Iodine-induced Hyperthyroidism Research Articles

A Case of Iodine-induced Thyrotoxicosis with Acromegaly

Hyperthyroidism is seen in 3.5-26% of subjects with acromegaly. Hyperthyroidism can be developed by thyroid stimulating hormone (TSH) dependent mechanism in TSH-secreting adenomas with acromegaly or by TSH independent mechanism through the stimulation of thyroid cells by growth hormone (GH). So, confirming the cause of hyperthyroidism is important to treat that. We report a case of a 56-year-old man who had acromegaly with iodine-induced thyrotoxicosis. He took the sea tangle for 4 years because he had constipation. His face and hands indicated acromegaly. Thyroid function test showed that T3 and free T4 were increased and TSH was decreased. Ultrasonography of neck showed diffuse enlargement of thyroid gland and thyroid scan showed decreased uptake of thyroid gland. So we could confirm iodine-induced thyrotoxicosis due to excessive iodine intake. Serum GH and insulin-like growth factor (IGF)-1 were markedly increased and brain MRI showed heterogenous 1 cm sized pituitary mass in right side. Acromegaly was confirmed by brain MRI, pituitary stimulation test and increased level of GH, IGF-1. He stopped iodine intake. After 6 months, T3, free T4 and TSH were normalized and he is waiting for the surgical removal of pituitary adenoma (J Kor Soc Endocrinol 21:63~67, 2006).

Thyrotoxicosis

<h2>Abstract</h2> Thyrotoxicosis affects 1% of women and 0.1% of men. The most common causes are Graves' disease and toxic nodular thyroid disease (caused by a multinodular goitre or an adenoma), but it is important to distinguish these types of disease from destructive thyrotoxicosis, which is usually self-limiting and caused by transient autoimmune destruction, viral infection or amiodarone. About one-half of patients with Graves' disease treated with antithyroid drugs are cured, whereas these drugs achieve only temporary biochemical control of hyperthyroidism in toxic nodular disease. Carbimazole is the first-line treatment in the UK, whereas methimazole and propylthiouracil are more commonly used elsewhere. Relapse is usually treated with radioactive iodine or surgery, both of which carry a high rate of subsequent hypothyroidism. Radioiodine may also cause worsening of thyroid-associated ophthalmopathy, particularly in patients who smoke. Radioiodine is first-line treatment in toxic nodular disease. Corticosteroids are used to treat severe cases of viral thyroiditis and the destructive thyroiditis that can accompany amiodarone treatment, though the latter must be distinguished from iodine-induced hyperthyroidism, which can also occur with this drug, and may require treatment with potassium perchlorate in addition to high doses of antithyroid drugs.

Reappraisal of the risk of iodine-induced hyperthyroidism: An epidemiological population survey

The occurrence of iodine-induced hyperthyroidism (IIH) has been reported after iodine supplementation from clinics and hospitals, but not following an epidemiologic survey. We studied the prevalence of thyroid derangement in a population following iodine supplementation. One yr after more than 75% of the population had been consuming 40 ppm iodized salt; information regarding history of endemic goiter and iodized salt production, distribution, consumption and monitoring were collected in four cities of the Islamic Republic of Iran. A total of 6048 subjects were randomly selected. All subjects were assessed for size of goiter, and urinary iodine and serum T4, T3, TSH, anti-thyroglobulin and anti-thyroperoxide were measured. Before iodine supplementation, all four cities were areas of endemic goiter. The rate of household consumption of iodized salt was 50, 75 and 90% in 1994, 1995 and 1996, respectively. Ninety-one percent of the salt samples contained 15-55 ppm iodide. Total goiter rate was 57, 62 and 68%; median urinary iodine was 188, 197 and 190 microg/l in the age groups of 6-18, 19-40 and >40 yr, respectively. Prevalence of clinical and subclinical hyperthyroidism was 0.34 and 0.41 and those of clinical and subclinical hypothyroidism were 0.51 and 1.07%, respectively. Nine point eight and 18% in the 19-40 yr age group and 17.6 and 25.6% in >40 yr old subjects had positive anti-thyroperoxidase and anti-thyroglobulin, respectively. This systemic epidemiologic study in an iodine deficient population showed that, following a well-executed iodine supplementation program, the occurrence of IIH is rare.

