The effect and mechanism of excessive iodine on the endothelial function of human umbilical vein endothelial cells.

Iodine excess (IE) can cause thyroid dysfunction, thyroid diseases can adversely affect cardiovascular function. Accordingly, this study was to explore the direct and indirect effects of IE on endothelial function. Nthy-ori 3-1 and HUVECs cells were treated with potassium iodide (KI). CCK-8, LDH leakage, Elisa, RT-PCR and Western blotting were used to detect relevant indicators. Results showed that a certain level of KI can directly and indirectly reduce the viability of HUVECs and increase cytotoxicity. KI decreased the expression of ET-1 and VWF in HUVECs, inhibited the secretion of ET-1 in culture medium, and increased the expression of IL-6 and TNFα in HUVECs or Nthy-ori 3-1 cells alone. In the co-culture system, KI decreased the expression of ET-1 and THBD and increased the expression of TNFα and IL-6. Collectively, IE can directly and indirectly inhibit endothelial function of endothelial cells, which may be related to its induced inflammatory response.

Effect of iodinated contrast media on peripheral blood mononuclear cells in terms of cell viability, cell cycle and oxidative stress in an in vitro system.

Iodine contrast agents are essential for diagnostic purposes in radiology and have significant medical benefits. However, they pose a risk of causing allergic reactions or adverse cellular effects. In this study, we examine the in vitro effects of iodine contrast agents (Iopamiro 370, Ultravist 370, Visipaque 320, and Optiray 350) on cellular functions of human peripheral blood mononuclear. The findings reveal that a concentration of 50 mgI/ml of iodine contrast agents causes a 50% reduction in cell viability, but lower concentrations of 2.5, 5.0, and 10.0 mgI/ml do not affect the cell cycle. Furthermore, the contrast agents decrease oxidative stress levels in cells. In conclusion, this study demonstrates that iodine contrast agents can be used safely in appropriate concentrations for diagnostic purposes without affecting the cell cycle and preventing oxidative stress on normal cells. The insights gained from this study could aid in the development of diagnostic contrast agents in the future of medicine.

3-Methyladenine alleviates excessive iodine-induced cognitive impairment via suppression of autophagy in rat hippocampus.

Drinking water with high levels of iodine has been identified as the key contributor to iodine excess, but the mechanisms of neurotoxicity induced by excessive iodine remain elusive. The present study aimed to explore the role of autophagy in the neurotoxic effect induced by excessive iodine in vivo. The Morris water maze test results demonstrated that excessive iodine impaired the learning and memory capabilities of rats, which were associated with marked body weight and brain weight abnormalities. In addition, iodine treatment increased malondialdehyde accumulation, decreased superoxide dismutase activity and glutathione (GSH) level, and enhanced levels of autophagy markers in the hippocampus. Notably, inhibition of autophagy with 3-methyladenine (3-MA) could significantly alleviate excessive iodine-induced cognitive impairment. These data imply that autophagy is involved in the cognitive impairment elicited by excessive iodine as a pathway of cell death, and inhibition of autophagy via 3-MA may significantly alleviate the above damage.

Influence of iodine in excess on seminiferous tubular structure and epididymal sperm character in male rats.

Excess iodine induced public health problems are now emerging in many iodine sufficient regions for indiscriminate intake of iodine through various iodized products. It has been reported that excess iodine can disrupt overall male reproductive physiology by generating oxidative stress in the testis. However, information on the possible effect of iodine in excess on spermatozoa found less. In the present investigation flow cytometric techniques and scanning electron microscopy (SEM) have been used to study the spermatozoal functional as well as structural status under the influence of excess iodine; generation of ROS in the spermatozoa as evident by DCFDA, altered acrosomal integrity as observed by fluorescence lectin staining method and depolarized mitochondrial membrane potential (ΔΨm ) noticed by JC-1 staining. Ultrastructure of seminiferous tubule after excess iodine exposure indicated severe deterioration of seminiferous tubular surface architecture. Significant increase in spermatozoal DNA fragmentation and apoptotic sperms were found by acridine orange and Annexin V, respectively, however the plasma membrane integrity/viability was decreased as evident by propidium iodide staining in various incremental doses and durations under iodine excess. The study reveals that excess iodine could cause apoptosis of spermatozoal cells by inducing ROS that ultimately affects male fertility potential.

The effect of experimentally induced hypothyroidism on the isoflurane minimum alveolar concentration in dogs.

