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      Iodine Status among Subclinical and Overt Hypothyroid Patients by Urinary Iodine Assay: A Case–Control Study

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          Abstract

          Objectives:

          The objective of the study was to assess the differences of iodine status as measured by urinary iodine excretion (UIE) between cases of hypothyroidism and healthy controls.

          Materials and Methods:

          The study was conducted in cases with subclinical hypothyroidism ( n = 58) and overt hypothyroidism ( n = 41) and compared with age- and sex-matched healthy euthyroid controls ( n = 52) attending Universal College of Medical Sciences Teaching Hospital, Bhairahawa, Nepal. Serum free triiodothyronine (fT 3), free thyroxine (fT 4), and thyroid-stimulating hormone (TSH) were estimated by competitive ELISA and sandwich ELISA, respectively (Diametra, Italy). The urinary iodine concentration (UIC) in urine samples was estimated by ammonium persulfate digestion method recommended by the WHO.

          Results:

          A significantly higher median UIC was observed among cases of subclinical hypothyroidism (224.90 μg/l) and overt hypothyroidism (281.0 μg/l) as compared to the controls (189.90 μg/l) ( P = 0.0001, P = 0.001). Serum TSH in the cases of subclinical hypothyroid was higher, whereas fT 3 was lower as compared to controls ( P = 0.028, P = 0.0001), respectively. Similarly, serum TSH in the cases of overt hypothyroid was higher and fT 3 and fT 4 were lower as compared to controls ( P = 0.0001, P = 0.0001, P = 0.015), respectively. There was positive correlation of UIC with TSH ( r = 0.269, P = 0.0001), whereas negative correlation was seen with fT 3 ( r = −0.328, P = 0.0001) and fT 4 ( r = −0.145, P = 0.076). The test of multiple regression has shown that fT 3 (β = −0.262, P = 0.012) as an independent predictor in association with UIE in cases.

          Conclusion:

          Excessive iodine intake was found in hypothyroid patients as assessed by UIE concluding that it may trigger the thyroid hypofunction. Cohort studies to generate further evidence should be done to explore potential mechanism of hypothyroidism in excess iodine intake.

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          Most cited references 16

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          Iodine deficiency.

          Iodine deficiency has multiple adverse effects in humans, termed iodine deficiency disorders, due to inadequate thyroid hormone production. Globally, it is estimated that 2 billion individuals have an insufficient iodine intake, and South Asia and sub-Saharan Africa are particularly affected. However, about 50% of Europe remains mildly iodine deficient, and iodine intakes in other industrialized countries, including the United States and Australia, have fallen in recent years. Iodine deficiency during pregnancy and infancy may impair growth and neurodevelopment of the offspring and increase infant mortality. Deficiency during childhood reduces somatic growth and cognitive and motor function. Assessment methods include urinary iodine concentration, goiter, newborn TSH, and blood thyroglobulin. But assessment of iodine status in pregnancy is difficult, and it remains unclear whether iodine intakes are sufficient in this group, leading to calls for iodine supplementation during pregnancy in several industrialized countries. In most countries, the best strategy to control iodine deficiency in populations is carefully monitored universal salt iodization, one of the most cost-effective ways to contribute to economic and social development. Achieving optimal iodine intakes from iodized salt (in the range of 150-250 microg/d for adults) may minimize the amount of thyroid dysfunction in populations. Ensuring adequate iodine status during parenteral nutrition has become important, particularly in preterm infants, as the use of povidone-iodine disinfectants has declined. Introduction of iodized salt to regions of chronic iodine deficiency may transiently increase the incidence of thyroid disorders, but overall, the relatively small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency.
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            Iodine-deficiency disorders.

            2 billion individuals worldwide have insufficient iodine intake, with those in south Asia and sub-Saharan Africa particularly affected. Iodine deficiency has many adverse effects on growth and development. These effects are due to inadequate production of thyroid hormone and are termed iodine-deficiency disorders. Iodine deficiency is the most common cause of preventable mental impairment worldwide. Assessment methods include urinary iodine concentration, goitre, newborn thyroid-stimulating hormone, and blood thyroglobulin. In nearly all countries, the best strategy to control iodine deficiency is iodisation of salt, which is one of the most cost-effective ways to contribute to economic and social development. When iodisation of salt is not possible, iodine supplements can be given to susceptible groups. Introduction of iodised salt to regions of chronic iodine-deficiency disorders might transiently increase the proportion of thyroid disorders, but overall the small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency. International efforts to control iodine-deficiency disorders are slowing, and reaching the third of the worldwide population that remains deficient poses major challenges.
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              Iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice.

              Excess iodine ingestion has been implicated in induction and exacerbation of autoimmune thyroiditis in human populations and animal models. We studied the time course and sex-related differences in iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R), spontaneously develops autoimmune thyroiditis but not diabetes. NOD-H-2h4 mice were given either plain water or water with 0.05% iodine for 8 weeks. Approximately 54% of female and 70% of male iodine-treated mice developed thyroid lesions, whereas only 1 of 20 control animals had thyroiditis at this time. Levels of serum thyroxin (T4) were similar in the treatment and control groups. Thyroglobulin-specific antibodies were present in the iodine-treated group after 8 weeks of treatment but antibodies to thyroid peroxidase were not apparent in the serum of any of the animals. Levels of thyroglobulin antibodies increased throughout the 8-week iodine ingestion period; however, no correlation was seen between the levels of total thyroglobulin antibodies and the degree of thyroid infiltration at the time of autopsy. The thyroglobulin antibodies consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA, IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b thyroglobulin-specific antibodies correlated well with the presence of thyroid lesions.
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                Author and article information

                Journal
                Indian J Endocrinol Metab
                Indian J Endocrinol Metab
                IJEM
                Indian Journal of Endocrinology and Metabolism
                Medknow Publications & Media Pvt Ltd (India )
                2230-8210
                2230-9500
                Sep-Oct 2017
                : 21
                : 5
                : 719-723
                Affiliations
                Department of Biochemistry, Universal College of Medical Sciences, Bhairahawa, Nepal
                [1 ]Department of Internal Medicine, Universal College of Medical Sciences, Bhairahawa, Nepal
                Author notes
                Address for correspondence: Assoc. Prof. Narayan Gautam, Department of Biochemistry, Universal College of Medical Sciences, PO 53, Ranigaon, Bhairahawa, Nepal. E-mail: ng_bp22@ 123456yahoo.com
                Article
                IJEM-21-719
                10.4103/ijem.IJEM_413_16
                5628543
                Copyright: © 2017 Indian Journal of Endocrinology and Metabolism

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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