Search

The aim of the study was to investigate the iodine intake in the resident population in Xi'an and analyze the relationship between iodine nutritional status and the prevalence of subclinical hypothyroidism and thyroid nodules (TNs). A total of 2507 people were enrolled in Xi'an. Venous serum thyroid stimulating hormone (TSH), thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb), urinary iodine concentration (UIC), and thyroid ultrasonography were collected. Patients with abnormal TSH were checked for free thyroxine (FT4) and triiodothyronine (FT3). Adults in Xi'an had median UICs of 220.80 μg/L and 178.56 μg/l, respectively. A sum of 16.78% of people had subclinical hypothyroidism. Both iodine excess and iodine deficit increased the frequency of subclinical hypothyroidism. The lowest was around 15.09% in females with urine iodine levels between 200 and 299 μg/l. With a rate of 10.69%, the lowest prevalence range for males was 100-199 μg/l. In Xi'an, 11.37% of people have TNs. In comparison to other UIC categories, TN occurrences were higher in females (18.5%) and males (12%) when UIC were below 100 μg/l. In conclusion, iodine intake was sufficient in the Xi'an area, while the adults' UIC remains slightly higher than the criteria. Iodine excess or deficiency can lead to an increase in the prevalence of subclinical hypothyroidism. Patients with iodine deficiency are more likely to develop TNs., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

Background: Sri Lanka introduced universal salt iodization (USI) in 1995 after which we demonstrated a high thyroglobulin antibody (TgAb) prevalence in 1998. However, it is unclear whether thyroid autoimmunity persists in the long term in populations exposed to sustained USI and whether such populations have an excess of thyroid dysfunction. We evaluated the prevalence of thyroid autoantibodies and dysfunction in Sri Lankan children and adolescents after more than two decades of sustained USI. Methods: We selected 10- to 18-year-old subjects of both sexes (randomized cluster sampling) from all 9 provinces of Sri Lanka in this cross-sectional study. Blood, urine, and anthropometric data were collected and thyroid ultrasound scans were performed. Validated statistical methods were used to derive local population-specific reference ranges for all thyroid parameters. We also measured urine iodine concentration (UIC), salt, and water iodine concentrations. Results: Blood and urine samples from 2507 and 2473 subjects respectively, and ultrasound scans from 882 subjects were analyzed. Population-derived upper limits for thyroid peroxidase antibody (TPOAb) and TgAb, and reference ranges for triiodothyronine, thyroxine, and thyrotropin (total and age-year-related groups) were significantly different from manufacturer's reference ranges. Using these derived ranges, the prevalence of TPOAb was 10.3% and TgAb was 6.4%. Of the TPOAb-positive subjects, TPOAb were of low concentration in 66.2% (1-3 times the upper limit of the reference range [ULRR]) and showed the strongest association with subclinical hypothyroidism (SCH) at the highest concentrations (>4 ULRR). The prevalence of SCH was 3%. Median UIC (interquartile range) was 138.5 μg/L (79.4-219.0) with regional variability, and median thyroglobulin was 8.3 ng/mL (4.1-13.5). Goiter prevalence was 0.6% and 1.93% (thyroid volume compared to age and body surface area, respectively). Salt and water iodine concentrations were satisfactory. Conclusions: Sri Lanka has safely and effectively implemented USI with good sources of iodine, leading to sustained iodine sufficiency over more than two decades. The early postiodization TgAb surge (42.1%) has settled (6.4%), and despite a persistently high TPOAb prevalence (10.3%), SCH prevalence remains low (3%). Further studies should be undertaken to monitor thyroid autoimmune dysfunction in Sri Lankan children, using age-specific, population-derived reference ranges.

Iodine is an essential micronutrient for the synthesis of thyroid hormones. The proper functioning of the thyroid axis is essential for the normal development of the nervous system, especially in the first trimester of gestation. The aim of the present study was to analyze the perinatal outcomes, anthropometry, and APGAR test scores of newborns and to relate them to maternal thyroid status. A total of 190 newborns participated in the study. No correlation was found between thyroid stimulating hormone (TSH) and maternal ioduria values in the first trimester of gestation with the weight or length of the newborn, or the APGAR score at one minute after birth. However, we found significant differences between the APGAR scores of children whose mothers had an iodine sufficiency level in the first trimester compared to the children of mothers with iodine deficiency. Similarly, the APGAR scores of children whose mothers had a TSH > 4 have significantly better APGAR scores than the children of mothers with a TSH < 4. Likewise, we found significant differences between the measurements of the newborns depending on whether their mothers smoked. The children of mothers who took iodine supplements or iodized salt obtained the highest APGAR score at one and five minutes after birth. It is essential to focus on recommending adequate consumption of iodine supplements and iodized salt prior to gestation and at least during the first trimester to achieve better fetal well-being.

The studies on the increasing incidence of thyroid abnormalities are scarce. The aim of this current study was to ascertain the effects of geographical region on thyroid abnormalities under the context of universal salt iodization (USI). We randomly selected 1255 participants residing in inland and 1248 in coast, with the determination of urinary iodine concentration (UIC) and functional and morphological abnormalities of thyroid gland. The median UIC was significantly higher for the inland participants (188.5 μg/L) than the coastal participants (128.5 μg/L; p < 0.001), indicating iodine sufficiency in both populations according to the recommended assessment criteria by the World Health Organization. However, the spectrum of thyroid abnormalities varied between regions, with hypothyroidism prevalent in inland and thyroid nodules in coast. The associations between region and thyroid abnormalities via binary logistic regression models showed that the coastal participants were at a higher risk of total thyroid abnormalities than those from the inland (OR 1.216, 95% CI 1.020-1.449), after the adjustment of ten confounders (demographical characteristics, smoking status, metabolism syndrome, and hyperuricemia). These results indicated that further investigations of the adverse effects of hypothyroidism and thyroid nodules on health burden is urgently needed to sustain USI program.

Background: We aimed to examine the association of urinary iodine concentration with Hashimoto's thyroiditis (HT) risk, and particularly, to investigate whether the HT-related genetic variations might modify the effects of urinary iodine on HT in the Chinese Han population. Methods: We conducted a case-control study with 1723 Chinese (731 cases, 992 controls). The associations between urinary iodine concentration and HT risk were analyzed using logistic regression models. The effects of interactions between the genetic risk scores (GRSs) and urinary iodine on HT risk were assessed by including the respective interaction terms in the models. We also applied restricted cubic spline regression to estimate the possible nonlinear relationship. The multinomial logistic regression models were performed to determine the associations of urinary iodine with euthyroid-HT and hypothyroidism-HT. Results: After controlling for potential confounders, the odds of HT increased with increasing quartiles of urinary iodine concentration: adjusted odds ratios (ORs) and 95% confidence intervals [CIs] were 1.45 [1.06-1.99], 1.66 [1.17-2.34], and 2.07 [1.38-3.10] for the quartiles 2, 3, and 4, respectively, compared with the first quartile ( p for trend <0.001). Multivariable restricted cubic spline regression analysis further demonstrated that there was a near-linear association between urinary iodine concentration and HT risk ( p -overall <0.001; p -nonlinear = 0.074). However, we did not find significant interactions between urinary iodine and GRSs on the risk of HT (all p for interaction >0.05). Interestingly, we found that each increment of urinary iodine was associated with a more than twofold increase in the odds of hypothyroidism-HT (adjusted OR = 2.64 [CI = 1.73-4.05]), but not with euthyroid-HT ( p  > 0.05). Conclusions: Higher urinary iodine concentration was associated with increased risk of HT, and this association was near linear, indicating that increased urinary iodine has a continuous and graded impact on HT risk. Moreover, the iodine-HT association was not modified by genetic predisposition to HT. Interestingly, urinary iodine concentration was significantly associated with increased risk of hypothyroidism.

