Placenta lesions common in lupus pregnancies with small for gestational age infants
Click Here to Manage Email Alerts
Key takeaways:
- Rates of increased perivillous fibrin deposition were notably higher in SLE pregnancies with SGA vs. without SGA.
- The finding should prompt screening for maternal autoimmune disease.
Among pregnancies in patients with systemic lupus erythematosus, those with small for gestational age infants were significantly more likely to demonstrate increased perivillous fibrin deposition in the placenta, according to data.
“Pregnant women with SLE face an elevated risk of adverse pregnancy outcomes, including miscarriages, preeclampsia, preterm birth and having [intrauterine growth restriction (IUGR)]/[small for gestational age (SGA)] infants,” Rashmi Dhital, MD, of Vanderbilt University Medical Center, and colleagues wrote in Rheumatology. “Available placental studies in SLE patients have primarily focused on those with antiphospholipid antibody positivity, and have noted features of [maternal vascular malperfusion], including extensive infarction, and decidual vasculopathy/thrombosis, as well as increased [perivillous fibrin deposition (PVFD)].
“However, there is an overall lack of data on placental findings on SLE in general, but particularly those correlating with SGA infants, which is a common adverse outcome, affecting up to a quarter of SLE pregnancies,” they added.
To learn more about the placental pathology associated with SGA in SLE, Dhital and colleagues retrospectively analyzed 70 SLE deliveries at the University of California, San Diego, 28 of which had placental analysis available. The researchers compared SLE pregnancies resulting in SGA with those that did not, as well as to matched pregnancies without SLE that still resulted in SGA.
According to the researchers, 75% of the 28 SLE deliveries with placental analysis demonstrated adverse outcomes. Meanwhile, all showed at least one histopathologic abnormality. In addition, all seven SLE placentas that demonstrated increased PVFD resulted in SGA, the researchers wrote.
Important factors that separated the 12 SLE placentas resulting in SGA from the 16 without SGA included small placental disc for gestational age (100% vs. 56%, P = .01) and placental disc infarct (50% vs. 6%, P = .02).
Compared with 36 matched, non-SLE pregnancies with SGA, higher prevalence of increased PVFD was the only distinguishing placental lesion in SLE-associated SGA, according to the researchers.
“The finding of increased PVFD in SLE-associated SGA (58%), a rate notably higher than SLE pregnancies without SGA infants (0%) and SGA cases unrelated to SLE (22%), may indicate a specific mechanism of placental injury leading to SGA in SLE,” Dhital and colleagues wrote. “We propose that the presence of this lesion in the placenta, particularly in the setting of SGA, should warrant a closer look for potential underlying maternal autoimmune disease, such as SLE.
“The poor overall outcome associated with this finding, and the high risk of recurrence, should alert the clinicians of high risk of [adverse pregnancy outcomes] in subsequent pregnancies, which may potentially be mitigated with use of certain therapies,” they added.
Perspective
Back to Top
David A. McLain, MD, MACR, FACP, FRCP
The interaction of pregnancy with immune mediated inflammatory diseases is an area that rheumatologists are often consulted on for expertise. The present study reviewed cases where the placenta was obtained after delivery and sectioned for pathology. There was discovery in some cases of massive perivillous fibrin deposition (MPVFD).
This condition has extensive fibrin deposits in the intervillous space potentially interfering with the exchange function of the trophoblast, and therefore contributing to placental dysfunction. Most placentas contain some perivillous fibrin, increasing with gestational age.
It is suggested that MPVFD should be diagnosed when perivillous fibrinoid material involves 25% or more of the villi. This is a rare condition. It has been proposed that women with severe MPVFD in the placenta more often have a history of autoimmune disease, especially primary antiphospholipid syndrome (PAPS). MPVFD in the placenta is associated with an increased risk for intrauterine growth retardation, intrauterine fetal death and preterm birth. The recurrence of MPVFD in first-trimester miscarriages is thought to be high (50%), but later in pregnancy it seems to be lower (less than 20%).
This condition has been treated or prevented with low dose aspirin and heparin. However, the increased prevalence of late pregnancy complications in patients with PAPS and a history of early miscarriage suggests that aspirin and heparin therapy does not eradicate the underlying pathological process, but merely reduces the severity, allowing the pregnancy to proceed to delivery.
Collapse
Read more about
Click Here to Manage Email Alerts