Protection Against Epithelial Ovarian Cancer, Medicine
Dr. Álvaro Monterrosa Castro, MD
Due to the lack of effective strategies for the early diagnosis and treatment of ovarian cancer:
Prevention is of capital importance. This pathology is an important cause of morbidity and mortality. It was estimated that by 1980, 137,600 new cases occurred in the world.
The American Cancer Society estimated that in the United States in 1999 there were 25,200 cases of ovarian cancer, the disease being localized in only 25% of the cases and 50% of the women dying as a result of the disease.
Ovarian cancer is the most fatal gynecologic malignancy with 5-year survival rates of less than 50% for whites and 46% for African Americans. Nulliparity and family history are risk factors.
The existence of a hereditary factor in ovarian cancer has been suggested, evidenced by the mutation of the BRCA-1 and BRCA-2 genes, involved in 10% of invasive ovarian cancers. Recent studies, including the “Hereditary Ovarian Cancer Clinical Study Group (HOCSG) (93), a large transnational case-control study that included 207 women with ovarian cancer and 161 of their healthy sisters.
Of the women with cancer, 179 were BRCA-1 and 28 were BRCA-2 positive.
The main results were published in 1998 and the relationship between heredity and ovarian cancer was pointed out. Carrying the BRCA-1 and BRCA-2 mutation increases the risk by 45% and 25% respectively (93).
Past use of oral contraceptives confers a 50% risk reduction. OR: 0.5 (CI: 0.3-0.8). After six or more years of use, protection reaches 60%. OR: 0.4 (CI: 0.2- 0.7). When restricting the analysis to positive controls for both BRCA mutations, a 60% reduction was also observed. OR: 0.4 (CI: – 0.2- 0.7), for the BRCA-1 mutation the reduction is 50% and for BRCA-2 it is 60%.
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Large-scale studies by the US Centers for Disease Control and the UK Royal College of General Practitioners (RCGP) indicate that suppression of ovulation caused by oral contraceptives protects against the development of epithelial ovarian cancer. (10).
This beneficial effect is directly proportional to the time of use and persists many years after planning with this method is suspended (94).
The Cancer and Steroid Hormone Study (CASH), a case-control study of women ages 20 to 50, conducted by the Centers for Disease Control (CDC) between 1980 and 1982, which included 494 women with ovarian cancer and 4,754 controls taken from the community, demonstrated that the use of oral anovulatories for one to five years reduces the risk of ovarian cancer by 50 to 70% (95).
Although the majority of women involved in CASH used Macrodosis combined oral contraceptives, no loss of protective effect was observed when doses of 30 or 35 ug/day of ethinyl estradiol were considered (43). This protective effect increases the longer the time of use and extends at least up to ten years after discontinuation (81,83).
The World Health Organization also conducted a multicenter study confirming the protective effect of oral contraceptives against epithelial ovarian cancer. Two cohort studies carried out in Great Britain confirmed the protective effect of the pill by finding relative risks of 0.3 and 0.6 in women who had used the method at some point. The protective effect is for both malignant tumors and Bordenline and each of the main histological subtypes of epithelial cancer (81). No protective effect has been observed against mucinous tumors (81).
The relative risk for women who had used pills for 10 or more years compared with those who had never used the pill was 0.2 (95). The lower risk of epithelial ovarian cancer is both in young women and in other ages, both in nulliparous women and in those who have had one or more children (81). Results from the study of cancer and steroid hormones suggest that the protective effect does not depend on the dose of estrogen or progestin, although new evaluations are needed using microdoses and especially the new triphasic preparations (812).
In 1992, a meta-analysis by Hankinson, Colditz, Hunter, et al (96) was published, which included 17 case-control studies and 3 cohort studies, observing in 18 studies a protective effect of combined oral contraceptives on ovarian cancer. One study found no effect and another a non-significant increase in risk. The overall result of the study establishes a RR: 0.64 (CI: 0.57- 0.73).
As noted, the protective effect increases with the duration of use, going from 12% in the first year to approximately 50% after five years of use of the pill, and the protection persists at least ten years after ending. the use of oral contraceptives. The same conclusions have been pointed out in more recent studies (97). There is no protection against non-epithelial ovarian cancer. In the Cancer and Hormones Study (95) the relative risk of ovarian germ cell cancer in women who had ever used oral contraceptives was 1.6 and 1.0 in those who had used oral contraceptives for five or more years.
In women with a family history of ovarian cancer, a reduction in risk is observed if the pill is used for at least ten years. No relationship between the use of oral contraceptives and the risk of Benign Ovarian Teratoma has been reported in the Walnut Creek study in the United States, nor in the Planned Parenthood Association study in Oxford in the United Kingdom. (98).
No relationship has been found between the use of oral contraceptives and the risk of ovarian cystadenoma (120,132), however the British evaluation (98) suggests that the risk of ovarian cystadenoma may be lower for patients who have recently received oral contraceptives. than for old users or those who have never received them.
In a recent publication it is stated verbatim (43) “combined oral contraceptives can be continued in appropriate women during the last years of reproductive life and be offered to women at high risk of ovarian cancer, as a primary indication, even when the benefits of contraception are not necessary.”
The Practice Committee of the American Society for Reproductive Medicine in its 2004 publication emphasizes that combined oral contraceptives offer protective benefits against the risk of hereditary ovarian cancer and assumes that the protection, although it appears to be similar, is not fully defined with the combinations that include new progestins, nor with triphasic, biphasic pills and doses equal to or less than 20 ug/day of ethinyl estradiol (10).
The following table presents a list of the most important studies where the estimated relative risk of ovarian cancer in users of combined oral contraceptives has been estimated, compared to women who had never used the pill.
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The pill usually eliminates the cramping that occurs during ovulation (82). This effect was achieved mainly with macrodose combined oral contraceptives. The recent combinations of very low doses and ultra-low doses, which do not completely suppress the ovary, allowing some follicular activity, are not usually related to improvement in menstrual cramps.
Dr. Álvaro Monterrosa Castro, MD
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