In light of the FDA's black box warning about potential bone loss in teenagers, how do you counsel teenagers about this highly effective birth control method? Recommendations from the World Health Organization provide a practical, evidence-based approach to weighing the risks.
Do you feel uneasy prescribing depot medroxyprogesterone acetate (DMPA) to adolescent patients in wake of the Food and Drug Administration's (FDA) recent black box warning? Are you grappling uncomfortably with this option when advising and treating teenagers who need contraception? If so, you're not alone.
For many adolescents, DMPA (150 mg intramuscularly every 12 weeks) continues to be the contraceptive of choice. The method is highly effective, reversible, and long acting. Moreover, adherence (often a major challenge in this age group) requires only a minimal effort. DMPA reduces menstrual symptoms like excessive bleeding and dysmenorrhea and improves anemia.1,2 The drug's other advantages include a progestin-only formulation that can be safely used by women with contraindications to estrogen and a unique injectable delivery system that offers your patient privacy.
Unfortunately, the FDA's recent black box warning about the adverse effects of DMPA on bone density in adolescents has left many clinicians at a loss for how to advise and treat their teenaged patients. Some clinicians have stopped providing DMPA to adolescents, while others have continued prescribing it but feel uneasy about this decision. With the United States lead-ing other developed countries in teenage pregnancy rates, clinicians need to carefully weigh concerns about the effects of DMPA on bone density against the consequence of withholding this important contraceptive option.3 The alternative, an unplanned pregnancy, could have a severely negative impact on-even ruin-a teen's future. To help interpret this information, let's examine the evidence behind the FDA decision.
IM DMPA works by inhibiting the pituitary gland from secreting gonadotropin, especially LH. It provides contraception by blocking the LH surge and thereby prevents ovulation.4 Additional mechanisms of contraception include a progestin-induced thickening of the cervical mucus (preventing sperm from penetrating) and thinning of the endometrial lining (creating an inhospitable environment for ovum and sperm).
Estrogen suppresses bone remodeling and resorption, and lower levels or a lack of estrogen (as occurs in menopause) can negatively impact bone density.4 Although DMPA suppresses FSH, this effect is typically not complete and most users' ovaries continue to produce some estradiol.4 However, since many of these young women experience symptoms of hypoestrogenism, we must consider the effect on bone density. An additional concern for teens is that peak bone mass in females occurs in late adolescence.5 Theoretically, lower levels of estrogen during DMPA use in the active phase of bone development might affect the skeleton more than use later in life. The reassuring news is that the recovery of bone density after DMPA use in teens appears to be no different than that of breastfeeding.6,7 In addition, bone mineral density (BMD) is only a surrogate for fracture risk, and no information exists on how this temporary decrease in BMD during DMPA use might translate to future fracture risk.
What does the literature show?
Table 1 summarizes the major research on DMPA and bone density.8-19 Most studies have focused on bone density in adults using DMPA and do show that prolonged use of DMPA decreases BMD over time. Compared to never or non-users of DMPA, however, the reduction in BMD among longer-term users is small (within one standard deviation) and clinically insignificant for most users.20 Importantly, the decrease in BMD also appears to be reversible when premenopausal women stop taking the drug.21