3Ds: decorin, discordance, and diamniotic dichorionic twins

aullimary Investigation: The cause of discordance in dichorionic diamniotic (DD) twins is still unknown. The authors aimed to compare decorin (DCN) and oxidative/antioxidative state levels between the placentas of discordant and concordant twins. Prospective study of 43 spontaneous DD twin pregnanci...

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Published in:Clinical and experimental obstetrics & gynecology 2017-01, Vol.44 (2), p.239-243
Main Authors: Ozler, S, Oztas, E, Guler, B Gumus, Ersoy, A O, Ergin, M, Uygur, D, Danisman, N
Format: Article
Language:English
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Summary:aullimary Investigation: The cause of discordance in dichorionic diamniotic (DD) twins is still unknown. The authors aimed to compare decorin (DCN) and oxidative/antioxidative state levels between the placentas of discordant and concordant twins. Prospective study of 43 spontaneous DD twin pregnancies included and placentas samples taken from each twin and prepared for homogenization. Total oxidant/antioxidant status levels in placental tissue were determined by automated colorimetric method. Decorin levels were detected by using ELISA method; 23 of these were discordant and 20 of them were concordant. DCN levels in the placentas of the low birth-weight twins were significantly lower than the levels of the placentas of appropriate gestational age twins (p = 0.006). There were no statistically significant differences in total antioxidant status (TAS), total oxidant status (TOS), or arylesterase (ARES) levels in discordant (p = 0.631, p = 0.370, and p = 0.079, respectively) and in the placental DCN, TAS, TOS, or ARES levels of the concordant twins (p = 0.407, p = 0.035, p = 0.194, and p = 0.979, respectively). When the authors compared the twins of similar birth weight, the DCN, TAS, and TOS levels were significantly lower in the discordant twins (p < 0.001, p < 0.001, and p = 0.002, respectively). Decreased levels of DCN in discordant twin fetuses compared to the same birth weight-concordant twins shows that it contributes to disease pathogenesis.
ISSN:0390-6663
2709-0094
DOI:10.12891/ceog3378.2017