2 I Epidemiology of Thyroid Dysfunction Hypothyroidism and Hyperthyroidism. Mark PJ Vanderpump. published by: Merck KGaA, Darmstadt, Germany

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1 2 I 2009 edited by: Peter PA Smyth, UCD, Dublin published by: Merck KGaA, Darmstadt, Germany Epidemiology of Thyroid D...

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2 I 2009

  edited by: Peter PA Smyth, UCD, Dublin

published by: Merck KGaA, Darmstadt, Germany

Epidemiology of Thyroid Dysfunction – Hypothyroidism and Hyperthyroidism Mark PJ Vanderpump

Thyroid International 2 2009

Epidemiology of Thyroid Dysfunction – Hypothyroidism and Hyperthyroidism Mark PJ Vanderpump Consultant Physician and Honorary Senior Lecturer in Endocrinology and Diabetes

Correspondence: Mark PJ Vanderpump Department of Endocrinology Royal Free Hampstead NHS Trust Pond Street London NW3 2QG United Kingdom Tel: +44 207 4726280 Fax: +44 207 4726487 Email: [email protected]

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Thyroid International 2 2009

Dr Mark Vanderpump has been a Consultant Physician and Honorary Senior Lecturer in Diabetes and Endocrinology at the Royal Free Hampstead NHS Trust in London since 1999. Having qualified at the University of Birmingham, his training was completed at posts in North East England and North Staffordshire. Whilst in Newcastle-upon-Tyne he was responsible for the 20-year follow-up of the Whickham survey. He has published on various aspects of thyroid disease and has been Secretary of the British Thyroid Association.

Description of Picture for Front Page The famous Champions Statue, commemorating three of West Ham's players who helped to win the 1966 World Cup for England. Captain Bobby Moore is held aloft with the cup. Geoff Hurst and Martin Peters, together with Ray Wilson (Fulham) are alongside him. It is located just outside Upton Park, the home ground of West Ham United Football Club in Newham, East London, near the site of the Olympic Stadium being built for 2012.

Thy­roid Inter­na­tional

­Editor-in-Chief: Peter PA Smyth, UCD, Dublin This is the ­title of a pub­li­ca­tion ­series by ­Merck KGaA, ­Darm­stadt, Germany. We are pub­lish­ing p ­ apers from renowned inter­na­tional thy­roid ­experts in ­order to pass on the exten­sive expe­ri­ence ­which the a­ uthors pos­sess in ­their ­field to a wide r­ ange of phy­si­cians ­dealing with the diagnosis and ther­apy of thy­roid dis­ ­­ eases. Respon­sible at M ­ erck KGaA, Darmstadt, Germany:  Sigrid Butz, M.D.

Thy­roid Inter­na­tional · 2–2009

­ erck KGaA, Darmstadt, Germany, D-64271 Darm­stadt M ISSN 0946-5464

H t Thyr idology

ETA’s journal on hot and controversial topics Free access:

www.hotthyroidology.com

Iodine Deficiency Disorders: Silent Pandemic

1. Introduction Thyroid disorders are amongst the most prevalent of medical conditions. Their manifestations vary considerably from area to area and are determined principally by the availability of iodine in the diet. Epidemiological studies of thyroid dysfunction have limitations, for example the definition of overt hypothyroidism and subclinical hypothyroidism, the selection criteria of the sample used, the influence of age, sex, genetic and environmental factors and the different techniques used for the measurement of thyroid hormones and the relative paucity of incidence data.1 Almost one-third of the world's population lives in areas of iodine deficiency.2 In areas where the daily iodine intake is below 50 μg, goitre is usually endemic, and when the daily intake falls below 25 μg, hypothyroidism is seen. The prevalence of goitre in areas of severe iodine deficiency can be as high as 80 %. Populations at particular risk tend to be remote and live in mountainous areas in South-East Asia, Latin America and Central Africa. Iodisation programmes are of proven value in reducing goitre size and in preventing goitre development and cretinism in children. Goitrogens in the diet, such as thiocyanate in incompletely cooked Cassava or thioglucosides in Brassica vegetables, can explain some of the differences in prevalence of endemic goitre in areas with similar degrees of iodine deficiency.

