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Nontoxic Goiter Treatment & Management

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD  more...
 
Updated: Feb 04, 2013
 

Medical Care

Nontoxic goiters usually grow very slowly over decades without causing symptoms. Without evidence of rapid growth, obstructive symptoms (eg, dysphagia, stridor, cough, shortness of breath), or thyrotoxicosis, no treatment is necessary. Therapy is considered if growth of the entire goiter or a specific nodule is present, especially if intrathoracic extension of the goiter, compressive symptoms, or thyrotoxicosis exists. The intrathoracic extension of the goiter cannot be assessed by palpation or biopsy. The goiter, if significant in size, should be removed surgically.[4] The currently available therapies include thyroidectomy, radioactive iodine therapy, and levothyroxine (L-thyroxine, or T4) therapy.

Radioactive iodine therapy - Radioiodine therapy of nontoxic goiters is often performed in Europe. It is a reasonable therapeutic option, particularly in patients who are older or have a contraindication to surgery.[5, 6, 7]

Radioactive iodine therapy for nontoxic goiters was reintroduced in the 1990s. Careful studies have shown a reduction in thyroid volume in nearly all patients after a single dose of therapy.[1] Of patients with nontoxic diffuse goiter treated with radioactive iodine, 90% have an average of 50-60% reduction in goiter volume after 12-18 months, with a reduction in compressive symptoms. The decrease in goiter size has positively correlated with the dose of iodine-131 (131 I). Reduction in goiter size is greater in younger patients and in individuals who have only a short history of goiter or who have a small goiter. Baseline TSH is not a predictor of response to radioactive iodine.

Obstructive symptoms improved in most patients who received radioactive iodine.

Adverse effects, including thyroiditis, occurred, but no patient reported worsening of compressive symptoms requiring treatment. No long-term follow-up reports on patients treated with radioactive iodine exist. Patients should always be monitored clinically after131 I therapy, for evidence of goiter regrowth.

Transient hyperthyroidism is rare and typically occurs in the first 2 weeks after treatment.

Unlike patients with Graves hyperthyroidism who almost all become hypothyroid after treatment with radioactive iodine, only a small percentage (~20%) of patients with nontoxic goiter develop hypothyroidism after radioactive iodine treatment

Recombinant human TSH (rhTSH) may have a role in radioactive iodine treatment for nontoxic goiter. Pretreatment with rhTSH 24 hours prior to therapy can reduce the amount of radioiodine needed to shrink the goiter (up to a 50% reduction).[8, 9, 10, 11]

Thyroid hormone suppressive therapy - The use of T4 in a euthyroid individual to shrink a nontoxic goiter is controversial.

One study showed that T4 therapy for nontoxic goiter reduced thyroid volume in 58% of patients, compared with 4% of patients treated with a placebo. However, these results have not yet proven to be reproducible, and the benefit of using T4 needs to be weighed against the risk of the resultant subclinical hyperthyroidism associated with an increased risk of decreased bone mineral density and increased atrial fibrillation. Goiter growth typically resumes after cessation of T4 therapy.

The American Thyroid Association and American Association of Clinical Endocrinologists have released guidelines for the management of hyperthyroid and other causes of thyrotoxicosis, including the use of radioactive iodine or surgery to treat toxic multinodular goiter.[12]

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Surgical Care

Thyroidectomy or surgical decompression causes rapid relief for obstructive symptoms.[1, 4, 13]

Most intrathoracic goiters may be removed from a cervical incision without sternotomy. Performing bilateral subtotal thyroidectomy has been recommended to reduce the risk of continued goiter growth. The rate of goiter recurrence depends on the extent of surgery but should not be higher than 10% in 10 years.

After bilateral subtotal thyroidectomy, all patients require thyroid hormone replacement therapy. The full replacement therapy should start immediately after surgery, with TSH levels checked 3-4 weeks postoperatively. Adjust thyroid hormone therapy, such as T4, to maintain a TSH level in the reference range. Some evidence exists that thyroid hormone replacement therapy prevents recurrence of nontoxic goiter after surgical removal.[14]

The use of total thyroidectomy to treat benign multinodular goiter has met with some concern, owing to the risk of parathyroid function damage and laryngeal nerve injury posed by the procedure. Nonetheless, total thyroidectomy is also seen as a means of avoiding the pitfalls of subtotal thyroidectomy, specifically, the recurrence of goiter and the inadequate treatment of thyroid cancers, which can occur in apparently benign goiters. Results from a 2008 literature review indicated that the rate of permanent complications is the same for subtotal and total thyroidectomy; consequently, the report's authors concluded that total thyroidectomy should be the procedure of choice for the surgical treatment of benign multinodular goiters.[4]