Abnormalities of thyroid function are common in patients with nephrotic syndrome (NS). However, a limited number of studies have reported on the association between clinicopathologic features and thyroid dysfunction in patients with NS. We retrospectively studied 317 patients who had been definitively diagnosed with NS. The NS patients with thyroid dysfunction showed higher urine protein, creatinine and lipid levels and lower albumin and hemoglobin than those with normal thyroid function, with no significant differences of pathological types. After dividing thyroid dysfunction groups into five subgroups, interestingly, membranous nephropathy was the most common pathologic type, both in normal thyroid group and in subclinical hypothyroidism group (40.4% and 46.7%, respectively), followed by minimal change disease (28.1% and 21.7%, respectively); while in the hypothyroid, low T3, and low T3T4 groups minimal change disease is now the leading type (48.8%, 33.3% and 38.6%, respectively). High levels of urinary protein, creatinine, cholesterol, and platelets were independent risk factors predicting thyroid dysfunction, while higher albumin and hemoglobin were protective factors. We demonstrated that the type of renal pathology was different among NS patients in different thyroid dysfunction subgroups. Interpretation of the interactions between thyroid and renal function is a challenge for clinicians involved in the treatment of patients with NS.

Background and Objectives: Iodine is an essential trace element for maintenance of normal thyroid function. Normal thyroid function is a prerequisite for neurocognitive development and growth in children. In the United States, iodine is not routinely added as a trace element in parenteral nutrition (PN). Our objective was to determine the prevalence of iodine deficiency and hypothyroidism in children on chronic PN., Methods: This was a cross-sectional study of children <17 years of age and using PN for >6 months at a tertiary children's hospital. Primary outcomes were spot urine iodine concentration (UIC), serum thyrotropin, and free thyroxine levels., Results: Twenty-seven patients were identified (74% male). The median age at screening was 48 months (range: 7-213 months). The median duration on PN was 27 months (range: 11-77 months). Seventeen out of 20 patients (85%) were iodine deficient (spot UIC <100 μg/L), whereas 11 out of 20 patients (55%) were severely iodine deficient (spot UIC <20 μg/L). The prevalence of acquired hypothyroidism (elevated thyrotropin, low free thyroxine, and UIC <100 μg/L) was 33% ( n = 8). None of the children with hypothyroidism screened for autoimmune thyroiditis had positive test results. There was no statistically significant association between duration of PN use and development of iodine deficiency ( P = .08) or hypothyroidism ( P = .96)., Conclusions: Children on chronic PN are at risk for developing iodine deficiency and resultant hypothyroidism; hence, these children should be screened for these outcomes. Further studies are needed to define the temporal onset of iodine deficiency and timing to thyroid dysfunction related to PN., Competing Interests: POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose., (Copyright © 2018 by the American Academy of Pediatrics.)

Purpose: To study oxidative stress status of early type 2 diabetic nephropathy (DN) patients with subclinical hypothyroidism (SCH) and to assess effect of L-thyroxine therapy on the oxidative stress in these patients., Methods: It is a randomized double-blind and placebo-controlled trial. A total of 48 patients with early type 2 DN were included as Euthyroid group, and 92 early type 2 DN with SCH were selected and randomly assigned to L-thyroxine treatment group (LT4 group) and placebo group (SCH group). Changes in urinary albumin excretion rate (UAER), serum malondialdehyde (MDA), superoxide dismutase (SOD) activity, urine 8-hydroxyl deoxyguanosine (8-OHdG), serum creatinine, estimated glomerular filtration rate, and lipid profile before and after 24 weeks of follow-up were examined and compared., Results: The levels of UAER, MDA, 8-OHdG were higher, while the SOD activity was lower in DN patients with SCH than in DN patients (p < 0.05 for all). In the LT4 group, the levels of UAER, MDA, 8-OHdG decreased significantly (p < 0.05) to levels no longer different from the Euthyroid group. The SOD activity increased significantly. But in SCH group, the levels of mAlb, MDA, 8-OHdG were greater after 24 weeks of follow-up and greater than patients in the Euthyroid group. SOD activity decreased significantly after 24 weeks in the SCH group (p < 0.05)., Conclusion: Oxidative stress is greater in the DN patients with SCH, and SCH may exacerbate kidney injury in early DN patients. The LT4 treatment may decrease the oxidative stress and attenuate renal injury in DN patient with SCH.

Context: The prevalence of thyroid disease in China is on the rise, and this could be partly associated with excessive iodine intake in some individuals; therefore, increased attention is being paid to individual iodine status. However, current indices are not appropriate for evaluating individual iodine status., Objective: To evaluate the association between serum iodine and urinary iodine (UI), as well as thyroid diseases, and provide an excellent base for future individual iodine status assessment., Design, Subjects and Measurements: A total of 902 adults were enrolled in this study including 325, 286 and 291 subjects from regions in China where iodine is adequate, sufficient and in excess, respectively. Serum iodine, UI and thyroid function were assessed, and ultrasonography performed in all subjects., Results: The median serum iodine values of adults with subclinical hypothyroidism, high serum autoantibody and thyroid nodules were significantly higher than those of euthyroid adults (P<0.05). A serum iodine level higher than 100 μg/L was considered as a risk factor for thyroid diseases. Serum iodine had strong nonlinear correlations with UI and thyroid function. When thyroid function was taken as a gold standard, the area under the receiver operating characteristic (ROC) curve for serum iodine was 0.752 and UI was 0.507 for subjects with lower serum iodine and UI levels. The area for serum iodine was 0.773 and UI was 0.638 for subjects with higher serum iodine and UI levels. The areas under these curves were significantly different (P<0.001)., Conclusion: In adults, serum iodine had a strong nonlinear correlation with UI and a high level of serum iodine was a risk factor for thyroid diseases., (© 2017 John Wiley & Sons Ltd.)

Background and Objectives: The treatment guidelines for thyroid dysfunction recommend defining reference ranges for thyroid hormones in each area through assessment of local population data considering the iodine nutritional status. The aim of this study was to define the reference ranges of free thyroxine (FT4), TSH, and thyroglobulin levels in a general population from Jaen, an area of southern Spain with an adequate iodine nutritional status, and whether they were associated with urinary iodine levels., Patients and Methods: A cross-sectional study was conducted in 1,003 subjects of the general population of the Jaen Health District. Levels of urinary iodine, FT4, TSH, thyroglobulin, and thyroid peroxidase (TPO) antibodies were measured according to age and sex., Results: Median and mean urinary iodine levels were 110.59μg/L and 130.11μg/L respectively. Median TSH level was 1.83μIU/mL (p2.5=0.56μIU/mL, p97.5=4.66μIU/mL). Median FT4 level was 0.84ng/dL (p2.5=0.62ng/dL, p97.5=1.18ng/dL). TPO antibodies were detected in 5.7% of subjects. There was no correlation between urinary iodine levels and FT4, TSH or TPO antibodies. Subjects with positive TPO antibodies had higher TSH levels (3.34μIU/L versus 2.14μIU/mL, P=.001; odds ratio=2.42)., Conclusions: Urinary iodine levels in Jaen are optimal according to World Health Organization standards. Reference ranges of FT4, TSH, and thyroglobulin do not differ from those reported in the literature and are no associated to urinary iodine levels. The prevalence of positive TPO antibodies was similar to that reported in other Spanish areas., (Copyright © 2017 SEEN y SED. Publicado por Elsevier España, S.L.U. All rights reserved.)