Autonomy can develop in nodular goitres leading occasionally to thyrotoxicosis and iodisation programmes can also induce thyrotoxicosis, especially in those aged over 40 years with nodular goitres. Autoimmune thyroiditis or hypothyroidism has not been reported to complicate salt iodisation programmes. Little prevalence data exists for autoimmune thyroid disease in areas of iodine deficiency.3 In iodine-replete areas, most persons with thyroid disorders have autoimmune disease, ranging through primary atrophic hypothyroidism, Hashimoto's thyroiditis to thyrotoxicosis caused by Graves' disease. Cross-sectional studies in Europe, the United States and Japan have determined the prevalence of hyperthyroidism and hypothyroidism and the frequency and distribution of thyroid autoantibodies in different, mainly Caucasian, communities.1 Recent data

from studies screening large population samples in the United States4,5 have revealed differences in the frequency of thyroid dysfunction and serum thyroid antibody concentrations in different ethnic groups, whereas studies from Europe have shown the influence of dietary iodine intake on the epidemiology of thyroid dysfunction.6 However studies of incidence of autoimmune thyroid disease have only been conducted in a small number of developed countries.7

2. Hypothyroidism In persons living in iodine-replete areas, the cause of acquired hypothyroidism is either chronic autoimmune disease (atrophic autoimmune thyroiditis or goitrous autoimmune thyroiditis [Hashimoto's thyroiditis]) or destructive treatment for thyrotoxicosis, but this is rarely discussed in the available studies. In iodinedeficient countries a daily iodine intake below 25 µg, particularly in preterm infants, is a more frequent cause of hypothyroidism accounting for many cases in Europe, Asia and Africa.

2.1 Congenital hypothyroidism Congenital hypothyroidism affects about one newborn in 3,500 to 4,000 births and is the most treatable cause of mental retardation.1 There is an inverse relationship between age at diagnosis and intelligence quotient (IQ) in later life. In iodine-replete areas, 85 % of the cases are due to sporadic developmental defects of the thyroid gland (thyroid dysgenesis) such as the arrested migration of the embryonic thyroid (ectopic thyroid) or a complete absence of thyroid tissue (athyreosis). The remaining 15 % have thyroid dyshormonogenesis defects transmitted by an autosomal recessive mode of

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Thyroid International 2 2009

inheritance. Clinical diagnosis occurs in less than 5 % of newborns with hypothyroidism because symptoms and signs are often minimal. As a result it is not possible to predict which infants are likely to be affected. Without prompt diagnosis and treatment most affected children gradually develop growth failure, irreversible mental retardation and a variety of neuropsychological deficits. The value of screening for congenital hypothyroidism in heel-prick blood specimens is unquestioned, and it is now done routinely in many countries. 2.2 Asymptomatic autoimmune thyroiditis The presence of high serum concentrations of thyroid antibodies (anti-thyroid peroxidase [microsomal] [TPOAb] and anti-thyroglobulin [TGAb]) correlates with the presence of focal thyroiditis in thyroid tissue obtained by biopsy and at autopsy from patients with no evidence of hypothyroidism during life. Early post-mortem studies confirmed histological evidence of chronic autoimmune thyroiditis in 27 % of adult women, with a rise in frequency over 50 years, and 7 % of adult men, and diffuse changes in 5 % of women and 1 % of men.1 Patients with hypothyroidism caused by either atrophic or goitrous autoimmune thyroiditis usually have high serum concentrations of these same antibodies. These antibodies also are often detected in serum of patients with Graves’ disease and other thyroid diseases, but the concentrations are usually lower. There is considerable variation in the frequency and distribution of thyroid antibodies because of variations in techniques of detection, definition of abnormal titres, and inherent differences in the populations tested. In the UK Whickham survey, the mean serum TSH concentrations were significantly higher in both men and women with positive serum antithyroid antibody tests, and 3 % of the subjects (5 % of women, 1 % of men) had both positive antibody tests and a serum TSH value greater than 6 mU/L.8 In the Third National Health and Nutrition Examination Survey (NHANES III) in the USA, the percentage of subjects with high serum TPOAb and TGAb concentrations increased with age in both men and women, and high concentrations were more prevalent in women than in men and less prevalent in

