Academic literature on the topic 'Urine iodine concentration'

Experimental groups of pigs were treated orally with 120 mg (Group O 120), or 480 mg (Group O 480) of iodine per animal, or intramuscularly with 240 mg (Group I 240) of iodine per animal. Iodine was administered in the form of iodised fatty acid esters (IFAE). The treatment resulted in significantly increased iodine concentrations in tissues and a single dose was sufficient to meet the requirement for the whole fattening period (180 days). Urinary iodine concentrations in all the experimental groups were higher than in the control group C receiving iodine only from conventional feed. Urinary excretion of iodine between days 2 and 5 was more distinctive in orally treated than in intramuscularly treated animals (Figure 1). Iodine concentrations at the end of the fattening period (day 180) were higher in the treated than in the control groups. The treatment effect was more marked in Groups O 480 and I 240 than in Group O 120. The dynamics of blood serum iodine concentrations was similar to urinary concentrations (Figure 2). Mean thyroid gland weights in the groups O 120, O 480, I 240, and C were 9.19, 8.51, 7.10, and 12.01 g, respectively. An opposite tendency was observed for iodine concentrations in thyroid gland dry matter (Figure 3). No effects of any of the treatments on total protein, albumin, total lipids, or cholesterol concentrations in blood serum were observed. Group C showed lower tissue iodine concentrations than any of the experimental groups. The only exception was hepatic tissue in which approximately the same iodine concentrations were found in all the groups. Data obtained in Groups O 120, O 480, and I 240 indicate that decisive for tissue concentrations was rather the dose of iodine than the route of administration. Iodine is stored above all in the thyroid gland and adipose tissue. As can be seen in Figure 4, its concentration was higher in muscles with a higher proportion of fat (neck) than in lean muscles (ham).

Iodine status in school-age children determined from iodine urine excretion and iodine intakeBackground: School-age children are more at risk if they experience deficiencies and excess iodine. The concentration of iodine in urine is a good biomarker for assessing iodine intake, 90% of iodine intake will be excreted through urine. Objective: This study aimed to analyze the iodine status of school-age children based on urinary iodine excretion (UIE) and iodine intake.Method: The study design used a cross-sectional study on 44 healthy school-aged children in Bogor Regency. Subject selection was done purposively in healthy 5th-grade elementary school students. The data taken in this study was urine iodine excretion concentration and food recall (1x24 hours). Data were analyzed using descriptive analysis and Pearson correlation test.Results: Median iodine excretion concentration in urine was 157 μg/l and the average daily iodine intake of children was 83.29 mg/day. Conclusion: The concentration of iodine excretion in the urine of the children is in the category of sufficient iodine as recommended by WHO / UNICEF / ICCID while the daily intake of iodine for children is still in the less category. The results showed that there was no association of iodine daily intake with iodine excretion concentration in urine(p=0.469).

Iodine is an essential component for fetal neurodevelopment and maternal thyroid function. Urine iodine is the most widely used indicator of iodine status. In this study, a novel validated ion-pair HPLC–UV method was developed to measure iodine concentration in clinical samples. A sodium thiosulfate solution was added to the urine sample to convert the total free iodine to iodide. Chromatographic separation was achieved in a Pursuit XRs C8 column. The mobile phase consisted of acetonitrile and a water phase containing 18-crown-6-ether, octylamine and sodium dihydrogen phosphate. Validation parameters, such as accuracy, precision, limits of detection and quantification, linearity and stability, were determined. Urinary samples from pregnant women were used to complete the validation and confirm the method’s applicability. In the studied population of 93 pregnant women, the median UIC was lower in the group without iodine supplementation (117 µg/L, confidence interval (%CI): 95; 138) than in the supplement group (133 µg/L, %CI: 109; 157). In conclusion, the newly established ion-pair HPLC–UV method was adequately precise, accurate and fulfilled validation the criteria for analyzing compounds in biological fluids. The method is less complicated and expensive than other frequently used assays and permits the identification of the iodine-deficient subjects.

