Iodine-induced Hyperthyroidism Research Articles

Risks of iodine-induced hyperthyroidism after correction of iodine deficiency by iodized salt.

Biochemical signs of hyperthyroidism, or even overt and possibly lethal clinical hyperthyroidism were reported in 2 severely iodine-deficient African countries (Zimbabwe and Democratic Republic of Congo, RDC) soon after the introduction of iodized salt. The 2 countries had access to iodized salt produced in Botswana, as well as 5 other countries in the region, namely Cameroon, Nigeria, Kenya, Tanzania, and Zambia. Therefore, a multicenter study was conducted in these 7 countries to evaluate whether the occurrence of iodine-induced hyperthyroidism (IIH) after the introduction of iodized salt was a general phenomenon or corresponded to specific local situations in the 2 affected countries. Two or 3 areas with a past history of severe iodine deficiency that had recently been supplemented with iodized salt were selected in each of the 7 countries. The prevalence of goiter was determined in 4423 schoolchildren in these areas and the concentration of urinary iodine in 2258. Salt factories and health structures were visited for the evaluation of the quality of iodized salt and the possible occurrence of IIH. The study showed that iodine deficiency had been eliminated in all areas investigated, and that the prevalence of goiter had markedly decreased since the introduction of iodized salt. This is a remarkable achievement in terms of public health. However, some areas were now exposed to iodine excess due mostly to a poor monitoring of the quality of the iodized salt and of the iodine intake of the population. In these areas or countries, IIH occurred only when the introduction of iodized salt had been of recent onset (<2 years), namely in Zimbabwe and RDC. In conclusion, the risk of IIH after correction of iodine deficiency is closely related to a recent excessive increment of iodine supply.

Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects.

In this study, the risk of iodine-induced thyrotoxicosis in unselected patients from an iodine-deficient area was investigated. The patients were consecutively enrolled. Thyroid hormone values and urinary iodine excretion were determined before, as well as 1, 4 and 12 weeks after iodine contamination by coronary angiography. Two of 788 unselected patients developed hyperthyroidism within 12 weeks. The two patients did not belong to a risk group for iodine-induced thyrotoxicosis (i.e. old people, patients with goiter or possible thyroid autonomy, low TSH). Both patients had normal TSH levels at baseline and ultrasound of the thyroid was without evidence of nodules. The study shows that in euthyroid unselected patients from an iodine-deficient area short-term iodine contamination by contrast media rarely leads to hyperthyroidism. On account of these facts, prophylactic therapy, e.g. by perchlorate or thiamazole, is not generally recommended, because the risk of side-effects is perhaps even greater than the risk of iodine-induced thyrotoxicosis.

Salt iodation and risk of neonatal brain damage

In the global effort to eliminate iodine-deficiency disorders WHO, in 1994, recommended iodation of salt at 50–100 parts per million at factory level to ensure 25–50 parts per million at consumer level.1 This approach was adopted in many African countries, including Tanzania, which has required that factories iodise salt at 75-100 parts per million since 1995. Findings of iodine-induced hyperthyroidism in parts of rural Africa, primarily in older women with large goitres,2,3 started discussion on salt iodine at consumer level.

SYNDROMES OF THYROTOXICOSIS WITH LOW RADIOACTIVE IODINE UPTAKE

It is very important to diagnose correctly the etiology of thyrotoxicosis, because the course and treatment of thyrotoxicosis with low radioactive iodine uptake differ significantly from that of hyperthyroidism due to Graves' disease or toxic nodular goiter. Many causes of subacute thyroiditis have been identified producing a characteristic course of transient hyperthyroidism, followed by hypothyroidism, and usually recovery. Ectopic hyperthyroidism includes factitious thyroid hormone ingestion, struma ovarii, and, rarely, large deposits of functioning thyroid cancer metastases. Iodine-induced hyperthyroidism may be associated with low radioiodine uptakes. Amiodarone-associated hyperthyroidism may be the result of subacute thyroiditis or iodine-induced hyperthyroidism; assessment and treatment can be quite challenging.

The prevention and management of iodine-induced hyperthyroidism and its cardiac features.

