Version May 2024
INTRODUCTION — Hypothyroidism can result from a defect anywhere in the hypothalamic-pituitary-thyroid axis. In the vast majority of cases, it is caused by thyroid disease (primary hypothyroidism). Much less often it is caused by decreased secretion of thyroid-stimulating hormone (TSH) from the anterior pituitary gland or by decreased secretion of thyrotropin-releasing hormone (TRH) from the hypothalamus (table 1).
The cause of hypothyroidism should be identified in every patient for the following reasons:
●Hypothyroidism may be transient and require no or only short-term therapy, as in patients with painless thyroiditis or postpartum thyroiditis. (See "Overview of thyroiditis".)
●It may be caused by a drug, such as lithium or an iodine-containing drug, and disappear when the drug is discontinued.
●It may be the first or only manifestation of hypothalamic or pituitary disease.
The cause can often be identified, or at least strongly inferred, from the history and physical examination.
This topic will review the major causes of hypothyroidism. The diagnostic approach to and treatment of hypothyroidism are discussed separately. (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults" and "Treatment of primary hypothyroidism in adults".)
PRIMARY HYPOTHYROIDISM — In patients with hypothyroidism caused by disease of the thyroid gland, decreased secretion of thyroxine (T4) and triiodothyronine (T3) leads to a reduction in the serum concentrations of the two hormones, which results in a compensatory increase in TSH secretion. Thus, the combination of a low serum T4 and a high serum TSH concentration both confirms the diagnosis of hypothyroidism and indicates that it is due to primary thyroid disease.
We recognize two degrees of primary hypothyroidism:
●Subclinical hypothyroidism – Subclinical hypothyroidism is defined as a high serum TSH concentration in the presence of normal serum free T4 and T3 concentrations. This combination of findings reflects the great sensitivity of TSH secretion to very small reductions in thyroid secretion. These patients have few, if any, symptoms and signs of hypothyroidism. (See "Subclinical hypothyroidism in nonpregnant adults".)
●Overt hypothyroidism – Overt hypothyroidism is defined as a high serum TSH concentration in the presence of a low serum free T4 concentration. Most of these patients have symptoms and signs of hypothyroidism. (See "Clinical manifestations of hypothyroidism".)
All of the thyroid disorders considered below can cause either subclinical or overt hypothyroidism.
Chronic autoimmune (Hashimoto's) thyroiditis — The most common cause of hypothyroidism in iodine-sufficient areas of the world is chronic autoimmune (Hashimoto's) thyroiditis, which is caused by cell- and antibody-mediated destruction of thyroid tissue [1]. The disorder has two forms: goitrous and atrophic. They differ in the extent of lymphocytic infiltration, fibrosis, and thyroid follicular cell hyperplasia of the thyroid gland but not in their pathophysiology.
Both cellular and humoral factors may contribute to the thyroid injury and hypothyroidism in chronic autoimmune thyroiditis. Cytotoxic T cells may directly destroy thyroid cells. In addition, more than 90 percent of patients with chronic autoimmune thyroiditis have high serum concentrations of autoantibodies to thyroglobulin, thyroid peroxidase (thyroid microsomal antigen) [2,3], or the thyroid sodium-iodide transporter (table 2) [4]. These antibodies have little, if any, functional activity. Many patients also have antibodies that block the action of TSH on the TSH receptor or that are cytotoxic to thyroid cells [5,6]. (See "Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)".)
Serum antithyroid antibodies need not be measured routinely in patients with overt primary hypothyroidism, because almost all have chronic autoimmune thyroiditis. However, a test for antithyroid peroxidase antibodies may be useful to predict the likelihood of progression to permanent overt hypothyroidism in patients with subclinical hypothyroidism or those with painless (silent) thyroiditis or postpartum thyroiditis.
Prevalence — In community surveys, high serum antithyroid peroxidase antibody concentrations are found in approximately 5 percent of adults and approximately 15 percent of older women (table 2) [7-9]. The frequency of subclinical hypothyroidism is similar and that of overt hypothyroidism varies from 0.1 to 2 percent [10]. In one population-based study, the overall incidence of autoimmune thyroiditis was 46.4 per 1000 subjects during a 20-year period [11].
