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.