Objective-To determine if the use of the injectable contraceptive depot medroxyprogesterone (DMPA), which reduces ovarian oestrogen production, is associated with changes in bone density.Design-Population study. DMPA Main outcome measure-Lumbar spine and femoral neck bone mineral density assessed by dual energy x ray absorptiometry.Results-Compared with premenopausal controls matched for age, race, and body mass index, DMPA users had significantly reduced bone density in the lumbar spine (mean difference 7 5% (95% confidence interval 1-9% to 13-1%), p=0.002) and in the femoral neck (6-6%, (0.8% to 12-3%), p=0007). Compared with postmenopausal controls matched for body mass index and duration of oestrogen deficiency, DMPA users had greater bone density in the lumbar spine (8-9% (4.3% to 13.5%), p=0001), but in the femoral neck the difference in bone density was less (4-0% (-0-4% to 8.5%), p=004).

While there was no obvious bias in rates of referral, there is clearly a need for better ways to support Māori and Pacific people, and men in particular, to complete bariatric surgery. Further research is needed to clarify the socio-economic and cultural barriers that underlie this phenomenon.

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Despite the widespread use of the C21 progestin medroxyprogesterone acetate (MPA) in hormone replacement therapy and gynecological practice, its effects on bone density are uncertain, with contradictory reports in the literature. We have examined the short term changes in bone density at the lumbar spine (a predominantly trabecular site) and the femoral neck (a predominantly cortical site) in 13 premanopausal women prescribed high dose MPA (50 mg/day) for gynecological disorders and in 12 control subjects. Compared to basal values, lumbar spine bone mineral density (measured by dual energy x-ray absorptiometry) fell progressively by a mean 2.4% at 6 months and 4.1% at 12 months (both P < 0.01); in five subjects who continued the drug, it had fallen by a mean 5.9% at 20 months (P < 0.002). The spinal bone loss in the MPA users was significantly greater than that in controls (P < 0.005 at 6 months; P < 0.01 at 12 months) and occurred despite a significant gain in body weight in the women using MPA (median, 3.5 kg at 6 months; P < 0.01). In four subjects in whom bone density was measured 6 months after cessation of MPA, spinal bone density showed significant recovery (mean increment, 2.8%; P < 0.025). Femoral neck bone density measurements did not differ between the groups. MPA induced amenorrhea in all subjects who continued with it beyond 6 months, and the amenorrheic subjects were estrogen deficient (median plasma estradiol, 70 pmol/L). We conclude that, when given in doses sufficient to induce hypogonadism, MPA use is associated with significant early loss of trabecular bone, which is probably the consequence of estrogen deficiency.

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