COMMENT
We found the evidence supporting
postfertilization effects for OCs in
the prevention of clinically recognized
pregnancy to range from poor
(level III) to very good (level II.2).
Specifically, evidence based on alterations
in endometrial biochemistry
and histology (level III), evidence
based on endometrial
thickness and endometrial receptivity
from research studying in vitro
fertilization (level II.2), and evidence
based on endometrial integrins
(level II.3) all support the possibility
of peri-implantation or
postimplantation effects. Furthermore,
evidence based on ectopic-tointrauterine
risk ratios from multiple
case-control studies (level II.2)
supports the possibility of postfertilization
preimplantation, periimplantation,
or postimplantation effects.
However, we could identify few
data that would assist in quantifying
these postfertilization effects. It
seems likely that for perfect use of
COCs, postfertilization mechanisms
would be likely to have a small
but not negligible role. For POPs,
COCs with lower doses of estrogen,
and imperfect use of any OCs,
postfertilization effects are likely
to have an increased role. In any
case, the medical literature does not
support the hypothesis that postfertilization
effects of OCs do not
exist.