The role that adequate iodine intake could have on the male reproductive function is not entirely known. The aim of this study is to determine whether there is a relation between male infertility and urinary and semen iodine levels in 96 couples who underwent consultation for infertility. The median of semen iodine was higher in men who consumed iodized salt than in those who consumed non-iodized salt (p=0.019). Men with a higher semen iodine level had more morphological alterations in spermatozoa (p=0.032). Men with a higher urinary iodine level had a lower motile sperm count according to the "direct swim-up" technique (p=0.044). Men >3years without successfully achieving pregnancy had a higher urinary iodine level than those with ≤ 3years (p=0.035). In conclusion, iodine may play a role in the quality of semen: an increase in semen iodine levels is associated with different variables related to male infertility., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Purpose: Studies suggest that subclinical hypothyroidism (SCH) is related to cardiovascular mortality (CVM). We explored the role of microalbuminuria (MIA) as a predictor of long-term CVM in population with and without SCH with normal kidney function., Materials and Methods: We examined the National Health and Nutrition Education Survey - III database (n = 6,812). Individuals younger than 40 years, thyroid-stimulating hormone levels ≥20 and ≤0.35mIU/L, estimated glomerular filtration rate <60mL/minute/1.73m 2 and urine albumin-to-creatinine ratio of >250mg/g in men and >355mg/g in women were excluded. SCH was defined as thyroid-stimulating hormone levels between 5 and 19.99mIU/L and serum T4 levels between 5 and 12µg/dL. MIA was defined as urine albumin-to-creatinine ratio of 17-250mg/g in men and 25-355mg/g in women. Patients were categorized into the following 4 groups: (1) no SCH or MIA, (2) MIA, but no SCH, (3) SCH, but no MIA and (4) both SCH and MIA., Results: Prevalence of MIA in the subclinical hypothyroid cohort was 21% compared to 16.4% in those without SCH (P = 0.03). SCH was a significant independent predictor of MIA (n = 6,812), after adjusting for traditional risk factors (unadjusted odds ratio = 1.75; 95% CI: 1.24-2.48; P = 0.002 and adjusted odds ratio = 1.83; 95% CI: 1.2-2.79; P = 0.006). MIA was a significant independent predictor of long-term all-cause (adjusted hazard ratio = 1.7, 95% CI: 1.24-2.33) and CVM (adjusted hazard ratio = 1.72, 95% CI: 1.07-2.76) in subclinical hypothyroid individuals., Conclusions: In a cohort of subclinical hypothyroid individuals, the presence of MIA predicts increased risk of CVM as compared to nonmicroalbuminurics with SCH. Further randomized trials are needed to assess the benefits of treating microalbuminuric subclinical hypothyroid individuals and impact on CVM., (Copyright © 2017 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Context: Iodine nutrition is a global event, especially for pregnant women., Objective: To develop applicable index of iodine intake for population during pregnancy., Design, Setting, and Participants: From 2012 to 2014, pregnant women at less than 8 weeks of gestation (n = 222) and reproductive-age women (n = 827) participated in this study. The pregnant women were evaluated at follow-up visits at 8, 12, 16, 20, 28, and 36 weeks of gestation and 3 and 6 months postpartum., Main Outcome Measures: Twenty-four-hour urine samples were collected at weeks 8 of gestation. Urine iodine (UI) and creatinine (Cr) and serum thyroglobulin were measured in all of the subjects. Circulatory iodine was measured using inductively coupled plasma-mass spectrometry at 8, 20, and 36 weeks of gestation and 6 months postpartum., Results: The median UI concentration decreased from 183.6 to 104.2 μg/L during pregnancy. The serum iodine (SI) changes were similar to the UI to creatinine ratio (UI/Cr). The SI level was lowest at the eighth week of gestation (60.5 μg/L), which rose significantly until 20 weeks (106.5 μg/L) and then began to decline (36 wk, 84.7 μg/L). The 24-hour UI excretion measurement was regarded as the gold standard. The area under the receiver-operating characteristic curve for UI/Cr was 0.92 for iodine deficiency diagnoses and 0.78 for SI. The area for SI was 0.82 for excessive iodine diagnoses and 0.75 for UI/Cr. The areas under these curves were significantly different (P < .001). The areas under the receiver-operating characteristic curve for UI were 0.61 (P = .11) and 0.65 (P = .08) for iodine deficiency and excessive iodine diagnoses, respectively. Additionally, for thyroglobulin, these values were 0.54 (P = .53) and 0.53 (P = .74), respectively., Conclusions: Iodine intake, as assessed by spot UI concentration in pregnant women, is inaccurate and increases the prevalence of iodine deficiency. The UI/Cr better reflects the 24-hour iodine excretion and circulating iodine levels during pregnancy and the postpartum period.

In animals, long-term feeding with peanut (Arachis hypogaea) seed coats causes hypertrophy and hyperplasia of the thyroid gland. However, to date there have been no detailed studies. Here, we explored the thyroidal effects of dietary peanut seed coats (PSC) in rats. The PSC has high levels of pro-goitrogenic substances including phenolic and other cyanogenic constituents. The PSC was mixed with a standard diet and fed to rats for 30 and 60 days, respectively. Animals fed with the PSC-supplemented diet showed a significant increase in urinary excretion of thiocyanate and iodine, thyroid enlargement, and hypertrophy and/or hyperplasia of thyroid follicles. In addition, there was inhibition of thyroid peroxidase (TPO) activity, 5'-deiodinase-I (DIO1) activity, and (Na+-K+)-ATPase activity in the experimental groups of rats as compared to controls. Furthermore, the PSC fed animals exhibited decreased serum circulating total T4 and T3 levels, severe in the group treated for longer duration. These data indicate that PSC could be a novel disruptor of thyroid function, due to synergistic actions of phenolic as well as cyanogenic constituents.

Objective: Thyroid dysfunction is associated with impaired cognitive development. Perchlorate decreases thyroidal iodine uptake, potentially reducing thyroid hormone production. It is unclear whether perchlorate exposure in early life affects neurodevelopment., Design: Historical cohort analysis., Patients: From 2002 to 2006, 21,846 women at gestational age <16 weeks recruited from antenatal clinics in Cardiff, UK and Turin, Italy were enrolled in the Controlled Antenatal Thyroid Screening Study (CATS). We undertook a retrospective analysis of 487 mother-child pairs in mothers who were hypothyroid/hypothyroxinemic during pregnancy and analyzed whether first trimester maternal perchlorate levels in the highest 10% of the study population were associated with increased odds of offspring IQ being in the lowest 10% at 3 years of age., Main Outcome Measures: Maternal urinary perchlorate, offspring IQ., Results: Urine perchlorate was detectable in all women (median 2.58 μg/L); iodine levels were low (median 72 μg/L). Maternal perchlorate levels in the highest 10% of the population increased the odds of offspring IQ being in the lowest 10% OR = 3.14 (95% CI 1.38, 7.13) P = .006 with a greater negative impact observed on verbal OR = 3.14 (95% CI 1.42, 6.90) P = .005 than performance IQ. Maternal levothyroxine therapy did not reduce the negative impact of perchlorate on offspring IQ., Conclusions: This is the first study using individual-level patient data to study maternal perchlorate exposure and offspring neurodevelopment and suggests that high-end maternal perchlorate levels in hypothyroid/hypothyroxinemic pregnant women have an adverse effect on offspring cognitive development, not affected by maternal levothyroxine therapy. These results require replication in additional studies, including in the euthyroid population.

Objective: To study the associations between intakes of iodine and water chemicals and the thyroid gland status of schoolchildren living in the coastal city of Port Sudan., Design: In our previous nationwide study on goitre, it was observed that the prevalence of goitre was high in Port Sudan city despite high urinary iodine excretion. A cross-sectional study including schoolchildren aged 6–12 years was designed. Measurements determined the prevalence of goitre, urinary iodine concentration and thiocyanate secretion in casual urine samples, serum levels of thyroxine, triiodothyronine, thyroid-stimulating hormone and thyroglobulin, as well as the levels of Cl⁻, F⁻, Ca²⁺, Mg²⁺ and total hardness of drinking water., Subjects: Schoolchildren (n 654) aged 6–12 years., Setting: Port Sudan city is located at the western bank of the Red Sea. The city is surrounded by a mountainous area known as the Red Sea Hills. It is the main sea port in the Sudan, inhabited by ethnically and socio-economically heterogeneous populations., Results: The prevalence of goitre in Port Sudan was 34.86% while the median urinary iodine concentration was 46,4μg/dl. Out of thirty-one pupils from Port Sudan, twenty-four (77.42 %) were found to have urinary iodine concentration greater than 30μg/dl and twelve (38.71 %) had different degrees of biochemical hypothyroidism. Excessive concentrations of Cl⁻, Ca²⁺, Mg²⁺ and water hardness (369.2, 116.48, 60.21 and 539.0mg/l, respectively) were detected in drinking water samples collected from Port Sudan that exceeded levels permitted by the WHO., Conclusions: The coastal city of Port Sudan is a goitre-endemic area. In contrast to other Sudanese cities in which endemic goitre is related to iodine deficiency, goitre in Port Sudan is associated with iodine excess. Water chemicals seemed to have no effects on thyroid status.

