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Impact of bariatric surgery on serum urate targets in people with morbid obesity and diabetes: a prospective longitudinal study
  1. Nicola Dalbeth1,2,
  2. Peggy Chen1,
  3. Marie White3,
  4. Gregory D Gamble2,
  5. Caran Barratt-Boyes4,
  6. Peter J Gow1,
  7. Brandon Orr-Walker4
  1. 1Department of Rheumatology, Counties Manukau District Health Board, Auckland, New Zealand
  2. 2Department of Medicine, University of Auckland, Auckland, New Zealand
  3. 3Centre for Clinical Research and Effective Practice, Middlemore Hospital, Auckland, New Zealand
  4. 4Department of Endocrinology and Diabetes, Counties Manukau District Health Board, Auckland, New Zealand
  1. Correspondence to Dr Nicola Dalbeth, Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, 85 Park Rd, Grafton, Auckland 1023, New Zealand; n.dalbeth{at}auckland.ac.nz

Abstract

Objectives Weight loss leads to reduced serum urate (SU) in people with obesity. However, the clinical relevance of such reductions in SU is unknown. This study examined the impact of non-surgical weight loss and bariatric surgery on SU targets in people with morbid obesity and diabetes.

Methods The study was a single-centre, prospective study of 60 people with type 2 diabetes and body mass index ≥35 kg/m2. Following 6 months of non-surgical weight loss, all participants had laparoscopic sleeve gastrectomy, with a further 1 year of follow-up. Serial SUs were measured throughout the study.

Results Participants experienced mean (SD) weight loss of 5.5 (4.1) kg prior to surgery and 34.3 (11.1) kg following surgery. SU did not change following non-surgical weight loss (0.38 (0.09) mmol/L at baseline and 0.38 (0.10) mmol/L at follow-up), but increased to 0.44 (0.15) mmol/L in the immediate postoperative period and reduced to 0.30 (0.08) mmol/L 1 year after surgery (p<0.05 for both compared with baseline). Baseline SU, cessation of diuretics, female sex and change in creatinine independently predicted change in SU at the final visit. In participants without gout, SU above saturation levels (≥0.41 mmol/L) were present in 19/48 (40%) at baseline and 1/48 (2%) 1 year after surgery (p<0.0001). In participants with gout, SU above therapeutic target levels (≥0.36 mmol/L) were present in 10/12 (83%) at baseline and 4/12 (33%) 1 year after surgery (p=0.031).

Conclusions Clinically relevant reductions in SU occur following bariatric surgery in people with diabetes and WHO class II or higher obesity.

  • Gout
  • Epidemiology
  • Lipids

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