Exposure To Non-Persistent Pesticides And Thyroid Hormone Levels: A Systematic Review Of The Epidemiological Evidence

2015 ◽  
Vol 2015 (1) ◽  
pp. 365
Author(s):  
Élida De Albuquerque Campos ◽  
Carmen Freire Warden
2020 ◽  
Vol 33 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Mahshid Gheidarloo ◽  
Roya Kelishadi ◽  
Silva Hovsepian ◽  
Mojtaba Keikha ◽  
Mahin Hashemipour

AbstractIn this systematic review, the association between prenatal exposure to organochlorine pesticides (OCPs) and neonatal thyroid hormone levels was studied. A systematic search of scientific literature was performed from the PubMed, SCOPUS and ISI web of science electronic bibliographic databases. The search strategy for the review was [(organochlorine OR “organochlorine pesticides” OR “organochlorine pollutants” OR “organochlorine pollutant”) AND (“thyroid hormone” OR triiodothyronine OR Thyroxine OR “fetal thyroid function” OR “thyroid function” OR “Thyroid Stimulating Hormone” AND “prenatal” AND “maternal exposure”)] in English sources. In this review, 305 papers (PubMed: 30; Scopus: 29; ISI: 246) were identified through an electronic database search. Twenty-seven articles were assessed for eligibility, from which 16 qualified articles were selected for the final evaluation. The most common OCP metabolites which were evaluated in order were hexachlorobenzene (HCB) (13 studies), pp-dichlorodiphenyldichloroethylene (pp-DDE) (13 studies), hexachlorocyclohexane (HCH) (10 studies) and dichlorodiphenyltrichlorethane (DDT) (eight studies). A review of the documents related to the association of prenatal exposure of OCPs with fetal or neonatal thyroid function tests provides us with heterogeneous data in this field. Factors such as differences in the studied populations and their area, ethnic and genetic background, time and rate of exposure, possible interaction of other thyroid-disrupting environmental factors and dietary intake of micronutrients such as iodine and/or selenium are considered the main limitations for making an accurate conclusion. For some OCPs including DDT, DDE, HCH and HCB, there are supporting evidences, and it is suggested that their exposure could potentially alter the fetal thyroid function and consequently impair the neurodevelopment process of the infants.


2014 ◽  
Vol 171 (3) ◽  
pp. R123-R135 ◽  
Author(s):  
Herman Verloop ◽  
Olaf M Dekkers ◽  
Robin P Peeters ◽  
Jan W Schoones ◽  
Johannes W A Smit

Iodothyronine deiodinases represent a family of selenoproteins involved in peripheral and local homeostasis of thyroid hormone action. Deiodinases are expressed in multiple organs and thyroid hormone affects numerous biological systems, thus genetic variation in deiodinases may affect multiple clinical endpoints. Interest in clinical effects of genetic variation in deiodinases has clearly increased. We aimed to provide an overview for the role of deiodinase polymorphisms in human physiology and morbidity. In this systematic review, studies evaluating the relationship between deiodinase polymorphisms and clinical parameters in humans were eligible. No restrictions on publication date were imposed. The following databases were searched up to August 2013: Pubmed, EMBASE (OVID-version), Web of Science, COCHRANE Library, CINAHL (EbscoHOST-version), Academic Search Premier (EbscoHOST-version), and ScienceDirect. Deiodinase physiology at molecular and tissue level is described, and finally the role of these polymorphisms in pathophysiological conditions is reviewed. Deiodinase type 1 (D1) polymorphisms particularly show moderate-to-strong relationships with thyroid hormone parameters, IGF1 production, and risk for depression. D2 variants correlate with thyroid hormone levels, insulin resistance, bipolar mood disorder, psychological well-being, mental retardation, hypertension, and risk for osteoarthritis. D3 polymorphisms showed no relationship with inter-individual variation in serum thyroid hormone parameters. One D3 polymorphism was associated with risk for osteoarthritis. Genetic deiodinase profiles only explain a small proportion of inter-individual variations in serum thyroid hormone levels. Evidence suggests a role of genetic deiodinase variants in certain pathophysiological conditions. The value for determination of deiodinase polymorphism in clinical practice needs further investigation.


