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Reprinted with permission from: "Archives of Family Medicine", February 2000, Volume 9 Number 2, Pages 126 - 133, Copyright: March 18, 1999, American Medical Association.
Postfertilization Effects of Oral Contraceptives and Their
Relationship to Informed Consent
Walter L. Larimore, MD; Joseph B. Stanford, MD, MSPH
The primary mechanism of
oral contraceptives is to inhibit ovulation, but this mechanism is not always
operative. When breakthrough ovulation occurs, then secondary mechanisms
operate to prevent clinically recognized pregnancy. These secondary mechanisms
may occur either before or after fertilization. Postfertilization effects would
be problematic for some patients, who may desire information about this
possibility. This article evaluates the available evidence for the
postfertilization effects of oral contraceptives and concludes that good
evidence exists to support the hypothesis that the effectiveness of oral
contraceptives depends to some degree on postfertilization effects. However,
there are insufficient data to quantitate the relative contribution of
postfertilization effects. Despite the lack of quantitative data, the
principles of informed consent suggest that patients who may object to any
postfertilization loss should be made aware of this information so that they
can give fully informed consent for the use of oral contraceptives.
Arch Fam Med.
2000;9:126-133
Oral contraceptives (OCs)
are among the most extensively studied and used medications in the world,1 and are
accessible without a prescription in some countries, although still virtually
unavailable in others. In America, OCs have contributed to an increased
acceptability of birth control,2 although,
for many patients, decisions about contraception still have moral, ethical, and
religious implications.3, 4 For
patients who believe that human life begins at fertilization (conception), a
method of birth control that has the potential of interrupting development
after fertilization (a postfertilization effect) may not be acceptable.5, 6
Postfertilization effects are operative for emergency (postcoital)
contraception (when it is administered too late to prevent ovulation),7, 8
luteolytic agents (ie, RU-486),9 and
intrauterine devices,5 and these
methods therefore are unacceptable to some patients. Although postfertilization
effects have been cited as a secondary mechanism of OCs,10-12 the
evidence for such effects has not been systematically reviewed. The purpose of
this article was to review and grade the available evidence for
postfertilization effects of OCs and discuss the implications for informed
consent, based on the premise that patients to whom postfertilization effects
are important have the right to make decisions based on the best available
evidence.13-15
Our analysis of the
evidence involved a review of the abstracts of all studies of OCs published
since 1970 available on MEDLINE that discussed the commonly used OCs, including
low-dose (<50 µg of estrogen) phasic combined oral contraceptives (COCs),
low-dose monophasic COCs, and progestin-only OCs (progestin-only pills [POPs]).
We also reviewed the patient handouts provided by OC manufacturers and the most
recent editions of several medical textbooks and reference books.
Since there is variability
in the definitions and use of terminology in reproductive medicine, we used the
American Academy of Obstetrics and Gynecology Committee on Ethics' definitions
for fertilization, implantation, embryo, and preembryo.16 Preembryo
is a general term that includes the human developmental stages that occur after
fertilization but prior to the appearance of the primitive streak about 14 days
after fertilization. From that point until the end of the eighth week after
fertilization, the term embryo is used. Implantation is the process
whereby the preembryo attaches to the endometrial lining of the uterus. This
process begins 5 to 7 days after fertilization and may last several days. For
this review, we defined postfertilization effects to include mechanisms
of action that operate after fertilization to prevent a clinically recognized
intrauterine pregnancy. We looked specifically for studies referencing any
postfertilization effects of OCs. When many studies indicated similar findings,
we listed the most recent or most methodologically sound references or other
systematic or general reviews of particular subjects.
