eMedicine Specialties > Endocrinology > Thyroid

Goiter, Nontoxic: Treatment & Medication

Author: Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Coauthor(s): Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Contributor Information and Disclosures

Updated: May 5, 2009

Treatment

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.2 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.3,4
    • 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.
    • Of patients with nontoxic diffuse goiter, 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 hyperthyroidism who are treated with radioactive iodine, only a small percentage of patients with nontoxic goiter develop hypothyroidism after radioactive iodine treatment
    • Recombinant human TSH (rhTSH)5,6,7 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).
  • 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.

Surgical Care

Thyroidectomy or surgical decompression causes rapid relief for obstructive symptoms (see image below and Image 4).2

  • 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.8
  • 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.2
  • 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.9
Nontoxic goiter of the thyroid gland with trachea...

Nontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast computed tomography scan through the thyroid shows significant tracheal compression.

Nontoxic goiter of the thyroid gland with trachea...

Nontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast computed tomography scan through the thyroid shows significant tracheal compression.


Consultations

  • Consult an endocrinologist in the complicated nontoxic goiter with nodule formation or obstructive symptoms.
  • If a high index of suspicion for malignancy exists in a patient with hoarseness, lymphadenopathy, and previous radiation exposure as a child, consult a thyroid surgeon.

Diet

Diets low in iodine need supplementation, especially in developing countries where government-supported iodine supplementation is not available. Patients taking iodine supplements may need a reduction to avoid iodine-induced thyroid disease in predisposed individuals.

Medication

No specific treatment for nontoxic goiter exists. Childhood or adult goiter that is established because of iodine deficiency does not shrink after supplementation with iodine. Goiters due to a defect in thyroid hormone synthesis, dyshormonogenesis, are often reduced in size by thyroid hormone therapy. Attempting to shrink nontoxic goiters with T4 has been standard practice, but this therapy has generally fallen out of favor because of the risks of hyperthyroidism, with its detrimental effects on bone and cardiac function.

Thyroid hormones (L-thyroxine)

T4 has been used to reduce the size or suppress the further growth of goiters.


Levothyroxine (Synthroid, Levoxyl, Unithroid, Levothroid)

Minimal excess doses of T4 suppress thyrotropin (TSH) secretion from the pituitary. TSH is the primary stimulator of thyroid gland growth and thyroid hormone synthesis. For many years, the standard therapy of nontoxic goiter has been suppression of thyroid function by exogenous T4 therapy. This practice has been largely abandoned because of data showing cortical bone loss with chronic excess of thyroid hormone therapy and lack of benefit in suppressing growth of large nodular goiters. Studies have shown that T4 therapy is most effective in decreasing the size of small diffuse goiters in patients with a basal TSH within the reference range.

Adult

50-75 mcg/d PO; evaluate TSH in 6 wk; adjust dose to keep the TSH low in the reference range (ie, approximately 0.3-1 µIU/mL)
Coronary artery disease: 12.5-25 mcg/d PO; evaluate for worsening of angina; dose can be increased slowly by 25 mcg q4-6wk until TSH is suppressed to lower limits of the reference range

Pediatric

Not established

Cholestyramine may decrease absorption; concomitant administration with calcium or iron supplements may decrease absorption; estrogens may increase the requirement for thyroid hormone therapy in patients with nonfunctioning thyroid glands; increases effect of anticoagulants; activity of some beta-blockers may decrease when the hypothyroid patient is converted to a euthyroid state

Documented hypersensitivity; uncorrected adrenal insufficiency; subclinical hyperthyroidism at baseline; unstable angina; unregulated atrial tachyarrhythmias

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Caution in angina pectoris or cardiovascular disease; monitor thyroid status periodically; menopausal women may develop bone loss and osteoporosis; large goiters frequently have areas of hyperfunction; before starting T4 therapy, check the TSH level to eliminate subclinical hyperthyroidism; T4 therapy should not be used if TSH is low; after instituting T4 therapy, a repeat TSH should be checked after 6 wk with the goal of suppressing TSH to the lower limit of the reference range (ie, 0.1-0.5 µIU/mL) without causing subclinical thyrotoxicosis; repeating laboratory evaluation is important because exogenous thyroid hormone therapy in the presence of thyroid autonomy may lead to significant thyrotoxicosis; because of the risk of coronary artery disease in older patients, start thyroid hormone therapy slowly because of the stimulatory effect on cardiac function and oxygen consumption

Antithyroid agents

Reduce goiter size.


