Thyroid, Diet, and Alternative Approaches.

BACKGROUND: Increasingly, patients are asking their physicians about the benefits of dietary and alternative approaches to manage their diseases, including thyroid disease. We seek to review the evidence behind several of the vitamins, minerals, complementary medicines, and elimination diets that patients are most commonly using for the treatment of thyroid disorders. SUMMARY: Several trace elements are essential to normal thyroid function, and their supplementation has been studied in various capacities. Iodine supplementation has been implemented on national scales through universal salt iodization with great success in preventing severe thyroid disease, but can conversely cause thyroid disorders when given in excess. Selenium and zinc supplementation has been found to be beneficial in specific populations with otherwise limited generalizability. Other minerals, such as vitamin B12, low-dose naltrexone, and ashwagandha root extract, have little to no evidence of any impact on thyroid disorders. Avoidance of gluten and dairy has positive impacts only in patients with concomitant sensitivities to those substances, likely by improving absorption of levothyroxine. Avoidance of cruciferous vegetables and soy has little proven benefit in patients with thyroid disorders. CONCLUSION: While many patients are seeking to avoid conventional therapy and instead turn to alternative and dietary approaches to thyroid disease management, many of the most popular approaches have no proven benefit or have not been well studied. It is our responsibility to educate our patients about the evidence for or against benefit, potential harms, or dearth of knowledge behind these strategies.

Combining Network Pharmacology with Molecular Docking for Mechanistic Research on Thyroid Dysfunction Caused by Polybrominated Diphenyl Ethers and Their Metabolites.

Network pharmacology was used to illuminate the targets and pathways of polybrominated diphenyl ethers (PBDEs) causing thyroid dysfunction. A protein-protein interaction (PPI) network was constructed. Molecular docking was applied to analyze PBDEs and key targets according to the network pharmacology results. A total of 247 targets were found to be related to 16 PBDEs. Ten key targets with direct action were identified, including the top five PIK3R1, MAPK1, SRC, RXRA, and TP53. Gene Ontology (GO) functional enrichment analysis identified 75 biological items. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis identified 62 pathways mainly related to the regulation of the thyroid hormone signaling pathway, MAPK signaling pathway, PI3K-Akt signaling, pathways in cancer, proteoglycans in cancer, progesterone-mediated oocyte maturation, and others. The molecular docking results showed that BDE-99, BDE-153, 5-OH-BDE47, 5'-OH-BDE99, 5-BDE47 sulfate, and 5'-BDE99 sulfate have a good binding effect with the kernel targets. PBDEs could interfere with the thyroid hormone endocrine through multiple targets and biological pathways, and metabolites demonstrated stronger effects than the prototypes. This research provides a basis for further research on the toxicological effects and molecular mechanisms of PBDEs and their metabolites. Furthermore, the application of network pharmacology to the study of the toxicity mechanisms of environmental pollutants provides a new methodology for environmental toxicology.

Safety of oil-based contrast medium for hysterosalpingography: a systematic review.

Recent meta-analyses have shown that a hysterosalpingography (HSG) with oil-based contrast increases pregnancy rates in subfertile women. However, the frequency of complications during or after an HSG with oil-based contrast in subfertile women and/or their offspring is still unclear. This systematic review and meta-analysis, without restrictions on language, publication date or study design, was performed to fill this knowledge gap. The results show that the most frequently reported complication was intravasation of contrast, which occurred in 2.7% with the use of oil-based contrast (31 cohort studies and randomized controlled trials [RCT], 95% CI 1.7-3.8, absolute event rate 664/19,339), compared with 2.0% with the use of water-based contrast (8 cohort studies and RCT, 95% CI 1.2-3.0, absolute event rate 18/1006). In the cohort studies and RCT there were 18 women with an oil embolism (18/19,339 HSG), all without serious lasting consequences. Four cases with serious consequences of an oil embolism were described (retinal oil embolism [n = 1] and cerebral complaints [n = 3]); these reports did not describe the use of adequate fluoroscopy guidance during HSG. In conclusion, the most frequently reported complication after an HSG with oil-based contrast is intravasation occurring in 2.7%. In total four cases with serious consequences of oil embolisms in subfertile women were published.

Frequency of thyroid dysfunction in pediatric patients with congenital heart disease exposed to iodinated contrast media - a long-term observational study.