The literature discusses several mechanisms for OCs. While
the primary effect of OCs is the inhibition of ovulation via suppression of
pituitary gonadotropin secretion (this mechanism is operative most of the
time),1, 10, 12
secondary effects are implicated at times of breakthrough ovulation to prevent
clinically recognized pregnancy.17, 18 We
classified these secondary effects as occurring either prefertilization or
postfertilization. Secondary prefertilization effects may include alterations
in cervical mucus that limit sperm penetration2, 17-20 and
changes in the endometrium and fallopian tube that may impede normal sperm
transport.2,
17, 18, 21
Breakthrough ovulation rates vary by the form and the dose
of the OC used.2,
10, 12, 18, 22 With
OCs, breakthrough ovulation is more likely with lower doses of estrogen and
with imperfect rather than perfect use.10, 12, 16, 17, 23-25
Perfect use of OCs implies taking them consistently and correctly (ie, in the
correct order, on time, each and every day, and without other medications that
might diminish the effectiveness of OCs). Typical use is described as
the full range of usage patterns for OCs that actually occur in women.1, 11, 12, 18 While
some smaller studies that evaluated small numbers of women for 6 or fewer
cycles have reported breakthrough ovulation rates of near 0, studies that
evaluated women for at least 6 cycles demonstrated ovulation rates ranging from
1.7%25
to 28.6%23
per cycle. For POPs, reported breakthrough ovulation rates range from 33%26 to 65%.20, 27, 28
Obviously, breakthrough ovulation can result in unintended
pregnancy1,
17, 18;
however, the pregnancy rates with typical use vary widely and are often
underestimated.29
Unadjusted analyses of unintended pregnancies while using COCs report rates of
0.1 to 1.0 per 100 woman-years of use in perfect use and 3 per 100 woman-years
in the first year of typical use.1, 10, 12, 17, 18, 20 Most of
these data do not account for elective abortions. One national analysis that
accounted for the underreporting of elective abortions estimated that the
unintended pregnancy rates during the first year of OC use were 4% for
"good compliers," 8% for "poor compliers," and up to 29%
for some users.29 Rates
of pregnancy are higher with POPs than with COCs.1, 17, 18
Unadjusted analyses of pregnancies while taking POPs reported rates of 0.5 to
1.0 per 100 woman-years of perfect use and 3 to 7 per 100 woman-years in the
first year of typical use.1, 10, 12, 17, 18, 20
However, these rates have not been adjusted for elective abortions and are
almost certainly underestimated.29
Progestin-only pills are reported to have potent effects on both cervical mucus
and the endometrium.19-21, 30, 31 While
this has led to speculation that "the principal mode of action is . . . to
make the cervical mucus hostile to the transport of the sperm,"17 animal
model data32
and data on ectopic pregnancy rates (reviewed below) suggest that
postfertilization effects also play a role.
In theory, postfertilization effects of OCs could involve
any 1 or more of the following 3 mechanisms of action: (1) A postfertilization
preimplantation effect would consist of a slower transport of the preembryo
through the fallopian tube, preventing the preembryo from implanting in the
uterus; this could result either in the unrecognized loss of the preembryo or
in an ectopic (tubal) pregnancy if the preembryo had slower tubal transport and
ended up implanting in the fallopian tube. (2) A peri-implantation effect would
be the alteration of the endometrium, such that a preembryo that reached the
uterus was unable to successfully implant into the endometrial lining of the uterus.
(3) A postimplantation effect could result from alteration of the endometrium
not sufficient to prevent implantation but unfavorable for maintenance of the
pregnancy; a preembryo or embryo already implanted in the endometrial lining of
the uterus would be unable to maintain itself long enough to result in a
clinically recognized pregnancy.
Direct evidence of postfertilization preimplantation and
peri-implantation effects would require methods that directly measured the rate
of fertilization and the loss of the preembryo in women taking OCs.
Transcervical tubal washings have been used in women using intrauterine devices
to quantify the rate of ova fertilization33 and
could theoretically be done for women taking OCs. However, there is no proven
method to measure the loss of the preembryo prior to implantation, even though
a number of possible methods have been investigated that involve maternal
hormones that may be produced or altered after fertilization.34-36
Probably the most promising method is the isolation of "early pregnancy
factor."37-39
Direct evidence of a postimplantation effect on the
preembryo or embryo prior to clinically recognized pregnancy would require
measurement with ultrasensitive assays for β–human chorionic gonadotropin
(β-HCG) or other pregnancy-related hormones.40
Although ultrasensitive assays for β-HCG have been done with normally
fertile women not using OCs,41-44 as
well as with women using nonhormonal methods of contraception,45 we
could find no such studies in women using OCs. Despite the lack of these data,
at least 3 lines of evidence have been suggested to support the hypothesis that
1 or more postfertilization effects are operative in at least some women taking
OCs. Using a standard quality of evidence table46 (Table 1), we graded the available evidence.
