Alloimmune Causes of Recurrent Pregnancy Loss

Porter, T. Flint; Scott, James R.

doi:10.1055/s-2000-13729

Cited by 29 publications

(19 citation statements)

References 53 publications

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“…5,6 Studies suggest that immune dysfunction underlies a proportion of RM. 7,8 This is evidenced by increased risk in women with some autoimmune diseases, including antiphospholipid syndrome. 9 In addition, maternal-paternal immunogenetic relationships appear to influence pregnancy outcomes, 10,11 with a beneficial effect of disparity in human leukocyte antigen (HLA) genes in successful pregnancies, and a number of studies showing that excess HLA-sharing in a couple may be a risk factor for RM.…”

Section: Introductionmentioning

confidence: 99%

Microchimerism in recurrent miscarriage

et al. 2014

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Maternal-fetal cell exchange during pregnancy results in acquisition of microchimerism, which can durably persist in both recipients. Naturally acquired microchimerism may impact maternal-fetal interaction in pregnancy. We conducted studies to ask whether microchimerism that a woman acquired from her own mother is detectable before or during pregnancy in women with recurrent miscarriage. Fetal microchimerism was also assayed. Women with primary idiopathic recurrent miscarriage (n523) and controls (n531) were studied. Genotyping was conducted for probands, their mothers and the fetus, a non-shared polymorphism identified and quantitative polymerase chain reaction performed to measure microchimerismin peripheral blood mononuclear cells. Preconception comparisons were made between recurrent miscarriage subjects and controls, using logistic regression and Wilcoxon rank sum. Longitudinal microchimerism in subsequent pregnancies of recurrent miscarriage subjects was described. There was a trend toward lower preconception detection of microchimerism in recurrent miscarriage versus controls, 6% vs. 19% (1/16 vs. 6/31, P50.2). During pregnancy, 3/11 (27%) of recurrent miscarriage subjects who went on to have a birth had detection of microchimerism from their own mother, whereas neither of two subjects who went on to miscarry had detection (0/2). This initial data suggest that microchimerism from a woman's own mother, while detectable in women with recurrent miscarriage, may differ from controls and according to subsequent pregnancy outcome. Further studies are needed to determine the cell types, quantities and any potential functional role of microchimerism in recurrent miscarriage.

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Section: Introductionmentioning

confidence: 99%

Microchimerism in recurrent miscarriage

et al. 2014

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“…Results of multiple studies have failed to show benefit in improving pregnancy outcomes in patients with RPL [132][133][134]. One randomized study noted no difference in birth outcomes of patients taking IVIG versus placebo [135].…”

Section: So How Could This Data Impact Treatment?mentioning

confidence: 99%

Immunogenetic contributions to recurrent pregnancy loss

Grimstad

Krieg

2016

J Assist Reprod Genet

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While sporadic pregnancy loss is common, occurring in 15 % of pregnancies, recurrent pregnancy loss (RPL) impacts approximately 5 % of couples. Though multiple causes are known (including structural, hormonal, infectious, autoimmune, and thrombophilic causes), after evaluation, roughly half of all cases remain unexplained. The idiopathic RPL cases pose a challenging therapeutic dilemma in addition to incurring much physical and emotional morbidity. Immunogenetic causes have been postulated to contribute to these cases of RPL. Natural Killer cell, T cell expression pattern changes in the endometrium have both been shown in patients with RPL. Human leukocyte antigen (HLA) and cytokine allelic variations have also been studied as etiologies for RPL. Some of the results have been promising, however the studies are small and have not yet put forth outcomes that would change our current diagnosis and management of RPL. Larger database studies are needed with stricter control criteria before reasonable conclusions can be drawn.

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“…Thus, it can be speculated that normal pregnancy is built on maternal immune response to paternally derived fetal antigens. If there is insufficient or no maternal alloimmune response to these fetal antigens, pregnancy loss can be anticipated [4]. This hypothesis gives rise to therapeutic strategies aiming at immunizing RSA patients with their husbands' or partner's leucocytes [5].…”

Section: Introductionmentioning

confidence: 99%