Repeated Spontaneous Abortion. Cooperative Effects of ADA and ACP1 Genetic Polymorphisms
Article first published online: 25 APR 2007
American Journal of Reproductive Immunology
Volume 58, Issue 1, pages 1–10, July 2007
How to Cite
Nicotra, M., Bottini, N., La Torre, M., Amante, A., Bottini, E. and Gloria-Bottini, F. (2007), Repeated Spontaneous Abortion. Cooperative Effects of ADA and ACP1 Genetic Polymorphisms. American Journal of Reproductive Immunology, 58: 1–10. doi: 10.1111/j.1600-0897.2007.00483.x
- Issue published online: 25 APR 2007
- Article first published online: 25 APR 2007
- Submitted November 15, 2006; revised February 16, 2007; accepted February 19, 2007.
- repeated spontaneous abortion;
- signal transduction
In consideration of the effect of adenosine deaminase (ADA) and ACP1 (a low-molecular-weight protein tyrosine phosphatase) on T-cell receptor activity, we have analysed the joint distribution of these polymorphisms in a sample of women with primary repeated spontaneous abortion (RSA) to search for possible interactive effects on susceptibility to RSA.
Method of study
ACP1 and ADA phenotypes were determined in 170 women with primary RSA in 79 healthy consecutive puerperae and in 160 female newborns from the Caucasian population of Rome and in 357 healthy consecutive puerperae from the Caucasian population of Penne. Chi-square test of independence and three way contingency table analysis by a log-linear model were performed.
Women with low-ADA activity and high-ACP1 activity show the lowest susceptibility to RSA. Women with high-ADA activity and low-ACP1 activity, on the contrary, show the highest susceptibility to RSA and also the highest incidence of auto antibodies and of A blood group incompatibility.
The data are in agreement with those expected on the basis of the effects of ACP1 and ADA genetic variability on T-cell receptor activity and suggest a cooperative effect of the two polymorphic systems in the susceptibility/resistance to repeated spontaneous abortion.