Thyroid functional features after diagnostic studies with iodine-containing X-ray contrast substances

Iodine-containing radiopaque preparations have been widely used for diagnostic purposes. The absolute amount of iodine introduced in this case is 200,000 to 350,000 times the daily requirement for the element. Throughout life, a person consumes only about 3-5 g of iodine, while during coronary angiography the dose of parenterally administered iodine is about 25-52 g. In this regard, the possibility of development should be taken into account when conducting diagnostic studies using radiopaque drugs iodine-induced conditions, especially in people of an older age group, among which the prevalence of thyroid pathology is especially high. The presence of autonomous formations in the thyroid gland (thyroid gland), often unrecognized, can lead to the development of iodine-induced thyrotoxicosis (IIT) after the introduction of pharmacological doses of iodine, which in turn can lead to deterioration in the course of IHD and the development of arrhythmic complications. We continue discussion the need for screening for the detection of functional thyroid dysfunctions and an ultrasound of the thyroid gland before the introduction of iodine-containing radiopaque drugs. The controversial issue remains the need for preventive treatment with thyreostatic drugs of people at risk of developing IIT.

Iodine status as determined by urinary iodine excretion in Lesotho two years after introducing legislation on universal salt iodization

Objective Mildto severe iodine deficiency has been documented in Lesotho since 1960.To eliminate the persisting iodine deficiency, legislation on universalsalt iodization was introduced in 2000 as a long-term public healthintervention strategy. We assessed the urinary iodine status of schoolchildren and women of child-bearing age in Lesotho 2 y afterthe introduction of legislation on universal saltiodization. Methods A31-cluster national survey was conducted in 2002 by using theproportion to population size method. In each cluster, 30 women ages 15to 30 y and 30 primary school children ages 8 to 12y were randomly selected to provide urine samples for urinary iodineanalysis. Data were interpreted according to criteria of the WorldHealth Organization, United Nations Children's Fund, andInternational Council for Control of Iodine Deficiency Disorders(2001). Statistical analysis was performed usingSAS. Results Weanalyzed 912 urine samples from children and 924 from women. The medianurinary iodine concentrations were 214.7 μg/L for children and280.1 μg/L for women, indicating more than adequate iodineintake. Median iodine concentration was higher in the lowlands (256.0μg/L in children and 329.9 μg/L in women) than in themountains (99.30 μg/L in children and 182.6 μg/L inwomen). Analysis of the distribution of the data showed values below 50μg/L in 10.1% of children and in 9.8% of women. Inaddition, 21.5% of children and 17.9% of women hadurinary iodine excretion values below 100 μg/L. In contrast,36% of children and 47.2% of women had urinary iodineconcentrations in excess of 300μg/L. Conclusion Results of urinary iodineexcretion measurements indicated that iodine deficiency has beeneliminated as a public health problem in Lesotho. However, the highmedian urinary iodine concentration of women in the lowlands indicatedthe possibility of a risk of iodine-induced hyperthyroidism invulnerablepeople.

Scintigraphy for Risk Stratification of Iodine-Induced Thyrotoxicosis in Patients Receiving Contrast Agent for Coronary Angiography: A Prospective Study of Patients with Low Thyrotropin

The risk of iodine-induced thyrotoxicosis in euthyroid patients receiving iodine-containing contrast agents is known to be low, but data on this risk in patients with latent hyperthyroidism are scarce. We investigated the role of thyroid scintigraphy using Tc-99m preceding the application of iodine-containing contrast material to estimate the risk of iodine-induced thyrotoxicosis in patients with low levels of TSH. In a prospective study on 91 patients, thyroid scintigraphy was performed before coronary angiography (CA). In patients with technetium thyroid uptake (TCTU) less than 1%, CA was done without prophylactic drugs (n = 56). Patients with TCTU greater than 1% were treated either with 900 mg of perchlorate or, depending on the autonomous volume, combined with 20 to 60 mg thiamazole. In the 56 patients with TCTU less than 1%, no case of iodine-induced hyperthyroidism occurred within 4 wk after CA. In the patients who received prophylactic drugs, two cases of mild thyrotoxicosis were observed. Our data suggest that in patients with low levels of TSH, the risk of hyperthyroidism after application of iodine-containing contrast media is negligible if TCTU is less than 1%. In these patients, CA can be performed without administration of prophylactic drugs.