AbstractObjective: To present data on the relationship between the concentration of thyroid-stimulating hormone (TSH) in whole blood or serum from neonates and the concentration of iodine in their mother's urine collected at birth to contribute to the contention that the recommended iodine intake during pregnancy should be increased.Design and Setting: Data were provided by current programmes of neonatal screening of congenital hypothyroidism in Bangkok and rural areas of Thailand.Subjects: A total of 5144 cord serum samples were collected in 2003 and measured for TSH concentrations. Paired samples of blood and urine were collected in 2000 from 203 infants and their mothers and from 1182 infant-mother pairs in 2002-03 in six rural provinces. Iodine was measured in the urine and TSH was measured in cord serum.Results: The urinary iodine concentration of mothers in rural Thailand is adequate, with a median of 103 μg l-1. However, in 2000, the median urinary iodine concentration of mothers in Bangkok was only 85 μg l-1. The concentration of TSH in whole blood collected on filter paper from neonates was not sensitive enough to be used as a monitoring tool for iodine nutrition in the neonates, as there was no relationship with the concentration of iodine in the urine of the children's mothers. This was in contrast to the concentration of TSH in serum collected from cord blood.Conclusions: Several conclusions were drawn from this data: 1) Neonatal TSH screening using whole blood collected from a heel prick at 3 days of age is not sensitive enough to assess the iodine nutrition of neonates; 2) Neonatal TSH screening using cord sera can be used to assess iodine nutrition in neonates; 3) The optimum median maternal urinary iodine concentration in Thailand appears to be 103 μg l-1; 4) The criteria proposed by WHO, UNICEF, and ICCIDD to assess iodine nutrition using data on neonatal TSH concentrations should be reassessed; and 5) Neonatal TSH screening can be effectively performed by collecting cord serum in district hospitals in Thailand.

Mild to moderate iodine deficiency is common among women of childbearing age. Data on iodine status in infants are sparse, partly due to the challenges in collecting urine. Urinary iodine concentration (UIC) is considered a good marker for recent dietary iodine intake and status in populations. The aim of this study was to investigate the reliability of iodine concentration measured in two spot-samples from the same day of diaper-retrieved infant urine and in their mothers’ breastmilk. We collected urine and breastmilk from a sample of 27 infants and 25 mothers participating in a cross-sectional study at two public healthcare clinics in Norway. The reliability of iodine concentration was assessed by calculating the intraclass correlation coefficients (ICC) and the coefficient of variation (CV). The ICC for infants’ urine was 0.64 (95% confidence interval (CI) 0.36–0.82), while the ICC for breastmilk was 0.83 (95% CI 0.65–0.92) Similarly, the intraindividual CV for UIC was 0.25 and 0.14 for breastmilk iodine concentration (BIC). Compared to standard methods of collecting urine for measuring iodine concentration, the diaper-pad collection method does not substantially affect the reliability of the measurements.

BACKGROUND The importance of adequate iodine status in pregnancy is undoubted as its deficiency is associated with adverse pregnancy outcomes for the mother as well as the foetus and neonate. Although median urine iodine concentration can assess iodine status of the population but not at an individual level. The purpose of this study was to assess the nutritional status of iodine and identify its effects on thyroid function during the first trimester of pregnancy. METHODS The study was carried out on 341 euthyroid healthy pregnant women using urine iodine concentration and other parameters of thyroid panel at a tertiary care hospital. RESULTS Median (interquartile range) urine iodine concentration and thyroid stimulating hormone (TSH) were 227.37 (161.7, 343.86) μg / L and 1.8 (1.1, 2.7) mIU / L respectively and Mean ± SD of free thyroxine and thyroid peroxidase antibodies were 14.53 ± 2.02 pmol / L and 38.23 ± 9.29 kIU / L respectively. Only thyroid peroxidase antibodies showed significant difference across groups with different iodine status. A positive correlation of urine iodine concentration (UIC) with thyroid peroxidase antibodies was observed (r = 0.137, P = 0.011). Multiple regression analysis revealed that thyroid peroxidase antibodies can serve as an independent predictor of iodine status in the presence of normal levels of TSH and FT4 (t - 3.063, CI; 0.880, 4.038, P = 0.002). CONCLUSIONS Thyroid peroxidase antibodies progressed positively with increase in urine iodine concentration indicating its role as a marker of iodine nutritional status and for early identification of women who can develop autoimmune thyroiditis resulting in hypothyroidism even prior to elevation of thyroid stimulating hormone levels. KEY WORDS Anti-TPO Ab, Free Thyroxine, Thyroid Stimulating Hormone, Urine Iodine Concentration

