Association between fetal interleukin-1 receptor antagonist gene polymorphism and unexplained fetal death - 18/08/11
, Santosh Vardhana, AB b, Kathleen Meagher-Villemure, MD c, Yvan Vial, MD a, P. Hohlfeld, MD a, Steven S. Witkin, PhD b
Reprint requests: Dr Stefan Gerber, Maternity–CHUV, 1011 Lausanne, Switzerland.Abstract |
Objective |
In spite of extensive clinical examinations or autopsies, as many as 15% to 40% of stillbirths remain unexplained. A systemic fetal inflammatory response is an independent risk factor for severe neonatal morbidity, mediated by proinflammatory cytokines. As a major anti-inflammatory cytokine, interleukin-1 receptor antagonist (IL-1ra) plays a crucial role modulating the proinflammatory response. The gene coding for IL-1ra (IL1RN) is polymorphic. We hypothesized that fetal possession of a specific allele, IL-1RN2, associated with increased proinflammatory responses, may increase susceptibility to intrauterine fetal death.
Study design |
Fetal kidney cells were obtained from paraffin blocks of 27 unexplained stillbirths. DNA was isolated and tested for IL-1RN genotypes by polymerase chain reaction. As a control group, DNA from 302 live births was also tested.
Results |
There was an enhanced rate of IL-1RN2 homozygocity, 41%, among unexplained stillbirths compared with the control group, 8.6% (P < .001). Histologic analysis of fetal tissues demonstrated a predominant proinflammatory response in IL-1RN2 homozygote fetuses. Extensive screening (microbiology, maternal serology, placenta histology) did not identify any specific trigger agent.
Conclusion |
There is an association between unexplained stillbirth and fetal homozygous IL1RN2 carriage.
Key words : Stillbirth, Intrauterine death, Inflammation, Interleukin-1receptor antagonist
Plan
| Supported in part by NIH grant HD41676. |
Vol 193 - N° 4
P. 1472-1477 - octobre 2005 Retour au numéro
Article précédent
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