Maternal and neonatal epidemiological features in clinical subtypes of preterm birth

Abstract

Objective This study was designed to characterize and compare the maternal and newborn epidemiological characteristics through analysis of environmental factors, socio-demographic characteristics, and clinical characteristics between the different clinical subtypes of preterm birth (PTB): Idiopathic (PTB-I), premature rupture of the membranes (PTB-PPROM) and medically indicated (PTB-M). The two subtypes PTB-I and PTB-PPROM grouped are called spontaneous preterm births (PTB-S). Methods A retrospective, observational study was conducted in 1.291 preterm non-malformed singleton live-born children to nulliparous and multiparous mother’s in Tucumán-Argentina between 2005 and 2010. Over 50 maternal variables and ten newborn variables were compared between the different clinical subtypes. The comparisons were done to identify heterogeneity between subtypes of preterm birth: (PTB-S) vs. (PTB-M), and within spontaneous subtype: (PTB-I) vs. (PTB-PPROM). In the same way, two conditional logistic multivariate regressions were used to compare the odds ratio (OR) between PTB-S and PTB-M, as well as PTB-I and PTB-PPROM. We matched for maternal age when comparing maternal variables and gestational age when comparing infant variables. Results The PTB-I subtype was characterized by younger mothers of lower socioeconomic status, PTB-PPROM was characterized by environmental factors resulting from inflammatory processes, and PTB-M was characterized by increased maternal or fetal risk pregnancies. Conclusions The main risk factor for PTB-I and PTB-M was having had a prior preterm delivery, however previous spontaneous abortion was not a risk factor, suggesting a reproductive selection mechanism.

Association of candidate gene polymorphisms with clinical subtypes of preterm birth in a Latin American population

“…The etiology of PTB-M is difficult to establish because the determinants of this condition are very heterogeneous and include preeclampsia, fetal distress, small-for-gestational (SGA), and placental abruption( 8 ). Despite the limitations of this clinical subtype, the current study identified that a marker in KCNN3 was associated with PTB-M. KCNN3 is expressed in tissues responsible for maintaining gestation and inducing parturition( 31 ) and is subject to regulation by estrogen( 32 ), providing a feasible biological mechanism for KCNN3 in the etiology of preterm labor( 33 – 34 ).…”

“…Given the heterogeneity observed in PTB, it is helpful to examine these categories separately with regard to etiology, prevention, and intervention( 7 ). However, differences among these preterm birth subtypes have not been fully explored in Latin American populations, and few epidemiological and genetic association studies of clinical subtypes in any population have been completed( 8 – 10 ).…”

Causal models: Specification, fitting, reporting, and interpretation

“…Thus, the effect of previous preterm birth in Bandoli et al's analysis represents a contrast between multiparous women who had a previous preterm birth versus nulliparous women, and multiparous women without a history of previous preterm birth. The latter two types of women have different risks of preterm birth and especially preeclampsia …”

“…The latter two types of women have different risks of preterm birth and especially preeclampsia. [7][8][9][10] Other limitations in the example by Bandoli et al relate to clinical issues and some unexpected causal assumptions. The reference to preterm birth subtypes as "indications" for preterm birth suggests some lack of attention to substantive details.…”

Should phenotype of previous preterm birth influence management of women with short cervix in subsequent pregnancy? Comparison of vaginal progesterone and Arabin pessary

“…An autoimmune/hormonal regulation axis may exist for spontaneous PTL‐IM, whilst pathways implicated in the etiology of PPROM include hematological/coagulation function disorder, collagen metabolism, matrix degradation and local inflammation. Additionally, the dissimilarity of clinical risk factors for PPROM and PTL‐IM suggests that there are different underlying pathophysiological pathways.…”