Interpretation
Uterine myomas during pregnancy increased the risk of PTB, which is consistent with findings of recent studies.1,2,8,9 A previous retrospective cohort study found that uterine myomas during pregnancy significantly increased PTB before 37 weeks (aOR, 1.5; 95% CI, 1.3–1.8) and before 34 weeks (aOR, 1.4; 95% CI, 1.0–1.8).1 However, another retrospective cohort study, in which the prevalence of uterine myomas was 1.5%, and the risk estimates were based on only 183 women with uterine myomas, showed no such association.17 In contrast, the present study was based on a sample of 5,354 women with uterine myomas (uterine myomas prevalence of 6%), which is comparable to the composition of recent studies.1,2 Overall, these findings support the hypothesis that uterine myomas during pregnancy increase the risk of PTB.
The risk of pPROM in the myoma group was greater than that in the control group. Previous studies on this association produced conflicting results.2,5–8,17 One retrospective cohort study reported higher incidence of pPROM (aOR, 1.3; 95% CI, 1.0–1.7)1; our findings are consistent with those of that study. Because pPROM precedes 40–50% of PTB cases,27,28 it is also likely to induce PTB in women with uterine myomas. Because the rate of neonatal mortality, and morbidity associated with PTB is higher in groups affected by pPROM than in any other subgroup of PTB,28 pPROM is likely to increase the risk of adverse neonatal outcomes in women with uterine myomas. These findings suggest that obstetricians should communicate the risk of pPROM and PTB to pregnant women with uterine myomas.
Compared to the control group, we found no increased risk of II in the myoma group; additionally, II did not increase the risk of PTB, or pPROM in the myoma group. No study to-date has shown any association between uterine myomas and increased risk of II in pregnancy. Previous studies have shown II to be a major risk factor for PTB13 and pPROM prior to labor.27 Moreover, microbiological studies suggested that II might account for 25–40% of PTB cases, while approximately 70% of pPROM cases were associated with II.13 The present study showed that II was a significant risk factor of PTB, and pPROM in the control group, but not in the myoma group. Although the sample size with II was small, and there were ambiguities regarding the classification and diagnosis of II owing to confusion of clinical characteristics, biomarkers, and pathological findings,29 the present study was the first large cohort analysis to evaluate the association between uterine myomas during pregnancy and II.
We found that the risk of GH was greater in the myoma group than in the control group. Other evidence on this association is conflicting,2,5–8,17 and the etiology of GH in women with uterine myomas is unknown. Although GH is a risk factor for PTB, the underlying mechanism of its effect on PTB remains unclear, as this study did not evaluate the mechanism of PTB. Concurrently, while we defined GH as only elevated maternal blood pressure, we did not account for hypertensive disorders of pregnancy (HDP) in the present analysis, because subtypes of HDP differ in characteristics,21,30 and extraction of HDP in the present data set with lacking laboratory data may lead to inaccurate analysis. Because of these unclarified issues, future studies should consider the specific mechanisms of PTB and differentiate between GH and HDP. Nevertheless, our findings suggested that maternal complications such as GH might be risk factors for PTB in women with uterine myomas.