OBJECTIVE: To determine the effect of experimentally induced hypothyroidism on isoflurane (ISO) minimum alveolar concentration (MAC) in dogs. STUDY DESIGN: Prospective experimental study. ANIMALS: Eighteen adult female mongrel dogs, age 2-4 years and weighing 8.2-13.1 kg. METHODS: Hypothyroidism was induced in nine dogs by the intravenous administration of 1 mCi kg(-1) of (131) Iodine. The remaining nine dogs served as controls. Dogs were studied 9-12 months after the induction of hypothyroidism. Anesthesia was induced with ISO in oxygen via a mask. The trachea was intubated, and anesthesia was maintained using ISO in oxygen using a semi-closed rebreathing circle system. The dogs were mechanically ventilated to maintain an end-tidal carbon dioxide concentration between 35 and 45 mmHg. End-tidal ISO concentrations were measured with an infrared gas analyzer. The MAC was determined in duplicate using a tail clamp technique. The mean values for the groups were compared using a two sample t-test. RESULTS: The mean ± SD MAC of isoflurane in the hypothyroid and euthyroid dogs was 0.98 ± 0.31% and 1.11 ± 0.26%, respectively. The mean MAC of isoflurane in hypothyroid dogs was not significantly different from the mean MAC of isoflurane in the control dogs (p = 0.3553). CONCLUSION AND CLINICAL RELEVANCE: The MAC of ISO in dogs was not significantly affected by experimentally induced hypothyroidism. The dose of ISO in dogs with hypothyroidism does not need to be altered.

Radiocontrast-induced thyroid dysfunction: is it common and what should we do about it?

There has been a substantial increase in the use of radiocontrast-enhanced imaging studies in the past two decades (particularly computed tomography and coronary angiography). Sudden exposure to high levels of iodide may result in thyroid dysfunction (hyperthyroidism and hypothyroidism alike). Although the adverse-event rate is not very high, the condition is notable considering the large number of contrast-enhanced radiographic studies performed. Clinicians often have to decide on the most suitable diagnostic modality and the safest contrast medium when it comes to certain patients. In this study, we stress that the thyroid function of the patients should also be taken into consideration while making such decisions. We discuss in detail the prevalence and types (hypothyroidism and hyperthyroidism) of radiocontrast-induced thyroid dysfunction. We list the subsets of the population that are at a higher risk of radiocontrast-induced thyroid dysfunction and summarize the necessary prophylaxis and possible treatment. The presented principles apply to intravenous, intra-arterial and enteral (endoscopic retrograde cholangiopancreatography) routes of iodinated contrast medium administration.

Leaching of organic matter and iodine, formation of iodinated disinfection by-products and toxic risk from Laminaria japonica during simulated household cooking.

Iodinated disinfection by-products (I-DBPs) exhibited potential health risk owing to the high toxicity. Our recent study demonstrated that I-DBPs from Laminaria japonica (Haidai), the commonly edible seaweed, upon simulated household cooking condition were several hundred times more than the concentration of drinking water. Here, the characterization of Haidai and its leachate tandem with the formation, identification and toxicity of I-DBPs from the cooking of Haidai were systemically investigated. The dominant organic matter in Haidai leachate were polysaccharides, while the highest iodine specie was iodide (∼90% of total iodine). Several unknown I-DBPs generated from the cooking of Haidai were tentatively proposed, of which 3,5-diiodo-4-hydroxybenzaldehyde was dominant specie. Following a simulated household cooking with real chloraminated tap water, the presence of Haidai sharply increased aggregate iodinated trihalomethanes, iodinated haloacetic acids, and total organic iodine concentrations to 97.4 ± 7.6 µg/L,16.4 ± 2.1 µg/L, and 0.53 ± 0.06 mg/L, respectively. Moreover, the acute toxicity of Haidai soup to Vibrio qinghaiensis sp.-Q67 was around 7.3 times higher than that of tap water in terms of EC50. These results demonstrated that the yield of I-DBPs from the cooking of Haidai and other seaweed should be carefully considered.

Effect of chronic excess iodine intake on thyroid function and oxidative stress in hypothyroid rats.