Review of available literature and experience supports a recommended daily iodine intake of 150 microg for adults, 200 microg during pregnancy, 50 microg for the first year of life, 90 microg for ages 1 to 6, and 120 microg for ages 7 to 12. The amount of iodine added to salt in fortification programs should be adjusted to achieve these intakes. Iodine-induced hyperthyroidism (IIH) is an occasional consequence of the correction of iodine deficiency, occurring most frequently in older subjects with multinodular goiter. This complication is usually mild and self-limited, but may be serious and occasionally lethal. The most important clinical manifestations are cardiovascular. Thyrotoxicosis can aggravate pre-existing cardiac disease and can also lead to atrial fibrillation, congestive heart failure, worsening of angina, thromboembolism, and rarely, death. In the absence of pre-existing cardiac disease, treatment of thyrotoxicosis usually returns cardiac function to normal. Heightened awareness on the part of the health sector will promote early detection and prompt treatment of IIH. Monitoring should be an important part of a successful program of iodization, and in addition it offers the best opportunity for recognizing and treating IIH. Further research to improve the characterization and prevention of IIH is strongly encouraged. The most important conclusion is that IIH, while an issue that needs serious address, is not a reason to stop iodine supplementation in deficient regions. The benefits to the community from correcting iodine deficiency and avoiding its associated disorders far outweigh the damage from IIH.

Iodine-Induced Hyperthyroidism: Occurrence and Epidemiology

We have critically reviewed the available information on iodine-induced hyperthyroidism (IIH) from published sources and other reports as well as the experience of the authors in Tasmania, Zaire, Zimbabwe, and Brazil. Administration of iodine in almost any chemical form may induce an episode of thyrotoxicosis (IIH). This has been observed in epidemic incidence in several countries when iodine has been given as prophylaxis in a variety of vehicles, but the attack rate as recorded has been low. IIH is most commonly encountered in older persons with long standing nodular goiter and in regions of chronic iodine deficiency, but instances in the young have been recorded. It customarily occurs after an incremental rise in mean iodine intake in the course of programs for the prevention of iodine deficiency, or when iodine-containing drugs such as radiocontrast media or amiodarone are administered. The biological basis for IIH appears most often to be mutational events in thyroid cells that lead to autonomy of function. When the mass of cells with such an event becomes sufficient and iodine supply is increased, the subject may become thyrotoxic. These changes may occur in localized foci within the gland or in the process of nodule formation. IIH may also occur with an increase in iodine intake in those whose hyperthyroidism (Graves' disease) is not expressed because of iodine deficiency. The risks of IIH are principally to the elderly who may have heart disease, and to those who live in regions where there is limited access to medical care. More information is needed on the long-term health impact of IIH or "subclinical" IIH, especially in the course of prophylaxis programs with iodized salt or iodinated oil in regions where access to health care is limited.

Workshop on Iodine-Induced Hyperthyroidism: Prefatory Note

Workshop on Iodine-Induced Hyperthyroidism: Prefatory Note

Lithium treatment in amiodarone-induced thyrotoxicosis

Amiodarone hydrochloride is an iodine-rich drug effective in the control of various tachyarrhythmias. It is known to cause refractory to thyrotoxicosis, which usually does not respond to regular antithyroid drugs. Lithium bicarbonate is a medication used to treat psychiatric disorders; it also influences thyroid production and release of hormones. We tried it in combination with propylthiouracil (PTU) for the treatment of amiodarone-induced thyrotoxicosis. Twenty-one patients were studied. The first group (n = 5) was treated by amiodarone withdrawal only. The second group (n = 7) received PTU (300 to 600 mg), and the third (n = 9) PTU (300 mg) and lithium (900 to 1350 mg) daily. Patient selection was not randomized. The PTU + lithium group had more severe symptoms and signs of thyrotoxicosis, as well as thyroxine levels at least 50% above the upper limit of normal. They also had been on a longer course of amiodarone treatment (34.3 +/- 11.9 months) than the PTU-only (11.4 +/- 7.5) and the no-treatment (7.8 +/- 4.2) groups. While there was no difference between the first two groups in time until recovery (10.6 +/- 4.0 versus 11.6 +/- 0.5 weeks, respectively), the group receiving lithium normalized their thyroid function tests in only 4.3 +/- 0.5 weeks (P < 0.01 versus both other groups). T3 levels normalized even earlier-by 3 weeks of lithium treatment. No adverse effects of lithium were encountered, and the medication was stopped 4 to 6 weeks after achieving a normal clinical and biochemical state. We conclude that lithium is a useful and safe medication for treatment of iodine-induced thyrotoxicosis caused by amiodarone. We would reserve this treatment for severe cases only. Further studies are needed to find out whether in patients with this troublesome complication lithium therapy could permit continuation of amiodarone treatment.

The many causes of subclinical hyperthyroidism.