Background The thyroid gland of patients with congenital heart disease may be exposed to large doses of iodine from various sources. We assessed the thyroid response after iodine exposure during conventional angiography in cardiac catheterization and angiographic computer tomography in childhood. Methods Retrospective mid- to long-term follow-up of 104 individuals (24% neonates, 51% infants, 25% children) with a median age and body weight of 104 days [0-8 years] and 5.3 kg [1.6-20]. Serum levels of thyroid-stimulating hormone, free triiodthyronine and free thyroxine were evaluated at baseline and after excess iodine. We also assessed risk factors that may affect thyroid dysfunction. Results Baseline thyroidal levels were within normal range in all patients. The mean cumulative iodinate contrast load was 6.6 ± 1.6 mL/kg. In fact, 75% had experienced more than one event involving iodine exposure, whose median frequency was three times per patient [1-12]. During the median three years follow-up period [0.5-10], the incidence of thyroid dysfunction was 15.4% (n=16). Those patients developed acquired hypothyroidism (transient n=14, long-lasting n=2 [both died]) with 10 of them requiring temporary replacement therapy for transient thyroid dysfunction, while four patients recovered spontaneously. 88 individuals (84.6%) remained euthyroid. Repeated cardiac interventions, use of drugs that interfere with the thyroid and treatment in the intensive care unit at the index date were strong predictors for acquired thyroid dysfunction. Conclusions The incidence of acquired hypothyroidism after iodine excess was 15.4%. However, most patients developed only transient hypothyroidism. Systemic iodine exposure seems to be clinically and metabolically well tolerated during long-term follow-up.

Effect of Launaea procumbens on thyroid glands lipid peroxidation and hormonal dysfunction: a randomized control trial.

BACKGROUND: Launaea procumbens (Roxb.) Amin is traditionally used in Pakistan for the treatment of hormonal disorders and oxidative stress. The present study was aimed to evaluate the efficacy of Launaea procumbens methanol extract (LPME) against KBrO3-induced oxidative stress and hormonal dysfunction in thyroid. METHODS: To examine the effects of LPME against the oxidative stress of KBrO3 in thyroid tissue, 36 male albino rats were used. Protective effects of LPME were observed on thyroid hormonal levels, activities of antioxidant enzymes, lipid peroxidation (TBARS) and DNA damage. RESULTS: Treatment with KBrO3 significantly (P < 0.01) reduced the levels of T3 (55.13 ± 1.93) and T4 (14.7 ± 1.78) and increased TSH (55.13 ± 1.93) levels. KBrO3 exposure in rats reduced the activities of antioxidant enzymes viz.; CAT (1.16 ± 0.08); SOD (12.0 ± 0.08), GST (17.7 ± 1.1) and GSR (54.3 ± 2.1) but increased lipid peroxidation (20.3 ± 0.71) and DNA (30.4 ± 2.0) damage. Co-administration of LPME significantly (P < 0.01) improved these alterations with respect to hormonal levels, activities of antioxidant enzymes and lipid peroxidation close to those seen in control rats. CONCLUSION: These results suggest that LPME can protect thyroid tissue against oxidative damage, possibly through the antioxidant effects of its bioactive compounds.

A new insight on the role of zinc in the regulation of altered thyroid functions during lithium treatment.

BACKGROUND: Lithium salts are widely used for the treatment of mental disorders but cause thyroid dysfunctions while zinc is an essential trace element and is required for a broad range of biological activities. The present study was designed to explore the potential of zinc in regulating 131I biokinetics and thyroid functions following lithium therapy. METHODS: To carry out the investigations, 40 female sprague dawley rats weighing 110-140g were segregated into four groups viz. Group I animals served as untreated controls, group II animals were given lithium (Li2CO31.1 g/kg diet), group III animals were supplemented with zinc (227 mg ZnSO4/L drinking water) and animals in group IV were given a combined treatment of lithium and zinc. The treatments were given for durations of 1, 2 and 4 months. RESULTS: Following intraperitoneal administration of 0.37 MBq carrier- free-131I, a significant depression in the thyroidal 131I uptake both at 2 and 24 hrs was observed following lithium treatment for all the durations which however was brought to within normal levels following zinc supplementation. Lithium treatment caused a significant elevation in the thyroidal biological half lives of 131I which was appreciably attenuated following 2 and 4 months of zinc supplementation. Lithium administration for 2 and 4 months significantly decreased serum T3 and T4 levels which however were increased following zinc supplementation. Lithium treatment for 4 months caused a significant decrease in the thyroidal activities of Na+ K+ ATPase and monoamine oxidase which were brought to near normal levels by zinc. Further, lithium treatment for 4 months raised thyroidal levels of lipid peroxidation and catalase which however were normalized by zinc supplementation. On the contrary, thyroidal levels of reduced glutathione and glutathione S transferase decreased significantly following 2 and 4 months of lithium treatment but were significantly increased following zinc treatment. CONCLUSIONS: The present study concludes that zinc supplementation is helpful in attenuating the adverse effects caused by lithium on thyroid functions and can effectively regulate the biokinetics of 131I.

