While the occurrence of HLA sharing, cytotoxic/FcR-blocking antibodies and IgG-ACA did not correlate with the outcome of pregnancy, TNF-alpha levels were found to be significantly higher in patients with subsequent miscarriage than in those with successful pregnancy.
The 4 allele was associated with significantly higher concentrations of luteinizing hormone (LH) (means +/- SE) (19.2 +/- 2.2 versus 12.3 +/- 1.3 mIU/ml, P < 0.02) and follicle stimulating hormone (FSH) (13.2 +/- 2.0 versus 10.0 +/- 0.6 mIU/ml, P < 0.05), significantly lower concentrations of prolactin (7.9 +/- 0.8 versus 14.9 +/- 3.5 ng/ml, P < 0.02) and higher parity (1.4 +/- 0.12 versus 0.92 +/- 0.13) and lower miscarriage rates (0.89 +/- 0.1 versus 1.33 +/- 0.24, P < 0.04).
Chorionic villi from the normal pregnancy and the sporadic miscarriage group exhibited co-localized TNF-alpha protein and mRNA in the syncytiotrophoblast and cytotrophoblast.
We have shown that the common missense mutation in the factor V gene, the Leiden mutation, which renders factor Va resistant to cleavage inactivation by activated protein C, predisposes to placental thrombosis and spontaneous miscarriage.
With respect to the HLA-Bw epitopes recognized by NKB1 clones, in 46% of the couples with recurrent miscarriage none of the spouses carried the HLA-Bw4 epitope compared with only 17% of the control couples (P < 0.02).
Since clones of NK-cells are inhibited differently by supertypic epitopes associated with HLA-C and -B alleles we found it of interest to study HLA-C and -Bw polymorphism in 35 couples with recurrent miscarriage and 30 control couples with normal fecundity.
We have investigated the potency of the C677T mutation in the methylene tetrahydrofolate reductase (MTHFR) gene as a genetic risk factor in women with a history of early (</=12 weeks gestation) and/or late (>12 weeks gestation) recurrent miscarriage (three or more consecutive pregnancy losses).Fifty-seven of the total 173 (32.
A corollary of this conclusion is that genotyping for point mutations in the structural gene for MBL would be a much less sensitive means of identifying couples at risk of experiencing recurrent miscarriage.
We conclude that carriers of factor V Leiden who are family members of probands with this mutation have a statistically significant and clinically important risk of late miscarriage or stillbirth.
Levels of TH-1 cytokines were significantly greater and higher in women with recurrent miscarriage compared with controls, whereas levels of TH-2 cytokine interleukin-6 were significantly lower in women with recurrent miscarriage than in controls.
The aim of this study was to investigate the relationship between recurrent miscarriages and factor V Leiden, prothrombin G20210A and C677T methylenetetrahydrofolate reductase (MTHFR) mutations.
Our results suggest that the presence of factor V Leiden and prothrombin G20210A polymorphism, but not MTHFRC677T homozygosity, could be additional risk factors for recurrent miscarriages.
This study was performed to test the hypothesis that an increased prevalence of activated protein C (APC) resistance in women with polycystic ovary syndrome (PCOS) puts them at increased risk of miscarriage and thrombosis.
We investigated the relation between idiopathic recurrent miscarriage and polymorphisms in the gene encoding for the interleukin 1 receptor antagonist, an indigenous modulator of proinflammatory immune response.
In contrast, the frequency of the factor V Leiden allele was similar among (i) women with recurrent early miscarriage (3.3%:60/1808; 58 heterozygotes and one homozygote), (ii) those with late miscarriage (3.9%:16/414; 14 heterozygotes and one homozygote) and (iii) the control group (4.0%:12/300; 12 heterozygotes).
This hypothesis is also supported by the observation that in couples with RSA, the delivery of a live born infant within 5 years from the first episode of miscarriage is negatively associated with the presence of a PGM1*2 allele in the husband.
We investigated the relationship between idiopathic recurrent miscarriage and a polymorphism of the gene encoding endothelial nitric oxide synthase (NOS3).