Subclinical hyperthyroidism, defined as serum thyroid hormone levels in the reference range with low serum TSH concentration, is a well recognized clinical entity, but little information is available concerning the prevalence of the disorders that produce it. We conducted a 24-month retrospective survey of subclinical hyperthyroidism patients referred to a university hospital nuclear medicine service for diagnostic studies. Twenty-four consecutive patients were evaluated (22 outpatients and 2 inpatients). All patients had highly sensitive TSH determination, thyroid hormone levels, radioiodine uptake and scan (except for 2 postpartum women), and, selectively, TSH-receptor antibody (TRAb), serum thyroglobulin, antithyroid antibodies, T3-suppression test, and erythrocyte sedimentation rate. A TSH value of about 0.1 microIU/mL was used as the cutoff. Only one patient in the group had a nonthyroidal disorder. In 14 patients (61%) subclinical hyperthyroidism was self-limited, due to silent thyroiditis (5 patients), iodine-induced hyperthyroidism (3 patients), postpartum thyroiditis (2 patients), subacute thyroiditis (2 patients), and probable hemorrhage into a functioning nodule (2 patients). Of the non-self-limited disorders (39%), Graves' disease accounted for 6 patients and solitary or multinodular goiter for 3. Graves' disease proved difficult to diagnose because the thyroid gland was normal in size in two of the six patients, TRAb was positive in only two of six, and the radioiodine uptake and gradient were normal in all six; the T3-suppression test was positive in two of two patients. We conclude that the causes of subclinical hyperthyroidism are the disorders that commonly produce overt thyrotoxicosis in medical practice, Graves' disease being the most frequent. However, the tests used to diagnose overt Graves' disease often fail in the setting of subclinical hyperthyroidism, except possibly the T3-suppression test.

Iodine-Induced Hyperthyroidism in a Newborn

In the article entitled Iodine-Induced Hyperthyroidism in a Newborn that appeared in the March 1995 issue of Pediatrics, the iodine content of povidone-iodine is estimated at 10 mg/mL rather than the estimate that we employed which was 10% or 10 g/dL. Thus, we are in agreement that the neonate in our report received 2.88 g rather than 28.8 g, which we reported. Donald Zimmerman, MD Mayo Clinic &amp; Mayo Foundation Pediatric Endocrinology Rochester, MN 55905

Hyperthyroidism After Radiographic Contrast in a Patient With Separate Cervical and Intrathoracic Multinodular Goiters

The authors report a case of multinodular goiter in both cervical thyroid and aberrant intrathoracic thyroid tissue which was associated with thyrotoxicosis after the use of radiographic contrast material. The role of correlative imaging in assessment of cervical and anterior mediastinal masses and the phenomenon of iodine-induced thyrotoxicosis are also discussed.

Iodine-Induced Hyperthyroidism in a Newborn

While hypothyroidism is a common result of neonatal iodine excess, hyperthyroidism may occur, possibly primarily in cases of marked iodine excess.

Iodine-induced hyperthyroidism caused by acne treatment

Iodine-induced hyperthyroidism caused by acne treatment

Systemic iodine absorption during endoscopic application of radiographic contrast agents for endoscopic retrograde cholangiopancreaticography.

Hyperthyroidism induced by contrast agents in a major problem in patients with pre-existing thyroid disease, particularly in patients with functional thyroid autonomy. The present study was undertaken to evaluate whether contrast media applied during endoscopic retrograde cholangiopancreaticography (ERCP) may result in a significant increase of serum iodine levels and thus may be associated with the risk of iodine-induced hyperthyroidism. The courses of serum concentrations of total iodine and free iodide, as well as of urinary iodine excretion, were measured in 15 patients before and up to 21 days after ERCP. During ERCP, the non-ionic contrast medium iopamidol was instilled in amounts resulting in a total iodine load of 57.4 +/- 22.8 mmol (7.3 +/- 2.9 g). In all patients, ERCP resulted in a highly significant increase in serum levels of total iodine from 0.8 +/- 0.5 to 85.2 +/- 116.9 mumol/l 4 h after application of the contrast agent. In parallel, serum iodide levels were raised from 0.06 +/- 0.04 to 5.42 +/- 6.09 mumol/l and urinary iodine excretion from 71.1 +/- 35.7 mumol/mol creatinine to 621,620.9 +/- 636,492.2 mumol/mol creatinine. Peak concentrations of serum iodine are well related to the total amount of iodine applied (p < 0.05). During follow-up, iodine levels returned to pre-exposure levels within 2-3 weeks. Levels of thyrotropin, free thyroxine, and free triiodothyronine remained unchanged during the follow-up period. In conclusion, endoscopic application of iodinated contrast agents during ERCP leads to significant increases of serum levels of total iodine and free iodide and of urinary iodine excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Treatment of amiodarone iodine-induced thyrotoxicosis with plasmapheresis and methimazole