Assessment of petroleum streams for thyroid toxicity.

The thyroid gland, and its associated endocrine hormones, is a growing area of interest in regulatory toxicology due to its important role in metabolism, growth and development. This report presents a review of the toxicology data on chemically complex petroleum streams for thyroid hormone effects. Toxicological summaries and studies from all available published and un-published sources were considered, drawing upon the European REACH regulatory submissions for 19 petroleum streams, with in depth review of 11 individual study reports and 31 published papers on related products or environmental settings. Findings relevant to thyroid pathology or thyroid hormone homeostasis were specifically sought, summarized, and discussed. A total of 349 studies of 28-days or longer duration were considered in the review, including data on mice, rats, rabbits, dogs, humans, and fish. The thyroid was almost invariably not a target organ in these studies. Three rodent studies did find thyroid effects; one on a jet fuel product (JP-8), and two studies on a heavy fuel oil product (F-179). The JP-8 product differs from other fuels due to the presence of additives, and the finding of reduced T4 levels in mice in the study occurred at a dose that is above that expected to occur in environmental settings (e.g. 2000mg/kg). The finding for F-179 involved thyroid inflammation at 10-55mg/kg that co-occurred with liver pathology in rats, indicating a possible secondary effect with questionable relevance to humans. In the few cases where findings did occur, the polycyclic aromatic hydrocarbon (PAH) content was higher than in related substances, and, in support of one possible adverse outcome pathway, one in-vitro study reported reduced thyroid peroxidase (TPO) activity with exposure to some PAH compounds (pyrene, benzo(k)fluoranthene, and benzo(e)pyrene). However, it could not be determined from the data available for this review, whether these specific PAH compounds were substantially higher in the JP-8 or F-179 products than in studies in which thyroid effects were not observed. Thus, a few products may carry a weak potential to affect the thyroid at high doses in rodents, possibly through secondary effects on the rodent liver or possibly through a pathway involving the inhibition of TPO by specific members of the PAH family. Human epidemiology evidence found weak and inconsistent effects on the thyroid but without identification of specific chemicals involved. Two studies in petroleum workers, which found a lower rate of morbidity and mortality overall, reported a statistically significant increase in thyroid cancer, but the small number of cases could not exclude confounding variables as possible explanations for the statistical findings. Overall, the available data indicates a low potential for thyroid hormone effects from exposure to petroleum streams, especially when the aromatic content is low. Because regulatory studies for most chemicals do not include detailed thyroid function or receptor studies, it remains possible that subclinical effects on this system may exist that were not detectable using conventional pathology or hormone measurements.

THE ABSENCE OF THYROID DISEASE IN AN AUSTRALIAN HEPATITIS C COHORT TREATED WITH TRIPLE COMBINATION THERAPY: A PARADIGM SHIFT.

OBJECTIVE: To assess the prevalence of thyroid disease in triple combination therapy with interferon (IFN)-α, ribavirin (RBV), and protease inhibitors (boceprevir and telaprevir) for the treatment of chronic hepatitis C virus (HCV) infection in an Australian hepatitis C cohort. Also, to compare with those who received dual RBV and IFN in the past. METHODS: A preliminary, retrospective, and nested case control study of thyroid disease in patients who underwent triple combination therapy for chronic HCV infection compared with dual therapy at a major tertiary referral hospital center. Fifty-nine patients were treated with such therapy at the Hunter New England Area Hepatitis C Treatment Center. Of these, 38 were treated with boceprevir and 21 with telaprevir. All had genotype 1 HCV infection. The main outcome measures included (1) the prevalence of thyroid disease (TD), including hyperthyroidism and hypothyroidism, and (2) thyroid outcome comparison with patients who had received dual therapy. RESULTS: There was no case of TD detected for the entire duration of therapy with triple anti-HCV therapy. There was a significant absence of TD in the protease inhibitor-treated group. CONCLUSION: No case of TD was detected during the treatment of HCV patients with protease inhibitor-based triple therapy. The reasons for this are unclear. Larger studies are necessary to confirm this finding.

