed in 6 patients, 5 with toxic multinodular goiter and one with Graves' disease. Three patients were initially treated with antithyroid drugs, but they were discontinued 20 days before radioiodine treatment. A progressive fall of the thyroid function tests was observed. Of 6 treated patients 3 became euthyroid and 3 developed hypothyroidism.
Non-suppressed thyroidal radioactive iodine uptake (RAIU) in thyrotoxic phase in a case of subacute thyroiditis with thyroid-stimulating antibodies (TSAb).
In this paper, we report a 49-year-old female with subacute thyroiditis who had thyroid-stimulating antibodies (TSAb) and thyroid-stimulation-blocking antibodies (TSBAb) in serum. Although she was in the thyrotoxic phase and TSH was suppressed in May, 1990, her radioactive iodine uptake (RAIU) was not suppressed (35.5%) and a thyroid scan disclosed a diffuse goiter with no defect. Serum assays revealed the presence of TSAb, but TSBAb were negative. In August, 1990, the right lobe became undetectable by thyroid scan when the RAIU was 20.7% with the TSH level remaining suppressed. At that time, TSAb were negative, while TSBAb were positive. When the RAIU was 31.1% in October, 1990, both thyroid lobes became visible and the TSH level was normalized. TSBAb became negative, and although TSAb reappeared it later became undetectable. These results indicate that the changes in the patient's thyroid scan and RAIU were attributable to the presence of TSAb.
Plasma levels of radioactive iodine (I131) in human tracer studies.
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[USE OF MINIMUM DOSES OF RADIOACTIVE IODINE I-131 FOR HISTOAUTORADIOGRAPHIC EXAMINATION OF NODULES AND EXTRANODULAR THYROID TISSUE IN ENDEMIC GOITER].
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[The effect of thiourea and thiouracil on radioactive iodine in the thyroid of two marine teleosts].
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Ki-ras mutational analysis in rat follicular-cell proliferative lesions of the thyroid gland induced by radioactive iodine and potassium perchlorate.
Although in both human and experimental pathology ras mutations have been related to the origin and progression of follicular-cell tumours, reports differ considerably with respect to the frequency of such mutations. The present paper reports, using direct sequencing, the incidence of Ki-ras mutations (codons 12 and 13) in follicular-cell carcinomas of the thyroid gland in Wistar rats induced by administration of radioactive iodine and potassium perchlorate. Direct sequencing revealed no mutations in the amplified gene segment of any of the 72 carcinoma samples studied. This absence of mutations agrees with some and is in sharp contrast with other previous reports in the literature, both for experimental animals and in studies of human thyroid follicular-cell carcinoma. Our results suggest that Ki-ras activation via mutations at codons 12 and 13 is neither a constant event nor an early event in the development of rat thyroid follicular-cell carcinoma.
Clinical outcome of patients with papillary thyroid carcinoma who have recurrence after initial radioactive iodine therapy.
BACKGROUND: Among patients with well differentiated papillary thyroid carcinoma who generally have an excellent prognosis and a near-normal lifespan, there exist subsets of patients who have significant risk for morbidity and mortality from this disease. It is important to define the patterns of disease progression and the clinical outcome of such patients to develop effective surveillance and treatment strategies. Patients with recurrence after surgery and therapeutic administration of radioactive iodine (RAI) for papillary thyroid carcinoma represent one such subset of high-risk patients. METHODS: At the University of Texas M. D. Anderson Cancer Center, 65 patients with papillary thyroid carcinoma were diagnosed between 1970 and 1990. Their medical records were reviewed with particular attention to disease recurrence and outcome as well as RAI imaging and treatment. RESULTS: Following diagnosis and initial therapy, 19 patients died from thyroid carcinoma after a median of 64 months; 34 had no evidence of disease for a median of 112 months of available follow-up; and 7 are alive with disease 61 to 153 months after diagnosis. Cervical lymph node metastases were present in 41 patients and extrathyroidal or extranodal tumor invasion was seen in 25 patients at the time of initial surgery; distant metastases (lung, bone, brain, liver, and adrenal) developed later in 18 patients. RAI uptake by recurrent tumor deposits in the neck was seen most frequently in patients with no direct invasion of adjacent tissues but with recurrence limited to cervical lymphadenopathy; this group of patients was the most likely to become clinically and radiologically disease free. RAI generally did not concertrate in invasive cancers with extrathyroidal or extranodal extension in the neck; patients with this type of invasive carcinoma were also more likely to die from the disease. CONCLUSIONS: We suggest that among patients with recurrent papillary thyroid carcinoma, invasive cancers are less likely to concertrate RAI, whereas patients with disease confined to lymph nodes are more likely to have RAI-avid tumors and to benefit from RAI therapy.
