The role of personality dimensions, depressive symptoms and other psychosocial variables in predicting postpartum suicidal ideation: a cohort study.

Suicidability has been associated with neuroticism and psychoticism, but its role during perinatal period has not been analyzed. We explore the association between personality dimensions, depressive symptoms, and other psychosocial variables in postpartum suicidal ideation. A cohort of 1795 healthy Spanish women from the general population was assessed for suicidal ideation (EPDS-Item10) in early postpartum, 8 and 32 weeks postpartum. Sociodemographic, obstetric, and reproductive variables, psychiatric history, social support, stressful life-events during pregnancy, depressive symptoms (EPDS), and the Eysenck's personality dimensions (EPQ-RS) were also assessed at baseline. A major depressive episode (DSM-IV) was confirmed in women with EPDS>10 at follow-up assessments. Descriptive, bivariate, and multivariate analyses were conducted. Adjusted logistic regression analysis was reported as odds ratio (ORs) with 95% confidence intervals (CIs). Seven percent of mothers reported suicidal ideation during the first 8 months postpartum. Sixty-two percent of women with suicidal ideation had a major depressive episode at 8 weeks, and 70% at 32 weeks postpartum. Neuroticism and psychoticism predicted suicidal ideation throughout the first 2 weeks after delivery (OR, 1.03; 95%CI 1.01-1.06; and OR, 1.03; 95%CI 1.01-1.05 respectively). Early postpartum depressive symptoms (OR 1.2; 95%CI 1.11-1.26), personal psychiatric history (OR 2.1; 95%CI 1.33-3.27), and stressful life events during pregnancy (OR 1.88; 95%CI 1.12-3.16) also emerged as predictors of postpartum suicidal ideation. Analysis of women for postpartum suicidal ideation should include not only psychiatric symptoms but also psychosocial assessment (i.e., covering psychiatric history, stressful events, or long-standing personality vulnerabilities) in order to identify those in need of early psychosocial or psychiatric care.

Are women with a history of abuse more vulnerable to perinatal depressive symptoms? A systematic review.

The objective of this paper is to examine the association between maternal lifetime abuse and perinatal depressive symptoms. Papers included in this review were identified through electronic searches of the following databases: Pubmed Medline and Ovid, EMBASE, PsycINFO, and the Cochrane Library. Each database was searched from its start date through 1 September 2011. Keywords such as "postpartum," "perinatal," "prenatal," "depression," "violence," "child abuse," and "partner abuse" were included in the purview of MeSH terms. Studies that examined the association between maternal lifetime abuse and perinatal depression were included. A total of 545 studies were included in the initial screening. Forty-three articles met criteria for inclusion and were incorporated in this review. Quality of articles was evaluated with the Newcastle-Ottawa-Scale (NOS). This systematic review indicates a positive association between maternal lifetime abuse and depressive symptoms in the perinatal period.

PACAP-PAC1R modulates fear extinction via the ventromedial hypothalamus.

Exposure to traumatic stress can lead to fear dysregulation, which has been associated with posttraumatic stress disorder (PTSD). Previous work showed that a polymorphism in the PACAP-PAC1R (pituitary adenylate cyclase-activating polypeptide) system is associated with PTSD risk in women, and PACAP (ADCYAP1)-PAC1R (ADCYAP1R1) are highly expressed in the hypothalamus. Here, we show that female mice subjected to acute stress immobilization (IMO) have fear extinction impairments related to Adcyap1 and Adcyap1r1 mRNA upregulation in the hypothalamus, PACAP-c-Fos downregulation in the Medial Amygdala (MeA), and PACAP-FosB/ΔFosB upregulation in the Ventromedial Hypothalamus dorsomedial part (VMHdm). DREADD-mediated inhibition of MeA neurons projecting to the VMHdm during IMO rescues both PACAP upregulation in VMHdm and the fear extinction impairment. We also found that women with the risk genotype of ADCYAP1R1 rs2267735 polymorphism have impaired fear extinction.

Mood changes after delivery: role of the serotonin transporter gene.

