Konstantinou Ger, Spyropoulou A, Zervas I
1st Department of Psychiatry, Medical School, National and Kapodistrian University of Athens, Eginition Hospital, Athens.
Department of Psychiatry, 251 Hellenic Airforce V. A. General Hospital, Athens, Greece.
Psychiatriki. 2020 Jan-Mar;31(1):47-56. doi: 10.22365/jpsych.2020.311.47.
Postpartum depression is a debilitating mental disorder with a high prevalence, usually related with a past psychiatric history of major depressive disorder, postpartum depression, bipolar disorder, premenstrual syndrome (PMS), and perinatal depressive symptoms during gestation. However, the existing literature does not sufficiently elucidate the pathophysiology of this clinical entity which appears in such a crucial period of woman's life. This review aims to search the available data regarding the involvement of immunological and autoimmune mechanisms in its onset. A literature review was conducted using web-based search engines provided by PubMed (for Medline database) and Google Scholar. Manuscripts in English and Greek language were included for the period 19902017. Nowadays, a large body of evidence indicates that depressive disorders are accompanied by activated neuro-immune, neuro-oxidative and neuro-nitrosative stress (IO&NS) pathways. However, clinical research regarding the biological mechanisms associated with PPD is a tough challenge as pregnancy and puerperium are periods of adaptive changes in pregnant women by definition. Two of the systems that have been studied as potentially contributing to the onset of PPD are: the activation of the Inflammatory Response System (IRS) and the deregulation of the Hypothalamic-PituitaryAdrenal axis (HPA). Controversial data indicate dysregulation of cytokines and other inflammatory agents in patients with PPD, as well as, a close correlation of immune-inflammatory mechanisms and kynurenine pathway. PPD has been closely associated with autoimmune diseases. It is notable that this entity shares many common traits with autoimmune diseases such as the genetic susceptibility, family history, the high correlation with other autoimmune diseases, clinical exacerbations and remissions, women's superiority in prevalence, and the possible re-occurrence during a future pregnancy. These facts suggest that the typical postpartum flare pattern, and other clinical characteristics, point towards an autoimmune etiology for PPD. There are indications that immune-inflammatory and autoimmune mechanisms may be the key to deciphering the complex pathophysiological pathways associated with the onset of PPD. Clinical studies have been insufficient to make clear the causative correlations of the underlying mechanisms involved. Future research could focus on the immune-inflammatory processes associated with the onset of the disease, as well as on potential biomarkers for an early diagnosis and an effective treatment of PPD.
产后抑郁症是一种患病率很高的使人衰弱的精神障碍，通常与既往的重度抑郁症、产后抑郁症、双相情感障碍、经前综合征（PMS）以及孕期围产期抑郁症状的精神病史有关。然而，现有文献并未充分阐明这种出现在女性生命如此关键时期的临床实体的病理生理学。本综述旨在搜索有关免疫和自身免疫机制在其发病过程中所起作用的现有数据。使用由PubMed（用于Medline数据库）和谷歌学术提供的基于网络的搜索引擎进行了文献综述。纳入了1990年至2017年期间的英文和希腊语文献。如今，大量证据表明，抑郁症伴有激活的神经免疫、神经氧化和神经亚硝化应激（IO&NS）途径。然而，由于妊娠和产褥期从定义上讲是孕妇适应性变化的时期，因此关于与产后抑郁症相关的生物学机制的临床研究是一项严峻的挑战。已被研究可能导致产后抑郁症发病的两个系统是：炎症反应系统（IRS）的激活和下丘脑 - 垂体 - 肾上腺轴（HPA）的失调。有争议的数据表明产后抑郁症患者体内细胞因子和其他炎症介质失调，以及免疫炎症机制与犬尿氨酸途径密切相关。产后抑郁症与自身免疫性疾病密切相关。值得注意的是，这个实体与自身免疫性疾病有许多共同特征，如遗传易感性、家族病史、与其他自身免疫性疾病的高度相关性、临床加重和缓解、女性患病率更高以及未来妊娠期间可能复发。这些事实表明，典型的产后发作模式和其他临床特征表明产后抑郁症存在自身免疫病因。有迹象表明，免疫炎症和自身免疫机制可能是解读与产后抑郁症发病相关的复杂病理生理途径的关键。临床研究不足以明确所涉及潜在机制的因果关系。未来的研究可以集中在与该疾病发病相关的免疫炎症过程，以及产后抑郁症早期诊断和有效治疗的潜在生物标志物上。
