Evidence-based management of toxic multinodular goiter (Plummer's Disease).
ABSTRACT Toxic multinodular goiter (Plummer's disease) has posed challenges to surgeons, endocrinologists, and radiation oncologists since its description in 1913. A literature review with evidenced-based methodology has not yet been reported.
A systematic review of the English literature from 1950 to 2007 and report of Mayo Clinic experience since 1950 was undertaken to establish evidence-based recommendations for management.
Surgery and radioactive iodine (RI) are both supported by level IV evidence in the treatment of solitary toxic nodules and toxic multinodular goiter, and treatment is determined by symptoms and co-morbidities. No evidence suggests a difference in treatment outcome based on pretreatment clinical or subclinical hyperthyroidism. Level IV evidence supports thyroidectomy over RI for large goiters. When compressive symptoms are present, level IV evidence supports thyroidectomy for maximal symptom relief in patients at moderate risk. Occult malignancies are found in 2-3% of thyroidectomy specimens for Plummer's disease. Despite technical reports of RI dose considerations, there are no prospective studies validating a dose formula. Ethanol ablation of toxic nodules in patients unfit for surgery is supported by level III evidence. Level V data suggest a cost benefit favoring surgery.
Treatment of Plummer's disease with antithyroid medications, ethanol ablation, RI ablation, or surgery must balance the goals of therapy, durability of cure, relief of symptoms, risk of malignancy, and risk of complications. Between 1950 and 2006, 948 (70%) of 1,356 patients with Plummer's disease have been treated surgically at Mayo Clinic.
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ABSTRACT: Since first discovered just 35 years ago, the incidence of spontaneous feline hyperthyroidism has increased dramatically to the extent that it is now one of the most common disorders seen in middle-aged to senior domestic cats. Hyperthyroid cat goiters contain single or multiple autonomously (i.e. TSH-independent) functioning and growing thyroid nodules. Thus, hyperthyroidism in cats is clinically and histologically similar to toxic nodular goiter in humans. The disease in cats is mechanistically different from Graves' disease, because neither the hyperfunction nor growth of these nodules depends on extrathyroidal circulating stimulators. The basic lesion appears to be an excessive intrinsic growth capacity of some thyroid cells, but iodine deficiency, other nutritional goitrogens, or environmental disruptors may play a role in the disease pathogenesis. Clinical features of feline toxic nodular goiter include one or more palpable thyroid nodules, together with signs of hyperthyroidism (e.g. weight loss despite an increased appetite). Diagnosis of feline hyperthyroidism is confirmed by finding the increased serum concentrations of thyroxine and triiodothyronine, undetectable serum TSH concentrations, or increased thyroid uptake of radioiodine. Thyroid scintigraphy demonstrates a heterogeneous pattern of increased radionuclide uptake, most commonly into both thyroid lobes. Treatment options for toxic nodular goiter in cats are similar to that used in humans and include surgical thyroidectomy, radioiodine, and antithyroid drugs. Most authorities agree that ablative therapy with radioiodine is the treatment of choice for most cats with toxic nodular goiter, because the animals are older, and the disease will never go into remission. Download here: http://joe.endocrinology-journals.org/content/223/2/T97.full.pdf+htmlJournal of Endocrinology 11/2014; 223(2):T97-T114. DOI:10.1530/JOE-14-0461 · 3.59 Impact Factor
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ABSTRACT: Iodine is essential for the synthesis of thyroid hormones. Iodine deficiency can affect human health in different ways, and is commonly referred to as iodine deficiency disorders (IDD). These range from defective development of the central nervous system during the fetal–neonatal life, to goitre in the adult. Only a few countries were completely iodine sufficient before 1990. Since then, a major effort has been made to introduce salt iodization to ensure sufficient intake of iodine in deficient areas. Iodine prophylaxis has been shown to exert a pivotal role in abating goitre and other iodine-deficiency disorders, and has also been shown to modulate the pattern of thyroid diseases. An increased frequency of thyroid autoimmunity and of hypothyroidism has been observed after introducing iodization programmes. Nevertheless, available evidence clearly confirms that the benefits of correcting iodine deficiency, consisting mainly of reducing nodular goitre and non-autoimmune hyperthyroidism, far outweigh the risks of iodine supplementation.Best Practice & Research: Clinical Endocrinology & Metabolism 08/2014; 28(4). DOI:10.1016/j.beem.2014.04.002 · 4.91 Impact Factor
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ABSTRACT: Persistent or recurrent hyperthyroidism after treatment with radioactive iodine (RAI) is common and many patiedlxnts require either additional doses or surgery before they are cured. The purpose of this study was to identify patterns and predictors of failure of RAI in patients with hyperthyroidism. We conducted a retrospective review of patients treated with RAI from 2007 to 2010. Failure of RAI was defined as receipt of additional dose(s) and/or total thyroidectomy. Using a Cox proportional hazards model, we conducted univariate analysis to identify factors associated with failure of RAI. A final multivariate model was then constructed with significant (p < 0.05) variables from the univariate analysis. Of the 325 patients analyzed, 74 patients (22.8 %) failed initial RAI treatment, 53 (71.6 %) received additional RAI, 13 (17.6 %) received additional RAI followed by surgery, and the remaining 8 (10.8 %) were cured after thyroidectomy. The percentage of patients who failed decreased in a stepwise fashion as RAI dose increased. Similarly, the incidence of failure increased as the presenting T3 level increased. Sensitivity analysis revealed that RAI doses < 12.5 mCi were associated with failure while initial T3 and free T4 levels of at least 4.5 pg/mL and 2.3 ng/dL, respectively, were associated with failure. In the final multivariate analysis, higher T4 (hazard ratio [HR] 1.13; 95 % confidence interval [CI] 1.02-1.26; p = 0.02) and methimazole treatment (HR 2.55; 95 % CI 1.22-5.33; p = 0.01) were associated with failure. Laboratory values at presentation can predict which patients with hyperthyroidism are at risk for failing RAI treatment. Higher doses of RAI or surgical referral may prevent the need for repeat RAI in selected patients.Annals of Surgical Oncology 07/2014; 21(13). DOI:10.1245/s10434-014-3858-4 · 3.94 Impact Factor