blacks than in other ethnic groups.5 Using a competitive immunoassay procedure, the reported prevalence of detectable TGAb and TPOAb levels were 10 % and 12 % of the healthy population. A hypoechoic ultrasound pattern or an irregular echo pattern may precede TPOAb positivity in autoimmune thyroid disease, and TPOAb may not be detected in more than 20 % of individuals with ultrasound evidence of thyroid autoimmunity.9 2.3 Prevalence of hypothyroidism In iodine-replete communities, the prevalence of spontaneous hypothyroidism is between 1 % and 2 %, and it is more common in older women and ten times more common in women than in men.1 In the Whickham survey, the prevalence of newly diagnosed overt hypothyroidism was 3 per 1000 women.8 The prevalence of previously diagnosed and treated hypothyroidism was 14 per 1000 women, increasing to 19 per 1000 women when possible but unproven cases were included. The overall prevalence in men was less than 1 case per 1000. One third had been previously treated by surgery or radioiodine for thyrotoxicosis. Excluding iatrogenic causes, the prevalence of hypothyroidism was 10 per 1000 women, increasing to 15 per 1000 when possible but unproven cases were included. The mean age at diagnosis was 57 years. Other studies in Northern Europe, Japan and the USA have found the prevalence to range between 0.6 and 12 per 1000 women and between 1.3 and 4.0 per 1000 in men investigated (see Table 1 and [1] for references). In the Colorado and NHANES III studies, the prevalence of newly diagnosed hypothyroidism was 4 per 1000 and 3 per 1000 respectively.4,5 In Pescopagano, Italy, an area of mild iodine deficiency (median urinary iodine excretion 55 μg/L), the prevalence of newly diagnosed overt hypothyroidism was 0.3 % of 573 women (autoimmune thyroiditis confirmed as aetiology) (there were no cases among 419 men), and no subject had been diagnosed and treated for hypothyroidism.10 In borderline iodine-deficient Copenhagen, Denmark, 6 per 1000 of the women and 2 per 1000 men had overt but undiagnosed hypothyroidism, and 1 % of all subjects were taking thyroxine.11

Iodine Deficiency Disorders: Silent Pandemic

Table 1. Prevalence of previously undiagnosed overt hypothyroidism and incidence of overt hypothyroidism in selected epidemiological surveys of thyroid dysfunction (see reference 1 unless stated) Study Name

N

Age (Years)

Test

2779

18+

TSH, T4

Colorado, USA4 NHANES III, USA5 Pescopagano, Italy10 Sapporo, Japan Copenhagen, Denmark11 Memphis/Pitttsburgh, USA14 Leiden, Netherlands12 Tayside, UK (1993–1997)16

25,862 16,533   992 4110 2656 2797   558 390,000

18+ 12+ 15+ 25+ 41–71 70–79 85–89 0+

Tayside, UK (1997-2001)17

390,000

0+

TSH TSH TSH, FT4 TSH TSH, FT4 TSH, FT4 TSH, FT4 Treatment for hypothyroidism As above

1283 1210 1148

44–66 60+ 70+

TSH TSH TSH

Whickham, UK8,15

Göteborg, Sweden Birmingham, UK Gothenburg, Sweden

The prevalence is higher in surveys of the elderly in the community.1 The overall prevalence of hypothyroidism,

including those already taking T4, in Birmingham, UK, of 1210 subjects aged 60 and over was 4 % of women and 0.8 % of men aged over 60 years. In subjects aged 60 years or more in Framingham, 4 % had serum TSH concentration greater than 10 mU/L, of whom one-third had low serum T4 concentrations.7 Overt hypothyroidism was found in 7 % of 558 subjects aged between 85 and 89 years in Leiden, Netherlands.12 2.4 Subclinical hypothyroidism

