May 1980, Volume 30, Issue 5

Case Reports

IODINE INDUCED THYROTOXICOSIS-CASE REPORTS AND REVIEW OF LITERATURE

S.M. Khan Paindakhel  ( Division of Nuclear Medicine, "IRNUM" Peshawar University Campus, Peshawar. )
Naseem Begum  ( Division of Nuclear Medicine, "IRNUM" Peshawar University Campus, Peshawar. )
Hikmat Shah  ( Division of Nuclear Medicine, "IRNUM" Peshawar University Campus, Peshawar. )
Iftikhar Ahmad  ( Division of Nuclear Medicine, "IRNUM" Peshawar University Campus, Peshawar. )

Abstract

Iodine in the form of Lugol\'s iodine is commonly prescribed for the treatment of goitre. Eighteen patients, who had positive history of ingestion of iodine are described. Some of the patients had hyperthyroidism when seen while others had thyrotoxicosis like symptoms after taking iodine. Hyperthyroidism was confirmed clinically, radio-isotopically and by response to treatment. Iodine was incriminated after exclusion of other causes of hyperthyroidism.

Introduction

Iodine in the form of cough mixtures, topical ointment, multivitamin mineral tablets, anti-diarrhoeal agents and lugol\'s iodine is commonly used. There are lack of facilities for investigation of goitre in Pakistan and lugol\'s iodine is commonly prescribed for patients having goitre.
The following patients had developed thyrotoxicosis or thyrotoxicosis like symptoms fol­lowing ingestion of iodine containing drugs.

Patients and Methods

There were 8 women and ten men. Their ages ranged from 20-71 years. All patients were referred to the thyroid clinic and they were examined before investigations. Thyroid uptake and P.B.1-131 were measured as previously reported (Khan et al., 1979). Thyroxine and triodothyronine were assayed using commercial kits (Radiochemical Centre, Amersham, U.K.).

Results

The clinical features, history of iodine ingestion and the results of investigations are given in the accompanying table.

Discussion

The role of iodine in the aetiology of hyperthyroidism has been well established since 1821 when Coindet described six goitrous patients who developed clinical features of thyrotoxicosis following treatment with iodine. Kocher (1910) drew attention to this phenomenon and called it Jod-Basedow. In 1920\'s, there were series of reports from the United States regarding increased incidence of thyrotoxicosis after iodisa-tion of salt (Kimball,1925; McClure, 1927). Connolly et al (1970) reported that the incidence of thyrotoxicosis on the island of Tasmania had more than doubled following the iodisation of bread. Vagenakis et al (1972) discussed the possible mechanisms for the iodide induced thyrotoxicosis. Iodine induced thyrotoxicosis may also occur in apparently normal persons (Savoie et al., 1975). Thyroid storm has also been reported after cardiac angiography (Blum et al., 1976) Livadas et al (1977) gave potassium iodide to sixteen cases of toxic adenoma and noted progressive increase in the serum T4 level. All patients in the present series had history of ingestion of commercially available LugoPs iodine except patients A.K. and A.W. (No. 8 and 18) who had 8 hydroxyquinoline derivatives. Diagnosis was confirmed by clinical feature radioisotope studies and by response to treatment and by exclusion of other thyrotoxic states (Graves, Disease, thyrotoxicosis factitia, thyrotoxicosis associated with hydatidi form mole and choriocarcinoma and thyrotoxicosis caused by ectopic thyroid tissue). There are no reports of 8 hydroxyquinoline induced thyrotoxicosis, but the iodine content in these drugs varies from 40 to 63.9 percent and thyroid enlargement has also been noted (Goodman and Gillman, 1975). The two patients (A.K. and A.W.) who self administered these drugs, used the drugs, for a long time (six and 3 years) as prophylaxis against amoebiasis. Prolonged use of these drugs not only induced hyperthyroidism as in the above two patients but can cause neurotoxicity (Oakley 1973).
The experience elsewhere in the world and the experience in Peshawar indicates that iodine may induce persisting hyperthyroidism in subjects with goitre. These studies also show that iodine should not be used in patients with goitre except in iodine deficiency goitre or in preoperative preparation of preexisting thyrotoxicosis.

Acknowledgements

We thank Manan Khan, M. Badshah, Z. Shah, Miss Fehmida and Saddique Bhatti, for technical and Miss T. Latif for secretarial help.

References

1. Blum, ML, Kranjac, T., Park, C.M. andEngleman, M. (1976) Thyroid storm after cardiac angiography with iodinated contrast medium occurrence in a patient with a previously euthyroid autonomous nodule of the thyroid. JAMA., 235:2324.
2. Coindet, J.E. (1821) Annales de chemie et de physique, 16:252, Cited by Nilsson (1973).
3. Connolly, R.J., Vidor, G.I. and Stewart, J.C. (1970) Increase in thyrotoxicosis in endemic goitre after iodation of bread. Lancet, 1:500.
4. Goodman, L.S. and Gillman, A. The pharmacological basis of therapeutics. 5th ed. New York, 1975, pp. 1073-4.
5. Kimball, O.P. (1925) JAMA., 85:1709.
6. Paindakhel, S.M.K., Ahmad, I. and Begum, F. (1979) Thyroid uptake in Peshawar: Analysis of 1100 cases JPMA., 29:75.
7. Kocher, T. (1910) Uber Jodbasedow. Archiv for Klinische, Chirurgie, 92:1166.
8. Livadas, D.P., Koutras, D.A., Souvatzoglou, A., Beckers, C. (1977) The toxic effects of small iodine supplements in patients with autonomous thyroid nodules. Clinical Endocrinology, 7:121.
9. McClure, R.D. (1927) Ann. Surg., 85:333.
10. Oakley, G.P. Jr. (1973) The neurotoxicosy of the halogena-ted hydroxyquinolines. JAMA., 225:395.
11. Sonkasen, P.H., Ekins, R.P., Stevens, H.G., Williams, E.S. and Nabarro, J.D.M. (1968) Serum levels of protein bound iodine and thyroxine after a course of Clioquinol. Lancet, 2:425.
12. Savoie, J.C., Massin, J.P., Thomopoulos, P. and Leger, F. (1975) Iodine-induced thyrotoxicosis in apparently normal thyroid glands. J. Clin. Endocrinol., 41:685.
13. Vagenakis, A.G., Wang, G., Burger, A., Maloof, F., Braverman, L.E. and Ingbar, S.H. (1972) Iodine induced thyrotoxicosis in Boston. N. Engl. J. Med., 287:523.

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