INTRODUCTION — Goiter refers to abnormal growth of the thyroid gland. Adults may have goiters that are diffuse or nodular, and the goiters may be associated with normal, decreased, or increased thyroid hormone production. The management of goiter depends upon the cause. This topic primarily focuses on the management of nontoxic, nonobstructive diffuse or multinodular goiter. Iodine deficiency goiter (the most common cause of goiter worldwide), obstructive or substernal goiter, toxic multinodular goiter, Graves' disease, and thyroiditis are reviewed separately:
●(See "Iodine deficiency disorders", section on 'Diffuse and nodular goiter'.)
●(See "Treatment of obstructive or substernal goiter".)
●(See "Treatment of toxic adenoma and toxic multinodular goiter".)
●(See "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment".)
●(See "Subacute thyroiditis".)
●(See "Painless thyroiditis".)
GENERAL APPROACH — Once goiter is detected (on physical exam or incidentally during a radiologic procedure performed for other purposes), an evaluation is performed to assess thyroid function and to identify the underlying cause, presence of obstructive symptoms, and presence of suspicious sonographic features in nodules within the goiter. These factors determine management. (See "Clinical presentation and evaluation of goiter in adults", section on 'Approach to evaluation'.)
For patients with benign, nontoxic, nonobstructive goiter (multinodular goiter, goitrous Hashimoto's thyroiditis, and iodine deficiency goiter), the goals of management are to correct underlying hypothyroidism (Hashimoto's, severe iodine deficiency), if present, and if the goiter is cosmetically concerning, to decrease the size or prevent further growth.
Hypothyroidism, if present, should be treated with thyroid hormone (levothyroxine) replacement therapy (see "Treatment of primary hypothyroidism in adults"). Over time, treatment with thyroid hormone may reduce the size of the goiter, particularly in patients with Hashimoto's thyroiditis with elevated serum thyroid-stimulating hormone (TSH) levels (see 'Goitrous Hashimoto's' below). In many cases, however, the goiter does not resolve completely, and additional therapy is required.
NONTOXIC NODULAR GOITER — Nontoxic nodular goiter refers to a nodular goiter not associated with increased thyroid hormone production. In the United States, benign multinodular goiter is the most common cause of nontoxic goiter in older adults, although over time, multinodular goiters may develop areas of autonomy and become associated with increased thyroid function. (See "Treatment of toxic adenoma and toxic multinodular goiter".)
Therapeutic options — The main options for management of nontoxic nodular goiter include:
●Observation with monitoring
●Thyroidectomy
●Radioiodine
Thyroid hormone suppression therapy may have a limited role in patients with nontoxic nodular goiter. (See "Thyroid hormone suppressive therapy for thyroid nodules and benign goiter", section on 'Nontoxic goiter'.)
There is no consensus on the ideal treatment of nontoxic benign goiter, and there are advantages and disadvantages of each treatment (table 1) [1-3]. The lack of consensus is due, in part, to the variable natural history of benign goiter. In up to 20 percent of women and 5 percent of men, the goiter stabilizes or spontaneously regresses over time [4]. However, in other patients, the goiter gradually increases in size over time with the development of additional nodules, compressive symptoms, and cosmetic concerns [5].
There are few trials comparing interventions. In one trial, 64 patients with sporadic nontoxic multinodular goiter (average size 60 mL) were randomly assigned to radioiodine (120 microcuries [4.44 megabecquerels]/g thyroid) or suppressive levothyroxine treatment (goal TSH between 0.01 and 0.1 mU/L). After two years, 97 percent of the patients treated with radioiodine and 43 percent of those treated with levothyroxine had a decrease in goiter size. The median decrease in goiter size (by ultrasound) was 41 percent in the group treated with radioiodine compared with a clinically insignificant 5 percent in the suppressive levothyroxine treatment group as a whole, but the responders in the suppressive levothyroxine group had a 22 percent reduction in goiter size [6]. Although none of the patients had overt hyperthyroidism at baseline, 17 had subclinical hyperthyroidism (low TSH, normal free thyroxine [T4]), which may bias the results in favor of radioiodine. Hypothyroidism developed in 45 percent of patients receiving radioiodine. Patients who were treated with suppressive doses of thyroid hormone were more likely to have thyrotoxic symptoms and a decrease in bone mineral density (BMD) (mean decrease of 3.6 percent at the lumbar spine, compared with no change in the radioiodine group).