ABSTRACT Background Iodine status surveys of women in Somaliland present widely conflicting results. Previous research indicates elevated concentrations of iodine (IQR 18–72 μg/L) in groundwater used for drinking and cooking, but the relation with iodine intake is not well characterized. Objectives We aimed to investigate the contributions of household water iodine concentration (WIC), breastfeeding, total fluid intake, hydration levels, and urine volume on urinary iodine concentration (UIC) and excretion (UIE) over a 24-h period and to define iodine status from iodine intake estimates and median UIC, normalized to a mean urine volume of 1.38 L/d (hydration adjusted). Methods The study sample comprised 118 nonpregnant, healthy women aged 15–69 y. All participants resided in Hargeisa, and 27 were breastfeeding. Data collection consisted of a 24-h urine collection, a 24-h fluid intake diary, a beverage frequency questionnaire, and a structured recall interview. We measured UIC and WIC in all urine and in 49 household water samples using the Sandell-Kolthoff reaction. Results WIC ranged between 3 and 188 μg/L, with significant median differences across the water sources and city districts (P < 0.003). Nonbreastfeeding women were borderline iodine sufficient [hydration-adjusted median urinary iodine concentration (mUIC) 109 μg/L; 95% CI: 97, 121 μg/L], whereas breastfeeding women showed a mild iodine deficiency (73 μg/L; 95% CI: 54, 90 μg/L). There were strong correlations (ρ: 0.50–0.69, P = 0.001) between WIC and UIC, with iodine from household water contributing more than one-half of the total iodine intake. Multivariate regression showed hydration and breastfeeding status to be the main predictors of UIC. Conclusions Iodine from household water is the main contributor to total iodine intake among women in Hargeisa, Somaliland. Variation in female hydration and spatial and temporal WIC may explain diverging mUIC between studies. Water sources at the extremes of low and high iodine concentrations increase the risk of subpopulations with insufficient or more than adequate iodine intake.

AbstractObjectives:The most important risk factor of cardiovascular disease is hypertension and high salt intake contributes to high blood pressure. However, to prevent iodine deficiency disorders, the iodisation of salt is a proven strategy. So, on one hand, we suggest people reduced salt consumption but on the other hand, we also fear an increase in the prevalence of iodine deficiency disorders. In the present study, we investigated the possibility of salt intake at WHO recommended levels resulting in higher or lower iodine status in India by assessing the urinary iodine status and its relation with blood pressure.Design:It was a cross-sectional study.Setting:It was a community-based study.Participants:We collected 24-hour urine samples for estimation of iodine concentrations in urine from 411 adult hypertensives in the Mandla district of central India. Urinary iodine was estimated using Thermo ORION make ion-selective electrodes.Results:The median urinary iodine excretion was 162·6 mcg/l. Interestingly 371 (90·26 %) subjects were observed with > 200 mcg/l urinary iodine concentration level indicating iodine sufficiency. Individuals with high urine Na significantly had high blood pressure as compared with individuals with low urinary Na excretion (P < 0·01). There is a higher probability of high urine iodine levels among individuals with higher urine Na levels.Conclusion:The study revealed that 90 % of the population were excreting excessive iodine in urine, which is more than adequate iodine uptake. This excess uptake enables a scope for reduction in salt intake to control hypertension.

Iodine is an essential trace element for humans and animals. The incidence of iodine poisoning in cattle is low. In the present study, we evaluated the clinical findings, serum glucose and cholesterol, thyroid hormone and urine iodine levels in cattle exposed to excess iodine. All of the clinical data were determined following the addition of potassium iodide to the drinking water. Inappetence, cough, and hyperthermia were notable clinical findings. We detected a very high iodine level (470 μg /L) in an analysis of the drinking water samples. A biochemical analysis revealed that the serum cholesterol levels in the affected cattle were significantly lower (p<0.05) than in healthy cattle. However, the serum glucose in the affected cattle was significantly higher (p<0.05) compared to healthy cattle. The iodine concentration in the urine of the affected animals was also significantly higher (p<0.05) than in the healthy animals. Importantly, a hematological analysis indicated leukocytosis with neutrophilia. Several clinical signs, including hyperthermia, tachycardia, alopecia, and a naso-oral discharge, based on suspected history can suggest iodine intoxication. In addition, biochemical parameters, such as urine iodine, serum glucose and cholesterol levels, were observed to be different between healthy and affected cattle. The thyroid function in affected cattle should also be studied.