The term subclinical hypothyroidism is used to describe the finding of a raised serum TSH but a normal FT4 in an asymptomatic patient. In the community, the most common aetiology is chronic autoimmune thyroiditis.1,9 In the original Whickham survey, 8 % of women (10 % of women over 55 years of age) and 3 % of men had subclinical hypothyroidism.8 In the Colorado, USA, study, 9.4 % of the subjects had a high serum TSH concentration, of whom 9.0 % had subclinical hypothyroidism.4 Among those with a high serum TSH concentration, 74 % had a value between 5.1 mU/L and 10 mU/L and

Prevalence n/1000 Men Women  0   3.3

Incidence n/1000/year Follow-up Men Women 20 years 0.6 3.5 (0.3–1.2) (2.8–4.5)

4.0 2.0  0 2.4 2.0 5.4

  3.0   8.5   5.0 13.0







4 years

0.88 (0.80–0.95)

4.98 (4.81–5.17)

4 years

1.09 4.75 (0.95–1.25 (4.46–5.07) — 1–2 11.1 — 2

70 —

— 7.8 —



  6.4 20.5 —

4 years 1 year 10 years

26 % had a value greater than 10 mU/L. The percentage of subjects with a high serum TSH concentration was higher for women than men in each decade of age, and ranged from 4 to 21% in women and 3 to 16% in men. An increase in serum TSH concentrations was also found in men in the NHANES III study. In the same study serum TSH concentrations increased with age in both men and women and were higher in whites than blacks, independent of serum antithyroid antibody concentrations.5 Community studies of elderly persons have confirmed the high prevalence of subclinical hypothyroidism in this age group, with approximately 10 % of subjects over 60 years having serum TSH values above the normal range.6,9 A further analysis of the NHANES III data demonstrated that the 97.5 centile for those subjects aged over 80 was 7.49 mU/L and 70 % had a serum TSH greater than the population defined upper limit of the reference range of 4.5 mU/L of whom only 40 % were anti-thyroid antibody positive.13 Data from a US cohort aged 70 to 79 years found that black subjects had a significantly lower prevalence of subclinical hypothyroidism (2 % in men, 3 % in women), as compared with white subjects (4 % in men, 6 % in women).14