Sodium iodide, or131 I (Iodotope)

Ultrasonographic studies have shown a decrease in thyroid volume after131 I therapy in the majority of patients with nontoxic goiter. When administered at a dose of 100 µCi per g of goiter (corrected for percent uptake of131 I at 24 h), thyroid volume decreases an average of 50-60% in 12-18 mo. In most patients, radioactive iodine therapy reduces compressive symptoms. Commonly used in Europe and Latin America but is not standard therapy in the United States unless the patient has contraindication for surgery. Theoretical concerns of radiation-induced swelling and worsening of compressive symptoms have not been supported in European studies. Often, low-iodine diets are recommended for 5 d up to several wk before therapy.

Adult

100 µCi/g goiter corrected for 24 h131 I thyroid uptake

Pediatric

Not established and not recommended

Increases lithium toxicity by producing additive hypothyroid effects; uptake is affected by stable iodine, thyroid, and antithyroid agents; amiodarone may block radioactive iodine uptake into the goiter

Documented hypersensitivity; pregnancy; breastfeeding; critical obstruction from goiter (edema after131 I treatment and radiation thyroiditis theoretically may worsen condition)

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Contraindicated in pregnant and breastfeeding women because drug may pass through placenta and is secreted into milk; may cause bone marrow depression, acute leukemia, anemia, blood dyscrasias, leukopenia, thrombocytopenia, radiation sickness, angina, sinus tachycardia, pruritus, skin rash, and hives; high doses may cause radiation thyroiditis with painful thyroid or release of stored thyroid hormone, causing temporary thyrotoxicosis

More on Goiter, Nontoxic

Overview: Goiter, Nontoxic
Differential Diagnoses & Workup: Goiter, Nontoxic
Treatment & Medication: Goiter, Nontoxic
Follow-up: Goiter, Nontoxic
Multimedia: Goiter, Nontoxic
References
Further Reading

References

  1. Baloch ZW, LiVolsi VA. Fine-needle aspiration of the thyroid: today and tomorrow. Best Pract Res Clin Endocrinol Metab. Dec 2008;22(6):929-39. [Medline].

  2. Agarwal G, Aggarwal V. Is total thyroidectomy the surgical procedure of choice for benign multinodular goiter? An evidence-based review. World J Surg. Jul 2008;32(7):1313-24. [Medline].

  3. Weetman AP. Radioiodine treatment for benign thyroid diseases. Clin Endocrinol (Oxf). Jun 2007;66(6):757-64. [Medline].

  4. Baczyk M, Pisarek M, Czepczynski R, Ziemnicka K, Gryczynska M, Pietz L, et al. Therapy of large multinodular goitre using repeated doses of radioiodine. Nucl Med Commun. Mar 2009;30(3):226-31. [Medline].

  5. Duntas LH, Cooper DS. Review on the occasion of a decade of recombinant human TSH: prospects and novel uses. Thyroid. May 2008;18(5):509-16. [Medline].

  6. Medeiros-Neto G, Marui S, Knobel M. An outline concerning the potential use of recombinant human thyrotropin for improving radioiodine therapy of multinodular goiter. Endocrine. Apr 2008;33(2):109-17. [Medline].

  7. Braverman L, Kloos RT, Law B Jr, Kipnes M, Dionne M, Magner J. Evaluation of various doses of recombinant human thyrotropin in patients with multinodular goiters. Endocr Pract. Oct 2008;14(7):832-9. [Medline].

  8. Phitayakorn R, McHenry CR. Follow-up after surgery for benign nodular thyroid disease: evidence-based approach. World J Surg. Jul 2008;32(7):1374-84. [Medline].

  9. [Best Evidence] Worni M, Schudel HH, Seifert E, et al. Randomized controlled trial on single dose steroid before thyroidectomy for benign disease to improve postoperative nausea, pain, and vocal function. Ann Surg. Dec 2008;248(6):1060-6. [Medline].