[RADIOACTIVE IODINE I-131 IN THE TREATMENT OF THYROTOXICOSIS (6-YEAR STUDY)].
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[ON IN VIVO MEASUREMENT OF RADIOACTIVE IODINE I-131 IN THE HUMAN THYROID GLAND].
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Serum troponin I levels in hyperthyroid cats before and after treatment with radioactive iodine.
A raised concentration of serum cardiac troponin I (cTnI) is a sensitive marker of cardiac myocyte injury in the cat and assays developed for its measurement in human patients have been validated in the cat. Raised levels have been associated with a number of cardiac insults including hypertrophic cardiomyopathy and trauma. Hyperthyroidism is a common disease of older cats and excess thyroid hormone is known to produce significant cardiovascular effects in this species. This study evaluated the effect of treatment for hyperthyroidism with radioactive iodine on cTnI concentration, assessed the association between thyroxin levels and glomerular filtration rate (GFR) and cTnI concentration in cats treated for hyperthyroidism and described changes in echocardiographic parameters following treatment. Prior to the treatment serum cTnI was measured and echocardiography performed, thyroxin, cTnI, and echocardiography were then repeated at various time points following radioisotope therapy. The results show that higher thyroxin levels were significantly (P=0.002) associated with a higher likelihood of the cat presenting with detectable levels of cTnI. No significant association was found between GFR and presence of detectable levels of cTnI. Furthermore the results indicate that the effects of hyperthyroidism on echocardiographic parameters appear considerably less in this study than in previous studies and that the main outcome of treatment on these parameters is a significant reduction in fractional shortening (P=0.006). These results suggest that chronic exposure to excess thyroid hormone may induce myocyte damage of sufficient severity to raise serum cTnI concentration in a proportion of cats that resolves following establishment of a euthyroid state.
Pattern of recovery of the hypothalamic-pituitary-thyroid axis following radioactive iodine therapy in patients with Graves' disease.