Endometrial Changes That May Affect Endometrial Receptivity
Oral contraceptives directly affect the endometrium.1, 10, 12, 20, 21 These
effects have been presumed to render the endometrium relatively inhospitable to
implantation or to the maintenance of the preembryo or embryo prior to
clinically recognized pregnancy by producing a predecidual or decidualized
endometrial bed with diminished thickness and with widely spaced, exhausted,
and atrophied glands; by altering the cellular structure of the endometrium,
leading to the production of areas of edema alternating with areas of dense
cellularity18,
20, 21; and by
altering the biochemical and protein composition of the endometrium.47
Although these changes are consistently seen in women taking
OCs, there is currently no direct evidence to link these changes to preembryo
or embryo loss in women taking OCs. However, this hypothesized
postfertilization effect seems to be so well accepted that in many medical articles
and textbooks it has been explicitly listed as the third mechanism of OCs
(after suppressing ovulation and prefertilization effects).1, 10, 17, 18 For
example, the Food and Drug Administration–approved product information for OCs
in the Physicians' Desk Reference states,
Although the primary mechanism of this action is inhibition
of ovulation, other alterations include changes in the cervical mucus, which
increase the difficulty of sperm entry into the uterus, and changes in the
endometrium, which reduce the likelihood of implantation.11
An independent clinical pharmaceutical reference also
contains this assertion.12 We
considered this level III (poor to good) evidence (Table 1).
To assess the clinical significance of an altered endometrium,
it was helpful to examine data that compared endometrial thickness with the
receptivity of the endometrium to preembryos during in vitro fertilization
procedures. Magnetic resonance imaging scans of the uteri of women reveal that
the OC users have endometrial linings that are consistently thinner than the
endometrial linings of nonusers,48-50 up
to 58% thinner.51 Of the
first 4 ultrasound studies published, the first did not find a relationship
between endometrial thickness and in vitro fertilization implantation rates52;
however, subsequent studies noted a trend,53, 54 and one
demonstrated that a decreased thickness of the endometrium decreased the
likelihood of implantation.55 Larger,
more recent, and more technically sophisticated studies56-65 all
concluded that endometrial thickness is related to the functional receptivity
of the endometrium. Furthermore, when the endometrial lining becomes too thin,
then implantation does not occur.56-58, 64, 65 The
minimal endometrial thickness required to maintain a pregnancy in patients
undergoing in vitro fertilization has been reported, ranging from 5 mm55 to 9 mm65 to 13
mm,53
whereas the average endometrial thickness in women taking OCs is 1.1 mm.50 These
data would seem to lend credence to the Food and Drug Administration–approved
statements that " . . . changes in the endometrium . . . reduce the
likelihood of implantation."11 We
considered this level II.2 (good to very good) evidence (Table 1).
Integrin Changes Affecting Fallopial Tube and Endometrial
Receptivity for Implantation
Integrins are a family of cell adhesion molecules that are accepted as markers
of uterine receptivity for implantation.66, 67
Temporal and spatial expression of these endometrial peptides is believed to
contribute to the establishment and maintenance of a cyclical endometrial
receptivity. Three cycle-dependent integrins (α1β1, α4β1,
αVβ3) have been shown to be " . . . coexpressed apparently only
for a brief interval of the cycle that corresponds with the putative window of
maximal uterine receptivity" and " . . . have emerged as reliable
markers of normal fertility."68 Of
these 3, the αVβ3 integrin seems "to be an excellent marker to
study the molecular events leading to the establishment of uterine receptivity
and successful implantation."68, 69 These 3
integrins are conspicuously absent in the endometrium of most patients with
luteal phase deficiency, endometriosis, and unexplained infertility.68
In addition, integrin expression is significantly changed by
OCs. Integrins have been compared using endometrial biopsy specimens from
normally cycling women and women taking OCs. In most OC users, the normal
patterns of expression of the integrins are grossly altered, leading Somkuti et
al68
to conclude that the OC-induced integrin changes observed in the endometrium
have functional significance and provide evidence that reduced endometrial
receptivity does indeed contribute to the contraceptive efficacy of OCs. They
hypothesized that the sex steroids in OCs alter the expression of these
integrins through cytokines and therefore predispose to failure of implantation
or loss of the preembryo or embryo after implantation. We considered this level
II.3 (good) evidence (Table 1).