Gadolinium as an alternative contrast agent during cardiac catheterization in patient with iodine-induced hyperthyroidism

We report the first case of a male patient with iodine-induced hyperthyroidism and unstable angina pectoris in whom a diagnostic cardiac catheterization with gadolinium as contrast agent was chosen. N.K., a 63-year-old caucasian male, underwent percutaneous transluminal angioplasty requiring visualisation with an iodinated contrast agent. Subsequent to this intervention he developed symptomatic hyperthyroidism with persistent arrhythmia and chest pain, necessitating hospitalization. The patient was started on high dose thiamazole and propronolol. During hospitalization coronary angiography seemed necessary. As the iodine load of conventional angiography was decided to pose a high risk of thyroid storm, the procedure was performed with the non-iodine based gadolinium. Gadolinium is not nephrotoxic and does not affect thyroid function. The exam was completed without side effects, revealing no significant stenoses of the coronary arteries. Three months later, when the patient had normal thyroid levels, cardioversion succeded to revert the atrial fibrillation to sinus rhythm. Patients with iodine induced hyperthyreoidism may develop cardiac complications such as unstable angina pectoris up to an acute coronary syndrome. A diagnostic or therapeutic coronary angiography with iodinated contrast agent often aggravates hyperthyroidism. Although imaging quality with gadolinium is not as good as with iodinated contrast agent, clinically useful angiogramms can be produced. Thus, gadolinium appears to be a low risk alternative for angiography, especially in patients with overt hyperthyroidism.

Hyperthyroidism in Patients Older than 55 Years: An Analysis of the Etiology and Management

Background: Hyperthyroidism is a common disease in the elderly. Although some studies on the prevalence of this thyroid disorder have been performed in the aged population, several aspects of hyperthyroidism, such as etiology and treatment effectiveness, have not been fully characterized in large series of aged patients. Objective: The aims of the present study were to determine the frequency of the diverse etiologies of hyperthyroidism, and to assess the effectiveness of therapy in adult patients older than 55 years. Methods: We performed a descriptive, observational, cross-sectional study in the setting of a hospital endocrinology clinic. We studied a group of 313 patients with hyperthyroidism. There were 246 women (78.6%, age 67.02 ± 8.35 years) and 67 men (21.4% age 63.34 ± 7.63 years). Overt hyperthyroidism was diagnosed in 167 patients (53.4%) and subclinical hyperthyroidism in the remaining 146 subjects (46.6%). In every patient we studied: the etiology; presence or absence of goiter; time of evolution from diagnosis; previously and presently used treatments; current thyroid functional status (free thyroxine and thyrotropin concentrations); adequacy of disease control, and thyroid autoimmune status. Results: The different etiologies of hyperthyroidism were as follows: toxic multinodular goiter 43.1%; Graves’ disease 21.4%; iatrogenic thyrotoxicosis 16.0%; toxic adenoma 11.8%; iodine-induced thyrotoxicosis 1.2%; subacute thyroiditis 1.0%; painless thyroiditis 0.3%; factitious thyrotoxicosis 0.3%; TSH-secreting pituitary adenoma 0.6%, and unknown etiology 3.8%. Etiology was related to age, sex, presence of goiter, degree of hyperthyroidism and autoimmune status. 77.6% of patients had been diagnosed in the last 5 years, and 91.3% in the last 10 years. Preferred therapies were thionamide drugs in patients with Graves’ disease and radioiodine in patients with hyperthyroidism due to nodular disease. Surgery was performed in a limited number of patients. Periodic follow-up was used in patients with subclinical hyperthyroidism. Control of the disease was adequate in 65.3% and inadequate in 34.7% of patients who received any kind of previous therapy. In this group of patients, logistic regression analysis showed that the probability of attaining good control of hyperthyroidism was greater in patients with overt thyrotoxicosis compared to patients with subclinical thyrotoxicosis. Conclusion: In patients older than 55 years, toxic multinodular goiter is the most frequent etiology of spontaneous hyperthyroidism, followed by Graves’ disease and toxic adenoma. Most patients with thyroid hyperfunction can be adequately controlled, provided that effective therapy is administered. Patients with overt hyperthyroidism seem to have a higher probability of attaining adequate control of their disease than patients with subclinical hyperthyroidism, regardless of age, sex or etiology.