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In Pescopagano, there was a slightly lower prevalence ratios (with 95 % CI) of developing spontaneous hypoof subclinical hypothyroidism (4 % of women and 3 % thyroidism in surviving women are shown in Table 2. of men), but high serum antithyroid antibody concenEither raised serum TSH or positive thyroid antibodies trations were as prevalent, although at lower titres, as in alone or in combination are associated with a signifi10 iodine-replete communities. In Copenhagen (median cantly increased risk of hypothyroidism. The odds are urinary iodine excretion 70 μg/L), only 0.7 % of subjects greatly increased when both risk factors are present had subclinical hypoand each had a similar Table 2. D  evelopment of spontaneous hypothyroidism in surviving thyroidism, and 83 % effect. The smaller women and men at 20-year follow-up of Whickham survey: of them had serum number of observed odds ratios (with 95 % CI)7 antithyroid antibody cases in men resulted concentrations greater Women in wide but highly 11 14 (9–24) than 200 kU/L. Other TSH raised, regardless of thyroid antibody status significant confidence 13 (8–19) studies of elderly per- Thyroid antibody + , regardless of TSH status limits but also did not If thyroid antibody , effect of raised TSH alone   8 (3–20) sons in iodine-deficient allow the independent   5 (2–11) areas have suggested a If thyroid antibody + , additional effect of raised TSH effects of these risk   8 (5–15) high prevalence of sub- If TSH normal, effect of thyroid antibody + alone factors to be calcuIf TSH raised, additional effect of thyroid antibody +   5 (1–15) clinical hypothyroidlated. In the surviving TSH raised and thyroid antibody + combined 38 (22–65) ism with approximatewomen the annual risk ly 10 % of subjects over of spontaneous overt 60 years having serum Men hypothyroidism was TSH raised, regardless of thyroid antibody status   44 (19–104) TSH values above 4 % in those who had Thyroid antibody + , regardless of TSH status   25 (10–63) the normal range. both high serum TSH 173 (81-370) Subclinical hypothy- TSH raised and thyroid antibody + combined and antithyroid antiroidism is found at body concentrations, higher frequency (18 % in Iceland and 24 % in Hungary) 3 % if only their serum TSH concentrations was high, in areas where iodine intake is high, but most cases are and 2 % if only their serum thyroid antibody concentranot of autoimmune origin.1 tion was high; at the time of follow up the respective rates of hypothyroidism were 55 %, 33 %, and 27 %. The probability of developing hypothyroidism was higher 2.5 Incidence of overt hypothyroidism in those women who had serum TSH concentrations above 2.0 mU/L and high serum titres of antithyroid The 20 year follow up of the Whickham cohort promicrosomal antibodies during the first survey. vided incidence data and allowed the determination of risk factors for spontaneous hypothyroidism in this period.15 The mean annual incidence of spontaneous hypothyroidism in the surviving women during the 20 year follow up period was 3.5 per 1000 (95 % confidence interval [CI] 2.8 to 4.5), increasing to 4.1 per 1000 (95 % CI 3.3 to 5.0) if all cases including those who had received destructive treatment for thyrotoxicosis were included. The mean annual incidence during the 20-year follow-up period in men (all spontaneous except for one case of lithium-induced hypothyroidism) was 0.6 per 1000 (95 % CI 0.3 to 1.2). The risk of having developed hypothyroidism was examined with respect to risk factors identified in the first survey. The odds

The other incidence data for hypothyroidism are from short (and often small) follow-up studies.7 In elderly subjects, the annual incidence rate of hypothyroidism varies widely between 0.2 and 7 % in the available studies (see Table 1 and [1] for references). Data from the large population study in Tayside, UK, has demonstrated that the standardised incidence of primary hypothyroidism varied between 3.90 and 4.89 per 1000 women per year between 1993 and 2001. The incidence of hypothyroidism in men significantly increased from 0.65 to 1.01 per 1000 per year (P = 0.0017). The mean age at diagnosis of primary hypothyroidism decreased in women from 1994 to 2001.16,17

Iodine Deficiency Disorders: Silent Pandemic

Spontaneous recovery has also been described in subjects with subclinical hypothyroidism, although the frequency of this phenomenon is unclear. In one study, 37 % of patients normalised their serum TSH levels over a mean follow-up time of 31.7 months. Normalisation of serum TSH concentrations were more likely to occur

in patients with negative antithyroid antibodies and serum TSH levels less than 10 mU/L, and within the first two years after diagnosis.9 However, all studies indicate that the higher the serum TSH value, the greater the likelihood of development of overt hypothyroidism in subjects with chronic autoimmune thyroiditis.

3. Hyperthyroidism The most common causes of hyperthyroidism are Graves' disease, followed by toxic multinodular goitre, whilst rarer causes include an autonomously functioning thyroid adenoma, or thyroiditis. In epidemiological studies, however, the aetiology is rarely ascertained. 3.1 Prevalence of hyperthyroidism

79 years in the US found evidence of hyperthyroidism (defined biochemically as a serum TSH concentration less than 0.1 mU/L and a serum free T4 concentration greater than 23 pmol/L in only five subjects (one man and four women).14 In Leiden only 2 of 558 subjects aged between 85 and 89 years had newly diagnosed overt hyperthyroidism.12