The present report illustrates the clinical and biochemical outcome in two amiodarone iodine-induced thyrotoxicosis (AIIT) patients submitted to plasmapheresis. Amiodarone was discontinued, and treatment with MMI (40 mg/day) was started. In addition, patients were submitted to two sessions of plasma-exchange, with a one-day interval between the two session. In both patients serum total T3 (TT3) and free T3 (FT3) concentrations decreased promptly but in contrast to the serum TT3, FT3 levels remained steadily above the normal range. A similar behaviour was observed for total T4 and free T4 plasma concentrations. Interestingly, a clearcut clinical amelioration was observed in both patients even before a reduction of circulating free thyroid hormone concentrations could be documented. In conclusion, our experience indicates that plasmapheresis may be useful in order to obtain a rapid amelioration of severe clinical picture of thyrotoxicosis, but cannot be considered as a definite therapy in AIIT. It should be considered that plasmapheresis is not devoid of risks and is also a very expensive procedure.

Iodine-induced hyperthyroidism due to nonionic contrast radiography in the elderly

purpose: To identify the number of cases of hyperthyroidism that followed the performance of contrast radiography in elderly patients at a geriatric hospital in a non-iodine-deficient area and to determine the clinical course of the condition. patients and methods: All patients over a 20-month period with biochemical hyperthyroidism (plasma free thyroxine level greater than 25.0 pmol/L and thyroid-stimulating hormone level less than 0.10 IU/L) were identified. Clinical features of hyperthyroidism and exposure to nonionic contrast media radiographs within the previous 12 months were sought. Follow-up extended from 6 to 22 months. results: A total of 28 patients with hyperthyroidism (aged 70 to 96 years) were identified. Seven patients (25%) had documented biochemical development of hyperthyroidism (five) or subsequent hyperthyroidism (two) 3 to 8 weeks after nonionic contrast media radiography. The four patients who underwent scanning had a multinodular thyroid, and thyroid antibodies were not detected in five of five patients. Although the condition appeared self-limited and six of six patients were euthyroid after 18 months, the condition was not benign; progress and recovery were adversely affected by hyperthyroidism. Four patients had a good response to treatment with an antithyroid drug (carbimazole). conclusions: Iodine-induced thyrotoxicosis following contrast radiography was found in 7 of 28 cases of hyperthyroidism seen at a geriatric hospital. Although the condition appears ultimately self-limited, pharmacologic control of severe clinical features may be required. The frequency of this condition in a non-iodine-deficient area appears related to the more common occurrence of autonomous thyroid nodules in the elderly. Because performance of contrast radiography is more common in this age group, the recognition and treatment of iodine-induced thyrotoxicosis are of increasing clinical importance.

Hyperthyroidism With a Low Radioactive Iodine Uptake-Reply

In Reply.— The alternative explanations given by Denker regarding normal radioiodine uptake in our patient with thyrotoxicosis induced by topical iodine application 1 is entirely plausible. However, the temporal relationship between iodine application and subsequent onset of clinical hyperthyroidism tends to favor iodine-induced thyrotoxicosis. The point we want to emphasize in our article is that povidone-iodine soaks are commonly used in the treatment of pressure sores and caution is necessary when used in patients with thyroid disorders, because they may cause abnormal thyroid hormone secretion or difficulty in interpreting the results of thyroid function tests, especially radioiodine uptake.

The effects of plasmapheresis on thyroid hormone and plasma drug concentrations in amiodarone‐induced thyrotoxicosis [letter