Our objective was to investigate the effects of chronic excess iodine intake on thyroid functions and thyroid oxidative stress state in hypothyroid rats. Sixty rats were divided into euthyroid and hypothyroid (thiocyanate-induced) groups with or without administration of excess iodine (3000 or 6000 µg/L) for 8 weeks. Serum thyroxine (T(4)), triiodothyronine (T(3)), thyroid-stimulating hormone (TSH), thyroid antioxidants (catalase, superoxide dismutase enzymes, and total antioxidants), and lipid peroxide (malondialdehyde; MDA) were measured. Reverse transcription - PCR gene expression for thyroidal Na(+)/I(-) symporter (NIS), D1 deiodinase, and thyroid peroxidase (TPO) were performed. Thiocyanate significantly decreased thyroid hormones (T(3), T(4)), increased lipid peroxides and antioxidants, and increased gene expression of NIS, D1 deiodinase, and TPO. Excess iodine intake in hypothyroid rats increased T3 and T4. Also, high iodine intake by hypothyroid rats significantly decreased NIS, D1 deiodinase, and TPO genes expression. Excess iodine significantly increased MDA and antioxidants in euthyroid and hypothyroid rats. In conclusion, thiocyanate-hypothyroidism increases gene expression of NIS, TPO, and TPO and induces oxidative stress. High iodine intake decreases NIS and D1 deiodinase gene expression in hypothyroid rats. Moreover, excess iodine increase thyroid hormones, lipid peroxides, and antioxidants in hypothyroid rats.

The impact of high iodine intake on thyroid function in ewes and lambs.

OBJECTIVES: The objective of the study was to assess the metabolic risk of excessive dietary iodine intake in ewes and neonatal lambs. DESIGN: Pregnant Sumava ewes received an experimental diet containing 3.1 mg iodine per kg of dietary dry matter in Group A (control, n=13, 6 ewes and 7 lambs) and 5.1 mg iodine per kg of dietary dry matter in Group B (experimental, n=12, 6 ewes, 6 lambs) for eight months. Iodine was administered to ewes as calcium iodate. TSH in blood serum; TT3, TT4, fT3, and fT4 in blood plasma were examined in both groups of ewes and lambs to assess the risks of iodine intake above the permitted limit, as it applies to thyroid gland activity. RESULTS: Group B ewes showed a significant increase in TSH and TT4 only on day 1 after parturition. The highest values of TT4, TT3, and fT3 in lambs were recorded on day 1 after birth. The lowest values of fT3 and fT4 in lambs were measured on day 60 after birth with no differences observed between the groups. In lambs of Group B the lower concentration of TSH until day 3 after birth was followed by a significant increase from day 10 after birth. CONCLUSION: Our results indicate a risk of postnatal hypothyroidism among lambs from pregnant and lactating ewes having a high iodine intake.

Assessing the skin irritation and sensitizing potential of concentrates of water chlorinated in the presence of iodinated X-ray contrast media.

Chemical disinfection of water provides significant public health benefits. However, disinfectants like chlorine can react with naturally occurring materials in the water to form disinfection byproducts (DBPs). Natural levels of iodine have been reported to be too low in some source waters to account for the levels of iodinated DBPs detected. Iodinated X-ray contrast media (ICM) have been identified as a potential source of iodine. The toxicological impact of ICM present in source water at the time of disinfection has not been fully investigated. Iopamidol, iohexol, iopromide, and diatrizoate are among the ICM most frequently detected in water. In this study, source water containing one of these four ICM was chlorinated; non-chlorinated ICM-containing water samples served as controls. Reactions were conducted at an ICM concentration of 5 µM and a chlorine dose of 100 µM over 72 hr. Water concentrates (20,000-fold) were prepared by XAD-resin/ethyl acetate extraction and DMSO solvent exchange. We used the MatTek® reconstituted human epithelial skin irritation model to evaluate the water concentrates and also assessed the dermal irritation and sensitization potential of these concentrates using the LLNA:BrdU ELISA in BALB/c mice. None of the water concentrates tested (2500X) resulted in a skin irritant response in the MatTek® skin irritation model. Likewise, none of the concentrates (2500X, 1250X, 625X, 312.5X, 156.25X) produced a skin irritation response in mice: erythema was minimal; the maximum increase in ear thickness was less than 25%. Importantly, none of the concentrates produced a positive threshold response for allergic skin sensitization at any concentration tested in the LLNA:BrdU ELISA. We conclude that concentrates of water disinfected in the presence of four different ICM did not cause significant skin irritation or effects consistent with skin sensitization at the concentrations tested.

Iodine: it's important in patients that require parenteral nutrition.

