PubMed · 6013713
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G Rieben. 1966-03-31. [Clinical demonstrations].. https://pubmed.ncbi.nlm.nih.gov/6013713/
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Increased parental Human Leukocyte Antigen (HLA) sharing has been repeatedly reported in recurrent spontaneous abortions (RSA). Parental HLA sharing increases the chance of feto-maternal histocompatibility and potentially affects maternal allo-recognition of the fetus. However, strong linkage disequilibrium across the whole Major Histocompatibility Complex (MHC) region makes it difficult to interpret parental HLA sharing conclusively. It is not known whether the shared HLA gene as such or an unknown gene(s) in linkage disequilibrium or a combination of several loci are causing the disease. Interestingly, in mouse and rat MHC-linked, recessive genes are known to control the reproduction, development and growth of the fetus. Human analogs have not been identified. Compared to HLA genes, MHC Class III has been studied much less in RSA. However, there are some observations of an increased number of unexpressed complement C4 alleles in RSA spouses. Complement C4 genes are located in a chromosomal region characterized by extremely high gene density and frequent gene rearrangements. C4 "null" alleles can act as markers of gene rearrangements in Class III unfavorable for pregnancy outcome. Many of the novel genes located in this region by sequencing serve as new candidates for RSA, since they have housekeeping functions and some of them are highly expressed in human reproductive organs.
We report on a female carrier of der(15) t(Y;15)(q12;p13) who had two pregnancy losses with trisomy 15 and one with tetraploidy. Molecular analysis showed that both non-disjunction events resulting in the trisomy 15 pregnancies occurred in maternal meiosis I. This finding raises the possibility that there may be an increased risk for trisomy 15 in some carriers of unbalanced t(Y;15) which, if followed by trisomic zygote rescue, may lead to uniparental disomy (UPD).
PURPOSE: The aim of this study was to investigate the effect of thromboprophylactic therapy on fetal and maternal Doppler flow parameters in pregnant women with severe complications in previous pregnancies and evidence of acquired or congenital thrombophilia in the current pregnancy. METHODS: Sixty-five patients with a history of recurrent abortions, intrauterine fetal death, intrauterine growth restriction (IUGR), and severe early-onset preeclampsia were tested for the presence of acquired or congenital thrombophilia. Those with positive findings were prescribed low-dose aspirin plus low-molecular-weight heparin (LMWH) (enoxaparin); the remainder received low-dose aspirin only. A Doppler flow study was performed before and after treatment and in the third trimester of pregnancy. RESULTS: Of the 65 pregnancies, four ended in spontaneous abortion and were excluded from the analysis. Of the 61 women with completed pregnancies, 37 (61%) had evidence of acquired or congenital thrombophilia: 22 (36%) protein S deficiency; 1 (2%) protein C deficiency; 2 (3%) activated protein C resistance (APC-R); 2 (3%) IgG for antiphospholipid antibodies; 1 (2%) circulating anticoagulant; and 9 (15%) a combined defect. This group showed a significant decrease in mean uterine artery pulsatility index (PI) before and after treatment (1.32+/-0.36 vs. 1.04+/-0.23, P=.006), whereas the remaining 24 patients treated with low-dose aspirin only had nonsignificant changes. Pearson's correlation test yielded no correlations of the pregnancy outcome parameters with Doppler flow values in the umbilical or uterine arteries. CONCLUSIONS: Thromboprophylactic therapy transiently improves maternal circulation parameters in patients with thrombophilia at risk of fetal loss and other severe complications of pregnancy, but not in correlation with their pregnancy outcome. Therefore, Doppler examination of maternofetal circulation in the second trimester is not predictive of pregnancy outcome.