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      TSH cut off point based on depression in hypothyroid patients

      research-article
      1 , 2 , , 1 , 1 , 1
      BMC Psychiatry
      BioMed Central
      TSH, Cut off, Hypothyroid, Depression

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          Abstract

          Background

          The prevalence of depressive symptoms in hypothyroidism is high. Considering that hypothyroidism and depression share some clinical features, some researchers use the “brain hypothyroidism” hypothesis to explain the pathogenesis of depression. We aimed to detect a new TSH cut-off value in hypothyroidism based on depression symptoms.

          Methods

          A cross-sectional study was conducted on hypothyroid patients referred to endocrine clinics. Individuals who had developed euthyroid state under treatment with levothyroxine with TSH levels of 0.5–5 MIU/L with no need for dosage change were included in the study. After comprehensive history taking, laboratory tests including TSH, T4 and T3 were performed. Beck depression questionnaire was completed for all patients by trained interviewers. TSH cut-off values based on depression was determined by Roc Curve analysis.

          Results

          The participants were 174 hypothyroid patients (Female; 116: 66.7%, Male; 58: 33.3%) with mean age 45.5 ± 11.7 (19–68) years old. Based on Beck depression test, scores less than 10 was considered healthy and more than 10 were considered depressed. According to Roc curve analysis, the optimal cut- off value of TSH was 2.5 MIU/L with 89.66% sensitivity. The optimal TSH cut- off based on severe depression was 4 MIU/L.

          Conclusion

          The present study suggests that a clinically helpful TSH cut-off value for hypothyroidism should be based on associated symptoms, not just in population studies. Based on the assessment of depression, our study concludes that a TSH cutofff value of 2.5 MIU/L is optimal.

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          Most cited references31

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          Neurodevelopmental and neurophysiological actions of thyroid hormone.

          For over 100 years, thyroid hormones have been known to be essential for neonatal neurodevelopment but whether they are required by the foetal brain remains a matter of controversy. For decades, the prevailing view was that thyroid hormones are not necessary until after birth because circulating levels in the foetus are very low and the placenta forms an efficient barrier to their transfer from the mother. Clinical observations of good neurological outcome following early treatment of congenital hypothyroidism were used to support the view that thyroid hormones are not required early in neurodevelopment. Nevertheless, the issue remained contentious because of findings that the severity of foetal neurological deficit due to maternal iodine deficiency correlated with the degree of maternal thyroxine (T4) deficiency. Furthermore, neurological damage in these cases could be prevented by correction of maternal T4 deficiency before mid-gestation. This observation led to the opposing view, supported by epidemiological studies of neurological cretinism, that maternal thyroid hormones are important and necessary for early foetal neurodevelopment. It is now clear that thyroid hormones are essential for both foetal and post-natal neurodevelopment and for the regulation of neuropsychological function in children and adults. In recent years, this controversial subject has progressed very rapidly following remarkable progress in understanding of the molecular mechanisms of thyroid hormone action. This article reviews the contributions of molecular biology and genetics to our new understanding of the physiological effects of thyroid hormones on neurodevelopment and in the adult brain.
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            Psychological well-being in patients on 'adequate' doses of l-thyroxine: results of a large, controlled community-based questionnaire study.