British Journal of Clinical PharmacologyVolume 31, Issue 3 p. 371-372 Free Access The effects of plasmapheresis on thyroid hormone and plasma drug concentrations in amiodarone-induced thyrotoxicosis [letter] B. Uzzan, B. Uzzan St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorE. Pussard, E. Pussard St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorA. Leon, A. Leon St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorD. Bekhechi, D. Bekhechi St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorA. Krivitzky, A. Krivitzky St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorE. Modigliani, E. Modigliani St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorG. Perret, G. Perret St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorR. Vassy, R. Vassy St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorA. Berdeaux, A. Berdeaux St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorJF Giudicelli, JF Giudicelli St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this author B. Uzzan, B. Uzzan St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorE. Pussard, E. Pussard St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorA. Leon, A. Leon St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorD. Bekhechi, D. Bekhechi St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorA. Krivitzky, A. Krivitzky St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorE. Modigliani, E. Modigliani St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorG. Perret, G. Perret St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorR. Vassy, R. Vassy St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorA. Berdeaux, A. Berdeaux St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this authorJF Giudicelli, JF Giudicelli St Mary's Hospital, Newport, Isle of Wight.Search for more papers by this author First published: March 1991 https://doi.org/10.1111/j.1365-2125.1991.tb05548.xCitations: 27AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References Berdeaux, A., Roche, A., Labeille, T., Giroux, B., Edouard, A. & Giudicelli, J. F. (1984). Tissue extraction of amiodarone and N-desethylamiodarone in man after a single oral dose. Br. J. clin. Pharmac., 18, 759– 763. Bonati, M., Galetti, F., Volpi, A., Cumetti, C., Rumolo, R. & Tognoni, G. (1983). Amiodarone in patients on long-term dialysis. New Engl. J. Med., 308, 906. Holt, D. W., Tucker, G. T., Jackson, P. R. & Storey, G. C. A. (1983). Amiodarone pharmacokinetics. Am. Heart J., 106, 840– 847. Leger, A. F., Massin, J. P., Laurent, M. F., Vincens, M., Auriol, M., Helal, O. B., Chomette, G. & Savoie, J. L. (1984). Iodine-induced thyrotoxicosis: analysis of 85 consecutive cases. Eur. J. clin. Invest., 14, 449– 455. Mason, J. W. (1987). Amiodarone. New Engl. J. Med., 316, 455– 466. Pellissier, J. F., Pouget, J., Cros, D., de Victor, B., Serratrice, G. & Toga, M. (1984). Peripheral neuropathy induced by amiodarone chlorhydrate. A clinicopathological study. J. neurol. Sci., 63, 251– 266. Russel, D. C., Paton, L. & Douglas, A. C. (1983). Amiodarone-associated alveolitis and polyarthropathy. Treatment by plasma exchange. Br. Heart J., 50, 491– 494. Citing Literature Volume31, Issue3March 1991Pages 371-372 ReferencesRelatedInformation

Plasma Exchange and Hemoperfusion in Iodine-Induced Thyrotoxicosis

Iodine-induced thyrotoxicosis is a life-threatening disease. Plasma exchange and hemoperfusion are the available means of detoxication. Both methods were applied repeatedly to 4 patients with iodine-induced thyrotoxicosis, and the efficacy of these treatment methods was compared. Thyroxine plasma levels were decreased by 33%, while the calculated body stores were reduced by 18% during plasma exchange. Hemoperfusion was less effective. With both methods, a rebound of plasma levels was seen. Improvement of the clinical condition was delayed for 1 week after discontinuation of treatment. One patient died, probably because detoxication was discontinued too soon after the thyroid hormone levels had normalized. Plasma exchange by using albumin (120 g/4,000 ml = 30 g/l) as replacement fluid is superior to that by using fresh-frozen plasma (2,000 ml/4,000 ml), since less thyroxine is administered (19 vs. 160 nmol).

Nativer 99mTc-Uptake in der Differentialdiagnostik von unauffälliger Schilddrüse, Struma mit Euthyreose und Schilddrüsenautonomie in einem Jodmangelgebiet

Global TcTU was determined in 568 patients without any specific thyroid drug intake - 54 with normal thyroid, 274 with goitre and euthyroidism and 240 with thyroid autonomy. 57 patients with autonomy and overt hyperthyroidism were the only group with TcTU values significantly higher than normals. Common to all groups was a large scatter of the TcTU values. In 332, the effects of individual iodine supply were studied by measuring the iodine concentration in spot urine samples. There was a significant inverse correlation between the TcTU values and the urinary iodine excretion in the groups of normal thyroids and of goitres with euthyroidism. In the group with autonomy an effect of iodine supply could only be seen in cases of greatly increased urinary iodine excretion, resulting in very low TcTU values. Out of 20 patients with autonomy and iodine contamination, only 4 showed overt hyperthyroidism. The large scatter of TcTU values in all groups may be explained by the persistent iodine deficiency as well as by the frequent exposure to unknown amounts of iodine in patients with thyroid disease. Therefore, the spontaneous TcTU alone cannot identify a small group of patients with autonomy and high risk of iodine-induced hyperthyroidism, from a very large group of patients with goitre.