Iodine deficiency has multiple adverse effects on growth and development because of inadequate thyroid hormone production. Four methods are generally recommended for assessment of iodine nutrition: urinary iodine concentration, thyroid size, and blood concentrations of thyroid-stimulating hormone and thyroglobulin. Iodine intakes < or = 1 mg/d are well tolerated by most adults, because the thyroid is able to adjust to a wide range of intakes. A daily dose of 1 microg iodine/kg body weight is recommended for infants and children receiving parenteral nutrition (PN), but this is far below their requirement. Daily iodine requirements in adults receiving enteral nutrition or PN are estimated to be 70-150 microg, but most PN formulations do not contain iodine. Despite this, deficiency is unlikely because absorption from iodine-containing skin disinfectants and other adventitious sources can provide sufficient iodine. However, if chlorhexidine replaces iodine-containing disinfectants for catheter care, iodine deficiency may occur during long-term PN, and periodic testing of thyroid functions may be prudent. Infants may be particularly vulnerable because of their small thyroidal iodine store, but available data do not yet support routine supplementation of preterm infants with iodine. Adults may be less vulnerable because thyroidal iodine stores may be able to support thyroid hormone production for several months. More studies to clarify this issue would be valuable.

[Thyroiditis: What's new in 2019?] / Thyroïdites : où en est-on en 2019 ?

Thyroiditis is a frequent and mostly benign disease that can sometimes disrupt the thyroid balance. Their diagnosis, as well as their aetiology, is a necessary step in the management of the patients. Painful thyroiditis includes acute thyroiditis of infectious origin and subacute thyroiditis. The first one can be treated by antibiotics or antifungals depending on the germ found. The second one will be treated with non-steroidal anti-inflammatory drugs or corticosteroids. In cases of Hashimoto's thyroiditis with overt hypothyroidism, replacement therapy with L-thyroxine will be adapted to the TSH level. As amiodarone treatment provides dysthyroidism, the thyroid status should be monitored regularly. Hypothyroidism will be treated using thyroid replacement therapy. Hyperthyroidism imposes a stop of amiodarone when it is possible. Treatment with synthetic antithyroid drugs (propyl-thio-uracil) or corticosteroids could be used whether there is an underlying thyroid disease or not. Immunotherapies with anti-PD-1/PDL1 or anti-CTLA-4 can also provide dysthyroidism. A monitoring of the thyroid assessment needs to be done in these patients, even if there are no clinical signs, which are not very specific in this context. The treatment of hypothyroidism will be based on thyroid replacement therapy according to the TSH level and the presence or absence of anti-TPO antibodies. Treatment of symptomatic hyperthyroidism may involve a prescription of beta-blockers, or synthetic antithyroid drugs in case of positive anti-TSH receptor antibodies. In all cases, it is desirable to contact an endocrinologist to confirm the diagnosis hypothesis and to decide on a suitable treatment.

Excess iodine impairs spermatogenesis by inducing oxidative stress and perturbing the blood testis barrier.

Approximately 2 billion people worldwide are susceptible to iodine deficiency. Iodine deficiency has largely been tackled by iodine fortification in salt; however indiscriminate use of iodine raises the risk of iodine toxicity. In this study, we aimed to investigate the molecular mechanisms underlying adverse effect of excess iodine on spermatogenesis. Sprague Dawley (SD) rats were orally administered with 0.7 mg potassium iodide (KI)/100 g Bw and 3.5 mg potassium iodide (KI)/100 g Bw for a period of 60 days. This resulted in significant loss of sperm count and motility. Molecular investigations provided evidence for the generation of oxidative stress with high SOD levels, reduced Nrf2, HO-1 and increased NF-kB and Follistatin. Further investigations showed increased apoptosis evidenced by reduced expression of anti-apoptotic (BCL-2, Survivin), increased expression of pro-apoptotic (Bid, Bax) markers, and increased expression of p53 and other modulators/effectors of apoptosis (cytochrome c, cleaved PARP, caspase3 and caspase9). Analysis of the blood testis barrier proteins showed reduced expression of tight junction (JAM-A, Tricellulin), ectoplasmic specialization (Integrin- ß1), adherens junction (N-Cadherin, E-cadherin, ß-catenin) proteins, and reduced expression of other junction protein coding genes (Claudin1, Claudin 5, Occludin, ZO-1, Testin, Fibronectin, CAR-F). Focal adhesion kinase (FAK) and key regulators of spermatogenesis (c-Kit receptor, androgen receptor) were also parallelly decreased. Further investigation showed reduced expression of germ cell proliferation and differentiation markers (PCNA, Cyclin D1, c-Kit, Cdk-4). These findings collectively explain the loss of spermatogenesis under excess iodine conditions. In conclusion, excess iodine causes loss of spermatogenesis by inducing oxidative stress and disrupting the blood testis barrier and cytoskeleton.