In an observational study examining quality-of-life indicators in patients with nontoxic benign goiter, the treatment modality (predominantly surgery or radioiodine) did not affect change in scale scores, which improved posttreatment but remained worse than those in the general population [7].
In the absence of adequate randomized trial data, management decisions should be individualized based upon patient factors, regional medical practices, and the following general principles (table 1):
●The decision to perform thyroidectomy is based upon the results of fine-needle aspiration (FNA) biopsy of any nodule(s) that may be present, the presence of cosmetic concerns, or other concomitant conditions such as hyperparathyroidism requiring surgery. Patients with nodules that are malignant or suspicious for malignancy on FNA biopsy require surgery. (See 'Surgery' below and "Diagnostic approach to and treatment of thyroid nodules", section on 'Management'.)
●Radioiodine has traditionally been used to treat patients with hyperthyroidism or thyroid cancer, but it is, in fact, both safe and effective for select patients with nontoxic nodular goiter. (See 'Radioiodine therapy' below.)
●The use of thyroid hormone suppressive therapy has declined primarily due to concerns about potential side effects, particularly atrial arrhythmias and decreased bone density, as well as controversy regarding its efficacy. Studies on the use of thyroid hormone suppressive therapy demonstrate that it is efficacious in some patients ("responders"), while continued goiter growth occurs in other patients. Thyroid hormone suppressive therapy is not an option for patients with serum TSH concentrations at the lower limit of or just below the normal range, because these patients already have endogenous suppression of TSH. When suppressive therapy is used, overt hyperthyroidism should be avoided, targeting a TSH of approximately 0.1 mU/L or higher. This topic is reviewed in detail separately. (See "Thyroid hormone suppressive therapy for thyroid nodules and benign goiter".)
Asymptomatic, stable goiter — Asymptomatic, euthyroid patients with benign multinodular goiters (<80 mL) do not require any specific treatment but should be monitored for the development of thyroid dysfunction or for continued growth of the thyroid gland and/or the development of obstructive symptoms.
We perform annual neck exams and obtain yearly thyroid function tests (TSH). We also monitor with thyroid ultrasound (initially annually, then at increasing intervals over time assuming stability [eg, two to five years] to evaluate for growth). Nodules with indeterminate or suspicious ultrasound features should be considered for biopsy because the prevalence of cancer in an individual nodule in a goiter is independent of the number of sonographically identified nodules. The evaluation and management of thyroid nodules are reviewed separately. (See "Diagnostic approach to and treatment of thyroid nodules".)
If the inferior extent of the goiter is not well seen on neck ultrasound, periodic neck noncontrast computed tomography (CT) or magnetic resonance imaging (MRI) may be necessary to monitor for tracheal compression or if there is retrosternal extent of the goiter, as these findings warrant additional testing (eg, flow-volume loop) and, potentially, surgical management. (See "Clinical presentation and evaluation of goiter in adults", section on 'Radiologic testing' and "Treatment of obstructive or substernal goiter", section on 'Our approach'.)
Very large or growing goiters — For patients with very large goiters (>80 to 100 mL) or goiters that continue to grow, we prefer active treatment rather than monitoring because of concern regarding continuous growth and possible development of thyroid autonomy. For euthyroid patients with very large goiters or goiters that continue to grow and potentially cause obstructive signs, symptoms, or cosmetic concerns, we prefer surgery over radioiodine. The reduction in thyroid volume with radioiodine is only moderate, the treated goiter requires continued monitoring for growth, and periodic imaging may raise concerns of a missed malignancy. Nevertheless, radioiodine therapy is an option for patients who are poor surgical candidates, for those who prefer to avoid surgery, or for those in whom the primary concern is autonomy with risk of developing subclinical or overt hyperthyroidism. (See "Treatment of obstructive or substernal goiter" and "Treatment of toxic adenoma and toxic multinodular goiter".)
Surgery — For most patients, we prefer surgery to radioiodine for patients with nontoxic, nonobstructive goiters that continue to grow and potentially cause obstructive signs, symptoms, or cosmetic concerns. (See 'Very large or growing goiters' above.)
Total or near-total thyroidectomy is preferred over subtotal thyroidectomy. In a Cochrane review of four randomized trials including 1305 patients, recurrent goitrous growth occurred in 0.2 percent of patients after total thyroidectomy and 8.4 percent of patients after a subtotal thyroidectomy [8].