The same conclusion was reached in a study of 600 patients with nontoxic multinodular goiter. Barczynski et al compared outcomes from total thyroidectomy (200 patients), the Dunhill procedure (unilateral total lobectomy plus contralateral subtotal lobectomy; 200 patients), and bilateral subtotal thyroidectomy (200 patients). The authors found that over a 5-year follow-up period the incidence of recurrent goiter after total thyroidectomy was 0.52%, while that following the Dunhill operation was 4.71%, and recurrence after bilateral subtotal thyroidectomy was 11.58%. The frequency of completion thyroidectomies was also lower in total thyroidectomy than in the other operations.

The incidence of transient hypoparathyroidism in the above study, as well as that of transient and permanent laryngeal nerve injuries, was greater in total thyroidectomy than in the other types of surgery. Nonetheless, the authors concluded that, owing to the fact that following total thyroidectomy there was a reduced incidence of goiter recurrence requiring repeat thyroidectomy, total thyroidectomy should be considered the procedure of choice for patients with nontoxic multinodular goiter.[15]

Results from a Swiss study of 72 patients indicated that a single dose of steroid prior to thyroidectomy for benign disease can, within 48 hours postsurgery, significantly reduce pain, nausea, vomiting, and voice alteration related to the procedure.[16]

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Consultations

Consult an endocrinologist in the complicated nontoxic goiter with obstructive symptoms, rapid growth, and/or evaluation for thyroid malignancy within the nontoxic goiter.

If a high index of suspicion for malignancy exists in a patient with hoarseness, lymphadenopathy, and previous radiation exposure as a child, consult an endocrinologist or a surgeon specializing in thyroid disease.

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Diet

Diets low in iodine need supplementation, especially in developing countries where government-supported iodine supplementation is not available. Adult patients require 150 mcg/day, which has been the average intake in the United States, but patients should be encouraged to use iodized salt at home and take multivitamins with iodine to ensure adequate intake. Patients should not take iodine supplements such as seaweed, as the amount of iodine is excessive and may result in iodine-induced thyroid hormone dysfunction in predisposed individuals.

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Contributor Information and Disclosures
Author

Stephanie L Lee, MD, PhD Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD Assistant Professor of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center, Boston University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Kent Wehmeier, MD Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, St Louis University School of Medicine

Kent Wehmeier, MD is a member of the following medical societies: American Society of Hypertension, Endocrine Society, International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Steven R Gambert, MD Professor of Medicine, Johns Hopkins University School of Medicine; Director of Geriatric Medicine, University of Maryland Medical Center and R Adams Cowley Shock Trauma Center

Steven R Gambert, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American College of Physicians, American Geriatrics Society, Endocrine Society, Gerontological Society of America, Association of Professors of Medicine

Disclosure: Nothing to disclose.

References
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Intrathoracic goiter causing obstruction. This patient has a visible goiter on physical examination. In addition, he has distension of his left external jugular vein, facial erythema (when compared with his shoulder), and cutaneous varicosities of venous blood draining from his head into his chest because of jugular obstruction from his goiter.
Technetium-99m (99mTc) thyroid scan of a large, nontoxic multinodular goiter. Multiple cold and hot nodules are observed in the enlarged thyroid gland. The white arrow indicates sternal notch marker.
Areas of autonomy with excess thyroid hormone secretion in a large nodular goiter. This technetium-99m (99mTc) thyroid scan shows hot and cold nodules in a multinodular goiter. Although the patient's thyroid-stimulating hormone level had become progressively suppressed, it was within the reference range, at 0.4 mU/mL (reference range 0.35-5.5 mU/mL).
Nontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast computed tomography scan through the thyroid shows significant tracheal compression.
Relief of tracheal compression after subtotal thyroidectomy of large, obstructive, nontoxic multinodular goiter. (A) Laryngoscopy demonstrating critical tracheal narrowing before thyroidectomy; (B) laryngoscopy showing widened patent trachea after thyroidectomy.
Multinodular goiter. On visual inspection of the neck (image on left), this patient appears to have a goiter. The computed tomography scan (image on right) shows the asymmetrical goiter, measuring 9.3 x 7.4 cm, with tracheal deviation, although no tracheal obstruction is present.
 
 
 
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