Hypothyroidism is much (five to eight times) more common in women than men. The majority of those who are hypothyroid have a goiter, but not all who have a goiter and circulating antithyroid antibodies have hypothyroidism.
In the United States National Health and Nutrition Examination Survey (NHANES III), 13,344 people without known thyroid disease had measurements of serum TSH, T4, thyroglobulin antibodies, and thyroid peroxidase antibodies with the following results [12]:
●Hypothyroidism was found in 4.6 percent (0.3 percent overt and 4.3 percent subclinical).
●Hyperthyroidism was found in 1.3 percent (0.5 percent overt and 0.7 percent subclinical).
●Serum thyroglobulin antibody concentrations were high in 10 percent and serum thyroid peroxidase antibody concentrations were high in 11 percent. The latter were associated with hypo- or hyperthyroidism, while the former were not.
●Mean serum TSH concentrations were significantly lower in Black (1.7 percent) than in White or Mexican Americans.
Thus, a significant proportion of the United States population has laboratory evidence of thyroid disease, suggesting that routine screening would be useful.
Natural history — The usual course of Hashimoto's thyroiditis is gradual loss of thyroid function. Among patients with this disorder who have mild (subclinical) hypothyroidism, exhibited as slight increases in TSH and the presence of thyroid antibodies, overt hypothyroidism occurs at a rate of approximately 5 percent per year [8,13]. Chronic autoimmune thyroiditis is usually, but not always, permanent. Repeat biopsies reveal little histologic change, nor do serum antithyroid antibody concentrations change in most patients [14]. However, a few patients have remissions and no longer need T4 therapy, indicating that the hypothyroidism is not always caused by destruction of the thyroid gland. One study, as an example, evaluated 15 Japanese patients with TSH-receptor blocking antibodies in whom the antibodies later disappeared; six remained euthyroid for several years after T4 therapy was discontinued [5]. Whether disappearance of antithyroid peroxidase antibodies can be used to predict remission of hypothyroidism is not known.
Susceptibility and risk factors — Chronic autoimmune thyroiditis is more common in women, especially older women. Whether the increase in risk in the latter group is due to estrogen deficiency or age is not known. Chronic autoimmune thyroiditis is also the most common cause of hypothyroidism in children, being reported as early as one and two years of age [15].
Chronic autoimmune thyroiditis is associated with several polymorphisms in the genes for human leukocyte antigen (HLA), T-cell antigen receptors, and other immunomodulatory molecules, suggesting a role for genetic susceptibility [16,17]. However, the relative risk is approximately two for most of the associations, which also vary considerably among different racial and ethnic groups. Turner syndrome and Down syndrome are both associated with a higher than expected rate of autoimmune thyroiditis [18,19]. (See "Pathogenesis of autoimmune adrenal insufficiency".)
Whatever the factors mediating genetic susceptibility, patients with chronic autoimmune thyroiditis are more likely to have a personal or family history of other autoimmune diseases, such as adrenal insufficiency and insulin-dependent diabetes mellitus [20]. Chronic autoimmune thyroiditis is one of the components of polyglandular autoimmune syndrome 2. (See "Causes of primary adrenal insufficiency (Addison disease)", section on 'Type 2 (polygenic)'.)
Other risk factors include the following:
●High iodine intake has been associated with Hashimoto's thyroiditis. Serum antithyroid antibody concentrations increase after dietary iodine intake is increased in endemic goiter regions [21]. Pharmacologic amounts of iodine are known to cause hypothyroidism in patients with chronic autoimmune thyroiditis. (See 'Iodine' below and "Iodine-induced thyroid dysfunction".)
●Relative selenium deficiency has been associated with Hashimoto's thyroiditis and hypothyroidism [22].
●Childhood weight gain and being overweight or obese at age 14 years have been associated with thyroid autoimmunity and hypothyroidism [23].
●Cigarette smoking increased the risk of hypothyroidism in patients with autoimmune thyroid disease [24]. However, in a population-based study, smoking was associated with a lower prevalence of hypothyroidism and a higher prevalence of hyperthyroidism [25].
