Fetal infection triggers systemic inflammation, preterm labor. ('Hostile Intrauterine Environment').

OSLO - Preterm labor is often triggered by microbial invasion of the fetus and the resulting fetal systemic inflammatory response syndrome, Dr. Roberto Romero said at the 18th European Congress of Perinatal Medicine.

These infections are largely subclinical and occur in patients with premature labor and intact membranes and preterm premature rupture of membranes (PROM), said Dr. Romero, chief of the perinatology research branch, National Institutes of Health, Bethesda, Md.

He and his associates conducted a prospective study in which 41 pregnant women were divided into four groups according to the presence or absence of inflammation in the amniotic cavity, the fetus, both compartments, or neither.

"The duration of pregnancy was related to the state of inflammation in the fetal compartment rather than in the amniotic fluid. Moreover, neonatal complications were more common in fetuses with a systemic inflammation, defined as the presence of an elevated concentration of interleukin-6," he said.

"The clinical implication is that a fetus presenting with premature labor or premature rupture of membranes can no longer be considered healthy and its complications attributed solely to untimely birth. A more accurate description is that many fetuses presenting with premature labor are critically ill and that the onset of labor is a mechanism to exit a hostile in-trauterine environment," Dr. Romero said.

A meeting attendee asked if physicians should stop preterm labor in the context of infection or deliver as soon as possible if there is evidence of fetal inflammation.

Dr. Romero answered that the obstetrician managing the patient with a fetal inflammatory response syndrome (FIRS) has three choices: immediate delivery to remove the fetus from the inflammatory environment; antibiotic treatment with the hope of prolonging pregnancy and reducing the rate of complications as was observed in randomized clinical trials of preterm PROM; and administering agents to downregulate the fetal inflammatory response.