Iodised salt for preventing iodine deficiency disorders.

Iodine deficiency is the main cause for potentially preventable mental retardation in childhood, as well as causing goitre and hypothyroidism in people of all ages. It is still prevalent in large parts of the world. To assess the effects of iodised salt in comparison with other forms of iodine supplementation or placebo in the prevention of iodine deficiency disorders. We searched the Cochrane Library, Medline, the Register of Chinese trials developed by the Chinese Cochrane Centre, and the Chinese Med Database. We performed handsearching of a number of journals (Chinese Journal of Control of Endemic Diseases, Chinese Journal of Epidemiology, Chinese Journal of Preventive Medicine, and Studies of Trace Elements and Health up to February 2001), and searched reference lists, databases of ongoing trials and the Internet. Date of latest search: November 2001. We included prospective controlled studies of iodised salt versus other forms of iodine supplementation or placebo in people living in areas of iodine deficiency. Studies reported mainly goitre rates and urinary iodine excretion as outcome measures. The initial data selection and quality assessment of trials was done independently by two reviewers. Subsequently, after the scope of the review was slightly widened from including only randomised controlled trials to including non-randomised prospective comparative studies, a third reviewer repeated the trials selection and quality assessment. As the studies identified were not sufficiently similar and not of sufficient quality, we did not do a meta-analysis but summarised the data in a narrative format. We found six prospective controlled trials relating to our question. Four of these were described as randomised controlled trials, one was a prospective controlled trial that did not specify allocation to comparison groups, and one was a repeated cross-sectional study comparing different interventions. Comparison interventions included non-iodised salt, iodised water, iodised oil, and salt iodisation with potassium iodide versus potassium iodate. Numbers of participants in the trials ranged from 35 to 334; over 20,000 people were included in the cross-sectional study. Three studies were in children only, two investigated both groups of children and adults and one investigated pregnant women. There was a tendency towards goitre reduction with iodised salt, although this was not significant in all studies. There was also an improved iodine status in most studies (except in small children in one of the studies), although urinary iodine excretion did not always reach the levels recommended by the WHO. None of the studies observed any adverse effects of iodised salt. The results suggest that iodised salt is an effective means of improving iodine status. No conclusions can be made about improvements in other, more patient-oriented outcomes, such as physical and mental development in children and mortality. None of the studies specifically investigated development of iodine-induced hyperthyroidism, which can be easily overlooked if just assessed on the basis of symptoms. High quality controlled studies investigating relevant long term outcome measures are needed to address questions of dosage and best means of iodine supplementation in different population groups and settings.

The continuing importance of thyroid scintigraphy in the era of high-resolution ultrasound.

At the molecular level, the uptake of radioiodine and pertechnetate is proportional to the expression of the thyroidal sodium/iodine symporter (NIS). Qualitative and quantitative scintigraphic evaluation of the thyroid is performed with a gamma camera fitted with an on-line computer system and enables determination of the iodine uptake or the technetium uptake (TCTU) as an iodine clearance equivalent. Despite new molecular genetic insights into congenital hypothyroidism, the iodine-123 or pertechnetate scan remains the most accurate test for the detection of ectopic thyroid tissue. Following the identification of specific mutations of the genes coding for the NIS, thyroid peroxidase and pendrin, the discharge test has lost its role in establishing the diagnosis of inherited dyshormonogenesis, but it is still of value in the assessment of defect severity. In PDS mutations the test can be used to establish the diagnosis of syndromic disease. Quantitative pertechnetate scintigraphy is the most sensitive and specific technique for the diagnosis and quantification of thyroid autonomy. The method has proved to be valuable in risk stratification of spontaneous or iodine-induced hyperthyroidism, in the estimation of the target volume prior to radioiodine therapy and in the evaluation of therapeutic success after definitive treatment. In iodine deficiency areas the thyroid scan remains indispensable for the functional characterisation of a thyroid nodule and is still a first-line diagnostic procedure in cases of suspected thyroid malignancy. This is especially of importance in patients with Graves' disease, among whom a relatively high prevalence of cancer has been found in cold thyroid nodules. While determination of the TCTU is without any value in the differentiation between autoimmune thyroiditis and Graves' disease in most cases, it is of substantial importance in the differentiation between hyperthyroid autoimmune thyroiditis and Graves' disease.

