Effect of Lugolʼs iodine on the vascularity of thyroid gland in hyperthyroidism

Rangaswamy, M; Padhy, Ajit Kumar; Gopinath, P. G.; Shukla, N.K.; Gupta, Kiran; Kapoor, M M

doi:10.1097/00006231-198909000-00007

Cited by 11 publications

(9 citation statements)

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“…The thyroid gland is a highly vascularized tissue in which a fine capillary network surrounds each follicle [28]. The function of the thyroid gland is linked to the control of the vascular network and, as noted earlier, iodide is used to suppress thyroid function as well as blood flow in patients [9,10,11,12]. A high concentration of iodide decreases the blood flow in the thyroid gland as well as vascular permeability by its paracrine action [13,14,15].…”

Section: Discussionmentioning

confidence: 99%

“…Excess iodide has also been shown to decrease vascularity of the thyroid gland [9,10,11,12], so much so that most endocrine surgeons administer Lugol’s solution [a mixture of molecular iodine (I 2 ) and potassium iodide (KI) in distilled water] to prepare patients with Graves’ disease for thyroidectomy [10,11]. Vascular endothelial growth factor (VEGF) is produced by thyroid cells upon stimulation with TSH or antibodies that stimulate the TSH receptor [13,14,15].…”

Section: Introductionmentioning

confidence: 99%

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Excess iodide decreases transcription of NIS and VEGF genes in rat FRTL-5 thyroid cells

Suzuki

Kimura²,

et al. 2010

Biochemical and Biophysical Research Communications

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Although it is well known that an excess of iodide suppresses thyroid function and blood flow in vivo, the underlying molecular mechanisms are not fully known. The functional effect of iodide occurs at multiple steps, which include inhibition of sodium/iodide symporter (NIS) expression, transient block of organification, and inhibition of hormonal release. The vascular effect likely involves suppression of the vascular endothelial growth factor (VEGF) gene. In this report, we show that excess iodide coordinately suppresses the expression of the NIS and VEGF genes in FRTL-5 thyroid cells. We also demonstrate that the mechanism of iodide suppression of NIS gene expression is transcriptional, which is synergized by the addition of thyroglobulin. Based on the findings of reporter gene assays and electrophoretic gel mobility shift analysis, we also report two novel DNA binding proteins that responded specifically to iodide and modulated NIS promoter activity. The results suggest that excess iodide affects thyroid vascular function in addition to iodide uptake. This study provides additional insights into the mechanism of action of excess iodide on thyroid function.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Excess iodide decreases transcription of NIS and VEGF genes in rat FRTL-5 thyroid cells

Suzuki

Kimura²,

et al. 2010

Biochemical and Biophysical Research Communications

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“…Dosage and administration — last paragraph) is erroneous. While short‐term high‐dose iodide does temporarily inhibit thyroid hormone release and reduces the vascularity of the gland in Graves disease, it has no beneficial effect on thyroid blood flow in toxic multinodular goitre (quality of evidence: III‐2, B) 23 . It should be noted that sustained iodide excess can exacerbate thyrotoxicosis and can impair the response to antithyroid drugs, with the potential for severe drug‐resistant thyroid overactivity that may require emergency surgery (quality of evidence: IV, B) 24 …”

Section: Recommendations On the Use Of Iodidementioning

confidence: 99%

Barriers in the quest for quality drug information: salutary lessons from TGA‐approved sources for thyroid‐related medications

Stockigt

2007

Medical Journal of Australia

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Product information (PI) for thyroid‐related medications endorsed by the Therapeutic Goods Administration, as reproduced in the commonly used compilation publications June 2006 MIMS (Monthly index of medical specialties) annual, MIMS Online and the Australian prescription products guide 2006, was evaluated to see whether it reflects contemporary therapeutic practice. Compared with current medical literature, these PI‐based sources provide inadequate, inaccurate or outdated therapeutic directives. Examples include: ➢Incorrect advice that thyroxine therapy should always begin at very low dosage. ➢Failure to recommend increased thyroxine dosage early in pregnancy (thus placing the offspring of women being treated for hypothyroidism at risk of impaired fetal brain development). ➢Incorrect and potentially unsafe advice to treat thyrotoxicosis with stable iodide in late pregnancy. ➢Failure to advise serial adjustment of antithyroid drug dosage until after a patient becomes euthyroid (this can result in iatrogenic thyroid dysfunction). ➢Outdated advice that antithyroid drugs are not compatible with breastfeeding. Recent initiatives to upgrade consumer medicine information (CMI) appear to accept PI‐based sources as a reliable benchmark for CMI. That inference is not warranted for thyroid‐related medications. Accountability for the updating of clinical information in PI needs to be defined, and the process for updating PI may need to be modified. Quality drug information, both PI and CMI, depends on fluent, evidence‐based collaboration between suppliers, regulators, prescribers, specialist clinicians and consumers.

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“…On two-dimensional and Doppler color flow imaging, Ralls et al 7and Li et al (16) have noted accelerated thyroid parenchymal blood velocity in patients with Graves' disease. Similarly, by using the first passage of a radioactive bolus, Rangaswamy et al (17) reported an increased thyroid vascular index in patients with toxic goiter. This increased vascularity might be responsible for the decreased echogenicity of the thyroid gland.…”

Section: Discussionmentioning

confidence: 95%

Ultrasonographic and Doppler Study of the Thyroid Gland in Graves’ Disease Before and After Treatment with Antithyroid Drugs

et al. 1997

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Objective: To determine the effects of medical treatment on the thyroid gland, peripheral circulation, and laboratory findings in patients with Graves' disease. Methods: Twenty patients with Graves' disease were treated with either carbimazole and propranolol (group I) or carbimazole only (group II). Serum free thyroxine (FT 4), thyroid-stimulating hormone (TSH), and thyrotropin-binding inhibitory immunoglobulins (TBII) were estimated before and after 6 weeks of treatment. Duplex Doppler ultrasonographic examination of the thyroid, inferior thyroid artery (ITA), and common carotid artery (CCA) was performed before and after 2, 4, and 6 weeks of therapy. Results: Serum FT 4 and TBII decreased after treatment in both groups, whereas serum TSH increased in group I only. The volume of the thyroid gland and parenchymal blood velocity were increased in these patients and diminished only with addition of propranolol to carbimazole. A diffuse hypoechogenic pattern in the thyroid gland and increased ITA blood flow and peak velocity were observed in all patients and persisted throughout treatment. The mean CCA peak blood velocity was accelerated in Graves' disease and diminished after 6 weeks of therapy in both groups, whereas increased CCA blood flow diminished only in group I. Conclusion: A 6-week period of therapy with carbimazole and propranolol has no effect on the diffuse low echogenic pattern in the thyroid gland and the accelerated ITA blood flow in Graves' disease. The addition of propranolol is associated with early decrements in thyroid volume, parenchymal vascularity, and CCA blood flow as well as early recovery of TSH suppression, but it has no additional effect on thyroid hormone secretion or TBII levels.

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Effect of Lugolʼs iodine on the vascularity of thyroid gland in hyperthyroidism

Cited by 11 publications

References 0 publications

Excess iodide decreases transcription of NIS and VEGF genes in rat FRTL-5 thyroid cells

Excess iodide decreases transcription of NIS and VEGF genes in rat FRTL-5 thyroid cells

Barriers in the quest for quality drug information: salutary lessons from TGA‐approved sources for thyroid‐related medications

Ultrasonographic and Doppler Study of the Thyroid Gland in Graves’ Disease Before and After Treatment with Antithyroid Drugs

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