Altered expression of TCR-CD3zeta induced by sera from women with preeclampsia.

OBJECTIVE: To investigate TCR-CD3zeta expression by cultured T lymphocytes exposed to midtrimester sera from pregnant women in whom preeclampsia developed at term compared with normotensive pregnant control subjects. STUDY DESIGN: Sera obtained at 24 to 28 weeks' gestation from 16 nulliparous women in whom preeclampsia developed at term and from 32 gestational age-matched control subjects without preeclampsia were evaluated for TCR-CD3zeta chain expression with use of Jurkat cells. Subsets of serum samples from 6 women with preeclampsia and 6 control subjects were then evaluated for their ability to induce apoptosis and to suppress interleukin-2 production. Groups were compared by use of the Kruskal-Wallis test, and P <.05 was considered significant. RESULTS: TCR-CD3zeta chain expression in cultured T lymphocytes was suppressed in approximately 60% of untreated control subjects after incubation with sera from normotensive pregnant women compared with 30% after incubation with sera from women with preeclampsia (P <.001). T-cell apoptosis was significantly higher after incubation with sera from normotensive control subjects, as was the expression of the proapoptotic regulator Bax, compared with sera from women with preeclampsia. Interleukin-2 levels were higher in T cells incubated with sera from women in whom preeclampsia later developed compared with sera from normotensive pregnant women (27.7 ng/mL versus 72.5 ng/mL; P <.001). CONCLUSIONS: Nulliparous women in whom preeclampsia developed did not suppress TCR-CD3zeta levels to the extent of normotensive control subjects, which may be linked to decreased lymphocyte apoptosis. This occurs remotely from the manifestation of clinical disease and suggests a deficiency in a serum factor in preeclampsia that may induce T cell zeta chain suppression in normal pregnancy.

Fetal splenic rupture following transfusion.

BACKGROUND: Splenic rupture in the newborn is a rare complication in erythroblastosis fetalis. There are no reports of splenic rupture in the fetus affected by hemolytic disease of the newborn. CASE: A 41-year-old gravida 3, para 2-0-0-2 with severe rhesus alloimmunization was managed with serial intrauterine transfusions resulting in fetal death after the fourth procedure. Autopsy findings revealed intra-abdominal clotted blood and splenic capsular defects consistent with splenic rupture. CONCLUSION: Fetal splenic rupture might occur in hemolytic disease of the newborn associated with splenomegaly. Acute hemodynamic changes with increased intra-abdominal pressure from intrauterine transfusion might precipitate splenic rupture. (Obstet Gynecol 2001;97:824-5.

Sonographic methods to detect fetal anemia in red blood cell alloimmunization.

Published reports, case studies, and articles from the English language regarding ultrasonographic detection of fetal anemia in red blood cell alloimmunization were obtained from a MEDLINE search from 1966 to November 1999 using the keywords Rh disease, hemolytic disease of the newborn, ultrasound, and Doppler flow studies and combinations thereof. All articles were cross-referenced. Ultrasound techniques including early findings associated with immune hydrops fetalis, multiple morphologic ultrasound markers, and Doppler flow studies that have been used to detect fetal anemia are reviewed and critically evaluated. Noninvasive sonographic techniques may reduce the number of invasive procedures that traditionally are used to follow fetuses at risk for anemia and decrease the associated risks from these procedures.