Background: Disorders of thyroid function have been inconsistently described in cystic fibrosis (CF) patients and in CF transmembrane regulator protein knockout animals. The literature lacks reports on iodine status of CF individuals. We hypothesize, that iodine deficiency is common in CF and account for abnormal thyroid function in CF patients., Methods: We investigated 129 children, adolescents, and adults with CF, who were living in the northern part of Bavaria/Germany. Malnutrition and lung function were analyzed. Urinary iodine excretion, TSH (thyroid-stimulating hormone), and ft4 (free thyroxine) were measured and set in relation to population-based, age-adjusted reference ranges., Results: Subclinical hypothyroidism (normal fT4, elevated TSH) was found in 11.6% of subjects, and iodine deficiency in 83.7%. No correlations were found with age, BMI, status of malnutrition, or lung function., Conclusion: Dramatic iodine deficiency was found in our cohort of CF patients. This condition can cause subclinical hypothyroidism; therefore, an individual iodine supplementation program is necessary and should be started immediately., (Crown Copyright © 2012. Published by Elsevier GmbH. All rights reserved.)

Background: Hypothyroidism is a chronic condition of endocrine disorder and its precise molecular mechanism remains obscure. In spite of certain efficacy of thyroid hormone replacement therapy in treating hypothyroidism, it often results in other side effects because of its over-replacement, so it is still urgent to discover new modes of treatment for hypothyroidism. Sini decoction (SND) is a well-known formula of traditional Chinese medicine (TCM) and is considered as efficient agents against hypothyroidism. However, its holistic effect assessment and mechanistic understanding are still lacking due to its complex components., Methodology/principal Findings: A urinary metabonomic method based on ultra performance liquid chromatography coupled to mass spectrometry was employed to explore global metabolic characters of hypothyroidism. Three typical hypothyroidism models (methimazole-, propylthiouracil- and thyroidectomy-induced hypothyroidism) were applied to elucidate the molecular mechanism of hypothyroidism. 17, 21, 19 potential biomarkers were identified with these three hypothyroidism models respectively, primarily involved in energy metabolism, amino acid metabolism, sphingolipid metabolism and purine metabolism. In order to avert the interference of drug interaction between the antithyroid drugs and SND, the thyroidectomy-induced hypothyroidism model was further used to systematically assess the therapeutic efficacy of SND on hypothyroidism. A time-dependent recovery tendency was observed in SND-treated group from the beginning of model to the end of treatment, suggesting that SND exerted a recovery effect on hypothyroidism in a time-dependent manner through partially regulating the perturbed metabolic pathways., Conclusions/significance: Our results showed that the metabonomic approach is instrumental to understand the pathophysiology of hypothyroidism and offers a valuable tool for systematically studying the therapeutic effects of SND on hypothyroidism.

Context: Experimental studies have shown that maternal hypothyroxinemia during early pregnancy is associated with poor neurodevelopment in affected offspring., Objective: The aim of this study was to assess the impact of maternal serum free T4 on psychomotor development of offspring., Materials and Methods: The study involved 147 women in the third trimester (week 37) of pregnancy. TSH and free T4 serum levels were measured at 37 week gestation. The children were evaluated between 38 and 60 months of age by the McCarthy Scales of Children's Abilities., Results: 54.4% of the women had a free T4 below the threshold of hypothyroxinemia. We find a significant effect of maternal hypothyroxinemia on the general cognitive index, and on perceptual-manipulative and memory coefficients., (Copyright © 2012 ISDN. Published by Elsevier Ltd. All rights reserved.)

Objectives: Determining the prevalence of hypothyroidism and its interrelationship with peroxidase antibodies and high urinary iodine levels as a means for devising a set of recommendations for health authorities regarding the consumption of iodised salt and the early detection of thyroid disease., Methods: 437 people in the municipality of Armenia (Quindío) participated in the study. ELISA tests were performed for free thyroxine, thyroid-stimulating hormone and thyroid peroxidase antibodies; a photocolorimetric analysis was carried out to determine urinary iodine levels., Results: Hypothyroidism prevalence was 18.5%. Thyroid peroxidase antibodies were positive in 28.9% of the study population, with significantly higher prevalence amongst those with levels > 10 mIU/mL thyroid-stimulating hormone compared to 5.1 to 10 mIU/mL in those without it (OR 3.2) and smokers (O.R 3,4). Free thyroxine was normal in 98.2% of participants (> 5 mIU/mL thyroid-stimulating hormone levels) and 92% in those in whom > 10 mIU/mL thyroid-stimulating hormone levels were found. The average iodine level was 565.1; levels above 300 µg/L were obtained in 81.8% of the participants., Conclusions: Increased positive thyroid peroxidase antibody prevalence with increasing thyroid-stimulating hormone values could demonstrate a high risk of developing autoimmune hypothyroidism in Armenia; despite high iodine levels, a relationship with thyroid peroxidase antibodies or thyroid-stimulating hormone levels could not be established.

Aims: It has been suggested that oxidative stress plays a key role in the pathogenesis of Down syndrome (DS). However, urinary biomarkers of oxidative stress have been little studied in this condition. Thus, we aimed to assess a set of urinary oxidative/nitrosative stress biomarkers in children with DS, with and without hypothyroidism, which comprise: 8-hydroxy-2'-deoxyguanosine (8-OHdG), isoprostane 15-F(2t)-IsoP, thiobarbituric acid-reacting substances (TBARS), advanced glycation end products (AGEs), dityrosine (diTyr), hydrogen peroxide (H(2)O(2)) and nitrite/nitrate (NOx)., Main Methods: Fluorimetric and spectrophotometric assays were performed in children with DS (n=26), some of them taking levothyroxine for hypothyroidism (n=7), and their non-Down siblings (n=19)., Key Findings: We found that only levels of diTyr were increased in DS, although no differences were obtained when hypothyroid DS children were excluded. Levels of 8-OHdG, 15-F(2t)-IsoP, TBARS, AGEs, H(2)O(2) and NOx did not differ neither between DS and controls nor between hypothyroid DS children and DS without hypothyroidism diagnosed. However, diTyr is increased in hypothyroid DS children compared with controls. Negative correlations with age were obtained for 8-OHdG, diTyr and NOx in DS and controls and for 8-OHdG, 15-F(2t)-IsoP, TBARS and AGEs in DS., Significance: Increased oxidative stress in children with DS cannot be explained by the urinary levels of 8-OHdG, 15-F(2t)-IsoP, TBARS, AGEs, diTyr, H(2)O(2) and NOx, at least with the assays used. Nonetheless, urinary diTyr could be used as oxidative/nitrosative stress biomarker in hypothyroid DS children. The present work presents evidence of a probable renal impairment in children with DS receiving levothyroxine for hypothyroidism., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: Postpartum thyroid dysfunction (PPTD) is characterized by an early hyperthyroid phase followed, with peak prevalence at 6 months, by a hypothyroid phase which carries a risk of long-term hypothyroidism. Iodine has a major effect on thyroid function. Western Australia has previously been shown to be iodine replete., Objective: To examine the iodine status of women with and without PPTD and the relationship of iodine status postpartum with long-term hypothyroidism., Design: Case-control with follow-up., Patients: A total of 149 women at 6 months postpartum (74 PPTD, 75 controls) with 98 (46 PPTD, 52 controls) followed up at 12 years., Measurements: Urinary iodine concentration (UIC) and thyroid function at 6 months postpartum; thyroid function at 12-year follow-up., Results: At 6 months postpartum, median UIC (quartiles) for observed TSH ranges were: for TSH < 0·4 mU/l 130·0 μg/l (82·0, 170·0); for TSH 0·4-4·0 mU/l 123·0 μg/l (80·5, 168·0); for TSH > 4·0 mU/l 85·0 μg/l (40·0, 141·5), P = 0·018. The odds ratio (OR) of hypothyroid PPTD with each unit of decreasing log iodine was 2·54, (95%CI: 1·47, 4·35), and with UIC < 50 μg/l, OR 4·22, (95%CI: 1·54, 11·55). In the long term, decreased log UIC significantly predicted hypothyroidism at 12-year follow-up (P = 0·002); as did UIC < 100 μg/l (P = 0·03) and UIC < 50 μg/l (P = 0·02). The association was independent of antibody status., Conclusion: Low UIC measured at 6 months postpartum is associated with hypothyroid PPTD and independently predicts long-term hypothyroidism. We believe that it results from more severe preceding destructive thyroiditis, with discharge of thyroidal iodine, and thereby predicts a greater risk of long-term hypothyroidism., (© 2011 Blackwell Publishing Ltd.)

