Amiodarone and thyroid autoimmunity in the United Kingdom.

Weetman, A. P.; Bhandal, Samarjit Kaur; Burrin, J. M.; Robinson, Karen A.; McKenna, WJ

doi:10.1136/bmj.297.6640.33

Cited by 25 publications

(7 citation statements)

References 4 publications

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“…The development of thyroid autoantibodies after amiodarone intake has been reported in some studies [23][24][25][26] but not in all [27]. Our data showed no predictive value of thyroid antibodies in patients who developed thyroid dysfunction, compared with participants who remained in the state of normal function.…”

Section: Discussioncontrasting

confidence: 81%

Incidence and predictability of amiodarone-induced thyrotoxicosis and hypothyroidism

Hofmann

Nawara

Ofluoglu

et al. 2008

Wien Klin Wochenschr

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Section: Discussioncontrasting

confidence: 81%

Incidence and predictability of amiodarone-induced thyrotoxicosis and hypothyroidism

Hofmann

Nawara

Ofluoglu

et al. 2008

Wien Klin Wochenschr

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“…Whether amiodarone can induce autoimmunity is uncertain (111,113). An early report that amiodarone induced a transient presence of TPO antibodies (114), could not be confirmed by others (115,116).…”

Section: Amiodaronementioning

confidence: 92%

The environment and autoimmune thyroid diseases

2004

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Genetic factors play an important role in the pathogenesis of autoimmune thyroid disease (AITD) and it has been calculated that 80% of the susceptibility to develop Graves' disease is attributable to genes. The concordance rate for AITD among monozygotic twins is, however, well below 1 and environmental factors thus must play an important role. We have attempted to carry out a comprehensive review of all the environmental and hormonal risk factors thought to bring about AITD in genetically predisposed individuals. Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders. The use of certain drugs (lithium, interferon-a, Campath-1H) also increases the risk of the development of autoimmunity against the thyroid gland. Further research is warranted into the importance of fetal microchimerism and of viral infections capable of mounting an endogenous interferon-a response.European Journal of Endocrinology 150 605-618

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“…This would explain the adverse effects of iodine prophylaxis in iodine-deficient patients in Argentina, where the prevalence of lymphocyte infiltration in thyroidectomy specimens increased from 8 to 31% in the 5 years after introduction of prophylactic iodine (27). A striking increase in thyroid antibodies was also reported after the use of amiodarone was initiated in Portugal, an area of low iodine intake (28), whereas no such effect was observed in the iodine-sufficient United Kingdom (29). Furthermore, an increase in thyroid antibodies was found 3 months after administration of iodine oil to patients with goitre in Greece (19).…”

Section: European Journal Of Endocrinology (1998) 139mentioning

confidence: 94%

Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial

Kahaly¹,

Dienes²,

Beyer³

et al. 1998

European Journal of Endocrinology

126

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Objective: Iodine is essential for normal thyroid function and the majority of individuals tolerate a wide range of dietary levels. However, a subset of individuals, on exposure to iodine, develop thyroid dysfunction. In this double-blind trial, we evaluated the efficacy and tolerability of low-dose iodine compared with those of levo-thyroxine (T 4 ) in patients with endemic goitre. Methods: Sixty-two patients were assigned randomly to groups to receive iodine (0.5 mg/day) or T 4 (0.125 mg/day) for 6 months. Subsequently, both groups were subject to placebo for another 6 months. Thyroid sonography, determination of thyroid-related hormones and antibodies, and urinary excretion of iodine were carried out at baseline and at 1, 6 and 12 months. Results: At 6 months, markedly increased urinary values of iodine were found in patients receiving iodine (36 mg/24 h at baseline, 415 mg/24 h at 6 months) compared with those receiving T 4 (47 mg/ 24 h at baseline, 165 mg/24 h at 6 months; P < 0.0001 compared with iodine group). T 4 administration engendered a greater (P < 0.01) decrease in thyroid volume (from 32 ml to 17 ml, P < 0.0001) than did intake of iodine (33 ml to 21 ml, P < 0.005). High microsomal and thyroglobulin autoantibody titres were present in six of 31 patients (19%) receiving iodine, and iodine-induced hypo-and hyperthyroidism developed in four and two of them, respectively. Fine-needle biopsy revealed marked lymphocyte infiltration in all six. After withdrawal of iodine, thyroid dysfunction remitted spontaneously and antibody titres and lymphocyte infiltration decreased markedly. Follow-up of these six patients for an additional 3 years showed normalisation of antibody titres in four of them. Conclusion: Although nearly comparable results were obtained with both treatment regimens regarding thyroid size, partly reversible iodine-induced thyroid dysfunction and autoimmunity were observed among patients with endemic goitre.

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Amiodarone and thyroid autoimmunity in the United Kingdom.

Cited by 25 publications

References 4 publications

Incidence and predictability of amiodarone-induced thyrotoxicosis and hypothyroidism

Incidence and predictability of amiodarone-induced thyrotoxicosis and hypothyroidism

The environment and autoimmune thyroid diseases

Iodide induces thyroid autoimmunity in patients with endemic goitre: a randomised, double-blind, placebo-controlled trial

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