Pistacia chinensis: a potent ameliorator of CCl4 induced lung and thyroid toxicity in rat model.

In the current study protective effect of ethanol extract of Pistacia chinensis bark (PCEB) was investigated in rats against CCl4 induced lung and thyroid injuries. PCEB dose dependently inhibited the rise of thiobarbituric acid-reactive substances, hydrogen peroxide, nitrite, and protein content and restored the levels of antioxidant enzymes, that is, catalase, peroxidase, superoxide dismutase, glutathione-S-transferase, glutathione reductase, glutathione peroxidase, γ-glutamyl transpeptidase, and quinone reductase in both lung and thyroid tissues of CCl4 treated rats. Decrease in number of leukocytes, neutrophils, and hemoglobin and T3 and T4 content as well as increase in monocytes, eosinophils, and lymphocytes count with CCl4 were restored to normal level with PCEB treatment. Histological study of CCl4 treated rats showed various lung injuries like rupture of alveolar walls and bronchioles, aggregation of fibroblasts, and disorganized Clara cells. Similarly, histology of CCl4 treated thyroid tissues displayed damaged thyroid follicles, hypertrophy, and colloidal depletion. However, PCEB exhibited protective behaviour for lungs and thyroid, with improved histological structure in a dose dependant manner. Presence of three known phenolic compounds, that is, rutin, tannin, and gallic acid, and three unknown compounds was verified in thin layer chromatographic assessment of PCEB. In conclusion, P. chinensis exhibited antioxidant activity by the presence of free radical quenching constituents.

[Dietary isolated isoflavone supplements for peri- and postmenopausal women: risks and questionable benefits]. / Risiken und fraglicher Nutzen von Nahrungsergänzungsmitteln mit isolierten Isoflavonen für Frauen in und nach der Menopause.

Isolated isoflavones are frequently offered as dietary supplements for the alleviation of peri- and postmenopausal complaints. These mainly soy-based secondary plant compounds are marketed with the claim of having numerous beneficial effects such as protection against breast cancer, osteoporosis, and cardiovascular diseases. Currently, there is no conclusive evidence for most of these health impacts. In addition, there is a controversial ongoing discussion about the safety of these products. After a long-term intake of high isoflavone doses, adverse effects on the breast tissue, the endometrium, and the thyroid, the last one especially under iodine-deficient conditions, cannot be excluded. Owing to their estrogenic effects, isoflavones may promote the growth of estrogen-sensitive malignant cells. The risk assessment of isoflavones is especially focused on peri- and postmenopausal women because they are the target group for dietary supplements based on isolated isoflavones and have, anyway, a higher risk for breast cancer. Since long-term treatment with isolated isoflavones, especially at high doses, is considered critical, we recommend that patients consume isoflavone-based supplements only after advice and under medical supervision.

Thyroid volume, iodine intake, autoimmune thyroid disorders, inborn factors, and endocrine disruptors: twenty-year studies of multiple effects puzzle in Slovakia.