Integrins have also been identified in the fallopian tube.69 Of
interest, the αV subunit is expressed in the fallopian tube epithelium
throughout the cycle, but the β3 subunit is only upregulated during the
period of endometrial receptivity. Therefore, it has now been postulated that
the normal tubal epithelium also has an implantation window that " . . .
affords the opportunity for trophoblast attachment should a 5-7 day preembryo
be unduly retained in the tube."69 As
discussed earlier, one of the postulated actions of the OCs is a slowing of
tubal peristalsis (via smooth muscle relaxation)70;
therefore, a reduction in tubal peristalsis that is associated with an
upregulation of the αVβ3 integrin in the epithelium of the fallopian
tube could theoretically lead to an increased risk of ectopic pregnancies in
women taking OCs.
If breakthrough ovulation occurs while using the COC, then
to some extent ovarian and blastocyst steroidogenesis could theoretically
"turn on" the endometrium, causing it to normalize prior to
implantation in the ovulatory cycle. However, after discontinuing use of COCs,
it usually takes several cycles for a woman's menstrual flow to approach the
volume of women who have not taken hormonal contraception,71
suggesting that the endometrium is slow to recover from its COC-induced
atrophy. Furthermore, in women who have ovulated secondary to missing 2
low-dose COCs, the endometrium in the luteal phase of the ovulatory cycle has
been found to be nonsecretory.23
Increased Extrauterine Pregnancy to Intrauterine Pregnancy
Ratio
If the action(s) of OCs on the fallopian tube and endometrium were such as to
have no postfertilization effects, then the reduction in the rate of
intrauterine pregnancies in women taking OCs should be proportional to the
reduction in the rate of extrauterine pregnancies in women taking OCs. If the
effect of OCs is to increase the extrauterine-to-intrauterine pregnancy ratio,
this would indicate that one or more postfertilization effects are operating.
All published data that we could review indicated that the ratio of
extrauterine-to-intrauterine pregnancies is increased for women taking OCs and
exceeds that expected among control groups of pregnant women not currently
using OCs. These case-controlled series come from 33 centers in 17 countries
and include more than 2800 cases and controls.72-77 The
odds ratios in these studies ranged from 1.7 (95% confidence interval [CI],
1.1-2.5)72
to 1.8 (95% CI, 0.9-3.4)73 to 4.3
(95% CI, 1.5-12.6)74 to 4.5
(95% CI, 2.1-9.6)75 to 13.9
(95% CI, 1.8-108.3).76 The
letter by Job-Spira et al74 seems
to represent the same data set of 279 cases and controls as the study by Coste
et al.76
The meta-analysis by Mol et al73
includes 2 of the publications,72, 75 but one
of these may include women taking POPs.72
Therefore, of the 5 publications, only 2 allow review of the association of
COCs with ectopic pregnancy.75, 76 These 2
studies from 7 maternity hospitals in Paris, France, and 3 in Sweden involved
484 women with ectopic pregnancies and 289 pregnant controls and suggest that
at least some protection against intrauterine pregnancy is provided via
postfertilization preimplantation effects. We recognize that studies that have
used nonpregnant controls have not shown a risk of increased ectopic pregnancy
for users of COCs. In our review, we restricted our analysis to studies using
pregnant controls, because we concur with researchers73, 76 in this
field that " . . . when considering the situation where a woman became
pregnant during contraceptive use, one should focus on pregnant controls."73
Therefore, COC use seems to be associated with an increased risk of ectopic
implantation or unrecognized loss of preembryos. We considered this level II.2
(good to very good) evidence (Table 1).
Ectopic pregnancy is a particular form of postfertilization
loss that involves substantial risks to the woman, and thus the absolute risk
of ectopic pregnancy for women taking OCs will be of interest to clinicians and
patients. Converting a relative risk of ectopic pregnancy to an absolute risk
has many inherent difficulties that have been reviewed elsewhere.78
Nevertheless, adapting the method suggested by Franks et al78 would
allow one to predict that the ectopic pregnancy rate for women taking OCs would
be the product of 3 factors: (1) the overall pregnancy rate per 1000
woman-years among those taking OCs, (2) the proportion of extrauterine
pregnancies compared with all pregnancies for a comparable control population
not taking OCs, and (3) the relative risk for ectopic pregnancy in women taking
OCs compared with the control population, which may be estimated by the odds
ratio from case-control studies. For factor 1, Potter29
suggests 40 for good compliers and 80 for poor compliers. For factor 2, the
proportion of ectopic pregnancies in the 1990s is estimated to range from 1 in
every 5679
to 6480,
81
pregnancies (0.0156 to 0.0179). A reasonable range for factor 3 would be 1.1 to
13.9, based on the studies discussed above. This model would predict an
absolute risk ranging from 0.7 (40 X 0.0156 X 1.1) to 19.9 (80 X 0.0179 X 13.9)
ectopic pregnancies per 1000 woman-years. We could only find one study, from
Zimbabwe, which reported an absolute risk of ectopic pregnancy in women taking
OCs of 0.582
per 1000 woman-years.