Background: Appropriate maternal intake of iodine during pregnancy is essential for maternal thyroxine production and thyroid status of the fetus. It should be possible to enhance iodine intake during pregnancy by using iodine fortified salt or taking iodine supplements. In the present report we determined the status of iodine nutrition in pregnant women who were stratified on the basis of their history of taking or not taking iodized salt or iodine supplements. The study was performed in Toledo (Spain), a region in which prior studies have noted borderline iodine sufficiency. Iodine nutrition was assessed by measuring urinary iodine concentration (UIC) and neonatal thyrotropin (TSH)., Methods: UIC was measured in 525 pregnant women. They were grouped according to their history of iodine intake. Diet Group 1 patients (n = 69) did not take iodized salt or iodine supplements during pregnancy. Diet Group 2 patients (n = 75) took iodized salt but not iodine supplements during pregnancy. Diet Group 3 patients (n = 381) took iodine supplements during pregnancy. Plasma determinations included TSH, free thyroxine, thyroid peroxidase antibody, and thyroglobulin antibody. UIC was measured in a single urine sample from all the pregnant women. Neonatal TSH was measured in capillary spot blood from all the neonates as part of a screening for congenital metabolic abnormalities., Results: The median UIC in all subjects was 164 μg/L (interquartile range [IR]: 116-245). The median UICs in Diet Groups 1, 2, and 3 were 134.5 (IR: 90-196), 146 (IR: 103-205), and 183 (IR: 124-261) μg/L, respectively (p = not significant [NS] for Diet Group 1 vs. 2; p < 0.01 for Diet Group 2 vs. 3; all other comparisons NS). The median (IR) TSH of the neonates in all Diet Groups was 1.0 (IR: 0.7-1.6) μU/mL. Only 2 neonates had blood TSH concentrations >5 mU/L. Neonatal blood TSH concentrations were similar in all Diet Groups., Conclusions: In a region with a history of borderline iodine deficiency the UICs were below 150 μg/L in a substantial percentage of pregnant women who did not take iodine supplements, regardless of whether or not they took iodized salt. Our results support the use of iodine supplements from the start of the pregnancy, or even before pregnancy in women who live in regions with a history of even small degrees of iodine deficiency. In addition, neonate TSH screening is not the best tool to assess whether the iodine status in populations is ideal.

Background: According to the World Health Organization, iodine excreted in urine is a measure of its supply. According to the International Council for Control of Iodine Deficiency Disorders (ICCIDD), the urinary iodine (UI) should be >100 microg I per 1 liter of urine. Severe deficiency (SID) is diagnosed when UI is <50 microg/L and a moderate deficiency (MID) when UI is <100 microg/L., Materials and Methods: UI analysis among 32 heart transplant recipients (26 men and 6 women); of overall mean age of 50.4 +/- 12.6 years was performed using the modified Program Against Micronutrient Malnutrition method, a spectrophotometric measurement based on the Sandell-Kolthoff reaction. Results were compared with those of thyroid stimulating hormone (TSH; microIU/mL), of free tri-iodothyronine (FT3; pg/mL), and thyroxine (FT4; ng/dL)., Results: The average UI among the whole group was 126.4 +/- 109.6 microg/L. SID occurred in 12 patients (37.5%) and MID in 4 (12.5%); namely, mean UI of 17.0 +/- 9.6 and 79.5 +/- 5.6, respectively. In the other 16 patients (50%), the average UI was high, namely, 220.1 +/- 72.1 IU/mL. TSH, FT3, and FT4 in the whole group were within normal ranges. However, FT4 values significantly differed when SID and MID patients were compared with those displaying the recommended UI: 0.8 +/- 0.2 and 0.9 +/- 0.1 versus 1.1 +/- 0.2 respectively (P < .05). We noted decreased values of TSH in 5 patients (15.6%) and of FT3 or FT4 in 6 subjects (18.8%)., Conclusion: There exists significant iodine deficiency among heart transplant recipients. Measurements of urinary iodine together with thyroid gland hormones may be essential to prevent thyroid gland disturbances in these patients.

Excessive iodine exposure was reported to be associated with thyroid dysfunctions. The aim of this study is to evaluate the link between excess urinary iodine as the prime indicator of excessive iodine intake and autoimmune subclinical hypothyroidism (SCH) among Egyptian women. Seventy three women with autoimmune SCH and 60 age- matched healthy women as controls were enrolled in this study. TSH, FT4, urinary iodine concentrations (UIC) and thyroid peroxidase antibody (TPOAb) were estimated. The levels of urinary iodine were significantly higher in patients with SCH as compared with control subjects, (326.97 112.98 vs. 274.45 98.75 microg/l, p<0.01). In patients with SCH, there was a significant correlation between UIC and TSH levels. Also, a significant correlation between UIC and TPOAb was found. We conclude that excessive iodine intake may trigger thyroid autoimmunity and eventually thyroid hypofunction among Egyptian women.

Acquired Immunodeficiency Syndrome (AIDS) is the final and most serious stage of the disease caused by human immunodeficiency virus. The Immune system is the target of AIDS. We investigate presently any possible involvement of thyroid hormone, the deficiency of which gives rise to oedema and susceptibility to nonspecific infections; with a view to finding the primary factor seeding the disease. It has been reported that circumcision reduced the incidence of HIV/AIDS infection. Beyond circumcision however there might be some constitutional factor that comprises HIV infection to clinical AIDS. It is against this background that our research team turned to possible dyshormonopoisis and to thyroid hormone as a prime suspect among other possible factors that cause clinical AIDS. Moreover the hormone has been reported to be crucial for optimum immune function. A population of 200 seropositive AIDS patients were investigated against a control of 50 subjects made up of 25 healthy circumcised males and 25 healthy females; all of who were seronegative for the disease. The parameters investigated include thyrotropin (TSH), Thyroxine (T4), Total protein (TP), Albumin (Alb), Globulin (Glob), Immune complex (IC3) and Bence Jones proteins (BJP) levels in serum or urine. All seropositive clinically HIV/AIDS patients were hypothyroid. Seronegatives had significantly higher T4, TP, and Alb levels at P < 0.001 and P < 0.05 for Glob than seropositives. Seropositive females exhibited significant (P < 0.001) higher levels of IC3 than seronegative males. The globulin levels of all HIV patients were significantly (P < 0.05) higher than control. BJP was also isolated in the urine of patients. The findings suggest that thyroid hormone deficiency is a primary culprit for the other inert or dormant factors to be activated.