In addition, patients with nodules within a goiter that are malignant or suspicious for malignancy on FNA biopsy require surgery. (See "Diagnostic approach to and treatment of thyroid nodules", section on 'Management' and "Differentiated thyroid cancer: Surgical treatment".)
Surgery for goiter is reviewed separately. (See "Treatment of obstructive or substernal goiter", section on 'Surgical approach' and "Thyroidectomy".)
Poor surgical candidates — For patients with nontoxic benign goiters that continue to grow but who are poor surgical candidates or who prefer to avoid surgery, radioiodine therapy is an alternative option. Radioiodine therapy is relatively infrequently used in the United States for the treatment of nontoxic goiter. Due to high dietary iodine intake, thyroid iodine uptake is typically low in patients with nontoxic goiter, and therefore, a relatively high dose of radioiodine is required for goiter reduction. Radioiodine for the treatment of nontoxic nodular goiter is more commonly used in Europe, and in particular Denmark and the Netherlands.
In the absence of a history of childhood neck radiation, we do not typically treat patients with nontoxic benign goiters who are poor surgical candidates with thyroid hormone suppressive therapy. The efficacy of thyroid hormone suppressive therapy in euthyroid patients with sporadic nontoxic goiter is controversial, and its use has declined due to concerns about potential long-term side effects from the induction of subclinical or overt hyperthyroidism. When used, thyroxine must be continued long term as any reduction in goiter size during therapy is lost upon discontinuation of thyroxine [9]. This topic is reviewed in detail separately. (See "Thyroid hormone suppressive therapy for thyroid nodules and benign goiter", section on 'Irradiated patients'.)
Radioiodine therapy — Radioiodine therapy is an option for patients who have nontoxic benign goiters that continue to grow but who are poor surgical candidates or prefer to avoid surgery.
There are several observational studies, mostly from Europe, describing the effects of radioiodine therapy in over 300 patients with nontoxic multinodular goiter (average goiter size ranging from 60 to 269 mL) [5,10-19]. In most studies, the patients were older; had respiratory symptoms, dysphagia, or recent thyroid growth; and were considered poor surgical candidates or had refused surgery. Overall, the reported reduction in goiter size (as measured by ultrasound) ranged from 40 to 60 percent within one to two years of therapy, with most of the effect occurring in the first three months [5]. Obstructive symptoms improved in most patients with increases in tracheal luminal diameter. There are fewer observational studies of radioiodine therapy for the treatment of nontoxic diffuse goiter [20,21]. In two studies, median thyroid volume reduction was 50 to 60 percent within one year of therapy.
The factors determining outcome were analyzed in one study of 50 patients in whom the mean reduction in goiter size was 47 percent (median follow-up 41 months) [17]. Eleven patients (22 percent) had no decrease in goiter size or a transient decrease and then re-enlargement of their goiter. The reduction in goiter size was greater in younger patients; those with smaller goiters, a shorter history of goiter, or dominant nodules; and those given higher doses of radioiodine. The baseline serum TSH concentration was not a determinant of reduction in goiter size, but a higher (but still normal) value was associated with a higher risk of hypothyroidism. (See 'Adverse effects' below.)
Dose — The dose of radioiodine in these studies ranged from 75 to 400 microcuries/g tissue (2.8 to 14.8 megabecquerels/g tissue). Most patients received doses between 100 and 200 microcuries/g (3.7 and 7.4 megabecquerels/g), similar to those used to treat hyperthyroidism. (See "Radioiodine in the treatment of hyperthyroidism".)
The dose was usually calculated by the following formula:
Dose (activity) = (thyroid weight x desired radioiodine delivery to thyroid) ÷ radioiodine uptake
The units are grams for thyroid weight and microcuries/g for radioiodine delivery; radioiodine uptake is expressed as a decimal (ie, 20 percent = 0.20).
The 24-hour thyroid radioiodine uptake is considerably lower in patients with nontoxic multinodular goiter than in patients with Graves' hyperthyroidism or toxic multinodular goiter. As a result, the dose of radioiodine needed may exceed that permissible for outpatients, which varies from state-to-state in the United States and also among other countries.
