Neoplasia and hormonal contraception.

Abstract

There are an estimated 8-10 million oral contraceptive (OC) users in the U.S. Investigation of the effects of OCs on neoplasia is not easy; currently 4 investigative methods are used: 1) case reports, 2) disease rate and trends, 3) case-control studies, which are the main source of careful retrospective information, and 4) cohort studies, which compare the incidence of disease in patients exposed to suspected environmental factors, and in those who are not exposed. Major risk factors for carcinoma of the breast are female sex, age, genetic predisposition, previous benign breast disease, and previous cancer of one breast; undetected breast cancer may be present for many years before diagnosis, and risk is increased in patients with chronic cystic mastitis or fibrocystic disease of the breast. Clinical observations have suggested a strong association between endocrine influence and the incidence or progression of breast cancer; current evidence tends to support the role of estrogens in the etiology of carcinoma of the breast with respect to long-term estrogen administration, but this evidence is not valid for young patients who are on combined OCs. Most studies have documented a decreased risk of benign breast disease with length of OC use persisting for 4 years; these studies, however, did not analyze lesions by histologic type. Studies that show a protective effect on benign disease do not show the same protective effect for breast cancer. Data from cohort studies show no association of OCs with breast cancer. Since 1972 a number of reports have associated OCs with liver tumors, stating that risk increases with duration of use. A national survey revealed that the frequency of malignant tumors increased with age, but that the frequency of benign lesions had a peak in the 26-30 age group which corresponds to increased use of OCs. Benign tumors are dangerous because they tend to rupture spontaneously. The association between pituitary adenoma, causing postpill amenorrhea, and OC use is very controversial. OC use may also cause endometrial hyperplasia; postmenopausal estrogen use has also been associated with endometrial carcinoma, although the causal relationship has never been proven; progestogens may be useful in the therapy of some endometrial carcinomas. Carcinoma of the cervix seems to be more influenced by age at 1st intercourse and by multiple sexual partners than by OC use; several case-control studies have shown that there is no significant difference between incidence among OC users and nonusers. Data about the association between OCs and ovarian carcinoma are reassuring but incomplete. OCs should not be used in patients with positive chorionic gonadotropin titers who have been treated for hydatidiform mole.