This study prospectively investigated the course of bone mineral density (BMD) in patients with anorexia nervosa (AN) and bulimia nervosa (BN) over a 3.6-yr follow-up period. From an initial sample of 47 female patients with an eating disorder (T1), 38 (n = 24 AN; n = 14 BN) were reassessed at follow-up (T2) (participation rate, 80.1%). For nonrecovered AN patients at T2, prevalence rates of osteopenia (-1.0 SD > or = T-score > -2.5 SD) and osteoporosis (T-score <or = -2.5 SD) at the lumbar spine were 54.2 and 20.8%, respectively. Due to an annual loss of lumbar spine BMD (-3.7 +/- 4.9%) in the chronic AN patients and a slight but insignificant annual increase (0.7 +/- 1.7%) for those who recovered, the difference in BMD between both outcome groups was more pronounced at follow-up (0.93 +/- 0.13 vs. 1.14 +/- 0.13 g/cm2; P <0.01). Nonrecovered AN patients with binge eating/purging type showed a significantly reduced BMD compared with patients with the restricting type (0.87 +/- 0.13 vs. 1.02 +/- 0.08 g/cm2; P = 0.02). Both at baseline and follow-up, AN patients had increased rates of bone resorption, as measured by urinary desoxypyridinoline, compared with a control group (n = 42) (11.4 +/- 4.4 vs. 10.4 +/- 7.8, P <0.001, vs. 5.6 +/- 2.4 and 10.4 +/- 7.8 nM/mM creatinine, P <0.05, respectively). The subtype of AN and body mass index were best predictors for BMD at the lumbar spine at follow-up (R2 = 0.576). With one exception, all bulimic patients had BMD and markers of bone turnover within the normal range. These results suggest that patients with chronic AN, particularly of the binge eating/purging type, are at high risk for osteoporosis and may need additional therapy to prevent bone loss.
This study prospectively investigated the course of bone mineral density (BMD) in patients with anorexia nervosa (AN) and bulimia nervosa (BN) over a 3.6-yr follow-up period. From an initial sample of 47 female patients with an eating disorder (T1), 38 (n = 24 AN; n = 14 BN) were reassessed at follow-up (T2) (participation rate, 80.1%). For nonrecovered AN patients at T2, prevalence rates of osteopenia (-1.0 SD > or = T-score > -2.5 SD) and osteoporosis (T-score <or = -2.5 SD) at the lumbar spine were 54.2 and 20.8%, respectively. Due to an annual loss of lumbar spine BMD (-3.7 +/- 4.9%) in the chronic AN patients and a slight but insignificant annual increase (0.7 +/- 1.7%) for those who recovered, the difference in BMD between both outcome groups was more pronounced at follow-up (0.93 +/- 0.13 vs. 1.14 +/- 0.13 g/cm2; P <0.01). Nonrecovered AN patients with binge eating/purging type showed a significantly reduced BMD compared with patients with the restricting type (0.87 +/- 0.13 vs. 1.02 +/- 0.08 g/cm2; P = 0.02). Both at baseline and follow-up, AN patients had increased rates of bone resorption, as measured by urinary desoxypyridinoline, compared with a control group (n = 42) (11.4 +/- 4.4 vs. 10.4 +/- 7.8, P <0.001, vs. 5.6 +/- 2.4 and 10.4 +/- 7.8 nM/mM creatinine, P <0.05, respectively). The subtype of AN and body mass index were best predictors for BMD at the lumbar spine at follow-up (R2 = 0.576). With one exception, all bulimic patients had BMD and markers of bone turnover within the normal range. These results suggest that patients with chronic AN, particularly of the binge eating/purging type, are at high risk for osteoporosis and may need additional therapy to prevent bone loss.