OBJECTIVE: The aim of this study was to evaluate multiple interrelations between several endogenous and exogenous effects and the thyroid volume and function in large groups of children, adolescents, and adults with a sufficient whole life intake of the iodine. SUBJECTS AND METHODS: The data were obtained either by cross sectioned or longitudinal studies in a total of 4998 children and adolescents (aged 7 to 17 years) and 2501 adults (1071 males and 1430 females aged 20-75 years). Thyroid volume (ThV) was measured by ultrasound, antibodies, and hormones by electrochemiluminiscent immunoassay, and endocrine disruptors (EDs, polychlorinated biphenyls-PCB, dichlorodiethyl-ichloroethylene-DDE, and hexachlorobenzene-HCB) by high resolution gas chromatography/mass spectrometry. RESULTS: 1. In large groups of boys and girls of age 7, 10, 13 or 17 years, the ThV was significantly higher in the 10th decile than in pooled nine lower deciles. Moreover, in 17-year old subjects significantly higher prevalence of hypoechogenicity by ultrasound, positive thyroperoxidase antibodies (TPOab), and increased thyrotropin (TSH) levels were found in the 10th decile. 2. In a small group of children, some individuals revealed consistently higher ThV during the whole 7-year follow-up period irrespective of supplementation with iodine. 3. In 325 sibling pairs of age 10-19 years, born within three years, three groups with different ThV/m2 of body surface were distinguished: Group A (183 pairs having both ThVs small), Group B (103 pairs having both ThVs large); Group C (33 pairs having one ThV small and the other one large). Similar aggregation of ThVs in three groups was observed in 13 pairs of discordant twins and 19 sibling triads in which all the siblings were born within four years. 4. In 42 concordant twins, several pairs had ThV nearly twice as high (in terms of both plain ThV or ThV/m2 of the body surface) as several other pairs of the same age which is assumed to be a result of a genetic background. 5. In large cohorts of males and females, a highly significant positive correlation was found between the ThV and high level of TPOab on one side and EDs on the other side. However, in nearly the same numbers of subjects with low TPOab, negative correlation was seen between ThV and disruptors. These observations may apparently support the synergic effect of the autoimmunity and EDs on the thyroid function. CONCLUSIONS: Several cases of an excessive thyroid growth in the iodine replenished children, adolescents, and adults may apparently result from the autoimmune thyroiditis, probably induced by immunogenic action of iodine in presumably disposed individuals. However, in some cases even simultaneous participation of EDs can not be excluded. Some observations have also suggested that excessive thyroid growth in the iodine replenished adolescent and adult population which was equally exposed to disruptors may also result from other reasons as the unfavorable hereditary background.

Hypothyroidism during treatment with tyrosine kinase inhibitors.

Tyrosine kinase inhibitors are relatively new targeted therapy drugs used for the treatment of metastatic clear cell kidney carcinoma, gastrointestinal stromal tumours, thyroid carcinoma and pancreatic neuroendocrine tumours during the progression of the disease. Hypothyroidism or thyroid dysfunction is often a side effect of this treatment. Therefore, monitoring of thyroid hormone levels before the beginning and during the treatment of tyrosine kinase inhibitors is a necessity. Hypothyroidism correlates with objective response to the treatment. Sunitinib. This is the most described tyrosine kinase inhibitor which causes hypothyroidism. The mechanism of hypothyroidism is still unclear. Sorafenib. Symptoms of hypothyroidism occur in 18% of patients treated with sorafenib due to metastatic renal cell carcinoma. Imatinib. Hypothyroidism is one of the most frequent side effects of the treatment. Emergent tracheotomy was necessary due to larynx swelling during marked hypothyroidism. Motesanib. Hypothyroidism or increased TSH level is diagnosed in 22% to 69% of patients with metastatic differentiated or medullary thyroid carcinomas. The management of patients with thyroid dysfunction and related symptoms such as fatigue is undoubtedly a challenge to an oncologist.

Iodine-induced thyroid dysfunction.

PURPOSE OF REVIEW: To summarize the mechanisms of iodine-induced hypothyroidism and hyperthyroidism, identify the risk factors for thyroid dysfunction following an iodine load, and summarize the major sources of excess iodine exposure. RECENT FINDINGS: Excess iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Sources of increased iodine exposure include the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients, excess seaweed consumption, and various miscellaneous sources. SUMMARY: Iodine-induced thyroid dysfunction may be subclinical or overt. Recognition of the association between iodine excess and iodine-induced hypothyroidism or hyperthyroidism is important in the differential diagnosis of patients who present without a known cause of thyroid dysfunction.

Vitamin E ameliorates iodine-induced cytotoxicity in thyroid.