Iatrogenic disease — Thyroidectomy, radioiodine treatment, and external radiation therapy are well-known causes of hypothyroidism.
Thyroidectomy — Because T4 has a half-life of seven days, hypothyroidism occurs within two to four weeks after total thyroidectomy. The time course after subtotal thyroidectomy in patients with Graves' hyperthyroidism is more variable. It occurs within the first year after surgery in the majority of patients; among those who are euthyroid at one year, approximately 0.5 to 1 percent become hypothyroid each year thereafter [26,27]. The late onset is presumably due to superimposed chronic autoimmune thyroiditis [28]. (See "Surgical management of hyperthyroidism".)
Radioiodine therapy — Radioiodine (I-131) therapy for Graves' hyperthyroidism can cause hypothyroidism weeks, months, or years later. The high-dose regimens preferred in most centers (to reduce the need for retreatment) result in hypothyroidism in the majority of patients within the first two to six months after therapy; the remainder become hypothyroid at a rate of 0.5 to 2 percent per year [26,27,29]. A significant minority of patients with toxic or nontoxic multinodular goiter or autonomously functioning thyroid adenomas also become hypothyroid after radioiodine therapy. (See "Radioiodine in the treatment of hyperthyroidism".)
External neck irradiation — External irradiation of the neck (in doses of 25 Gy [2500 rads] or more) also causes hypothyroidism. The effect is dose dependent, the onset is gradual, and many patients have subclinical hypothyroidism for several years before developing overt disease. (See "Endocrinopathies in cancer survivors and others exposed to cytotoxic therapies during childhood", section on 'Primary hypothyroidism'.)
●Hodgkin lymphoma – One study evaluated 1677 patients with Hodgkin lymphoma who were treated with neck radiation and were followed for up to 20 years; the cumulative incidence of hypothyroidism was 30 percent [30] and, in one study, was more common in patients who had lymphangiography [31].
●Hyperfractionated radiation therapy – Data from children suggest that hyperfractionated radiation may cause fewer cases of hypothyroidism than conventional therapy [32].
●Head and neck cancer – A thyroid-destructive effect is also seen with total body irradiation [33] and external radiation therapy in patients with head and neck cancer. In one study, 53 percent of irradiated patients with head and neck carcinoma developed hypothyroidism [34]. (See "Management of late complications of head and neck cancer and its treatment", section on 'Thyroid disease'.)
●Breast cancer – External radiation for breast cancer may also lead to hypothyroidism, depending on the area irradiated and whether the thyroid is shielded. In a small study (n = 40), 15 percent of irradiated patients and 5 percent of controls developed hypothyroidism [35].
●Nuclear accident – Thyroid irradiation also may promote the formation of antithyroid antibodies. Studies in children and adolescents from Belarus who were exposed to radioactive fallout after the nuclear accident at Chernobyl have noted an increased prevalence of antithyroglobulin or antithyroid peroxidase antibodies at six to eight years (19.5 versus 3.8 percent in unexposed children) [36]. Thyroid function was normal in these children; their future risk of hypothyroidism is not known. (See "Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)", section on 'Radiation exposure'.)
Iodine — Both iodine deficiency and excess can cause hypothyroidism. Iodine deficiency is the most common cause of hypothyroidism (and goiter) worldwide [37]. When defined as an iodine intake less than 100 mcg/day, it affects approximately two billion people, many of whom live in mountainous areas. Iodine deficiency is rare in North America because iodized salt is ubiquitous and there are many other sources of iodine in the diet; it persists in parts of Europe because iodized salt is less frequently consumed in some countries. In certain regions (Africa, South America), the effect of iodine deficiency is magnified by consumption of foodstuffs such as cassava roots that contain cyanoglucosides; these substances are metabolized to thiocyanate, which has antithyroid properties and magnifies the effects of iodine deficiency [38]. (See "Iodine deficiency disorders".)
