OTHER USES
Other clinical uses of
estrogens and progestins include the treatment of dysfunctional uterine
bleeding, dys-menorrhea, endometriosis, and rarely, metastatic pros-tate
cancer.
Administration of estrogen
alone or estrogen–progestin combinations multiplies by 1.2 to 1.8 the relative
risk of breast cancer in postmenopausal women. The risk is slightly greater in
women taking estrogen–progestin (conjugated equine estrogens plus
medroxyproges-terone acetate) compared with women taking estrogen alone
(conjugated equine estrogens). In addition, the risk is greater for lean women
(low body mass index) with either therapy. Thus, the ability of progestins to
protect the endometrium from cancer risk is not ob-served in breast tissue.
Oral contraceptive use in younger women does not seem to be associated with an
increased breast cancer risk.
Oral contraceptive use
lessens the incidence of ovarian cancer.
Hepatocellular carcinoma and
benign hepatomas are rare complications of oral contraceptive and tamoxifen
use.
Estrogen replacement therapy
is associated with an in-creased risk of thromboembolic disease, and
alternative therapies for osteoporosis and cardiovascular protec-tion are
recommended for individuals with prior throm-boembolic episodes. The problems
generally are more severe and/or more frequent when either of the syn-thetic
estrogens, ethinyl estradiol or mestranol, is used. These preparations alter
liver function more signifi-cantly than do the natural estrogens, such as the sulfate
conjugates or esterified estrogens. Alterations in the synthesis of specific
liver proteins, such as coagulation factors and fibrinogen, are implicated in
the formation of thromboembolisms. Conjugated estrogens, tamox-ifen, clomiphene
and raloxifene also increase the fre-quency of thromboembolic disease.
Current estimates are that
oral contraceptive use doubles to triples the overall risk of thromboembolic
disease. The increased use in recent years of oral con-traceptives with lower
estrogen content probably con-tributes to the decreased risk. However, the risk
is greater in women who smoke, who are over age 35, or who are diabetic.
Mild hypertension and fluid
retention frequently oc-cur in oral contraceptive users. Systolic blood
pressure is elevated 5 to 6 mm Hg; diastolic blood pressure in-creases are on
the order of 1 to 2 mm Hg. Hypertension is not commonly a problem in
postmenopausal women receiving conjugated estrogens.
A 0.5% incidence of migraines
has been reported among users of oral contraceptives. Migraine headaches may be
a warning signal for an oncoming stroke, and immediate discontinuation of oral
contraceptive use is recommended.
Diethylstilbestrol (DES) was
once given to prevent spontaneous abortion, but it no longer has such a
med-ical indication. There is a 0.01 to 0.1% incidence of a rare vaginal and
cervical clear cell adenocarcinoma among the daughters of mothers who received
DES during their first trimester of pregnancy. An increased cancer incidence in
male offspring of mothers who had received DES has also been noted.
Progestins may be teratogenic
during the first trimester of pregnancy. Therefore, if pregnancy is sus-pected,
oral contraceptive use should not be initiated or use should be stopped
promptly.
There is some delay in the
return of fertility after dis-continuation of oral contraceptive use.
Gonadotropin profiles should be normal 3 months after combination oral
contraceptive use is stopped. The incidence of pro-longed amenorrhea extending
beyond 6 months is 2 to 3%. This reaction is especially a problem with the use
of progestin-only minipills.
The use of oral
contraceptives may interfere with lacta-tion. In addition, the hormones may be
present in the mother’s milk, hence be taken in by the nursing child. If breast
feeding is planned, the use of oral contraceptives should be discontinued until
after weaning.
There is a 2.5-fold increased
incidence of gallbladder disease in postmenopausal women receiving estrogens.
This occurrence may be related to changes in plasma lipid metabolism.
Estrogen usage is associated
with a mild decrease in glucose tolerance. Estrogens do not cause diabetes, but
their concurrent use in the diabetic patient may neces-sitate adjustment in
insulin dosage.
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