Elevated amniotic fluid interleukin-6 levels at genetic amniocentesis predict subsequent pregnancy loss,☆☆,,★★

Presented at the Sixteenth Annual Meeting of the Society of Perinatal Obstetricians, Kamuela, Hawaii, February 4-10, 1996.
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Abstract

OBJECTIVE: Our purpose was to determine the proportion of pregnancy loss after genetic amniocentesis that is related to preexisting subclinical intrauterine inflammation. STUDY DESIGN: We accessed our bank of stored second-trimester amniotic fluid and maternal serum samples obtained from women undergoing genetic amniocentesis at our institution from 1988 to 1995 (N = 11,971). Interleukin-6 levels were measured by enzyme-linked immunosorbent assay in samples from every case resulting in spontaneous postprocedure loss (excluding fetal aneuploidy and anomalies) within 30 days after the procedure (n = 66) and from 66 normal control women delivered at term and matched for year of test, gestational age, maternal age, and indication for amniocentesis. RESULTS: Mean maternal serum interleukin-6 levels were the same in each group (0.02 ± 0.07 ng/ml for cases and 0.06 ± 0.25 ng/ml for controls, p = 0.45). Mean amniotic fluid interleukin-6 levels were higher in cases (4.0 ± 13.1 ng/ml) than in controls (0.5 ± 0.7 ng/ml, p = 0.04). The higher mean amniotic fluid interleukin-6 levels in the cases resulted from the inclusion of eight very high values (3 SD or 2.5 ng/ml). When these samples were excluded, the means and range of values were the same in each group (0.4 ± 0.4 ng/ml for cases and 0.5 ± 0.7 ng/ml for controls, p = 0.58). Twelve percent (8/66) of the cases and 3% (2/66) of the controls had amniotic fluid interleukin-6 levels 2.5 ng/ml (p = 0.048, odds ratio 4.1, 95% confidence interval 1.0 to 31.2). Although the overall correlation between maternal serum and amniotic fluid interleukin-6 levels was good (r = 0.50, p < 0.002), only one of the eight cases would have been identified by a maternal serum interleukin-6 level 3 SD above the mean (0.8 ng/ml). CONCLUSION: Analysis of our complete unselected group of postamniocentesis pregnancy losses indicates that up to 12% may result from preexisting subclinical intrauterine inflammation. This inflammation is most likely localized and may not be identified by a maternal serum interleukin-6 level before the procedure. (Am J Obstet Gynecol 1996;175:830-3.)

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MATERIAL AND METHODS

We accessed our bank of stored second-trimester amniotic fluid and maternal serum obtained from all women undergoing genetic amniocentesis at our institution from 1988 to 1995 (N = 11,971). All amniocenteses were performed by an experienced operator using a 22-gauge spinal needle and ultrasonographic guidance. All maternal serum was obtained just before the procedure as part of a larger, institutional review board - approved study of the multiple marker screening test. Every sample was stored

RESULTS

The overall unexplained postamniocentesis pregnancy loss rate was 0.55% (66/11,971). The mean maternal serum IL-6 levels were similar in cases and controls (0.02 ± 0.07 ng/ml in cases and 0.06 ± 0.25 ng/ml in controls, p = 0.45). However, mean amniotic fluid IL-6 levels were higher in cases (4.0 ± 13.1 ng/ml in cases and 0.5 ± 0.7 ng/ml in controls, p = 0.04). The highest amniotic fluid IL-6 levels tended to occur in cases with the earliest loss (<7 days, 8.9 ± 19.6 ng/ml; 7 to 13 days, 4.5 ±

COMMENT

In the >30 years since second-trimester genetic amniocentesis was first described, numerous innovations in technique have improved the safety of the procedure. The procedure-related pregnancy loss rate is generally quoted as 0.5%, the same incidence observed in our study. Although low, this persistent miscarriage rate is frustrating to many clinicians who use the safest techniques and yet cannot seem to avoid this occasional complication.

One explanation for postamniocentesis pregnancy loss is

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From the Center for Obstetric Research, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology,aand the Department of Nutrition Sciences,bUniversity of Alabama at Birmingham.

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Supported in part by Agency for Health Care Policy Research contract No. 282-92-0055.

Reprint requests: Katharine D. Wenstrom, MD, University of Alabama at Birmingham, Department of Obstetrics and Gynecology, 618 South 20th St., UAB Station, Birmingham, AL 35233-7333.

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