This research aimed to investigate the compensation mechanism of iodine deficiency and excess in the mammary gland during lactation. Female rats were divided into the low iodine group (LI), the normal iodine group (NI), the 10-fold high iodine group (10HI) and the 50-fold high iodine group (50HI). We measured the iodine levels in the urine, blood, milk, and mammary gland. The protein expression of sodium/iodide symporter (NIS), DPAGT1, and valosin-containing protein (VCP) in the mammary gland was also studied. The 24-hour urinary iodine concentration, serum total iodine concentration, serum non-protein-bound iodine concentration, breast milk iodine concentration, and mammary gland iodine content in the 50HI group were significantly higher than those in the NI group (p < 0.05). Compared with the NI group, NIS expression in the 50HI group significantly decreased (p < 0.05). DAPGT1 expression was significantly higher in the LI group than in the NI group (p < 0.05). The expression level of VCP was significantly increased in the 10HI and 50HI groups. In conclusion, milk iodine concentration is positively correlated with iodine intake, and the lactating mammary gland regulates the glycosylation and degradation of NIS by regulating DPAGT1 and VCP, thus regulating milk iodine level. However, the mammary gland has a limited role in compensating for iodine deficiency and excess.

Iodine is crucial for thyroid hormone production which is essential for growth and development. Iodine deficiency in pregnancy can lead to cognitive impairment, poor growth, congenital abnormalities and in severe situations cretinism. Mild iodine deficiency re-emerged in Australia in the last decade. To address this issue, in 2009 mandatory iodine fortification of bread was implemented and in 2010 routine iodine supplementation in pregnancy was recommended. Since mandatory iodine fortification there has been limited data on the iodine intake and iodine status of Australians, including pregnant women. Intervention trials in iodine deficient populations have shown a higher maternal and infant urine iodine concentration (UIC) in iodine supplemented groups compared to controls, with the effect on thyroid function being less clear. However, no studies have assessed the relationships between maternal iodine intake from food and supplements in pregnancy and maternal or infant iodine status and thyroid function in mildly iodine deficient or sufficient populations. The primary aims of the thesis were to examine the associations between maternal iodine intake/iodine status/thyroid function in pregnancy and markers of maternal and infant iodine status/thyroid function. The secondary aims were to examine the associations between maternal iodine intake/thyroid function in pregnancy and pregnancy/birth outcomes, infant growth and the general health of pregnant and postnatal women. 783 pregnant women in South Australia participated in the study. An iodine specific food frequency questionnaire (I-FFQ) was developed and validated to assess dietary iodine intake at baseline (<20 weeks’ gestation) and 28 weeks’ gestation. Maternal UIC, maternal thyroid function and the general health and wellbeing of pregnant and postpartum women was assessed at baseline, 28 weeks’ gestation and 3 months postpartum. Breast milk iodine concentration (BMIC) was assessed at birth and 3 months postpartum. Thyroid stimulating hormone (TSH) was collected from newborn screening at birth. Pregnancy/birth outcome data and infant anthropometrics at birth were collected from the women’s and infant’s medical records and infant UIC, infant thyroid function and infant growth was measured at 3 months of age. Based on the median UIC, pregnant women in this study were classified as iodine sufficient, both with or without the use of iodine supplements during pregnancy. Maternal iodine intake in pregnancy was positively associated with maternal UIC and BMIC (Chapter 4), while no association was found with maternal thyroid function (Chapter 4), infant UIC, infant thyroid function (Chapter 5) or clinical outcomes (Chapter 6). At 28 weeks’ gestation maternal free triiodothyronine (fT3) was positively associated with infant fT3 at 3 months of age, while maternal fT3 and thyroglobulin (Tg) was inversely associated with infant TSH at 3 months of age (Chapter 5). Furthermore, markers of maternal thyroid function at 28 weeks gestation was associated with the mental and physical health of women at 3 months postpartum as well as the severity of stress at 28 weeks gestation (Chapter 6). In summary, maternal iodine intake in pregnancy is not associated with maternal or infant thyroid function in an iodine sufficient population, although maternal thyroid function at 28 weeks’ gestation is associated with infant thyroid function at 3 months of age and with aspects of the general health and wellbeing of pregnant and postnatal women. Further research is needed to better understand these relationships in populations with various iodine status and their impact on infant development.
Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2015