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Infants exposed to selective antidepressants (SADs) in utero are at risk to develop poor neonatal adaptation (PNA) postpartum. As symptoms are non-specific and the aetiology of PNA is unknown, the diagnostic process is hampered. We hypothesised that the serotonin metabolism plays a role in the aetiology of PNA.
In this controlled study, infants admitted postpartum from February 2012 to August 2013 were included and followed for 3 days. Infants exposed to SADs during at least the last 2 weeks of fetal life were included in the patient group (n=63). Infants not exposed to psychotropic medication and admitted postpartum for another reason were included in the control group (n=126). The neonatal urinary 5-hydroxyindoleacetid acid (5-HIAA) levels of SAD-exposed infants who developed PNA, SAD-exposed infants who did not develop PNA and control infants were compared.
The course of the 5-HIAA levels over the first 3 days postpartum differed between infants with and without PNA (p≤0.001) with higher 5-HIAA levels in infants with PNA on day 1 (2.42 mmol/mol, p=0.001). Presence of maternal psychological distress modified this relationship.
A transient disturbance of the neonatal serotonergic system may play a role in the aetiology of PNA. Other factors, including the presence of maternal psychological distress, also seem to play a role.
Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis.
To evaluate the effects of antidepressant treatment compared with usual care in an effectiveness study.
In a multicentre randomised controlled trial, 2177 myocardial infarction patients were evaluated for ICD–10 depression and randomised to intervention (n=209) or care as usual (n=122). Both arms were evaluated at 18 months post-myocardial infarction for long-term depression status and new cardiac events.
No differences were observed between intervention and control groups in mean scores on the Beck Depression Inventory (11.0, s.d.=7.5 v. 10.2, s.d.=5.l, P=0.45) or presence of ICD-10 depression (30.5 v. 32.1%, P=0.68). The cardiac event rate was 14% among the intervention group and 13% among controls (OR=1.07, 95% CI 0.57-2.00).
Antidepressant treatment did not alter long-term depression post-myocardial infarction status or improve cardiac prognosis.
As depression is a considerable risk factor for an unfavourable course of myocardial infarction (MI), antidepressant treatment of post-MI depression and, inherent to MI status, polypharmacy has become an important issue.
The present study is the first to evaluate cognitive side effects of fluoxetine, as part of a placebo-controlled double-blind trial, in patients with post-first MI depression.
Cognitive performance of 54 depressed patients post first-MI, treated with fluoxetine or placebo was compared. Cognitive performance was tested before and after 9 weeks of treatment using the Visual Verbal Learning Test, Concept Shifting Task, Stroop Colour-Word Test and Letter-Digit-Substitution Test.
The median number of cardiovascular drugs taken by MI patients was 4.9. There were no differences between the fluoxetine and the placebo group on cognitive performance.
In sum, there were no negative side effects of fluoxetine compared with placebo on cognition in depressed MI patients, simultaneously treated with cardiac drugs.
In the present paper the association of stress-induced cortisol with memory impairment is discussed
An experiment is described in which an attempt is made to block stress-induced cortisol by lowering 5-HT neurotransmission by means of acute tryptophan depletion (ATD). Forty-five healthy control subjects participated in the experiment.
Stress-induced peak cortisol and immediate memory performance were negatively associated. ATD tended to block stress-induced cortisol response. ATD also blocked the association between peak cortisol response and memory impairment.
Stress-induced cortisol and its association with memory impairment is mediated at least partially by serotonin.
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