Objective: To explore the possibility of predicting decline or improvement in thyroid function over 1 year, and to investigate the correlations of serum TSH (s-TSH) with hypothyroidism-related symptoms and signs, serum thyroid peroxidase antibody (s-TPO-Ab) and urinary iodine excretion in individual patients with untreated subclinical hypothyroidism (SH)., Design: Monthly repeated measurement study without intervention., Methods: Twenty-one patients without former thyroid disease who had been identified with s-TSH between 5 and 12 mU/l and normal serum thyroxine (s-T4) at two occasions were enrolled. Subsequently, 13 monthly measurements of s-TSH, hypothyroidism-related symptoms and signs, serum free T4, s-TPO-Ab and urinary iodine excretion were performed., Results: Over the study year, s-TSH increased significantly in 5 patients, 16 had unchanged s-TSH, whereas none improved. From clinical and biochemical inclusion data, it was not possible to predict who would later increase in s-TSH. In individual patients, a highly significant correlation between s-TSH and s-TPO-Ab was found (r=0.37, P<0.0001) and also between s-TSH and urinary iodine excretion (r=0.14, P=0.034). No correlation between s-TSH and clinical symptoms and signs was observed. Time shift showed best correlation between s-TSH and s-TPO-Ab measured at the same time point, whereas urinary iodine excretion correlated best to s-TSH and s-TPO-Ab obtained 1 month later., Conclusion: At the time of inclusion, it was not possible to identify the 24% of SH patients who would show deterioration in thyroid function over the following year. Impairment in thyroid function varied in parallel with thyroid autoimmunity, whereas high urinary iodine excretion predicted high s-TSH and s-TPO-Ab 1 month later.

Objective: To describe a patient with excess urinary thyroxine (T4) excretion and worsening of preexisting hypothyroidism in the setting of nephrotic syndrome and to determine whether excess urinary T4 excretion is present in other patients with proteinuria., Methods: We present data regarding the patient's initial presentation, diagnostic studies, and course of her illness. We suspected urinary T4 loss to be the cause of her presentation and analyzed her urine sample for total T4. We also analyzed differences in urinary T4 excretion in 22 patients with proteinuria and 16 control patients without proteinuria. Relevant medical literature is reviewed., Results: A 44-year-old woman presented with a 3-month history of increasing fluid retention, weight gain, and fatigue. She had long-standing hypothyroidism on a stable levothyroxine dosage, 125 mcg/d. She had gained 27 kg and had developed significant edema. She had a grossly elevated thyroid-stimulating hormone level of 91 mIU/L. Her condition worsened, and a urinary protein measurement was 14.06 g/24 h-diagnostic of nephrotic syndrome. The levothyroxine dosage was increased to 225 mcg/d. Urinary total T4 concentration in a 24-hour sample was 59.0 microg/L (83.1 microg/24 h), indicating that a substantial fraction of her orally ingested T4 was lost in urine. Urinary total T4 excretion was significantly higher in patients with proteinuria (mean +/- standard deviation, 18.0 +/- 18.2 microg/L) vs control patients without proteinuria (mean, 3.8 +/- 1.8 microg/L) (P = .0014)., Conclusion: In the patient described, urinary T4 loss due to proteinuria and nephrotic syndrome resulted in a severe exacerbation of underlying hypothyroidism.

A 24-year-old woman complained of tiredness, sensitivity to cold, and feelings of depression. A diagnosis of hypothyroidism based on decreased 24 h urinary T3 and T4 excretion was made, and she was treated with levothyroxin. No blood tests were done. She was referred with the question if she had other endocrine disorders. Her periods were regular, and on physical examination no abnormalities except slight acne were found. Similarly, hypothyroidism was diagnosed by decreased thyroid hormone excretion in 24 h urine, again without blood tests, in a 68-year-old woman whose mother had a goitre, and who had already been prescribed liothyronine. She had no complaints, and physical examination was unremarkable. The thyroid gland was not palpable. Thyroid peroxidase antibodies were absent in both patients. After discontinuation of medication with thyroid hormones they both remained euthyroid. It is concluded that thyroid disease did not exist in those 2 patients. Measurement of 24 h urinary T3 and T4 excretion is not an accurate diagnostic test for hypothyroidism.

A sufficient amount of iodine in food is necessary for the thyroid gland to produce hormones during pregnancy. The aim of our work was to evaluate iodine and thyrotrophic hormone (TSH) concentration in urine, free triiodothyronine (fT3) and thyroxine (fT4) in complicated pregnancies in Upper Silesia (region of iodine deficiency in Poland) in comparison with normal pregnancies. In both groups the iodine content in urine was evaluated by a quick test and serous concentrations of TSH, fT3 and fT4 were determined by a radioimmunological method. We found the iodine excretion with urine below 100 microg/L in 29.15% of all women under study, i.e. an insufficient supply of this element. The reduced iodine concentration in urine was found to be more often in women with imminent premature delivery. Moreover, it was found that in II trimester the concentration of iodine excreted with urine had been significantly lower comparing to the patients examined in III trimester. We found significantly higher concentration of thyrotrophic hormone in pregnant women with iodine excretion below 100 microg/L of urine. Evaluation of the iodine concentration in urine may be a simple screening test to determine the supply of this element in a diet. Moreover, our studies demonstrate the necessity for the iodine supplementation in pregnant women in the Silesian region--an area of iodine deficiency in Central Europe.

The purpose of this study was to examine protein expression of renal aquaporins (AQP) and ion transporters in hypothyroid (HT) rats in response to an oral water load compared with controls (CTL) and HT rats replaced with l-thyroxine (HT+T). Hypothyroidism was induced by aminotriazole administration for 10 wk. Body weight, water intake, urine output, solute and urea excretion, and serum and urine osmolality were comparable among the three groups at the conclusion of the 10-wk treatment period. One hour after oral gavage of water (50 ml/kg body wt), HT rats demonstrated significantly less water excretion, higher minimal urinary osmolality, and decreased serum osmolality compared with CTL and HT+T rats. Despite the hyposmolality, plasma vasopressin concentration was elevated in HT rats. These findings in HT rats were associated with an increase in protein abundance of renal cortex AQP1 and inner medulla AQP2. AQP3, AQP4, and the Na-K-2Cl cotransporter were also increased. Moreover, 1 h following the oral water load, HT rats demonstrated a significant increase in the membrane-to-vesicle fraction of AQP2 by Western blot analysis. The defect in urinary dilution in HT rats was reversed by the V(2) vasopressin antagonist OPC-31260. In conclusion, impaired urinary dilution in HT rats is primarily compatible with the nonosmotic release of vasopressin and increased protein expression of renal AQP2. The impairment of maximal solute-free water excretion in HT rats, however, appears also to involve diminished distal fluid delivery.

Nitrate is a wide spread contaminant of ground and surface water. The source of nitrate in the ground water may be from run off or seepage from fertilized soil, municipal or industrial waste water, land fills, septic system, urban drainage or decaying plants. Human and animal systems are affected severely on nitrate exposure. The study was to investigate the effect of dietary nitrate exposure on the thyroid status along with the state of iodine nutrition. Rats were fed diet containing 3% potassium nitrate (KNO3) for 4 weeks and then thyroid status was evaluated by thyroid gland weight, urinary iodine excretion pattern, thyroid peroxidase (TPO) activity, serum levels of total thyroxine (T4), triiodothyronine (T3) and thyroid stimulating hormone (TSH) concentrations. In nitrate treated animals, the weight of thyroid gland was increased significantly (P<0.001) while thyroid peroxidase activity (P<0.01), serum T4 (P<0.01) and serum T3 levels (P<0.001) were reduced; but serum TSH level was increased (P<0.001) along with slightly elevated iodine excretion level (P<0.001) in comparison to control animals. The overall results indicated the development of a relative state of functional hypothyroidism with enlarged thyroid after nitrate exposure. This study can explain a part for the persistence of residual goitre in the post-salt iodization phase.