Clinical experience of amiodarone-induced thyrotoxicosis over a 3-year period: role of colour-flow Doppler sonography.

Current thinking is that amiodarone-induced thyrotoxicosis (AIT) might be either iodine-induced thyrotoxicosis in latent hyperthyroidism (Type 1) or destructive thyroiditis (Type 2), and also that colour-flow Doppler sonography (CFDS) of the thyroid and serum interleukin 6 (IL-6) are tools that can classify AIT and direct treatment. To assess the validity of this thinking, our objective was to determine whether CFDS and IL-6 identified AIT subgroups with distinct features. Retrospective case-note audit of all patients presenting with AIT to the Endocrine Department of a UK teaching hospital over a 3-year period. To assess proportions of Type 1 vs. Type 2 AIT and to compare and contrast their clinical features. 37 patients were identified with AIT (mean age 65, range 20-86 years). In 30 patients in whom AIT persisted, 25 underwent CFDS. In 25 patients who underwent CFDS, 10 (40%) were classified as Type 1, 10 (40%) as Type 2 and 5 (20%) as indeterminate type. In the patients classified by CFDS in whom AIT persisted, 40% of Type 1 patients were male vs. 90% of Type 2 patients. Also, free T4 tended to be lower in patients presenting with Type 1 AIT (52.1 +/- 7.5 pmol/l) compared to Type 2 (74.8 +/- 8.1 pmol/l, P = 0.08), free T3 was lower (8.8 +/- 0.9 vs. 15.6 +/- 3.0 pmol/l, P = 0.03) and the cumulative amiodarone dose was lower (66 +/- 20 vs. 186 +/- 28 g, P = 0.002). We used less prednisolone to achieve euthyroidism in patients with Type 1 AIT whereas carbimazole doses were not different and the time to euthyroidism was the same in both groups (81 +/- 21 vs. 88 +/- 13 days). IL-6 was raised in two patients with Type 1 and in one patient with Type 2 AIT. CFDS could characterize two distinct subtypes in patients with AIT. Conversely, IL-6 seemed to be an unhelpful test in this context.

Organophosphorous poisoning with intermediate syndrome

Organophosphorous poisoning with intermediate syndrome

Iatrogenic Thyrotoxicosis. Causal Circumstances, Pathophysiology and Principles of Treatment. Review of the Literature

.Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones. In most instances, thyrotoxicosis is due to hyperthyroidism, a term reserved for disorders characterized by overproduction of thyroid hormones by the thyroid gland. Nevertheless, thyrotoxicosis may also result from a variety of conditions other than thyroid hyperfunction. The present report focuses on the etiologies, pathophysiology and treatment of iatrogenic thyrotoxicosis. Iatrogenic thyrotoxicosis may be caused by 1) subacute thyroiditis (a result of lymphocytic infiltration, cellular injury, trauma or radiation) with release of preformed hormones into circulation, 2) excessive ingestion of thyroid hormones (“thyrotoxicosis factitia”), 3) iodine-induced hyperthyroidism (radiological contrast agents, topical antiseptics or other medications). Among these causes of iatrogenic thyrotoxicosis, that induced by the iodine overload and cytotoxicity associated with amiodarone represents a significant challenge. Successful management of amiodarone-induced thyrotoxicosis requires close cooperation between endocrinologists and endocrine surgeons. Surgical treatment may have a leading yet often underestimated role in view of the potential life-threatening severity of this disease, whereas others kinds of iatrogenic thyrotoxicosis are usually treated conservatively.

