Inflammation May Explain Antidepressants’ Link to Preterm Birth


Overview: Prozac (fluoxetine), a common antidepressant, causes an inflammatory response in the amniotic sac. This finding may shed light on the underlying factors why women taking SSRI antidepressants have an increased risk of premature birth.

sauce: Yell

A Yale University study found that exposure to Prozac, a common antidepressant, triggered an inflammatory response in the human fetal membrane, also known as the amniotic sac.

This effect may reveal an underlying factor in the known increased risk of preterm birth in people who use antidepressants during pregnancy, and potential therapeutic targets to reduce that risk. there is.

Findings will be announced on December 13th. Journal of Reproductive Immunology.

A previous study found that 13% of pregnant women use antidepressants during pregnancy. However, research has shown that a common type of antidepressant medication known as a serotonin reuptake inhibitor (SRI) can have a range of adverse effects on the fetus and pregnancy.

The strongest evidence shows that pregnant women’s membranes rupture too early, increasing the risk of subsequent premature birth.

Pregnant women with mental illness therefore face the difficult decision of whether to stop treatment.

“It’s difficult for a pregnant person to suddenly stop taking necessary medications,” said Vicky Abrahams, professor of obstetrics, gynecology, and reproductive sciences at Yale Medical School.

“If we can identify ways to prevent adverse pregnancy outcomes, we can reduce the risk of SRI treatment.”

Rupture of the membranes refers to the rupture of the amniotic sac, a sign that labor has begun or is about to begin. When it occurs before the pregnancy reaches full term, it is known as premature rupture of the membranes.

“Too early can trigger premature birth. We know that prematurity is really harmful to the baby and can have long-term effects on the health of the child later in life,” said Abrahams. .

Inflammation of the fetal membranes (the amniotic sac that encloses the fetus and amniotic fluid) is thought to contribute to premature rupture of the membranes. To determine whether inflammation played a role in her SRI’s adverse effects on pregnancy, Abrahams and her colleagues analyzed the effects of Prozac, also known as fluoxetine, on fetal membranes.

For this study, researchers used samples of human fetal membrane tissue donated to the Yale Reproductive Sciences Biobank and collected from uncomplicated pregnancies delivered by caesarean section. They exposed several tissue samples to Prozac and compared them to samples not exposed to the drug.

They found that Prozac increased the activity levels of a molecule called p38-MAPK, which mediates inflammation. The molecule then caused an increase in interleukin-6, a small protein called a cytokine that promotes inflammation.

The researchers then analyzed fetal membrane samples taken from people who used Prozac during pregnancy and compared them with samples from people who didn’t use antidepressants, and found that they also had elevated levels of active p38-MAPK. I discovered that you are

A previous study found that 13% of pregnant women use antidepressants during pregnancy.Image is in public domain

The findings reveal potential targets for therapy.

“There is evidence that targeting inflammatory cytokines may be an option in other disease models,” said Abrahams.

“People with lupus, for example, are at increased risk of adversely affecting fertility, and clinical trials are underway to treat these patients with antibodies that target specific cytokines. there may be.”

Ultimately, the study reveals signaling pathways that should be further investigated, which may provide even better therapeutic targets, she added.

Going forward, Abrahams will investigate how SRIs like Prozac act on fetal membranes to elevate p38-MAPK, how other SRIs affect fetal membranes, and how other types of antidepressants We are interested in clarifying whether there is a similar effect in

But for now, Abrahams said, knowing that SRIs can cause inflammation in fetal membranes can help decision-making and clinical management.

“This gives doctors and patients more information,” she said. “And it helps them make more informed choices.”

See also

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About this psychopharmacology and pregnancy research news

author: mallory locklear
sauce: Yell
contact: Mallory Locklear – Yale
image: image is public domain

Original research: open access.
“The serotonin reuptake inhibitor fluoxetine induces human fetal membrane aseptic inflammation via p38 MAPK activation.” Veronica A Fabrizio et al. Journal of Reproductive Immunology


Overview

The serotonin reuptake inhibitor fluoxetine induces sterile inflammation of human fetal membranes via p38 MAPK activation

Serotonin reuptake inhibitors (SRIs) are often used as first-line therapy for depression and other psychiatric disorders. Her use of SRIs during pregnancy has been associated with premature rupture of membranes (PPROM) and subsequent preterm birth.

The aim of this study was to investigate the mechanisms responsible for SRI-associated PPROM. Putative mechanisms underlying PPROM include fetal membrane (FM) inflammation, increased apoptosis, and/or accelerated senescence, the latter of which may be reversed by statins.

Human FM explants from normal delivery without delivery, infection, or antidepressant use were treated with or without SRIs, fluoxetine (FLX) alone, or with p38 MAPK inhibitors or statins, simvastatin, or treated in the presence of rosuvastatin. FMs were also collected from either her FLX-naive or FLX-exposed woman during pregnancy.

FLX significantly increased FM p38 MAPK activity and inflammatory IL-6 secretion. Inhibition of p38 MAPK decreased FM IL-6 secretion in response to FLX. Statins did not reduce SRI-induced FM IL-6 production.

FMs of women exposed to FLX during pregnancy had elevated levels of p38 MAPK activity compared with matched unexposed women. FMs exposed to FLX showed no signs of increased apoptosis and/or accelerated senescence.

These results demonstrate that the SRI, FLX, induces sterile FM inflammation through activation of the p38 MAPK pathway during pregnancy without apoptosis and senescence.

These findings may provide better information for clinicians and patients when weighing the risks and benefits of SRI antidepressant treatment during pregnancy.



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