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      Comorbidity of autoimmune thyroid disorders and psychiatric disorders during the postpartum period: a Danish nationwide register-based cohort study

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          Abstract

          Background

          The postpartum period is well-known risk period for the first onset of autoimmune thyroid disorders (AITDs) as well as first onset of psychiatric disorders. These two disorders are some of the most prevalent medical conditions postpartum, often misdiagnosed and disabling if left untreated. Our study was designed to explore the possible bidirectional association between AITDs and psychiatric disorders during the postpartum period.

          Methods

          A population-based cohort study through linkage of Danish national registers, which comprised 312 779 women who gave birth to their first child during 1997–2010. We conducted Poisson regression analysis to estimate the incidence rate ratio (IRR) of psychiatric disorders among women with first-onset AITDs, the IRR of AITDs among women with first-onset psychiatric disorders as well as the overlap between these disorders using a comorbidity index.

          Results

          Women with first-onset AITDs postpartum were more likely to have first-onset psychiatric disorders than women who did not have postpartum AITDs (IRR = 1.88, 95% confidence interval (CI): 1.25–2.81). Women with first-onset postpartum psychiatric disorders had a higher risk of AITDs than women with no psychiatric disorders (IRR = 2.16, 95% CI: 1.45–3.20). The comorbidity index 2 years after delivery was 2.26 (95% CI: 1.61–2.90), indicating a comorbidity between first-onset AITDs and psychiatric disorders.

          Conclusions

          First-onset AITDs and psychiatric disorders co-occur in the postpartum period, which has relevance to further studies on the etiologies of these disorders and why childbirth in particular triggers the onset.

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          Most cited references22

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          The role of reproductive hormones in postpartum depression.

          Despite decades of research aimed at identifying the causes of postpartum depression (PPD), PPD remains common, and the causes are poorly understood. Many have attributed the onset of PPD to the rapid perinatal change in reproductive hormones. Although a number of human and nonhuman animal studies support the role of reproductive hormones in PPD, several studies have failed to detect an association between hormone concentrations and PPD. The purpose of this review is to examine the hypothesis that fluctuations in reproductive hormone levels during pregnancy and the postpartum period trigger PPD in susceptible women. We discuss and integrate the literature on animal models of PPD and human studies of reproductive hormones and PPD. We also discuss alternative biological models of PPD to demonstrate the potential for multiple PPD phenotypes and to describe the complex interplay of changing reproductive hormones and alterations in thyroid function, immune function, hypothalamic-pituitary-adrenal (HPA) axis function, lactogenic hormones, and genetic expression that may contribute to affective dysfunction. There are 3 primary lines of inquiry that have addressed the role of reproductive hormones in PPD: nonhuman animal studies, correlational studies of postpartum hormone levels and mood symptoms, and hormone manipulation studies. Reproductive hormones influence virtually every biological system implicated in PPD, and a subgroup of women seem to be particularly sensitive to the effects of perinatal changes in hormone levels. We propose that these women constitute a "hormone-sensitive" PPD phenotype, which should be studied independent of other PPD phenotypes to identify underlying pathophysiology and develop novel treatment targets.
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            Perinatal depression--the fourth inflammatory morbidity of pregnancy?: Theory and literature review.

            Perinatal depression is one of the leading causes of maternal morbidity and mortality. The biological etiology of this disorder remains in question, despite considerable research into the contributions of hormonal imbalance, the role of monoamines, and dysregulation of the HPA axis. Because inflammation is known to be associated with major depression in men and non-perinatal women as well as with other important morbidities of pregnancy (such as preeclampsia, preterm birth, and gestational diabetes), and because these morbidities may correlate with perinatal depression, inflammation may be a common physiological pathway that can also help explain perinatal depression. In this paper, we review the theoretical background of inflammation in perinatal depression and then review the literature concerning immune and inflammatory factors in the etiology and course of perinatal depression. We close with recommendations for future studies in this still relatively unexplored area. Identification and understanding of a common pathophysiology between other pregnancy morbidities and perinatal depression would link physical and mental well-being, likely leading to better treatment and prevention. Copyright © 2013 Elsevier Ltd. All rights reserved.
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              From the third month of pregnancy to 1 year postpartum. Prevalence, incidence, recurrence, and new onset of depression. Results from the perinatal depression-research & screening unit study.

              Perinatal depression is a particular challenge to clinicians, and its prevalence estimates are difficult to compare across studies. Furthermore, to our knowledge, there are no studies that systematically assessed the incidence of perinatal depression. The aim of this study is to estimate the prevalence, incidence, recurrence, and new onset of Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, minor and major depression (mMD) in an unselected population of women recruited at the third month of pregnancy and followed up until the 12th month postpartum.
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                Author and article information

                Journal
                applab
                Psychological Medicine
                Psychol. Med.
                Cambridge University Press (CUP)
                0033-2917
                1469-8978
                June 2018
                September 20 2017
                June 2018
                : 48
                : 08
                : 1291-1298
                Article
                10.1017/S0033291717002732
                28929982
                0ca2c715-8afc-40a1-9e00-78c75a328b2a
                © 2018
                History

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