Acute and excessive iodine supplementation leads to iodine-induced thyroid cytotoxicity. Excessive oxidative stress has been suggested to be one of the underlying mechanisms in the development of thyroid cytotoxicity. The aim of this study was to investigate whether vitamin E (VE), an important antioxidant, could ameliorate iodine-induced thyroid cytotoxicity. A goiter was induced in rats by feeding a low-iodine (LI) diet for 12 weeks. Involution of hyperplasia was obtained by administering a twofold physiological dose of iodine in feeding water with/without the supplementation of 25-, 50-, or 100-fold physiological dose of VE in the LI diet for 4 weeks. In iodine-supplemented rats, thyroid epithelial cell ultrastructure injuries remained and were more severe. Relative weights of iodine-induced involuting glands were significantly reduced compared with the goiter, but still higher than control. Immunohistochemistry indicated that the expression of 4-hydroxynonenal, 8-hydroxyguanine, peroxiredoxin 5, and CD68 in thyroid increased (P<0.01), whereas thioredoxin reductase 1 decreased (P<0.01). VE supplementation attenuated thyroid cytotoxicity induced by iodine. A 50-fold VE dose was optimal in attenuating twofold iodine-induced thyroid cytotoxicity. However, VE supplementation did not reduce the weight or relative weight of the iodine-induced involuting gland. These results show that excess iodine leads to thyroid damage and VE supplementation can partly ameliorate iodine-induced thyroid cytotoxicity.

Thyroid disruption: mechanism and clinical implications in human health.

Exposure to specific environmental toxins, including polychlorinated biphenyls, dioxins, phthalates, polybrominated diphenyl ethers (PBDEs), and other halogenated organochlorines, has been shown to interfere with the production, transportation, and metabolism of thyroid hormones by a variety of mechanisms. A broad range of chemicals, with structural similarity to thyroid hormone, have been shown to bind to thyroid receptors with both agonist and antagonist effects on thyroid hormone signaling. The incidence of thyroid disease in the United States, particularly for thyroid cancer and thyroid autoimmune disease, is increasing substantially. The evidence for the significant effects of background levels of thyroid-disrupting chemicals, the known pathways for thyroid disruptors, and the evidence and implications for neurodevelopmental damage due to thyroid-disrupting chemicals is reviewed.

Thyroid function and changes in ultrasound morphology during antiviral therapy with pegylated interferon and ribavirin in patients with chronic hepatitis C.

SUMMARY: Thyroid disease is a common side-effect of interferon-based antiviral therapy for chronic hepatitis C, which may lead to dose reduction or discontinuation of therapy. The aim of this study was to investigate changes in ultrasound morphology, thyroid function, autoimmunity as well as predictive factors for the development of thyroid dysfunction in patients with hepatitis C virus infection treated with pegylated interferon-alpha (PEG-IFN-alpha) and ribavirin. A total of 59 patients with chronic hepatitis C assigned for antiviral treatment with PEG-IFN-alpha and ribavirin were enrolled into the study. All patients were subjected to an ultrasound examination of the thyroid gland before treatment, and after 1, 3 and 6 months of antiviral therapy. In addition, thyroid function and autoimmune status were determined at fixed time-points. Prior and during the course of therapy, 11 patients (19%) developed thyroid dysfunction (one hypothyroidism, nine hyperthyroidism, one hyperthyroidism followed by hypothyroidism). Hyperthyroidism was shown to be Graves' disease in one patient and destructive thyroiditis in nine patients. Power-Doppler ultrasound could differentiate between destructive thyroiditis and Graves' disease. A reduction in echogenicity suggestive for a destructive process of the thyroid gland was observed even before changes in thyroid function of antibody status could be measured. Risk factors for the development of thyroid dysfunction were age, female gender, pre-treatment thyroid volume, pre-existing thyroglobulin/thyroid peroxidase antibodies and viral load. Changes in thyroid function are a common side-effect occurring during antiviral therapy with PEG-IFN-alpha and ribavirin. Ultrasound presents a simple complementary tool for screening and follow-up during antiviral therapy, which helps to differentiate between the common types of hyperthyroidism and gives insight into morphological changes of the thyroid gland during antiviral therapy.

Reversal of cadmium-induced thyroid dysfunction by selenium, zinc, or their combination in rat.