BACKGROUND: Polymorphic variations in the serotonin transporter gene (5-HTT) moderate the depressogenic effects of tryptophan depletion. After childbirth there is a sharp reduction in brain tryptophan availability, thus polymorphic variations in 5-HTT may play a similar role in the post-partum period. AIMS: To study the role of 5-HTT polymorphic variations in mood changes after delivery. METHOD: One thousand, eight hundred and four depression-free Spanish women were studied post-partum. We evaluated depressive symptoms at 2-3 days, 8 weeks and 32 weeks post-partum. We used diagnostic interview to confirm major depression for all probable cases. Based on two polymorphisms of 5-HTT (5-HTTLPR and STin2 VNTR), three genotype combinations were created to reflect different levels of 5-HTT expression. RESULTS: One hundred and seventy-three women (12.7%) experienced major depression during the 32-week post-partum period. Depressive symptoms were associated with the high-expression 5-HTT genotypes in a dose-response fashion at 8 weeks post-partum, but not at 32 weeks. CONCLUSIONS: High-expression 5-HTT genotypes may render women more vulnerable to depressive symptoms after childbirth.

Coping strategies and postpartum depressive symptoms: A structural equation modelling approach.

BACKGROUND: Variables such as the mother's personality, social support, coping strategies and stressful events have been described as risk factors for postpartum depression. Structural Equation Modelling (SEM) analysis was used to examine whether neuroticism, perceived social support, perceived life events, and coping strategies are associated with postpartum depressive symptoms at the 8th and 32nd weeks. METHODS: A total of 1626 pregnant women participated in a longitudinal study. Different evaluations were performed 8 and 32weeks after delivery. Several measures were used: the Edinburgh Postnatal Depression Scale (EPDS), the Diagnostic Interview for Genetic Studies (DIGS), the Eysenck Personality Questionnaire (EPQ-RS), the St. Paul Ramsey life events scale and the Duke-UNC Functional Social Support Questionnaire. The brief COPE scale was used to measure coping strategies. SEM analysis was conducted for all women and in those women with a clinical diagnosis of postpartum depression. RESULTS: Passive coping strategies were associated with postpartum depressive symptoms at both visits (8th and 32nd weeks). Neuroticism was associated with more passive coping strategies and less active coping strategies. Neuroticism and life stress were positively correlated, and social support was negatively correlated with life stress and neuroticism. CONCLUSIONS: Early identification of potential risk for symptomatology of depression postpartum should include assessment of neuroticism, life events, social support and coping strategies.

[Casual diagnosis of Gitelman's syndrome]. / Diagnóstico casual de un síndrome de Gitelman.

Gitelman's syndrome is a renal tubule disease of recessive autosomal inheritance in which the fundamental alteration is found in the distal tubule, specifically at the level of the Na/Cl cotransporter, is sensitive to thiazides, and coded in chromosome 16q. It is characterised by a metabolic alkalosis with normal blood pressure, hypokalaemia, as well as hypomagnesaemia and hypocalciuria, which separate it from Bartter's syndrome. Its diagnosis can be delayed up to the adult age, as patients may remain asymptomatic for long periods of time. The treatment consists of oral supplements of potassium and magnesium, and the use of potassium-sparing diuretics and indomethacin has also been described.

Diagnóstico casual de un síndrome de Gitelman / Casual diagnosis of Gitelman's syndrome

El síndrome de Gitelman es una tubulopatía de herencia autosómica recesiva en el que la alteración fundamental se halla en el túbulo distal, concretamente a nivel del cotransportador Na/Cl, sensible a las tiazidas, codificado en el cromosoma 16q. Cursa con alcalosis metabólica con normotensión, hipopotasemia, así como hipomagnesemia e hipocalciuria que la diferencian del síndrome de Bartter. Su diagnóstico puede demorarse hasta la edad adulta ya que los pacientes pueden mantenerse asintomáticos durante largos períodos de tiempo. El tratamiento consiste en suplementos orales de potasio y magnesio, así como también se ha descrito la utilidad de diuréticos ahorradores de potasio e indometacina (AU)

Gitelman's syndrome is a renal tubule disease of recessive autosomal inheritance in which the fundamental alteration is found in the distal tubule, specifically at the level of the Na/Cl cotransporter, is sensitive to thiazides, and coded in chromosome 16q. It is characterised by a metabolic alkalosis with normal blood pressure, hypokalaemia, as well as hypomagnesaemia and hypocalciuria, which separate it from Bartter's syndrome. Its diagnosis can be delayed up to the adult age, as patients may remain asymptomatic for long periods of time. The treatment consists of oral supplements of potassium and magnesium, and the use of potassium-sparing diuretics and indomethacin has also been described (AU)