Iodine excess also can cause hypothyroidism by inhibiting iodide organification and T4 and T3 synthesis (the Wolff-Chaikoff effect). Normal subjects quickly "escape" from this effect of iodine. However, patients with abnormal thyroid glands do not, and they can become hypothyroid if given iodine for more than a few days. Patients at risk for iodine-induced hypothyroidism include those with chronic autoimmune thyroiditis and those who have had a partial thyroidectomy or a history of radioiodine therapy, painless, postpartum, or subacute granulomatous thyroiditis. The excess iodine can be derived from health tonics, cough medicines, kelp tablets and other dietary supplements, iodine-containing substances (eg, Betadine) applied to the skin or vagina, drugs such as amiodarone, and radiographic contrast agents (table 3). (See "Iodine-induced thyroid dysfunction".)
Drugs — The drugs given intentionally to decrease thyroid secretion (methimazole and propylthiouracil [and perchlorate]) can cause hypothyroidism. None have other uses and, therefore, should not be the cause of hypothyroidism in patients who do not have a history of hyperthyroidism. Ethionamide, an antimycobacterial drug used as a second-line agent for the treatment of multidrug-resistant tuberculosis, is structurally similar to methimazole and is a rare cause of hypothyroidism [39].
Drugs used to treat nonthyroid conditions that can cause hypothyroidism include lithium carbonate, amiodarone (an iodine-containing drug), interferon alfa, interleukin-2, tyrosine kinase inhibitors, and checkpoint inhibitor immunotherapy (eg, ipilimumab, pembrolizumab, and nivolumab) (table 4). Serum TSH should be measured when patients develop possible hypothyroid symptoms and, at minimum, every 6 to 12 months in patients taking these drugs. (See "Lithium and the thyroid" and "Amiodarone and thyroid dysfunction" and "Overview of thyroiditis", section on 'Drug-induced thyroiditis' and "Toxicities associated with immune checkpoint inhibitors", section on 'Autoimmune thyroid disease'.)
Oral tyrosine kinase inhibitors (eg, sunitinib, sorafenib, imatinib, motesanib) used for the treatment of gastrointestinal stromal tumors (GISTs), renal cell carcinoma, hepatocellular cancer, chronic myeloid leukemia, and in other cancers can cause hypothyroidism [40]. Of the kinase inhibitors, sunitinib appears to cause thyroid dysfunction most frequently, occurring in 15 of 42 patients (36 percent) in one report [41] and 21 of 40 patients in another report [42]. (See "Drug interactions with thyroid hormones", section on 'Tyrosine kinase inhibitors' and "Non-cardiovascular toxicities of molecularly targeted antiangiogenic agents", section on 'Thyroid dysfunction'.)
The RET inhibitor, selpercatinib, inhibits T4 to T3 conversion and can cause hypothyroidism, predominately in levothyroxine-treated patients [43].
In addition, patients with hypothyroidism who are taking T4 may become hypothyroid again, if given drugs that decrease T4 absorption (such as cholestyramine and iron salts), increase its clearance (such as phenytoin and carbamazepine), or decrease T4-to-T3 conversion (amiodarone). Thus, if the offending drug cannot be stopped, the T4 dose may need to be increased. (See "Drug interactions with thyroid hormones".)
Environmental exposures — Epidemiologic studies have reported an increased risk of hypothyroidism after exposure to some environmental toxins and contaminants [44]. As an example, polybrominated diphenyl ethers (PBDEs [flame retardants]) exposure has been associated with hypothyroidism (prevalence ratio 1.7, 95% CI 1-3) [45]. (See "Endocrine-disrupting chemicals", section on 'Thyroid disease'.)
Infiltrative disease — Infiltrative diseases, such as fibrous thyroiditis (Reidel's thyroiditis), hemochromatosis, scleroderma, leukemia, and cystinosis, are rare causes of hypothyroidism [46]. Amyloid goiter is likewise uncommon, although, when present, it often results in hypothyroidism. In one series, as an example, 5 of 19 patients (26 percent) with amyloid goiter were hypothyroid [47]. Infections of the thyroid, as with Mycobacterium tuberculosis and Pneumocystis carinii, occasionally damage the thyroid enough to cause hypothyroidism. (See "Infiltrative thyroid disease".)
Sarcoid infiltration can cause goiter. However, patients with sarcoidosis have a higher than expected prevalence of thyroid antibodies; thus, hypothyroidism in these patients also may have an autoimmune etiology [48].
