Longitudinal 5-Year Evaluation of Bone Density and Microarchitecture After Roux-en-Y Gastric Bypass Surgery

Katherine G. Lindeman; Logan B. Greenblatt; Caroline Rourke; Mary L. Bouxsein; Joel S. Finkelstein; Elaine W. Yu

Disclosures

J Clin Endocrinol Metab. 2018;103(11):4104-4112. 

In This Article

Abstract and Introduction

Abstract

Context: Bone health declines in the initial years after Roux-en-Y gastric bypass (RYGB), but long-term skeletal effects are unclear.

Objective: To document longitudinal changes in bone mineral density (BMD) and microarchitecture 5 years after RYGB.

Design, Setting, and Participants: Prospective 5-year observational study of 21 adults with severe obesity receiving RYGB at an academic medical center.

Main Outcome Measures: Spine and hip areal BMD were measured by dual-energy X-ray absorptiometry, and trabecular volumetric BMD (vBMD) of the spine was assessed by quantitative CT (QCT). We measured vBMD and microarchitecture of the distal radius and tibia by high-resolution peripheral QCT in a subset of subjects. Serum type I collagen C–terminal telopeptide (CTX) and procollagen type I N-terminal propeptide (P1NP) were also measured.

Results: Areal BMD declined by −7.8% ± 7.6% at the spine and −15.3% ± 6.3% at the total hip by 5 years after RYGB (P ≤ 0.001), although the rate of bone loss slowed in later years. Trabecular spine vBMD decreased by −12.1% ± 12.3% by 5 years (P ≤ 0.001). At peripheral sites, vBMD continued to decrease steadily throughout 5 years, with parallel declines in cortical and trabecular microarchitecture, leading to decreases in estimated failure load of −20% and −13% at the radius and tibia, respectively (P < 0.001). Five years after RYGB, CTX and P1NP were 150% and 34% above baseline (P < 0.001 and P = 0.017, respectively).

Conclusions: Sustained high-turnover bone loss and bone microarchitectural deterioration occur in the 5 years after RYGB. Adults receiving RYGB warrant assessment of bone health.

Introduction

The clinical management of severe obesity [body mass index (BMI) ≥40 kg/m2] has been transformed by the emergence of bariatric surgery procedures, which lead to improvements in a wide range of obesity comorbidities and are associated with decreased mortality.[1–3] Roux-en-Y gastric bypass (RYGB) has traditionally been one of the most commonly performed types of weight loss surgery[4] but is associated with negative skeletal effects. RYGB and other bariatric procedures with malabsorptive features have been shown to increase the risk of fractures at sites including the spine, hip, and upper extremity.[5–7]

This RYGB-associated skeletal fragility is mediated by accelerated high-turnover bone loss and has been documented in the short term in multiple longitudinal studies.[8–22] Collectively, these studies document that a decline in bone density up to 10% is common in the initial 1 to 2 years after RYGB. RYGB also leads to short-term declines in volumetric bone density of the axial and peripheral skeleton[18,23] and weakening of peripheral bone microarchitecture.[18–20,23] However, the long-term skeletal consequences of RYGB have not been well characterized beyond these initial postsurgical years. In particular, no studies have looked at changes in volumetric bone density or skeletal microarchitecture beyond 2 years. Furthermore, the mechanisms of bone loss after RYGB remain unclear but may involve a combination of mechanical unloading of the skeleton, calcium and vitamin D malabsorption, and changes in metabolic hormones that may affect the entero-osseous axis.[24,25]

We previously reported substantial bone loss by dual-energy X-ray absorptiometry (DXA) and a deterioration in both cortical and trabecular microarchitecture 2 years after RYGB.[22] To determine whether these skeletal changes progress, we assessed bone density and bone microarchitecture up to 5 years after RYGB. In addition, we assessed whether changes in weight, body composition, and calciotropic or entero-osseous hormones are associated with bone loss after RYGB.

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