Iodine excess and hyperthyroidism.

150 microg iodine are daily required for thyroid hormone synthesis. The thyroid gland has intrinsic mechanisms that maintain normal thyroid function even in the presence of iodine excess. Large quantities of iodide are present in drugs, antiseptics, contrast media and food preservatives. Iodine induced hyperthyroidism is frequently observed in patients affected by euthyroid iodine deficient goiter when suddenly exposed to excess iodine. Possibly the presence of autonomous thyroid function permits the synthesis and release of excess quantities of thyroid hormones. The presence of thyroid autoimmunity in patients residing in iodine-insufficient areas who develop iodine-induced hyperthyroidism has not been unanimously observed. In iodine-sufficient areas, iodine-induced hyperthyroidism has been reported in euthyroid patients with previous thyroid diseases. Euthyroid patients previously treated with antithyroid drugs for Graves' disease are prone to develop iodine-induced hyperthyroidism. As well, excess iodine in hyperthyroid Graves' disease patients may reduce the effectiveness of the antithyroid drugs. Occasionally iodine-induced hyperthyroidism has been observed in euthyroid patients with a previous episode of post-partum thyroiditis, amiodarone destructive or type II thyrotoxicosis and recombinant interferon-alpha induced destructive thyrotoxicosis. Amiodarone administration may induce thyrotoxicosis. Two mechanisms are responsible for this condition. One is related to excess iodine released from the drug, approximately 9 mg of iodine following a daily dose of 300 mg amiodarone. This condition is an iodine-induced thyrotoxicosis or type I amiodarone-induced thyrotoxicosis. The other mechanism is due to the amiodarone molecule that induces a destruction of the thyroid follicles with a release of preformed hormones. This condition is called amiodarone-induced destructive thyrotoxicosis or type II thyrotoxicosis. Patients developing type I thyrotoxicosis in general have preexisting nodular goiter whereas those developing type II thyrotoxicosis have a normal thyroid gland. The latter group of patients, after recovering from the destructive process, may develop permanent hypothyroidism as the consequence of fibrosis of the gland.

Iodine kinetics and effectiveness of stable iodine prophylaxis after intake of radioactive iodine: a review.

Ingestion of potassium iodide (KI) offers effective protection against irradiation of the thyroid after accidental exposure to radioactive iodine. This prophylaxis aims at rapidly obtaining maximal thyroid protection without adverse effects. This article reviews studies on iodine kinetics in humans and on the efficacy of KI in protecting the thyroid. In adults with normal thyroid function, ingestion of 100 mg of iodide just before exposure to radioactive iodine blocks at least 95% of the thyroid dose. If exposure persists after iodide ingestion (100 mg), the percentage of averted dose may decrease significantly. Daily ingestion of a dose of 15 mg of KI would then maintain the thyroid blockade at a level above 90%. The efficacy of iodide and the occurrence of antithyroid effects also depend on external and individual factors such as dietary iodine intake, thyroid function, and age. The KI dosage regimen should be adjusted for age at exposure. For the fetus, the newborn, children, and adolescents, the risk of radiation-induced thyroid cancer in case of accidental exposure to radioactive iodine justifies KI prophylaxis, despite the risk of hypothyroidism, especially in newborns. For the elderly, the benefits of KI may be lower than the risk of iodine-induced hyperthyroidism.

Iatrogenic thyrotoxicosis: causal circumstances, pathophysiology, and principles of treatment-review of the literature.

Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones. In most instances thyrotoxicosis is due to hyperthyroidism, a term reserved for disorders characterized by overproduction of thyroid hormones by the thyroid gland. Nevertheless, thyrotoxicosis may also result from a variety of conditions other than thyroid hyperfunction. The present report focuses on the etiologies, pathophysiology, and treatment of iatrogenic thyrotoxicosis. Iatrogenic thyrotoxicosis may be caused by (1) subacute thyroiditis (a result of lymphocytic infiltration, cellular injury, trauma, irradiation) with release of preformed hormones into circulation; (2) excessive ingestion of thyroid hormones ("thyrotoxicosis factitia"); (3) iodine-induced hyperthyroidism (radiologic contrast agents, topical antiseptics, other medications). Among these causes of iatrogenic thyrotoxicosis, that induced by the iodine overload and cytotoxicity associated with amiodarone represents a significant challenge. Successful management of amiodarone-induced thyrotoxicosis requires close cooperation between endocrinologists and endocrine surgeons. Surgical treatment may have a leading yet often underestimated role in view of the potential life-threatening severity of this disease, whereas others kinds of iatrogenic thyrotoxicosis are usually treated conservatively.

Update on the management of hyperthyroidism and hypothyroidism.

Clinical aspects, laboratory investigation, and treatment of hyperthyroidism and hypothyroidism are reviewed in light of recent information. Special circumstances, such as hyperthyroidism during pregnancy, Graves ophthalmopathy, iodine-induced hyperthyroidism, and subclinical hypothyroidism, are also considered.

Update on the Management of Hyperthyroidism and Hypothyroidism

Clinical aspects, laboratory investigation, and treatment of hyperthyroidism and hypothyroidism are reviewed in light of recent information. Special circumstances, such as hyperthyroidism during pregnancy, Graves ophthalmopathy, iodine-induced hyperthyroidism, and subclinical hypothyroidism, are also considered.

Iodine supplementation: benefits outweigh risks.

In 1990, iodine deficiency affected almost one-third of the world population and was the greatest single cause of preventable brain damage and mental retardation. Following a resolution adopted by the World Summit for Children in 1990. major programmes of iodine supplementation were implemented by the governments of the affected countries with the support of major donors. Iodisation of salt was recognised as the method of choice. Nine years later, by April 1999, 75% of the affected countries had legislation on salt iodisation and 68% of the affected populations had access to iodised salt. The prevalence of iodine deficiency disorders decreased drastically in most countries and the deficiency disappeared completely in some such as Peru. This result constitutes a public heath success unprecedented with a non-infectious disease. However, occasional adverse effects occurred. The principle effect is iodine-induced hyperthyroidism which occurs essentially in older people with autonomous nodular goitres, especially following iodine intake that is too rapid and of too massive an increment. The incidence of the disorder is usually low and reverts spontaneously to the background rate of hyperthyroidism or even below this rate after 1 to 10 years of iodine supplementation. The possible occurrence of iodine-induced thyroiditis in susceptible individuals has not been clearly demonstrated by large epidemiological surveys. Iodine supplementation is followed by an increased prevalence of occult papillary carcinoma of the thyroid discovered at autopsy but the prognosis of thyroid cancer is improved due to a shift towards differentiated forms of thyroid cancer that are diagnosed at earlier stages. Iodine-induced hyperthyroidism and other adverse effects can be almost entirely avoided by adequate and sustained quality control and monitoring of iodine supplementation which should also confirm adequate iodine intake. Available evidence clearly confirms that the benefits of correcting iodine deficiency far outweigh the risks of iodine supplementation.

Differential indications for thyroid gland operation

Although the case for thyroid surgery is based on morphologic and physiologic criteria, it is mainly based on individual therapeutic goals. The goals are influenced by various biographic, medical and personal facts and by many environmental conditions. Thus, there is no rationale for cataloguing indications. With the euthyroid goitre the indication for surgery is usually given by the size of the thyroid gland, especially since it has become clear in various studies that with drug therapy the achievable size reduction is rather small. With Graves' disease the pros and cons of the three main methods, surgery, medical treatment or radioiodine, have to be considered in each case. Surgery is mainly indicated when the goal is a rapid and reliable normalization of the hormonal status. Thyroid autonomy is a clear-cut case for radioiodine. Only isolated autonomous nodules can equally well be treated by surgery. In addition, a case for surgery is given when besides the autonomy a large goitre is present. A special indication is iodine-induced thyrotoxicosis that cannot be normalized by medical treatment. All kinds of thyroid carcinoma, with very few exceptions, usually have to be operated on as the first choice.