The aim of this study was to evaluate the potential benefit of combined treatment with zinc (Zn) and selenium (Se) in reversing cadmium (Cd)-induced thyroid dysfunction compared to Se or Zn treatment alone in rats exposed to Cd. For this purpose, 30 adult male Wistar albino rats were equally divided into control and four treated groups receiving either 200 ppm Cd (as CdCl2), 200 ppm Cd + 500 ppm Zn (as ZnCl2), 200 ppm Cd + 0.1 ppm Se (as Na2SeO3), or 200 ppm Cd + 500 ppm Zn + 0.1 ppm Se in their drinking water for 35 days. The results showed that Cd exposure increased significantly the relative thyroid weight (RTW), the thyroid Cd concentration, and the serum thyroid stimulating hormone (TSH) level, whereas the serum thyroxine (T4) level was decreased compared to control rats. The treatment of Cd-exposed rats with Se alone only partially protected from the Cd-induced decrease in serum T4 level. The treatment of Cd-exposed animals with Zn alone partially protected against Cd-induced thyroid dysfunction by maintaining normal RTW and by decreasing Cd concentration in the thyroid. It also partially prevents Cd-induced decrease in serum T4 level. The combined treatment of Cd-exposed animals with Se and Zn induced a more significant decrease in the thyroid Cd concentration than the Zn supplement and a total correction of the RTW. This treatment was also more effective than that with Se or Zn alone in reversing Cd-induced decrease in serum T4 level and Cd-induced increase in serum TSH level. Se and Zn can have a synergistic role against Cd-induced thyroid dysfunction.

Safe range of iodine intake levels: a comparative study of thyroid diseases in three women population cohorts with slightly different iodine intake levels.

Iodine excess may lead to thyroid diseases. Our previous 5-year prospective survey showed that the prevalence and incidence of hypothyroidism or autoimmune thyroiditis increased with iodine intake. The aim of the present study was to investigate the optimal range of iodine intake by comparing the prevalence of thyroid diseases in three areas with slightly different levels of iodine intake. In 2005, 778 unselected women subjects from three areas with different iodine intake levels were enrolled. Levels of serum thyroid hormones, thyroid autoantibodies, and urinary iodine were measured, and thyroid B ultrasounds were performed. Among the subjects with mildly deficient iodine intake, those with adequate intake, and those with more than adequate intake, the prevalence of clinical and subclinical hypothyroidism was 0, 1.13, and 2.84%, respectively (P = 0.014); that of thyroid goiter was 24.88, 5.65, and 11.37%, respectively (P < 0.001); that of serum thyrotropin values was1.01, 1.25, and 1.39 mIU/l, respectively; and that of serum thyrotropin/thyroglobulin ratio was 7.98, 6.84, and 5.11, respectively (P < 0.001). In conclusion, median urinary iodine 100~200 mug/l may reflect the safe range of iodine intake levels. Serum thyrotropin/thyroglobulin ratio might be a better index of evaluating iodine status.

Impact of organic solvents and environmental pollutants on the physiological function in petrol filling workers.

Long term exposure to solvents and air pollutants can lead to deleterious effects on respiratory, haematological and thyroid functioning. The aim of this study was to investigate whether chronic exposure to solvents like benzene and pollutants like carbon monoxide in petrol filling workers had adverse effect on blood parameters, thyroid and respiratory functions. The study group consisted of 42 healthy, non-smoker petrol filling workers, aged 20-50 years with work (exposure) duration from 2-15 years while 36 healthy subjects of the same age group served as controls. Physical examination and measurement of pulmonary functions by portable electronic spirometer were performed. Complete blood pictures (CBP) were determined by normal haematology lab procedure and hormones by Chemiluminescence immunoassay (CLIA) light absorption techniques. There was a significant decrease in the lung volumes and capacities; the restrictive pattern was more prevalent in the workers when compared with the control groups. But in the workers exposed for long period (more than 10 years) the restrictive pattern was changed to mixed pattern. A significant increase in haemoglobin (Hb) (>16 mg %) and red blood cells (RBC) (5.4 million cells/mm3) were observed in workers with longer period of exposure when compared with the control subjects (14.483 mg% and 4.83 million cells/mm3 for Hb and RBC respectively). White blood cell count except eosinophils and platelets were significantly lower in workers compared to controls. Marked increase in the tetra iodothyroinine (T4), free thyroxine (T4F) level and significant decrease in thyroid stimulating hormones (TSH), and tri-iodothyronine (T3) were observed between long term exposed and non-exposed groups. Till now researchers focused only on the effect of solvents in workers professionally exposed to solvents without considering the effect of concomittant air pollution. The result obtained from present study indicates that there is a significant toxic effect of solvents and air pollutants on workers exposed for longer duration. Improved detection and prevention technologies are needed to answer environmentally related health questions for petrol filling workers.