Unlabelled: The aim of the study was to define disturbances of thyroid function in adult population of the city of Cracow followed up for ten years. The analysis included the results obtained from 891 individuals, 571 females and 320 males aged 18-78 years examined prior to and after implementation of the obligatory model of iodine prophylaxis (years 1989-1990 and 1998-1999). After the exclusion of patients diagnosed earlier as having hyperthyroidism or hypothyroidism, the mean TSH level in the years 1998-1999 was significantly higher as compared to data obtained between 1989 and 1990 (1.44 microj/ml vs. 1.30 microj/ml) in the examined population. Our 10 years observation revealed an insignificant increase in frequency of hyperthyroidism only among females (1.6% vs. 0.9%) which did not indicate a clear, endemic in character increase at the population level. In the present investigations, hypothyroidism was demonstrated to occur more frequently as compared to the 1989-90 study (2.1% vs. 1.4% among females and 0.3% vs. 0% in males). Both differences were not statistically significant. As seen from the present results, over the investigated 10-year period, in the Cracow population, there occurred a clear, statistically significant (p<0.001) increase of the percentage of individuals with an elevated TPO antibody titter (3.8% vs. 11.8%). In our investigation no correlation was observed between anti-TPO antibodies and ioduria levels., Conclusions: The results reveal no statistically significant increase in incidence of hyperthyroidism and hypothyroidism after implementation of the obligatory model of iodine prophylaxis. The future studies are needed to clarify the mechanisms involved in increase of anti-TPO autoantibodies and verify its possible temporary nature.

In this study, we investigate how oxidative stress alters the urinary F2-isoprostanes' level and we examine the correlation between 8-isoPGF(2alpha) and thyroid hormones in female patients with Graves' hyperthyroidism. We quantitatively determined the concentrations of urinary F2-isoprostanes using gas chromatography-mass spectrometry in the selected ion-monitoring mode. We recruited individuals in the following three groups of subjects for this study: (1) female hyperthyroidism patients (n = 14, 21-71 years), (2) female hypothyroidism patients (n = 16, 16-66 years), and (3) female age-matched normal controls (n = 10, 20-61 years). The average concentration of 8-iso prostaglandin F(2alpha) (8-isoPGF(2alpha)) in hyperthyroidism patients was significantly higher than that in the healthy controls (P < 0.05). The concentration of 8-isoPGF(2alpha) in hypothyroidism patients was similar to that in normal controls. Although the level of 8-isoPGF(2alpha) in two of the patients was slightly elevated, the P value was not significant (NS). Our data suggest that the increased level of urinary 8-isoPGF(2alpha) may reflect possible oxidation injuries in hyperthyroidism patients due to the high level of thyroid hormones. Therefore, the elevated 8-isoPGF(2alpha) in patients could be used as an important biomarker for hyperthyroidism disease.

Hypothyroidism is associated with a number of functional renal disorders primarily affecting water and salt handling. In this study, we aim to investigate functional renal disorders in overt and subclinical hypothyroidism. We utilised urinary beta-2 microglobulin (beta2M) as a sensitive marker of tubular dysfunction. Urinary beta2M excretion and tests for renal functions were repeated before and after T4 replacement therapy. Forty-four patients (28 with overt disease, 16 with subclinical disease) and 31 healthy control subjects were involved in the study. There was a significant increase in urinary beta2M in both overt and subclinical hypothyroidism (p < 0.05 in both). TSH levels were correlated with beta2M excretion. Effects of hypothyroidism on renal functions were readily reversible by 3 weeks of thyroid hormone replacement therapy. Urinary beta2M was a sensitive marker of renal tubular dysfunction associated with overt and subclinical hypothyroidism.

Hypothyroidism patients have increased cardiovascular risk, although the mechanism is not defined. Endothelial dysfunction may initiate atherosclerosis, is present in patients with hypothyroidism, and therefore may link hypothyroidism and vascular disease. We are unaware of studies examining the effect of thyroid replacement therapy on endothelial function in hypothyroid patients. The present study examined the effect of treatment of hypothyroidism on brachial artery reactivity. Consequently, we measured endothelium-dependent (EDV) and endothelium-independent (EIV) vasodilation using brachial artery ultrasonography in 8 hypothyroid patients (5 men, mean age 48.9 +/- 5.5 years; mean thyrotropin [TSH] 49.0 +/- 37.0 mIU/L) before and after thyroxine treatment. Thyroxine treatment reduced average TSH to 2.9 +/- 0.5 mIU/L and improved EDV (8.0% +/- 4.4% v 3.4% +/- 2.5%, P <.05), whereas EIV was unchanged (20.3% +/- 6.1% v 19.2% +/- 9.4%, P = not significant [NS]). Thyroxine treatment did not alter serum lipids. Thyroid replacement therapy improves endothelium-dependent vascular reactivity in patients with hypothyroidism irrespective of lipid changes.

Bone turnover is reported to increase in favour of resorption in overt hyperthyroidism and the rate of resorption is associated with the levels of thyroid hormones. Hypothyroidism, on the other hand, was shown to cause no disturbance of calcium kinetics and found to associate lower trabecular resorption surfaces and increased bone cortical thickness. Similar studies are very rare in subclinical thyroid disorders and consequently we aimed to examine calcium and bone metabolism in subclinical thyroid disorders. Thirteen patients with subclinical hyperthyroidism secondary to untreated Graves' disease, 20 patients with subclinical hypothyroidism and 10 healthy subjects participated in this survey. Briefly calcium, phosphorus, and creatinine (Cre), urinary deoxypyridinoline (U-DPD) and serum osteocalcin (OC) were measured as biochemical markers for calcium metabolism. Concerning serum Ca and phosphorus levels, there were no differences between three of the groups, but urinary Ca excretion was higher in subclinical hyperthyroid patients compared to control and hypothyroid subjects. Hypothyroid patients had similar U-DPD levels with control subjects (p = 0.218). Serum OC and U-DPD were higher in subclinical hyperthyroid compared to control subjects (p<0.001 and p<0.001 respectively). We demonstrated a higher bone turnover and greater calcium excretion in subclinical hyperthyroid patients. Additionally, we found that subclinical hypothyroidism is not associated with disturbed calcium metabolism. As persistent increase in bone turnover is responsible for accelerated bone loss, patients with Graves' disease may have increased risk for osteoporosis.

Iodine is an essential element with unique role in organism: it is indispensable component of thyroid hormones. After binding with specific nuclear receptor, T3/T4 induce transcription of genetic code via mRNA and regulate proteosynthesis in most tissues. Thyroid hormones regulate rate of metabolic processes and consequently development of organism. Czech Republic was in past typical region with moderate to severe iodine deficiency. Therefore epidemiological survey was started in randomly selected samples of peoples. Thereafter a complex program of improving iodine supply was realized. Prompt effects of this changes were recorded, namely increase of ioduria and decrease of thyroid volume. Essential trace element selenium has a fundamental importance to the cell and body metabolism regulation by thyroid hormones. Activities of selenoenzymes deiodinases lead to the activation of prohormone T4 to active hormone T3 and the inactivation of T3 and of T4, as well. There is unfortunately moderate to mild Se deficit in the CR. Average serum Se concentrations for the populations from 6 to 65 years are in the regions of the CR between 42 and 62 micrograms/l and urine Se values are between 8 and 15 micrograms/l. We have found statistically significant correlations among indexes of selenium status and indexes of thyroid hormone metabolism and function. Especially dangerous are concomitant deficiencies of both key elements for thyroid hormone metabolism--I and Se--from the point of thyroid hormone regulative functions.

In a recent publication we hypothesized that increased bone metabolism induced by thyroid hormones should increase lead excretion even in lead unexposed subjects. To examine this hypothesis, 10 hypothyroid patients were investigated before and after substitution therapy with levothyroxine. After a mean of 9 wk after onset of therapy (patients were then in an euthyroid state), lead concentrations in urine (PbU) corrected by the individual creatinine in urine were increased (p = .007), while lead concentrations in blood (PbB) were slightly decreased (3.44 +/- 1.73 vs. 2.74 +/- 1.38, p = .008). Desoxypyridinoline cross-links (Pyr), a sensitive marker for bone degradation and excreted in urine, correlated with PbU (r = .64, p = .002) but not with PbB. Additionally PbU significantly correlated with serum concentrations of free circulating T3 (fT3) or free circulating T4 (fT4). Thus, we may suspect that increased lead excretion was induced by accelerated bone metabolism, since Pyr was increased after therapy (3.21 +/- 1.19 vs. 6. 10 +/- 1.81 nM/mM Cr, p < .001), too.