Micronucleus induction in mouse polychromatic erythrocytes by an X-ray contrast agent containing iodine.

In this article, the authors report the results of in vivo studies on bone marrow polychromatic erythrocytes (PCE) from mice treated with Urografina®292 (a mixture of sodium amidotrizoate and meglumine amidotrizoate) and with purified sodium amidotrizoate and meglumine amidotrizoate separately or in combination at the same ratio and concentration as that of the highest dose of Urografina®292 used in the experiment. The results showed that Urografina®292 significantly increased the frequencies of micronucleated polychromatic erythrocytes (MNPCEs) in both male (p=0.0082 and p=0.0062) and female (p=0.0350 and p=0.0101) mice treated with doses of 14.3 and 20.0 ml/kg body weight, respectively. When lower doses were used (5.7 and 8.6 ml/kg body weight), the treated mice did not show any significant increase in the frequencies of MNPCEs compared with the negative control group. The same result was observed for both male and female animals treated with purified sodium amidotrizoate and meglumine amidotrizoate separately or in combination. In addition, there was a significant positive correlation between the Urografina®292 doses used and the frequency of micronuclei. These results supported the hypothesis that small amounts of aryl amines present in all X-ray contrast agents containing diatrizoate and closely related triiodobenzoates were responsible for genotoxicity. The frequencies of PCEs in treated animals were determined to estimate the toxicity of Urografina®292, sodium amidotrizoate, and meglumine amidotrizoate to bone marrow, and the results indicated that they did not show any significant difference compared with the negative control group. The fact that mutagenic agents are also generally carcinogenic contributes to the concern with regard to the possible long-term risks of these agents in case of patients who are exposed to iodine-containing X-ray contrast agents during radiodiagnostic procedures.

Feasibility of disinfection kinetics and minimum inhibitory concentration determination on bacterial cultures using flow cytometry.

Disinfection kinetics has been well established for selected antimicrobial agents on isolated bacterial strains. Due to the difficulties of culturing most bacteria, the majority of these studies have been limited to readily cultivable microorganisms of a single type or family. This study explores the feasibility of using flow cytometry for characterising the disinfection kinetics and minimum inhibitory concentration (MIC) of an Escherichia coli culture and a microbial consortium. The proposed method relies on fluorescent dye molecules to indicate the morphological and physiological status of numerous individual cells. Biocides of varying effectiveness and inactivation mechanisms (chlorine, iodine, and silver) were used to evaluate this novel application. Using pseudo-first-order kinetics, the coefficients of specific lethality of chlorine and iodine on Escherichia coli were 4.71 and 3.78 x 10(-3) L mg(-1) min(-1) and MIC of silver ion was between 60 and 80 microg L(-1). The coefficients of specific lethality of chlorine and iodine on the microbial consortium were 4.96 and 8.89 x 10(-3) L mg(-1) min(-1) and MIC of silver ion was between 40 and 60 microg L(-1). This method can be used to provide a rapid and consistent way of determining disinfection kinetics and MICs for pure and mixed bacterial cultures and can potentially be used to examine water and wastewater disinfection efficiency. However, caution should be used to ensure that the physiological and morphological status characterised by cytodyes is a result of the inactivation mechanisms of the disinfectants evaluated.

[A study on the mechanism of iodine-induced thyroid epithelial cell injury in the induction of autoimmune thyroiditis].

OBJECTIVE: To investigate the effect of iodine excess on thyroid follicle epithelial ultrastructure and the relationship between thyroid injury and autoimmune thyroiditis. METHODS: NOD. H-2(h4) mice and Kunming mice were randomly divided into four groups receiving plain water, 5 fold, 10 fold, and 100 fold excessive iodine water. 4, 8 and 24 weeks after receiving iodine water, the mice were killed. After fixation with osmic acid and dual staining with uranyl chloride and citrate lead, thyroid gland ultrastructure was examined with electron microscopy. RESULTS: Iodine treated NOD. H-2(h4) mice exhibited marked accumulation of peroxisome and secondary lysosomes, apoptosis and necrosis of thyroid epithelial cell, damage of thyroid follicles and lymphocytic infiltration. The observed changes induced by iodine were in a dose dependent way. CONCLUSION: The oxidative injury on the thyroid epithelial cells induced by iodine excess might be the prerequisite for the creation of autoimmune thyroiditis.