The prevalence of hyperthyroidism in women is between 0.5 and 2 %, and is ten times more common in women than in men in iodine-replete communities. In the Whickham survey, the prevalence of undiagnosed hyperthyroidism was 4.7 per 1000 women.8 Hyperthyroidism had been previously diagnosed and treated in 20 per 1000 women, rising to 27 per 1000 women when possible but unproven cases were included, as compared with 1.6 to 2.3 per 1000 men, in whom no new cases were found at the survey. The mean age at diagnosis was 48 years. Other available cross-sectional studies of the adult population provide comparable data (see Table 3 and [1] for references). In NHANES III, in those subjects who were neither taking thyroid medication nor reported histories of thyroid disease, 2 per 1000 had “clinically significant” hyperthyroidism, defined as a serum TSH concentration less than 0.1 mU/L and a serum total T4 concentration greater than 170 nmol/L.5 Overt hyperthyroidism, defined as serum TSH concentration less than 0.01 mU/L, was present in only 1 per 1000 of those not taking thyroid medication in the cross-sectional survey of 25,682 subjects aged over 18 years attending the Health Fair in Colorado.4

The prevalence of undiagnosed hyperthyroidism in Pescopagano was higher, at 2 %, with a further 1 % of adults there having a history of toxic nodular goitre.10 Approximately one-third had a diffuse goitre; the frequency in men and women was similar. In a population sample of 2656 from Copenhagen, another area of mild iodine deficiency, newly diagnosed thyrotoxicosis was found in 1.2 % of women and no men, and the prevalence of known thyrotoxicosis was 1.4 %.11

The prevalence data in elderly persons show a wide range between 0.4 % to 2.0 %.1 A cross-sectional study of 2799 healthy community-dwelling adults aged 70 to

The reported overall prevalence ranges from 0.5 % to 6.3 %, with men and women over 65 years having the highest prevalence; approximately half of them are tak-

3.2 Subclinical hyperthyroidism Subclinical hyperthyroidism is defined as a low serum TSH concentration and normal serum T4 and T3 concentrations, in the absence of hypothalamic or pituitary disease, non-thyroidal illness, or ingestion of drugs that inhibit TSH secretion such as glucocorticoids or dopamine. The available studies differ in the definition of a low serum TSH concentration and whether the subjects included were receiving thyroxine therapy. The third generation assays have rarely been used in epidemiological studies.1

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ing thyroxine.1,9 Among these studies, the serum TSH cut-off value ranged from less than 0.1 mU/L to less than 0.5 mU/L and it is not clear how this difference affected the reported prevalence rates. Among subjects with subclinical hyperthyroidism, those with low but detectable serum TSH values may recover spontaneously when retested. In the Colorado study of 25,862 subjects (of whom 88 % were white), and in which the serum TSH cut-off value was 0.3 mU/L, the overall prevalence of subclinical hyperthyroidism was 2.1 %.4 In contrast, the NHANES III study, defining subclinical hyperthyroidism using a more stringent 0.1 mU/L as the serum TSH cut-off, reported an overall prevalence of 0.7 % in the total population and 0.2 % in the thyroid disease-free population (n = 13,344). The rates were highest in those subjects aged 20 to 39 years and those more than age 79 years. In this study the percentage of subjects with serum TSH concentrations less than 0.4 mU/L was significantly higher in women than men, and black subjects had significantly lower mean serum TSH concentrations, and therefore a higher prevalence of subclinical hyperthyroidism (0.4 %) than whites (0.1 %) or Mexican Americans (0.3 %). In the US study of subjects aged 71 to 79 years the prevalence was 1.1 % in women and 0.7 % in men and there was no difference between black and white residents.14 In the Leiden study of subjects aged over 85 years, the prevalence was 3 %.12 The prevalence of subnormal serum TSH concentrations (detection limit 0.01 mU/L and excluding those subjects taking thyroxine) was higher in the iodine-deficient population of Pescopagano (6 %), due to functional autonomy from nodular goitres.10 In Jutland, an area of mild iodine deficiency in Denmark, 10 % of a random sample of 423 subjects had low serum TSH concentrations, as compared with 1 % of 100 subjects of similar age in iodine-rich Iceland. Subclinical hyperthyroidism was not detected in a group of elderly nursing home residents in an iodine-rich region of Hungary.3 3.3 Incidence of hyperthyroidism The incidence data available for overt hyperthyroidism in men and women from large population studies are comparable, at 0.4 per 1000 women and 0.1 per 1000 men,