Aim: To evaluate renal function in correlation with lipid metabolism parameters in patients with primary hypothyroidism (HT) in compensation and decompensation., Material and Methods: 45 HT patients' examination included study of blood creatinine, urea, cholesterol, triglycerides, high and low density lipoproteins, urinary microalbumin, thyroid hormones and thyrotropin, beta 2-microglobulin levels, glomerular filtration rate (GFR), renal functional reserve (RFR). Also, Zimnitsky test and ultrasound investigation of the kidneys were made., Results: It was found that renal dysfunction in decompensated HT is characterized by normal renal concentration function, high intraglomerular pressure (low GFR and RFR), high concentration of beta 2-microglobulin in blood. Severe HT runs with negative correlation between GFR and total blood cholesterol, LDL. Albuminuria and low RFR in decompensated HT and marked hyperlipidemia suggest development of glomerulopathy related to abnormal physicochemical processes in glomerular endothelium., Conclusion: Patients with decompensated HT have apparant glomerular dysfunction and disturbances in lipid metabolism. Hyperlipidemia in HT is a factor of renal damage.

Background: The interaction of melatonin to sterility and anovulation as well as related hormonal disorders has not been sufficiently examined yet. We set out to investigate the interaction between melatonin and hyperprolactinemia, hyperandrogenemia, hypothyreosis and obesity in premenopausal females., Methods: We evaluated the overnight urinary excretion of 6-sulfatoxymelatonin (6-SMT) in a group of 155 women using a radioimmunoassay., Results: Melatonin levels in patients with hyperprolactinemia and hyperandrogenemia with normal body mass index are significantly higher compared to matched controls. Obese females without hormonal disorders showed statistically lower 6-sulfatoxymelatonin levels and in hypothyreotic females we found no difference in 6-sulfatoxymelatonin levels compared to controls., Conclusion: Melatonin plays an important role in patients with hormonal disorders such as hyperprolactinemia and hyperandrogenemia. Melatonin should be prescribed restrictively in all sterile patients. In patients with untreated hypothyreosis or obesity, melatonin seems to play a minor part; in those with hyperprolactinemia and hyperandrogenemia additionally to standard sterility treatment light therapy may improve the outcome.

This study was undertaken to confirm the importance of iodine excess in neonatal transient hypothyroidism. In 30 transient hypothyroid newborns at screening we measured urinary iodine excretion and TSH. They were divided into two groups: group A consisted of 21 newborns who had been exposed to iodine; group B of 9 non-exposed newborns. The two groups were significantly different only for median urinary iodine excretion (p = 0.001). In 61.5% of newborns of group A, iodine exposure caused iodine excess (urinary iodine excretion higher than 185 micrograms/l); this correlated with a higher prevalence of prematurity and a lower mean gestational age. Clinical records should reveal iodine exposure, but only urinary iodine excretion shows iodine excess. We suggest that evaluation at birth of urinary iodine excretion in every newborn with high TSH could help in predicting a good prognosis, since hypothyroidism due to the Wolff-Chaikoff effect is always spontaneously reversible, even if treatment may be suggested.

Aims: To define the aetiology of neonatal transient hypothyroidism (NTH) and recommend preventive measures., Methods: Maternal and perinatal clinical data on the use of antiseptics, drugs, and contrast agents containing iodine were collected from 40 subjects. Thyroid stimulating hormone (TSH), free thyroxine (FT4), thyroxine (T4), thyroglobulin (TG), TSH receptor antibodies, thyroid peroxidase antibodies and urinary iodine were measured in random neonatal samples. In the mothers with known or suspected thyroid disorders, TSH, FT4, TSH receptor antibodies and thyroid peroxidase antibodies were also measured., Results: The NTH aetiology was identified in 85% of cases. More than 50% of the babies with transient hypothyroidism had been exposed to iodine; maternal transfer of antibodies had occurred in a third of them., Conclusions: It is suggested that the practice of using iodine containing disinfectants should be withdrawn, and chlorhexidine substituted instead; that pregnant women should be advised of the adverse effects of using iodine products; and that thyroid function should be monitored whenever iodine is used.

Objective: Previously we reported 3,3'-diiodothyronine sulfate-like material (compound W) in maternal serum, and studies suggest that compound W is derived from thyroid hormones of fetal origin. In this study we characterized gestational changes of urinary compound W concentrations to correlate with changes in serum concentrations., Study Design: Urinary samples were collected from 94 women at various gestational ages ranging from 3 to 40 weeks. Urinary compound W was first identified biochemically. The concentrations of compound W (adjusted for creatinine levels) were assessed by a 3,3'-diiodothyronine sulfate radioimmunoassay in ethanol extracts of urine samples., Results: Compound W increased to 88 +/- 1.4 pmol (of 3,3'-diiodothyronine sulfate equivalent)/mmol creatinine in urinary samples obtained from 26 women in the first trimester of pregnancy compared with 40 +/- 6.9 pmol/mmol creatinine in 10 nonpregnant women. Excretion of compound W increased further during the second and third trimesters: 171 +/- 17 (n = 18) and 434 +/- 26 (n = 50) respectively. In contrast, urinary 3,3',5-triiodothyronine sulfate concentrations measured by radioimmunoassay were similar during pregnancy to values in nonpregnant women., Conclusions: Urinary compound W concentrations increase with the progression of normal pregnancy and correlate with the increase in serum levels. Random spot urine compound W concentrations, adjusted for creatinine levels, may be used in place of serum levels in conditions in which obtaining serum samples may be technically difficult, especially during population screening.

A high incidence of transient neonatal hypothyroidism has been observed in premature infants after routine skin cleansing with iodine. Because these reports have been predominantly from Europe, a borderline, iodine-deficient area, we wished to determine whether this was also true in North America, an iodine-sufficient area. A prospective, controlled study was performed in premature babies < or = 36 weeks gestation admitted to a neonatal intensive care nursery. Thyroxine (T4) and thyrotropin (TSH) were measured at day 1, days 4 to 6, and 10 to 12 after skin preparation with iodine or with a noniodine-containing antiseptic solution (chlorhexidine) that served as control. If repeat cleansing was required, this sequence was repeated. Urinary iodine was quantitated on days 1 to 3 to estimate iodine exposure. There was no difference in the mean T4 concentration at any of the time points evaluated nor in the incidence of transient hypothyroidism between the iodine-exposed (2/17) and control babies (0/14) despite urinary iodine excretion up to 88 times the control value. Unexpectedly 5 iodine-exposed but 0 control babies developed severe hypothyroxinemia (T4 < 40 nmol/L), compatible with the sick euthyroid syndrome; one of them died. We conclude that, unlike in Europe, transient hypothyroidism is not a common sequela of routine skin cleansing with iodine in premature newborn infants in North America. This difference in incidence may be due to prior iodine status. Whether excessive iodine absorption in premature infants is associated with thyroid-independent toxic effects remains to be clarified.

Owing to the progressive iodination of salt in Switzerland (5, 10, 20 mg KI/kg in the years 1922, 1965, 1980), iodine deficiency in former endemic goiter regions had nearly disappeared. In several areas of the country, urinary iodine had increased from below 30 micrograms/24 h (1920) to > 100 micrograms/g creatinine (1981-1990). In 1991-1992, however, the 24-h-iodinuria in a subgroup of 160 examinations out of a total of 289 persons in Berne was again insufficient (norm > 150 micrograms J/24 h): mean 121 micrograms/24 h (82 micrograms/l), median 107.8 micrograms/24 h (67 micrograms/l). Follow-up of one proband in 1991-1992 (n = 9) and 1996 (n = 11) yielded average 24-h-iodinurias in the slightly deficient domain of (mean +/- SD) 104 +/- 57 micrograms/ 24 h (75 +/- 30 micrograms/l) and 103 +/- 27 micrograms/24 h (44 +/- 17 micrograms/l) respectively, with a wide range (45-258 micrograms l/24 h globally). Possible reasons for the decreasing iodide intake in recent years, resulting in the 1990s in a marginally deficient supply, are reduced intake of salt in recent decades, increased consumption of foodstuffs prepared with non-iodized salt, dietary diversification, and frequent meals away from the family table. Therefore, intake of non-iodized salt should be avoided in Switzerland.