PURPOSE: To characterize the time course of recovery of the hypothalamic-pituitary-thyroid (HPT) axis by determining the frequency, onset, duration, and clinical attributes of the central hypothyroid phase following 131I therapy for Graves' disease and to examine whether the central hypothyroid phase is due to direct pituitary thyrotroph suppression or to hypothalamic thyrotropin-releasing hormone (TRH) deficiency. PATIENTS AND METHODS: Twenty-one hyperthyroid patients with Graves' disease evaluated at a university endocrine clinic and treated with radioactive iodine were prospectively studied. Serial thyroid function levels (serum thyroxine [T4], free thyroxine [free T4], triiodothyronine [T3], and thyroid-stimulating hormone [TSH]) were measured and TRH stimulation tests were performed at 2 to 4 week intervals for all subjects following 131I treatment. None of the patients was treated with thionamides after receiving 131I therapy. RESULTS: Nineteen (90%) of the patients with Graves' disease experienced a transient central hypothyroid phase defined as the presence of a suppressed or inappropriately normal TSH level despite a low free T4 level following 131I treatment. This phase occurred a mean of 62.8 +/- 5.1 days following 131I treatment, persisted for an average of 24.7 +/- 2.4 days, and was not predictive of eventual treatment outcome. All patients had concordantly low T4 and T3 levels during this period and exhibited a blunted TSH response to TRH compared to 29 euthyroid control subjects, suggesting primary feedback suppression at the level of the pituitary thyrotrophs. The suppressed thyrotrophs required a minimum of 2 weeks to recover once patients became hypothyroid. The length of preexisting hyperthyroidism, basal free T4 elevation, and administered dose of 131I failed to predict the duration of the central hypothyroid phase, although a higher dose of 131I was associated with an earlier onset of central hypothyroidism (r = -.51, P < 0.05). CONCLUSIONS: Clinicians should be aware of the delay in the recovery of the HPT axis that occurs in the majority of patients with Graves' disease treated with 131I and is manifested by a transient central hypothyroid phase. The blunted TSH response to TRH stimulation during this period suggests that suppression occurs primarily at the level of the pituitary thyrotrophs. The use of sensitive TSH measurements alone to monitor these patients during this period is not helpful and may be misleading.
Effect of radioactive iodine therapy on cytokine production in Graves' disease: transient increases in interleukin-4 (IL-4), IL-6, IL-10, and tumor necrosis factor-alpha, with longer term increases in interferon-gamma production.
Spontaneous and mitogen-stimulated production of interleukin-4 (IL-4), IL-6, IL-10, IL-12, interferon-gamma (IFNgamma), and tumor necrosis factor-alpha were evaluated by enzyme-linked immunospot assay of peripheral blood mononuclear cells from patients with Graves' disease immediately before and at 4, 17, and 59 days after treatment with radioactive iodine. Patients had significantly reduced IL-4 and IFNgamma production before treatment compared with healthy controls. Both cytokines were increased to normal levels by day 17 after treatment, and IFNgamma remained at normal levels on day 59, whereas IL-4 returned to subnormal levels at this time. IL-12 production was initially normal and was not significantly altered by therapy. IL-6, IL-10, and tumor necrosis factor-alpha were also normal before radiotherapy, but increased significantly on day 17, returning to pretreatment levels by day 59. Thus, radioiodine treatment induced a transient increase in both proinflammatory and antiinflammatory cytokines and a more prolonged increase in IFNgamma production, the latter representing a definite shift toward a type 1 cytokine profile.
Effect of destruction of thyroid glands by radioactive iodine on pancreatic diabetes in the dog.
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[BLOOD CHANGES IN PATIENTS WITH THYROTOXICOSIS DURING RADIOACTIVE IODINE TREATMENT ACCORDING TO DATA OF MORPHOLOGICAL AND MICROFLUORESCENT RESEARCH].
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Radioactive iodine exchange reaction of HIPDM: kinetics and mechanism.
In conjunction with single photon emission computed tomography (SPECT), iodine-123 (123I)-labeled N,N,N'-trimethyl-[2-hydroxy-3-methyl-5-iodobenzyl]-1,3-propanediamine (HIPDM) has been used clinically as a regional cerebral perfusion imaging agent. The [123I]HIPDM can be prepared by a simple aqueous exchange reaction in a kit form. We synthesized unlabeled HIPDM by condensation of 2-hydroxy-3-methyl-5-iodobezaldehyde and N,N,N'-trimethyl-1,3-propanediamine, followed by a sodium borohydride reduction reaction. The kinetics of the radioactive iodine exchange reaction for the preparation of [123I]HIDM is controlled by the pH, the temperature, and the presence of reductant (sodium bisulfite), and oxidant (sodium iodate). The reaction is a second order iodine-iodine exchange with an activation energy of 30.6 kcal/mole. The mechanism of this reaction probably involves the formation of an active 1+ or iodine free radical, which is sensitive to the presence of a reductant, such as sodium bisulfite.