[ Editorials | Departments and Series | Index ]

OB/GYN Editorial MAY 2005

Depot Medroxyprogesterone Acetate Injectable Contraception in Adolescents: Reassuring Data Regarding Skeletal Health

Andrew M. Kaunitz, MD

Data from the newly released 2002 National Surve`y of Family Growth indicate that more than 2 million US women are now using injectable depot medroxyprogesterone acetate (DMPA) for contraception.¹ Many of these users are adolescents and older teenagers. Use of DMPA not only prevents ovulation—making this a highly effective, long–acting method of birth control—but it also reduces ovarian production of estradiol,^2,3 an impact which can lead to lowered bone mineral density (BMD) during use.

Evidence showing that BMD declines during DMPA use led the US Food and Drug Administration (FDA) to mandate a “black box” warning in DMPA packaging in November 2004 due to concerns regarding its safety in teenagers and young women. However, DMPA use has not been linked to menopausal osteoporosis or fractures. In addition, cross-sectional data have been reassuring that, in former adult DMPA users, subsequent BMD recovers completely.^4,5 Even so, given that peak bone mass is attained during adolescence and early adulthood, the dearth of BMD data related to DMPA use in young women continued to cause apprehension about skeletal safety in teenaged users.

Fortunately, recent publications allow clinicians to offer DMPA to their teenaged contraceptive patients with confidence that they are not increasing the risk of osteoporosis later in life. In a 2-year, double-blind, randomized, controlled trial of 123 adolescents, Cromer et al⁶ found that when low-dose estradiol supplementation was added to DMPA, there was no decline in BMD. Cundy et al⁷ similarly observed that DMPA supplemented with estrogen resulted in stable BMD in adult women.

Another recently published study from Scholes et al⁸ noted reassuring observations regarding recovery of BMD following use of DMPA in teenagers. This cohort study followed 170 adolescents (including 80 who used DMPA at baseline), and found that recovery of BMD is complete within 12 months post-DMPA discontinuation. The authors stated that “Adjusted mean BMD values for discontinuers were at least as high as those of nonusers for all anatomic sites at 12 months and at all subsequent follow-up intervals.”⁸ Of note, BMD was ultimately observed to be higher in former DMPA users than in never-users. Likewise, the duration of DMPA use was not observed to affect the speed of BMD recovery following DMPA discontinuation. The authors concluded that “...these results in teens and those from our previous cohort provide reassurance that bone loss is regained, even in younger users.”⁸

The study by Cromer et al⁶ emphasizes that in teenagers, as in adult women, the transient loss of BMD associated with DMPA use can be attributed entirely to the contraceptive-related reduction in ovarian estradiol production. Although “add-back” estrogen supplementation indeed prevents BMD loss in DMPA users, the recovery of BMD that occurs after DMPA discontinuation in both teenagers and adults means that such supplemental estrogen is generally unnecessary. As Cromer et al⁶ and Scholes et al⁸ have pointed out, the transient impact of DMPA on endogenous estradiol levels and BMD is similar to trends noted with lactation, which has not been found to have a long-term effect on skeletal health.⁹ The observation from Scholes et al⁸—that following DMPA use in teenagers, BMD is higher than in never-users—correlates with similar postlactation BMD findings in teenagers.¹⁰ Therefore, concerns regarding skeletal health should not prevent clinicians from prescribing DMPA to adolescent or adult women. Likewise, monitoring BMD using dual X-ray absorptiometry or other bone imaging modalities is rarely of clinical value in young women. Although calcium supplementation is appropriate for teenagers, this recommendation applies regardless of contraceptive use.

Andrew M. Kaunitz, MD
Associate Advisory Board Member

back to top

References

1. Mosher WD, Martinez GM, Chandra A, Abma JC, Willson SJ. Use of contraception and use of family planning services in the United States: 1982-2002. Adv Data. 2004;(350):1-36.
2. Westhoff C. Depot-medroxyprogesterone acetate injection (Depo-Provera): a highly effective contraceptive option with proven long-term safety. Contraception. 2003;68(2):75-87.
3. Kaunitz AM. Injectable long-acting contraceptives. Clin Obstet Gynecol. 2001;44(1):73-91.
4. Petitti DB, Piaggio G, Mehta S, Cravioto MC, Meirik O. Steroid hormone contraception and bone mineral density: a cross-sectional study in an international population. The WHO Study of Hormonal Contraception and Bone Health. Obstet Gynecol. 2000;95(5):736-744.
5. Orr-Walker BJ, Evans MC, Ames RW, Clearwater JM, Cundy T, Reid IR. The effect of past use of the injectable contraceptive depot medroxyprogesterone acetate on bone mineral density in normal post-menopausal women. Clin Endocrinol (Oxf). 1998;49(5):615-618.
6. Cromer BA, Lazebnik R, Rome E, et al. Double-blinded randomized controlled trial of estrogen supplementation in adolescent girls who receive depot medroxyprogesterone acetate for contraception. Am J Obstet Gynecol. 2005;192(1):42-47.
7. Cundy T, Ames R, Horne A, et al. A randomized controlled trial of estrogen replacement therapy in long-term users of depot medroxyprogesterone acetate. J Clin Endocrinol Metab. 2003;88(1):78-81.
8. Scholes D, LaCroix AZ, Ichikawa LE, Barlow WE, Ott SM. Change in bone mineral density among adolescent women using and discontinuing depot medroxyprogesterone acetate contraception. Arch Pediatr Adolesc Med. 2005;159(2):139-144.
9. Sowers M, Corton G, Shapiro B, et al. Changes in bone density with lactation. JAMA. 1993;269(24):3130-3135.
10. Chantry CJ, Auinger P, Byrd RS. Lactation among adolescent mothers and subsequent bone mineral density. Arch Pediatr Adolesc Med. 2004;158(7): 650-656.

back to top