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Selective Serotonin-Reuptake Inhibitors and
Risk of Pulmonary Hypertension of the Newborn

New England Journal of Medicine
February 9, 2006

Researchers have expressed the opinion that SSRIs may cause PPHN because the lung acts as a reservoir for antidepressant drugs; and, in fact, substantial accumulation of SSRIs within the lungs has been reported.  In addition to this, serotonin has vaso-constrictive properties that increase pulmonary vascular resistance, and at the same time has mitogenic and comitogenic effects on pulmonary smooth-muscle cells.  Therefore, higher levels of serotonin circulating within the growing fetus and the accumulation of serotonin within the fetus’s lungs may result in the proliferation of smooth-muscle cells that is characteristic of PPHN.  Alternatively or perhaps, in addition, SSRIs have an inhibitory effect on the synthesis of nitric oxide, a vasodilator that may have a role in the regulation of vascular tone and reactivity both in utero and during postnatal life.

Irving Kirsh told 60 Minutes that the difference between the perceived benefit of a placebo compared with that of an antidepressant is minimal for most.

Less severe complications occur in 20 to 30 percent of all newborns with prenatal exposure to SSRIs late in the pregnancy.  These complications include the following:

Mild Respiratory Distress  

Transient tachypnea

A condition that occurs when there is extra fluid in the lungs, or the fluid in the lungs is absorbed too slowly. As a result, it is more difficult for the baby to take in oxygen properly, and the baby breathes faster and harder in order to compensate.

Failure to cry  


The bluish coloration of the skin due to the presence of de-oxygenated hemoglobin in blood vessels near the skin surface suggesting a circulatory or ventilatory problem.

According to researchers, it is possible that these respiratory problems represent the less severe end of the spectrum in a range of outcomes consistent with PPHN.


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