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Author: Admin | 2025-04-28
Per cent of adult bone mass is laid down during adolescence [13]. Bone demineralization exceeds bone mineralization as early as 25 years of age [14]. Thus, using a contraceptive method that can reduce bone mineralization in women under age 25 may negatively affect bone health in the longer term. DMPA has come under particular scrutiny because the hypoestrogenic state induced by this method has been associated with decreased bone mineralization [15]. There have been some reassuring findings, however: the decrease in bone mineral density (BMD) is highest in the first year of use and slows thereafter; and small studies have indicated that there is a rebound increase in bone mineral density after DMPA is discontinued [16]. When considering potential impact on BMD, remember that pregnancy is also associated with bone demineralization. The SOGC advises that providers include DMPA in their armamentarium, but that they weigh the risks and benefits of DMPA use with patients and advise youth who choose this method to optimize calcium and vitamin D intake, engage in weight-bearing exercise and reduce cigarette, caffeine and alcohol use to optimize bone health [17].Given the importance of bone mineralization, pills containing 30 mcg to 35 mcg of ethinyl estradiol (EE) should be prescribed preferentially because EE doses below 30 mcg may be associated with poorer bone mineralization in youth [18]. COCs with 20 mcg EE have not been found to have fewer side effects [19] or risks (see below) than 30 mcg to 35 mcg pills. While the transdermal patch releases 20 mcg of EE daily, the pharmacokinetics are different and the overall exposure is higher than that of a 30 mcg EE pill [20]. The intravaginal ring appears to cause less overall estrogen exposure than taking a 30 mcg EE pill, but its effect on bone mineral density in youth has not yet been evaluated.Hormonal contraceptives, thromboembolic events and strokeEstrogen-containing contraceptives increase risk for thrombosis. COC use increases the risk for venous thromboembolism (VTE) by two to four times [21] and for stroke by 1.5 to two times, compared with risk levels in nonusers [22]. The risk for VTE or stroke is not statistically different between pills containing 20 mcg and 30 mcg of EE [22][23]. Data are not yet available on COCs with 10 mcg of EE. Transdermal and transvaginal contraceptives have not been studied as extensively with respect to VTE. At worst, they may double the rate of VTE compared with COCs [24]. It is important to remember that despite the higher risk for VTE and stroke with using COCs, the baseline risk for such events in youth 15 to 19 years old is low (venous thrombosis: 4 to 11 per 100,000 per year [25]–[27]; stroke: 3 to 6 per 100,000 per year [28]). Therefore, the absolute risk posed by using hormonal therapy is also low [29].In the last decade, several studies have raised the possibility that VTE risk (but not stroke risk) is moderated by the type of progestin used in COCs [21]. The role of
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