2015 ◽  
Vol 16 (2) ◽  
pp. 78
Author(s):  
Umit Kervan ◽  
Anil Ozen ◽  
Utku Unal ◽  
Irfan Tasoglu ◽  
Mahmut Mustafa Ulas ◽  
...  

<p><b>Objective:</b> The aim of this study was to examine the effects of positive inotropic drugs, including adrenaline, dopamine, and dobutamine on thyroid hormone levels following open heart surgery.</p><p><b>Methods:</b> We analyzed free thyroid hormones (FT3 and FT4) and thyroid-stimulating hormones (TSH) in 200 consecutive patients undergoing open heart surgery. Patients were divided into 5 groups according to the inotropic drug administration as follows: Group A (n = 46) received dopamine alone; Group B (n = 40), dopamine and dobutamine; Group C (n = 36), dopamine, dobutamine, and adrenaline; Group D (n = 32), adrenaline alone; and Group E (n = 46), placebo. Procedural factors affecting thyroid hormones were recorded and included cardiopulmonary bypass (CPB) time, cross-clamping time, degree of hypothermia, and the duration and doses of positive inotropic drugs. Blood samples for hormone assays were collected before initiation of inotropic drug therapy (baseline) and postoperatively at 24, 72, and 120 hours after drug therapy.</p><p><b>Results:</b> FT3, FT4, and TSH levels at baseline were similar in all groups. Although there was a trend showing very slight increases in thyroid hormone levels from baseline to the 24th, 72nd, and 120th postoperative hours after drug therapy, these changes were not significant, and there were also no significant differences between the groups. There was also no significant statistical difference in CPB time, cross-clamping time, degree of hypothermia, and duration and doses of positive inotropic drugs between groups.</p><p><b>Conclusion:</b> Although thyroid hormone levels were affected by positive inotropic drug usage after open heart surgery, this effect was not significant and thyroid hormone levels remained within normal ranges.</p>


2020 ◽  
Vol 33 (5) ◽  
pp. 653-659
Author(s):  
Jia Song ◽  
Yun Cui ◽  
Chunxia Wang ◽  
Jiaying Dou ◽  
Huijie Miao ◽  
...  

AbstractBackgroundThyroid hormone plays an important role in the adaptation of metabolic function to critically ill. The relationship between thyroid hormone levels and the outcomes of septic shock is still unclear. The aim of this study was to assess the predictive value of thyroid hormone for prognosis in pediatric septic shock.MethodsWe performed a prospective observational study in a pediatric intensive care unit (PICU). Patients with septic shock were enrolled from August 2017 to July 2019. Clinical and laboratory indexes were collected, and thyroid hormone levels were measured on PICU admission.ResultsNinety-three patients who fulfilled the inclusion criteria were enrolled in this study. The incidence of nonthyroidal illness syndrome (NTIS) was 87.09% (81/93) in patients with septic shock. Multivariate logistic regression analysis showed that T4 level was independently associated with in-hospital mortality in patients with septic shock (OR: 0.965, 95% CI: 0.937–0.993, p = 0.017). The area under receiver operating characteristic (ROC) curve (AUC) for T4 was 0.762 (95% CI: 0.655–0.869). The cutoff threshold value of 58.71 nmol/L for T4 offered a sensitivity of 61.54% and a specificity of 85.07%, and patients with T4 < 58.71 nmol/L showed high mortality (60.0%). Moreover, T4 levels were negatively associated with the pediatric risk of mortality III scores (PRISM III), lactate (Lac) level in septic shock children.ConclusionsNonthyroidal illness syndrome is common in pediatric septic shock. T4 is an independent predictor for in-hospital mortality, and patients with T4 < 58.71 nmol/L on PICU admission could be with a risk of hospital mortality.


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