[Overdose of iodine on expression of CCK gene in rat brains].

OBJECTIVE: To observe the effect of overdose iodine on the expression of CCK gene in brains of rats and identify the possible mechanisms. METHODS: One-month weaning Wistar rats were randomly divided into five groups which were fed with normal feedstuff and water supplemented with different concentrations of potassium iodide, named A group (iodine ration was about 6.15 microg per day), B group (iodine ration was about 30.75 microg per day), C group (iodine ration was about 61.5 microg per day), D group (iodine ration was about 307.5 microg per day) and E group (iodine ration was about 615 microg per day). Rats were sacrificed after being fed for three or six months. Then serum thyroid hormones were measured by radioimmunoassay and the mRNA level of CCK gene was studied by using RT-PCR technique. RESULTS: At the end of three months, the values of thyroid hormones in E group [TT4 (45.2 +/- 13.7) nmol/L, TI'3 (0.65 +/- 0.20) nmol/L, FT3 (0.93 +/- 0.45) pmol/L, FT4 (7.07 +/- 2.43) pmol/L, rT3 (0.15 +/- 0.04) nmol/L] were all lower than those in A group [TT4 (76.0 +/- 18.8) nmol/L, TT3 (1.34 +/- 0.41) nmol/L, FT3 (2.45 +/- 0.62) pmol/L, FT4 (15.12 +/- 3.40) pmol/L, rT3 (0.24 +/- 0.04) nmol/L]. There were significant differences between E group and A group on the levels of serum TH (F values are 14.68, 16.03, 21.16, 20.25, 13.52 respectively, P < 0.01); FT3 levels in C and D groups were significantly decreased as compared to A and B groups (F = 21.16, P < 0.05). rT3 level in D group was significantly decreased compared with A,B and C groups (F = 13.52, P < 0.05). At the end of six months, the levels of serum TH in E group (TT4 (51.84 +/- 15.83) nmol/L, TT3 (0.77 +/- 0.22) nmol/L, FT4 (6.88 +/- 2.23) pmol/L, FT3 (0.74 +/- 0.28) pmol/L, rT3 (0.14 +/- 0.03) nmol/L) were lower than those in any other groups (F values were 6.05, 12.22, 11.25, 13.42, 5.89 respectively, P < 0.05). At the end of both three and six months, the mRNA levels of CCK gene in E group were lower than any other groups (F values were 4.04, 3.95 respectively, P < 0.01). The results of correlation analysis showed that serum FT4 had linear correlation with levels of CCK mRNA (r values were 0.990, 0.948 respectively; P < 0.05); However serum FT3 had no linear correlation with the levels of CCK mRNA (r values are 0.970, 0.932 respectively). CONCLUSIONS: Exposure to overdose of iodine (iodine ration was 100-fold higher than that of A group) could decrease the mRNA level of CCK gene. Compared with FT3, FT4 might have more important role on the regulation of CCK mRNA induced by excess of iodine.

Acute Kidney Injury and Iodinated Contrast Media.

Iodinated contrast agents used in computed tomography (CT) examinations have the potential to cause adverse reactions in patients. The possibility of acute kidney injury should be of concern to radiologic technologists performing CT examinations. Although prevention is paramount, identifying and treating contrast-induced nephropathy, for example, as well as following appropriate guidelines regarding the handling and usage of contrast material, are crucial. This article discusses recent research in these areas.

Iodine Deficiency and Toxicity Among School Children in Damoh District, Madhya Pradesh, India.

OBJECTIVE: To estimate the prevalence of Iodine Deficiency Disorders, and household consumption of adequately iodized salt in Damoh district, Madhya Pradesh in 2016. METHODS: Cross-sectional study with cluster sampling method was used among school-going children. 30 clusters, each with 90 children were selected to access Total Goiter rate (TGR). 540 salt samples were collected to estimate salt iodine content from their household and 270 on the spot urine samples were collected to estimate Urine Iodine Excretion level. RESULTS: TGR was 2.08%. The prevalence of iodine deficiency, adequate iodine nutrition, and either more than adequate or toxic level of Iodine was 26%, 28% and 46 %, respectively. 72.4% people were consuming adequately iodized salt. CONCLUSION: Damoh district is no more an endemic area for iodine deficiency. We recommend continuous monitoring to assess IDDs as well Iodine-induced toxicity in future.