The risk of ectopic pregnancy is higher with POPs, and
ectopic pregnancy has been discussed at length by a number of investigators as
a clinically significant potential complication of POPs.82-84 The
odds ratio of an extrauterine pregnancy for a woman taking a POP (compared with
pregnant controls) was reported in only one study and was 79.1 (95% CI,
8.5-735.1).74
Assuming an overall clinical pregnancy rate of 30 to 70 per 1000 woman-years,
this equates to a predicted absolute risk of 4 to 99 ectopic pregnancies per
1000 woman-years ([30 or 70] X [0.0156 or 0.0179] X [8.5 or 79.1]) in women
taking POPs. This is reasonably concordant with absolute rates of ectopic
pregnancy in women taking POPs, which have been reported to range from about 382, 83, 85 to
about 2084,
86 per
1000 woman-years.
Data from case-controlled series demonstrate that women with
clinically recognized pregnancy are no more or less likely to miscarry based on
whether they were taking an OC after their pregnancy was clinically recognized.87-90
However, the epidemiology, biology, and recognized risk factors of clinically
recognized embryo or fetal loss (spontaneous abortion after clinically
recognized pregnancy) do not seem to apply to early (unrecognized) preembryo or
embryo loss, as the available evidence suggests that the mechanisms of early
establishment and maintenance of pregnancy and later maintenance of pregnancy
are qualitatively and substantially different.90
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-to-intrauterine risk ratios from multiple case-control studies (level
II.2) supports the possibility of postfertilization preimplantation,
peri-implantation, 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.
Despite the evidence, which suggests that postfertilization
effects for OCs are operational at least some of the time, and the fact that a
postfertilization mechanism for OCs is described in the Physicians' Desk
Reference,11
in Drug Facts and Comparisons,12 and in
most standard gynecologic, family practice, nursing, and public health
textbooks, we anecdotally find that few physicians or patients are aware of
this possibility. Therefore, we believe that the potential for
postfertilization effects is probably not routinely presented to patients as part
of their informed consent to use an OC. Furthermore, it is of concern to us
that only one of the many OC patient information handouts we and others5 have
reviewed, including those produced by the OC manufacturers, mentions the
possible postfertilization mechanism, despite the fact that this information is
nearly always included in the professional labeling of these same OCs.
Since there is evidence to support the existence of
postfertilization effects and because it is impossible to know in advance which
patients would find the potential for this effect objectionable, we believe
that the lack of information regarding postfertilization effects in patient
information materials about OCs represents a potential failure to provide
complete informed consent. Furthermore, if this mechanism of an OC violates the
moral requirements of a woman, then failure to disclose this information
seriously jeopardizes her autonomy. If information about the mechanism of an OC
is deliberately withheld or misstated, then an unethical deception occurs.
Failure to disclose information that might lead a patient to choose a different
method of treatment is generally considered to be unethical.12, 13
Therefore, it seems clear to us that failure to inform patients of a possible
postfertilization mechanism of an OC is a failure to provide informed consent.
Many reproductive scientists have defined pregnancy as
occurring at the point of or at some point after implantation.16, 91, 92
However, this definition does not change the fact that some patients, for
personal, scientific, moral, or religious reasons, identify the start of human
life at fertilization. For such patients, a form of contraception that allows
fertilization and then causes loss of the preembryo or embryo may be
unacceptable. Regardless of the personal beliefs of the physician or provider
about the mechanism of OCs, it is important that patients have information
relevant to their own beliefs and value systems.