An alternative approach is to use multiple fractionated doses of radioiodine. When 60 millicuries (2.22 gigabecquerels) was given in four divided monthly doses to patients with obstructive goiter in one report, 71 percent had improvement in symptoms related to compression of neck structures and 92 percent had a reduction in goiter size, but 66 percent became hypothyroid [22]. Slightly over one-half of the patients had toxic nodular goiter. Thus, it is uncertain whether the higher rate of hypothyroidism was due to the fractionated doses or higher retention of isotope in the hyperthyroid patients.
Adverse effects — Radioiodine is generally well tolerated. In studies of radioiodine for the treatment of nontoxic benign goiter, the following findings were noted:
●Hypothyroidism occurred in 22 to 58 percent of patients within one to eight years after treatment [11-13,17,18]. An additional 10 to 40 percent of patients had subclinical hypothyroidism [10,13,15,17], and treatment with levothyroxine after radioiodine probably masked hypothyroidism in some other patients.
●Approximately 5 percent of patients had transient hyperthyroidism [10,11,13,15,16]. The mean serum free T4 and triiodothyronine (T3) concentrations transiently increased by 13 and 20 percent, respectively, in the first two weeks after treatment [14].
●Symptomatic radiation thyroiditis (thyroid pain and tenderness) was uncommon, occurring in 2 of 69 patients (3 percent) in one series [13] and 4 of 32 patients (13 percent) in another series [6]. (See "Overview of thyroiditis".)
●Concerns that radioiodine therapy in patients with nontoxic multinodular goiter might cause early goiter enlargement, thereby leading to acute airway obstruction, have not materialized [14,18]. However, in a study of patients with nonobstructive, toxic multinodular goiter given radioiodine, 8 percent had an increase in goiter size (mean increase 23 percent) [23], suggesting caution and careful monitoring in patients with severe tracheal narrowing.
●Two groups found that 4 to 5 percent of patients with nontoxic multinodular goiter treated with radioiodine developed Graves' hyperthyroidism, with high serum concentrations of TSH receptor antibodies 3 to 10 months later [24,25]. Another study of over 1350 patients found only 1.1 percent of patients developed autoimmune hyperthyroidism [26]. However, this occurred up to 10 times more commonly in patients with high serum antithyroid peroxidase antibody concentrations before treatment (TSH receptor antibody tests were negative then in all patients) [25,26]. These patients were treated with an antithyroid drug or additional radioiodine. (See "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment".)
●Based on measurements of whole-body radiation exposure, one group calculated slightly increased estimated lifetime risk of nonthyroid cancer of approximately 1.6 percent because of the large doses of radioiodine used in patients with very large goiters (mean size 222 g) [27]. The risk is much less (approximately 0.5 percent) in patients above the age of 65 years, the age of most patients with nontoxic multinodular goiters large enough to require therapy. The risk of nonthyroid and thyroid cancer after radioiodine treatment of hyperthyroidism is discussed separately. (See "Radioiodine in the treatment of hyperthyroidism", section on 'Cancer'.)
Pretreatment with recombinant human TSH to increase the radioiodine uptake — We do not administer recombinant human TSH (rhTSH, thyrotropin alfa) prior to radioiodine administration of nontoxic goiter. Neither regular nor modified-release rhTSH is approved by the US Food and Drug Administration (FDA) or European Medicines Agency (EMA) for use with radioiodine in the treatment of multinodular goiter. It is only available in kits of two vials of 0.9 mg (for use prior to administration of radioiodine to athyreotic thyroid cancer patients), and it is costly. The proposed rhTSH dosing for treatment of nontoxic multinodular goiter is much lower than for thyroid cancer, and a preparation designed for use in patients with nontoxic goiter is not currently available. (See "Differentiated thyroid cancer: Radioiodine treatment", section on 'Recombinant human TSH'.)
Pretreatment with rhTSH increases radioiodine uptake in nontoxic nodular goiter and results in a more homogeneous distribution of uptake by stimulating uptake in relatively cold areas more than in relatively hot areas, particularly in those with low serum TSH concentrations [28-30]. Thus, administration of rhTSH allows for treatment with lower doses of radioiodine without compromising efficacy [31,32]. It has been shown to be a useful adjunct to radioiodine for the treatment of nontoxic multinodular goiter, especially when the radioiodine uptake is low [33-35].