  10. Berghout A, Wiersinga WM, Drexhage HA, et al. Comparison of placebo with L-thyroxine alone or with carbimazole for treatment of sporadic non-toxic goitre. Lancet. Jul 28 1990;336(8709):193-7.

  11. Bonnema SJ, Bertelsen H, Mortensen J, et al. The feasibility of high dose iodine 131 treatment as an alternative to surgery in patients with a very large goiter: effect on thyroid function and size and pulmonary function. J Clin Endocrinol Metab. Oct 1999;84(10):3636-41. [Medline][Full Text].

  12. Braverman LE, Utiger RD, Hermus AR, Huysmans DA:. Clinical manifestations and treatment of nontoxic diffuse and nodular goiter. In: Werner & Ingbar's The Thyroid. Baltimore, Md: Lippincott Williams & Wilkins;. 2000;866-871.

  13. Hegedus L, Gerber H. Multinodular goiter. In: DeGroot LJ, Jameson JL, eds. Endocrinology. 2001;2:1517-1528.

  14. Hermus AR, Huysmans DA. Treatment of benign nodular thyroid disease. N Engl J Med. May 14 1998;338(20):1438-47. [Medline].

  15. Hollowell JG, Staehling NW, Hannon WH, et al. Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from National Health and Nutrition Examination Surveys I and III (1971-1974 and 1988-1994). J Clin Endocrinol Metab. Oct 1998;83(10):3401-8. [Medline][Full Text].

  16. Huysmans D, Hermus A, Edelbroek M, et al. Radioiodine for nontoxic multinodular goiter. Thyroid. Apr 1997;7(2):235-9. [Medline].

  17. Huysmans DA, Hermus AR, Corstens FH, et al. Large, compressive goiters treated with radioiodine. Ann Intern Med. Nov 15 1994;121(10):757-62. [Medline].

  18. Huysmans DA, Nieuwlaat WA, Erdtsieck RJ, et al. Administration of a single low dose of recombinant human thyrotropin significantly enhances thyroid radioiodide uptake in nontoxic nodular goiter. J Clin Endocrinol Metab. Oct 2000;85(10):3592-6. [Medline][Full Text].

  19. Netterville JL, Coleman SC, Smith JC, et al. Management of substernal goiter. Laryngoscope. Nov 1998;108(11 Pt 1):1611-7. [Medline].

  20. Perrild H, Hansen JM, Hegedus L. Triiodothyronine and thyroxine treatment of diffuse non-toxic goitre evaluated by ultrasonic scanning. Acta Endocrinol (Copenh). Jul 1982;100(3):382-7. [Medline].

  21. Rios A, Rodriguez JM, Canteras M, et al. Surgical management of multinodular goiter with compression symptoms. Arch Surg. Jan 2005;140(1):49-53. [Medline][Full Text].

  22. Ross DS. Thyroid hormone suppressive therapy of sporadic nontoxic goiter. Thyroid. Fall 1992;2(3):263-9. [Medline].

Keywords

nontoxic goiter, thyroidgoiter, TSH, hypothyroid, hypothyroidism, thyroid symptoms, thyroid disease, thyroid problems, thyroid hormonethyroxine, thyroid levels, thyroid treatment, thyroid function, thyroid medication, TSH levels, TSH T4, enlarged thyroid, thyroid stimulating hormone, thyroid-stimulating hormone, thyroid hormones, thyroid TSH, T3 thyroid, multinodular goiter, triiodothyronine, thyroidectomy, iodine deficiency, adenomatous goiter, endemic goiter, sporadic goiter, nodular hyperplasia, follicular epithelial hyperplasia, cretinism,dyshormonogenesis, diffuse or nodular enlargement of the thyroid gland, diffuse goiter

Contributor Information and Disclosures

Author

Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, and Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Steven R Gambert, MD, MACP, Chairman, Department of Medicine, Physician-in-Chief, Sinai Hospital of Baltimore; Professor of Medicine, Program Director, Internal Medicine Program, Johns Hopkins University School of Medicine
Steven R Gambert, MD, MACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors of Medicine, Endocrine Society, and Gerontological Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor 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, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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