            Over 1% of the UK population is receiving thyroid hormone replacement with l-thyroxine (T4). However, many patients complain of persistent lethargy and related symptoms on T4 even with normal TSH levels. To date there has been no large study to determine whether this is related to thyroxine replacement or coincidental psychological morbidity. We have therefore attempted to address this issue using a large, community-based study. Computerized prescribing records of five general practices were used to identify 961 patients who had been on thyroxine for a minimum of 4 months from a population of 63 000 (1.5%), along with age- and sex-matched controls. All 1922 individuals were sent a two-page questionnaire, made up of the short form of the General Health Questionnaire (GHQ-12), designed to detect minor psychiatric disorders in the community, and a 12-question 'thyroid symptom questionnaire' (TSQ) in the same format. A covering letter explained that we were interested in 'how patients felt on medication' and made no direct reference to thyroxine. Scores from the GHQ and TSQ were marked for each individual using the GHQ and Likert scoring methods. Patients' latest TSH measurements were obtained from laboratory records. Comparisons were then made on scores for the total GHQ-12, TSQ and individual questions between patients (P) and control (C) groups. Separate analyses were made comparing the patients with a normal TSH (nP) and the control group. Five hundred and ninety-seven (62%) of the patients (P) and 551 (57%) of the controls (C) responded and fully completed at least one of the two questionnaire. Three hundred and ninety-seven responding patients (nP) had a TSH estimation performed in the previous 12 months with the last result being in the local laboratory normal range for TSH (0.1-5.5 or 0.2-6.0 mU/l, according to the assay method used). The responding P, nP and C populations were well matched for age (59.96, 59.73, 59.35 years) and sex (85%, 83%, 87% female). The number of individuals scoring 3 or more on the GHQ-12 (indicating 'caseness') was 21% higher in P than C [185/572 (32.3%) vs. 137/535 (25.6%), P = 0.014] and 26% higher in nP than C [131/381 (34.4%) vs. 137/535 (25.6%), P < 0.005]. Stronger differences were seen with the TSQ scores [C = 187/535 (35.0%), P = 273/583 (46.8%), P < 0.001, P vs. C; and nP = 189/381 (48.6%), P < 0.001, nP vs. C]. Differences existed in chronic drug use and chronic disease prevalence between the control and patient groups, but the differences in GHQ and TSQ scores between the groups remained significant even after correction for these factors as well as age and sex in multiple regression analysis. This community-based study is the first evidence to indicate that patients on thyroxine replacement even with a normal TSH display significant impairment in psychological well-being compared to controls of similar age and sex. In view of the large numbers of people on thyroxine replacement, we believe that these differences, although not large, could contribute to significant psychological morbidity in a substantial number of individuals.
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              Common variation in the DIO2 gene predicts baseline psychological well-being and response to combination thyroxine plus triiodothyronine therapy in hypothyroid patients.

              Animal studies suggest that up to 80% of intracellular T(3) in the brain is derived from circulating T(4) by local deiodination. We hypothesized that in patients on T(4) common variants in the deiodinase genes might influence baseline psychological well-being and any improvement on combined T(4)/T(3) without necessarily affecting serum thyroid hormone levels. We analyzed common variants in the three deiodinase genes vs. baseline psychological morbidity and response to T(4)/T(3) in 552 subjects on T(4) from the Weston Area T(4) T(3) Study (WATTS). Primary outcome was improvement in psychological well-being assessed by the General Health Questionnaire 12 (GHQ-12). The rarer CC genotype of the rs225014 polymorphism in the deiodinase 2 gene (DIO2) was present in 16% of the study population and was associated with worse baseline GHQ scores in patients on T(4) (CC vs. TT genotype: 14.1 vs. 12.8, P = 0.03). In addition, this genotype showed greater improvement on T(4)/T(3) therapy compared with T(4) only by 2.3 GHQ points at 3 months and 1.4 at 12 months (P = 0.03 for repeated measures ANOVA). This polymorphism had no impact on circulating thyroid hormone levels. Our results require replication but suggest that commonly inherited variation in the DIO2 gene is associated both with impaired baseline psychological well-being on T(4) and enhanced response to combination T(4)/T(3) therapy, but did not affect serum thyroid hormone levels.
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                Author and article information

                Contributors
                98-86-34173612 , afsanehtalaeii@yahoo.com
                rafeenasrin@yahoo.com
                f.rafiei87@yahoo.com
                alichehrei@yahoo.com
                Journal
                BMC Psychiatry
                BMC Psychiatry
                BMC Psychiatry
                BioMed Central (London )
                1471-244X
                7 September 2017
                7 September 2017
                2017
                : 17
                : 327
                Affiliations
                [1 ]ISNI 0000 0001 1218 604X, GRID grid.468130.8, Department of Internal Medicine, School of Medicine, Endocrinology and Metabolism Research Center, , Arak University of Medical Sciences, ; Arak, Iran
                [2 ]Amiralmomenin Hospital, Arak, Iran
                Article
                1478
                10.1186/s12888-017-1478-9
                5590144
                28882111
                48178f7d-375a-43c1-9e8d-052b543dea86
                © The Author(s). 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 19 October 2016
                : 22 August 2017
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2017

                Clinical Psychology & Psychiatry
                tsh,cut off,hypothyroid,depression
                Clinical Psychology & Psychiatry
                tsh, cut off, hypothyroid, depression

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