ESPE2022 Poster Category 1 Bone, Growth Plate and Mineral Metabolism (46 abstracts)
1Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 2Region Västra Götaland, Sahlgrenska University Hospital, Queen Silvia Children’s Hospital, Department of Pediatrics, Gothenburg, Sweden; 3Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 4Department of Orthopedics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 5Department of Clinical Chemistry, Linköping University, Linköping, Sweden
Purpose: Anorexia nervosa (AN) increases the risk of impaired bone health, low areal bone mineral density (aBMD), and subsequent fractures. This study investigated the long-term effects on bone and biomarkers in young women with AN.
Methods: Twenty-five Swedish female AN patients, median age 21.0 years (16.1 to 24.3 years), median BMI 15.4 kg/m2, were included, 22 patients completed a high-energy in-patient treatment for 12 weeks, 20 of these were followed-up after 3 years. Bone mass and body composition were measured by dual-energy X-ray absorptiometry (DXA), peripheral quantitative computed tomography (PQCT), and DXA and laser before and after 12 weeks of nutrition therapy, and after 3 years. C-terminal collagen cross-links (CTX), osteocalcin, bone-specific alkaline phosphatase (BALP), leptin, and sclerostin, were analyzed at the same time points. An age-matched comparison group of 17 healthy women was recruited for the 3-year follow-up.
Results: Body mass index (BMI) and fat mass increased from baseline to 3 years in women with AN. Median total body aBMD among the AN patients remained stable over 3 years, but was significantly lower compared to healthy controls after 3 years. Trabecular volumetric BMD (vBMD) decreased during the first 12 weeks and over 3 years despite stable BMI and was significantly lower in AN patients than the controls. The trabecular vBMD was decreased in 42% of the AN patients and in 6% of the healthy controls. Median serum sclerostin decreased from 31.7 to 24.6 pmol/l after 12 weeks of nutrition therapy (P=0.033) and further decreased to 19.0 pmol/l over 3 years (P=0.042). From baseline to 3 years, median BALP increased from 8.0 to 15.0 µg/l (P=0.0029), but osteocalcin was stable. Median serum CTX decreased from 1.24 ng/ml at baseline to 0.34 ng/ml at the 3-year follow-up (P<0.0001). Leptin increased during nutrition therapy before decreasing at 3 years. There were no associations between the change in sclerostin from baseline to 3 years and the changes in other bone turnover markers, aBMD, or vBMD.
Conclusions: This longitudinal study demonstrated low aBMD in AN patients compared to healthy controls and a reduction in trabecular vBMD at the 3-year follow-up despite stable BMI, reduced sclerostin levels, and changes in bone turnover markers usually associated with increased bone mass. Our findings highlight the importance of early detection and organized long-term follow-up of bone health in young women with a history of AN.