●Short-term efficacy – In meta-analyses of trials, radioiodine with rhTSH (eg, 0.005 to 0.45 mg administered 24 hours prior to radioiodine) was significantly more effective in reducing goiter volume than radioiodine alone (weighted mean difference 11.9 to 19.66 percent) [36,37]. As examples:
•In a randomized trial of radioiodine treatment calculated to give a thyroidal dose of 100 grays administered 24 hours after rhTSH (0.3 mg) or placebo, patients receiving rhTSH had a greater reduction in goiter size at one year (62 versus 46 percent) [38]. The median radioiodine dose was similar in the two groups.
•In another trial, 90 patients with nontoxic nodular goiter (median size 63 mL) were randomly assigned to either 0.1 mg rhTSH and radioiodine (50 grays) or placebo and radioiodine (100 grays) [31]. After 12 months, the mean reduction in goiter volume was identical (35 percent), even though the rhTSH group received half the dose of radioiodine as the placebo group. Both groups reported improvement in goiter symptoms.
These results suggest that pretreatment with rhTSH allows a major reduction in radioiodine dose without changing efficacy. The reduction in radioiodine dose may facilitate outpatient treatment and reduce the risk of side effects.
●Long-term efficacy – Long-term follow-up in two of these trials [38,39] found that goiter volume was reduced further in all patients after a mean 71 months [40]. The reduction in goiter volume remained higher in the rhTSH group (70 versus 56 percent in the group who received radioiodine without rhTSH), and the number of patients requiring additional therapy for obstructive symptoms was lower in the rhTSH group (5 versus 20 percent in the group who were not pretreated with rhTSH). The prevalence of hypothyroidism remained higher in the rhTSH group (52 versus 16 percent).
●Adverse effects of rhTSH – Compared with radioiodine alone, the use of rhTSH prior to radioiodine is associated with a higher incidence of hypothyroidism (62 versus 11 percent in one trial [38]). However, in the trial described above in which patients who were pretreated with rhTSH received one-half the dose of radioiodine, the difference in the prevalence of hypothyroidism one year after treatment was not significant (12 versus 7 percent) [31].
A potential concern about pretreatment with rhTSH is an increase in goiter size after administration of rhTSH. This was illustrated in a study of 10 patients with nodular goiter given 0.3 mg of rhTSH who then experienced an increase in mean goiter size at 24 hours of 9.8 percent and at 48 hours of 24 percent, returning to baseline at one week, suggesting that rhTSH could cause obstructive symptoms in patients with near obstructive goiters and that candidates for this treatment should be carefully screened for near-critical obstructive signs or symptoms [9].
In another study using rhTSH to reduce goiter size in 14 patients with large goiters, the smallest cross-sectional area of the trachea measured by MRI was found to be 10.5 percent greater one week after radioiodine administration, although the forced vital capacity was slightly reduced [41]. A modified-release, very-low-dose rhTSH preparation (0.01 to 0.03 mg) has been studied that results in lower peak serum TSH levels and, therefore, might be associated with less risk of goiter enlargement [42].
Pretreatment with methimazole to increase the radioiodine uptake — Methimazole increases TSH by reducing thyroid hormone synthesis. One would anticipate that the higher level of TSH would be associated with a higher radioiodine uptake. This was demonstrated in a small randomized trial comparing methimazole 10 mg daily or placebo for six weeks prior to radioiodine administration (21.6 mCi [800 mBq]) [43]. Methimazole increased the TSH from 2.1 to 7.9 mIU/L, and the rate of radioiodine uptake from 29 to 65 percent. Reduction in gland size was 34 percent greater in the group that received methimazole, while there was no change in the rate of hypothyroidism at one year (31 versus 27 percent in the treatment versus placebo group, respectively).
GOITROUS HASHIMOTO'S — Hashimoto's thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas of the world. It is characterized clinically by gradual thyroid failure, diffuse goiter formation, or both, due to autoimmune-mediated destruction of the thyroid gland involving apoptosis of thyroid epithelial cells. The two major forms of the disorder are goitrous autoimmune thyroiditis and atrophic autoimmune thyroiditis. (See "Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)", section on 'Clinical phenotypes'.)