Hypothyroidism in infants and children — The most common causes of congenital hypothyroidism are agenesis and dysgenesis of the thyroid, but a few have inherited defects in thyroid hormone biosynthesis or are delivered by mothers who were receiving an antithyroid drug for hyperthyroidism [49]. Among children who become hypothyroid later, the most common cause is chronic autoimmune thyroiditis. (See "Clinical features and detection of congenital hypothyroidism".)
Transient hypothyroidism — Hypothyroidism occurs transiently during the course of several types of thyroiditis. (See "Overview of thyroiditis".)
●Patients with silent (or postpartum) thyroiditis and subacute (or granulomatous) thyroiditis have inflammation of thyroid tissue with transient hyperthyroidism, frequently followed by transient hypothyroidism, then recovery of thyroid function. The hypothyroidism is usually more severe in patients with subacute thyroiditis, while occasional patients with painless thyroiditis will present during the hypothyroid phase of the illness.
Transient hypothyroidism can last from a few weeks to as long as six months in these disorders. Patients with minimal symptoms may not require therapy. Those with symptomatic hypothyroidism should be treated with T4, which can be given for several months, then discontinued. A normal serum TSH value six weeks later will confirm the recovery of thyroid function.
●Among women with postpartum thyroiditis, approximately 20 to 30 percent have hyperthyroidism followed by transient hypothyroidism and 40 to 50 percent have only transient hypothyroidism. In either instance, the hypothyroidism lasts several weeks to a few months. These figures are based on serial biochemical testing; the proportion of women with symptoms is smaller, and fewer need replacement therapy. (See "Postpartum thyroiditis".)
●Some patients who undergo subtotal thyroidectomy become hypothyroid after four to eight weeks but recover several weeks or months later. The probable explanation is that they have enough remaining thyroid tissue to maintain normal thyroid secretion once its growth has been stimulated by TSH.
●Many patients with Graves' hyperthyroidism whose glands were not completely ablated by radioiodine and who have some remaining thyroid tissue may have transient hypothyroidism after radioactive iodine therapy because TSH secretion, previously low, does not increase appropriately in response to low serum T4 concentrations for several weeks or months.
Withdrawal of exogenous thyroid therapy in patients who do not have hypothyroidism and in whom the therapy suppressed endogenous pituitary-thyroid function is sometimes followed by transient hypothyroidism until TSH secretion and then thyroid secretion resumes [50].
SECONDARY AND TERTIARY (CENTRAL) HYPOTHYROIDISM — Secondary hypothyroidism is that caused by TSH deficiency, and tertiary hypothyroidism is caused by thyrotropin-releasing hormone (TRH) deficiency. Less than 1 percent of patients with hypothyroidism have one of these forms of central hypothyroidism. (See "Central hypothyroidism".)
Most patients with central hypothyroidism have low or normal serum TSH concentrations (but inappropriately low in the presence of low serum T4 and T3 concentrations). However, a few patients with TSH deficiency have slightly high serum TSH values because they secrete TSH that is less glycosylated and therefore has less biological activity than normal TSH (but is normally immunoreactive).
Secondary hypothyroidism can be caused by any of the causes of hypopituitarism, most often a pituitary tumor [51] (see "Causes of hypopituitarism"). Most patients with pituitary microadenomas are euthyroid, whereas 10 to 25 of those with macroadenomas are hypothyroid, either initially or after surgical or radiation therapy. (A few patients who are initially hypothyroid become euthyroid after resection of a pituitary macroadenoma.)
Other causes of secondary hypothyroidism include postpartum pituitary necrosis (Sheehan syndrome), trauma, hypophysitis, nonpituitary tumors such as craniopharyngiomas, infiltrative diseases, and inactivating mutations in the gene for either TSH or the TSH receptor [52-56] (see "Resistance to thyrotropin and thyrotropin-releasing hormone"). TSH deficiency may be isolated, but more often, it occurs in association with other pituitary hormone deficiencies. (See "Causes of hypopituitarism" and "Clinical manifestations of hypopituitarism".)