but the age-specific incidence varies considerably (Table 3 and [1] for references). The peak age-specific incidence of Graves’ disease was between 20 and 49 years in two studies, but increased with age in Iceland and peaked at 60 to 69 years in Malmö, Sweden. The peak age-specific incidence of hyperthyroidism caused by toxic nodular goitre and autonomously functioning thyroid adenomas in the Malmö study was over 80 years. The only available data in a black population, from Johannesburg, South Africa, also suggest a tenfold lower annual incidence of hyperthyroidism (0.09 per 1000 women and 0.007 per 1000 men) than in whites. In the survivors of the Whickham survey cohort, 11 women had been diagnosed and treated for hyperthyroidism after the first survey and five women were diagnosed at the second survey.15 The aetiology in these 16 new cases was Graves' disease in 10 subjects, multinodular goitre in three subjects, an autonomously functioning thyroid adenoma in one, chronic autoimmune thyroiditis in one and unknown in one. The mean annual incidence of hyperthyroidism in women was 0.8 per 1000 survivors (95 % confidence interval [CI] 0.5 to 1.4).9 The incidence rate was similar in the deceased women. No new cases were detected in men. Other cohort studies provide comparable incidence data, which suggests that many cases of hyperthyroidism remain undiagnosed in the community unless routine testing is undertaken.1 In the large population study in Tayside, Scotland, 620 incident cases of hyperthyroidism were identified with an incidence rate of 0.77/1000 per year (95 % CI 0.70 to 0.84) in women and 0.14/1000 per year (95 % CI 0.12 to 0.18) in men.16 The incidence increased with age, and women were affected two to eight times more than men across the age range. Recent further analysis suggested that the incidence of thyrotoxicosis was increasing in women but not in men between 1997 and 2001.17 Data on the risk of progression of subclinical hyperthyroidism to overt hyperthyroidism are limited. In the majority of subjects a detectable below normal serum TSH will eventually rise towards normal. In those subjects with an undetectable serum TSH and a confirmed aetiology due to Graves’ disease or nodular disease, it has been calculated from short follow-up studies that the annual incidence is approximately 5 %.1,9

Iodine Deficiency Disorders: Silent Pandemic

Table 3. Prevalence of previously undiagnosed overt hyperthyroidism and incidence of overt hyperthyroidism in selected epidemiological surveys of thyroid dysfunction (*TRAB = TSH receptor antibody, PBI =Protein-bound iodine, FT4I = Free thyroxine index). (See reference 1 unless stated) Study Name

N

Age (Years)

Test

2779

18+

T4, FT4I

Colorado, USA4 NHANES III, USA5 Pescopagano, Italy10 Sapporo, Japan Copenhagen, Denmark11 Memphis/Pittsburgh, USA14

25,862 16,533   922 4110 2656 2797

18+ 12+ 15+ 25+ 41–71 70–79

TSH TSH, TT4 TSH, FT4 TSH, TRAB* TSH, FT4 TSH, FT4

Leiden, Netherlands12 Tayside, UK (1993-1997)16

  599 390,000

85–89 0+

Tayside, UK (1997-2001)17

390,000

0+

TSH, FT4 Treatment for hyperthyroidism As above

Johannesburg, South Africa Birmingham, UK Gothenburg, Sweden Funen, Denmark Iceland Malmö, Sweden

? 1210 1148 450000 230000 257764

0+ 60+ 70+ 0+ 0+ 0+

T4 TSH TSH PBI, T4, T4 T4, T4 PBI

Whickham, UK8,15

Prevalence n/1000 Men Women 0 4.7

Incidence n/1000/year Follow-up Men Women 20 years
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