The thyroid enlargement that can occur in patients with goitrous autoimmune thyroiditis is usually asymptomatic. In patients with goitrous Hashimoto's and elevated serum TSH levels, treatment with thyroid hormone may reduce the size of the goiter. Rare patients have significant thyroid enlargement, sometimes with thyroid pain and tenderness. Such patients may require surgery for symptomatic relief. There is one report of the use of radioiodine in goitrous Hashimoto's thyroiditis unresponsive to levothyroxine-suppressive therapy [44]. Thirteen patients received two to six doses of 13 millicuries radioiodine at one- to six-month intervals, which resulted in a 59 percent reduction in goiter size.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Thyroid nodules and cancer".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Hyperthyroidism (overactive thyroid) (The Basics)" and "Patient education: Thyroid nodules (The Basics)" and "Patient education: Nodular goiter (The Basics)")
●Beyond the Basics topics (see "Patient education: Hyperthyroidism (overactive thyroid) (Beyond the Basics)" and "Patient education: Antithyroid drugs (Beyond the Basics)" and "Patient education: Thyroid nodules (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●For patients with nontoxic, nonobstructive goiter (including benign multinodular goiter, goitrous Hashimoto's thyroiditis, and iodine deficiency goiter), the goals of management are to correct underlying hypothyroidism, if present, and if the goiter is cosmetically concerning, to decrease the size or prevent further growth. (See 'General approach' above and "Treatment of primary hypothyroidism in adults".)
●The main options for management of benign nontoxic nodular goiter include observation with monitoring, thyroidectomy, or radioiodine. The role of thyroid hormone suppression therapy is controversial, and its use has declined primarily due to concerns about potential long-term side effects from the induction of subclinical or overt hyperthyroidism (table 1). In the absence of adequate randomized trial data, management decisions should be individualized based upon patient characteristics. (See 'Therapeutic options' above.)
●For asymptomatic, euthyroid patients with benign multinodular goiters (<80 mL), we suggest monitoring rather than active therapy (Grade 2C). Patients should be monitored for the development of thyroid dysfunction or for continued growth of the thyroid gland and/or the development of obstructive symptoms. We perform annual neck exams and obtain yearly thyroid function tests (thyroid-stimulating hormone [TSH]). For patients with benign multinodular goiter, we also monitor with thyroid ultrasound (initially annually, then at increasing intervals over time assuming stability [eg, two to five years] to evaluate for growth). (See 'Asymptomatic, stable goiter' above.)
●For patients with very large goiters (>80 to 100 mL) or goiters that continue to grow, we suggest surgery rather than monitoring because of concern regarding continuous growth and possible development of compressive symptoms and/or thyroid autonomy (Grade 2C). Radioiodine therapy is an alternative option, particularly for patients who are poor surgical candidates or for those who prefer to avoid surgery. In addition, radioiodine may be useful for those patients with low-normal or low serum TSH concentrations whose goiters have autonomous areas with relatively higher radioiodine uptake. However, the reduction in thyroid volume with radioiodine is only moderate, the treated goiter requires continued monitoring for growth, and periodic imaging may raise concerns of a missed malignancy. (See 'Very large or growing goiters' above and "Treatment of toxic adenoma and toxic multinodular goiter", section on 'Radioiodine therapy'.)
We are not routinely using recombinant human TSH (rhTSH, thyrotropin alfa) prior to radioiodine administration of nontoxic goiter. (See 'Pretreatment with recombinant human TSH to increase the radioiodine uptake' above.)
●In the absence of a history of childhood neck radiation, we do not routinely treat patients with thyroid hormone suppressive therapy. When suppressive therapy is used, overt hyperthyroidism should be avoided, targeting a TSH of approximately 0.1 mU/L or higher. The efficacy of thyroid hormone suppressive therapy in euthyroid patients with sporadic nontoxic goiter is controversial, and its use has declined primarily due to concerns about potential long-term side effects from the induction of subclinical or overt hyperthyroidism. (See 'Poor surgical candidates' above and "Thyroid hormone suppressive therapy for thyroid nodules and benign goiter".)
●In patients with goitrous Hashimoto's and elevated serum TSH levels, treatment with thyroid hormone may reduce the size of the goiter. Rare patients require surgery for significant thyroid enlargement, sometimes with thyroid pain and tenderness. (See "Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)", section on 'Clinical phenotypes' and 'Goitrous Hashimoto's' above.)
●Patients with nodules within a goiter that are malignant or suspicious for malignancy on fine-needle aspiration (FNA) biopsy require surgery. (See "Diagnostic approach to and treatment of thyroid nodules", section on 'Management'.)
●The treatment of obstructive or substernal goiter and the treatment of toxic multinodular goiter are reviewed separately. (See "Treatment of obstructive or substernal goiter" and "Treatment of toxic adenoma and toxic multinodular goiter".)