Tertiary hypothyroidism can be caused by any disorder that damages the hypothalamus or interferes with hypothalamic-pituitary portal blood flow, thereby preventing delivery of TRH to the pituitary [51]. It can also be caused by mutations in the gene for the TRH receptor [57,58]. Like TSH deficiency, TRH deficiency can be isolated or occur in combination with other hormonal deficiencies. Hypothalamic damage results from tumors, trauma, radiation therapy, or infiltrative diseases.
TSH deficiency and TRH deficiency cannot be distinguished by biochemical tests. Any patient with findings suggestive of central hypothyroidism should undergo magnetic resonance imaging (MRI) of the hypothalamus and pituitary. The results allow inferences to be made as to which hormone is deficient, but the distinction is of no practical importance with respect to the patient's hypothyroidism.
RESISTANCE TO THYROID HORMONE — Resistance to thyroid hormone (RTH) is a rare disorder, usually inherited as an autosomal dominant trait. It is caused by mutations in the gene for the beta form of the T3 nuclear receptor. The abnormal receptors have a decreased affinity for T3, the physiologically active hormone within cells; they can also inhibit the action of the normal receptors [59]. (See "Resistance to thyroid hormone and other defects in thyroid hormone action".)
This disorder is included here because a few patients with the syndrome have had findings indicating the presence of hypothyroidism in infancy, such as short stature, deafness, and intellectual disability. However, most patients with this disorder are euthyroid (some have a suggestion of hyperthyroidism, such as tachycardia). There may be an association between this disorder and attention deficit hyperactivity disorder (ADHD), and learning disabilities and hearing loss are significant problems [59,60].
These patients are often discovered by accident as a result of a thyroid test; the characteristic findings are high serum T4 and T3 concentrations, with a normal or high serum TSH concentration. These biochemical findings indicate that the pituitary thyrotroph cells are relatively resistant to T4 and T3 (as are other tissues) and also that high serum T4 and T3 concentrations can overcome the resistance.
Treatment is usually unnecessary, but T4 or T3 may be given if symptoms of hypothyroidism occur.
RESISTANCE TO THYROTROPIN AND THYROTROPIN-RELEASING HORMONE — These rare disorders are due to inactivating mutations in the TSH or thyrotropin-releasing hormone (TRH) receptor genes, PAX8 gene mutations, and mutations in the long arm or chromosome 15. Some of these patients are euthyroid due to compensation from high serum levels of TSH, while others are hypothyroid and benefit from treatment with levothyroxine. (See "Resistance to thyrotropin and thyrotropin-releasing hormone".)
CONSUMPTIVE HYPOTHYROIDISM — Consumptive hypothyroidism is a very rare form of hypothyroidism characterized by excessive degradation of thyroid hormone due to the ectopic production of the type 3 deiodinase, which metabolizes T4 to reverse T3 and T3 to T2. This has been described in vascular and fibrotic tumors and in patients with gastrointestinal stromal tumors (GISTs) [61,62].
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: Hypothyroidism".)
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: Hypothyroidism (underactive thyroid) (The Basics)")
●Beyond the Basics topics (see "Patient education: Hypothyroidism (underactive thyroid) (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●The cause of primary hypothyroidism in most patients is Hashimoto's thyroiditis. Other common causes should be evident because of a history of surgery, radioiodine, or external radiation to the neck, or the use of drugs associated with hypothyroidism (table 1 and table 4). (See 'Primary hypothyroidism' above.)
●Infiltrative disorders, inherited defects in biosynthesis of thyroid hormone, and generalized resistance to thyroid hormone (RTH) are rare causes of hypothyroidism. (See 'Infiltrative disease' above and 'Hypothyroidism in infants and children' above and 'Resistance to thyroid hormone' above.)
●Causes of transient hypothyroidism, such as painless or postpartum thyroiditis, should also always be considered to avoid unnecessary lifelong treatment with thyroxine (T4). (See 'Transient hypothyroidism' above.)
●It is critical that secondary or central hypothyroidism is not missed; measurement of both thyroid-stimulating hormone (TSH) and free T4 should avoid misdiagnosis. (See 'Secondary and tertiary (central) hypothyroidism' above.)
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