However, the objective presentation of the potential for
postfertilization effects of OCs may be complex; there are a variety of
potential interpretations of the postfertilization effects depending on which
aspect is emphasized: (1) One could state that OCs may significantly reduce the
absolute risk per woman-year of any possible postfertilization loss in the same
way that they reduce the absolute clinical pregnancy rate.78 For
some women or medical personnel who believe that human life begins at
fertilization, this view might render OCs, even with postfertilization loss,
morally acceptable. (2) One could emphasize that once fertilization has
occurred, OCs may cause at least an occasional postfertilization loss,
regardless of the rate of fertilization. For some women or medical personnel
who believe that human life begins at fertilization, the view that any
postfertilization loss could be attributed to the effects of OCs and therefore
could be considered induced rather than natural may render OCs morally
unacceptable to use, even if the absolute frequency of such an event is very
low.
Medical colleagues have suggested to us that
postfertilization loss attributed to OCs would not need to be included in
informed consent until it is either definitely proven to exist or proven to be
a common event. However, rare but important events are an essential part of
other informed consent discussions in medicine, primarily when the rare
possibility would be judged by the patient to be important. For example,
anesthesia-related deaths are extremely rare for elective surgery (<1:25,000
cases); nevertheless, it is considered appropriate and legally necessary to
discuss this rare possibility with patients before such surgery because the
possibility of death is so important. Therefore, for women to whom the induced
loss of a preembryo or embryo is important, failure to discuss this
possibility, even if the possibility is judged to be remote, would be a failure
of informed consent. Others feel that an overemphasis of possible
postfertilization effects might make women choose a less-effective method of
contraception and therefore increase the incidence of unplanned pregnancy. Both
of these views fail to acknowledge the value of a woman's autonomy in making
decisions based on informed consent. During informed consent discussions,
overemphasis of any single possible risk may not result in appropriate informed
consent; however, neither does choosing to not mention the possible risk result
in adequate informed consent. Therefore, discussion of this potential risk
should occur and should be kept within the perspective of the available medical
evidence.
One possible approach to this complex issue might be to
inquire of the patient whether she desires this information. The physician or
provider might say, for example: "Most of the time, the pill acts by
preventing an egg from forming. This prevents pregnancy. However, women on the
pill can still sometimes get pregnant. Some doctors think that the pill may
cause the loss of some of these pregnancies very early in the pregnancy, before
you would even know you were pregnant. Would knowing more about this
possibility be important to you in your decision about whether to use the
pill?"
If the answer is yes, further explanation of the issues
would be indicated and should occur in terms that are as understandable as
possible. Proper informed consent requires patient and physician comprehension
of information, the disclosure of this information, and the sharing of
interpretations.14, 15 If any
mechanism of any OC violates the morals of any particular woman, the failure of
the physician or care provider to disclose this information would effectively eliminate
the likelihood that the woman's consent was truly informed13, 14, 93 and
would seriously jeopardize her autonomy.13
Furthermore, there is a potential for negative psychological
impact on women who believe human life begins at fertilization, who have not
been given informed consent about OCs, and who later learn of the potential for
postfertilization effects of OCs.94 The
responses to this could include disappointment, anger, guilt, sadness, anger,
rage, depression, or a sense of having been violated by the provider.5 Further
research is necessary to identify the exact frequency of postfertilization
effects of OCs.
The available evidence supports the hypothesis that when
ovulation and fertilization occur in women taking OCs, postfertilization
effects are operative on occasion to prevent clinically recognized pregnancy.
Physicians should understand and respect the beliefs of patients who consider
human life to be present and valuable from the moment of fertilization. Since
it would be difficult to predict which patients might object to being given an
OC if they were aware of possible postfertilization effects, mentioning the
potential for postfertilization effects of OCs to all patients and providing
detailed information about the evidence to those who request it is necessary
for adequate informed consent.
Author/Article
Information
From the Department of Family Medicine, University of South Florida, Kissimmee
(Dr Larimore), and Department of Family and Preventive Medicine, University of
Utah, Salt Lake City (Dr Stanford).
Reprints: Joseph B. Stanford, MD, MSPH, Department of Family and Preventive
Medicine, University of Utah, 50 North Medical Dr, Salt Lake City, UT 84132
(e-mail: jstanford@dfpm.utah.edu).
Accepted for publication March 18, 1999.
We thank John R. Hartman, MD, Chris Kahlenborn, MD, G. Gayle
Stephens, MD, William Toffler, MD, and Randy Alcorn, MS, for their help with
conceptual development of this article and for identifying important
references.
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