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Weight Loss for Overweight and Obese Individuals with Gout: A Systematic Review of Longitudinal Studies

| Rheumatology
Authors:
Sabrina Mai Nielsen,1 Melanie Birger Morillon,1-3 Lisa K. Stamp,4 *Robin Christensen1
Disclosure:

Ms Nielsen and Dr Morillon have declared no conflicts of interest. Dr Stamp declares speaker fees from Amgen and grants from Ardea Biosciences outside the submitted work. Dr Christensen reports non-financial support from Board membership, grants from consultancy (AbbVie, Amgen, Axellus A/S, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Eli Lilly, Hospira, MSD, Norpharma, Novartis, Orkla Health, Pfizer, Roche, Sobi, and Takeda), personal fees from employment (Research Unit for Musculoskeletal Function and Physiotherapy, Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark), non-financial support from expert testimony, grants from/grants pending (Axellus A/S, AbbVie, Cambridge Weight Plan, Janssen, MSD, Mundipharma, Novartis, and Roche), grants from payment for lectures, including service on speakers’ bureaus (Abbott, Amgen, Axellus, Bayer HealthCare Pharmaceuticals, Biogen Idec, Bristol-Myers Squibb, Cambridge Weight Plan, Ipsen, Janssen, Laboratoires Expanscience, MSD, Mundipharma, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, Sobi, and Wyeth), grants from payment for manuscript preparation (Axellus, Bristol-Myers Squibb, Cambridge Weight Plan, and Aleris-Hamlet [via Norpharma]), non-financial support from patents (planned, pending, or issued), non-financial support from royalties, grants from payment for development of educational presentations (Bristol-Myers Squibb, MSD, and Pfizer), non-financial support from stock/stock options, grants from travel/ accommodations/meeting expenses unrelated to activities listed (Abbott, AbbVie, Axellus, Bristol-Myers Squibb, Cambridge Weight Plan, Celgene, Laboratoires Expanscience, Norpharma, Novartis, Pfizer, Roche, Rottapharm-Madaus, and Wyeth), and is involved in many healthcare initiatives and research that could benefit from wide uptake of this publication  (including Cochrane, OMERACT, IDEOM, RADS, and the GRADE Working Group). Musculoskeletal Statistics Unit, The Parker Institute is grateful for the financial support received from public and private foundations, companies and private individuals over the years. The Parker Institute is supported by a core grant from the Oak Foundation; the Oak Foundation is a group of philanthropic organisations that, since its establishment in 1983, has given grants to not-for-profit organisations around the world.

Acknowledgements:

We thank the Copenhagen University Library Frederiksberg, Copenhagen, Denmark for their work in retrieving full texts. We would like to thank several individuals for assistance with the translation of articles in Russian, Chinese, and Bulgarian: Dr Natalia Manilo, Department of Rheumatology, Rigshospitalet Glostrup and Frederiksberg, Copenhagen, Denmark; Dr Tao Ma, Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, Copenhagen, Denmark; and Dr Nora Vladimirova, Department of Rheumatology, Rigshospitalet Glostrup and Frederiksberg, Copenhagen, Denmark, respectively. We thank Prof Nicola Dalbeth, Department of Rheumatology, Counties Manukau District Health Board, Auckland, New Zealand, who responded to data and information requests.

Support:

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors; the Oak Foundation had no role in study design or the writing of this manuscript.

Citation
EMJ Rheumatol. ;4[1]:70-72. Abstract Review No. AR8.

Each article is made available under the terms of the .

It has been estimated that almost half of gout patients in Europe are obese.1 BMI is strongly correlated with serum urate (SU),2 and weight loss in people without gout has been shown to decrease SU.3 Hyperuricaemia is a critical factor in the development of gout, which is caused by deposition of monosodium urate crystals in the joints and tissues. Hence, lowering SU is considered central in the long-term management of gout. The recommended target for SU is <360 μmol/L (<6 mg/dL), and if this is sustained over time, it leads to dissolution of monosodium urate crystals, reduction in gout flares, and resolution of tophi.

Even though weight loss is commonly recommended for gout,4 no one has previously conducted a systematic review investigating the effects of weight loss. Therefore, our objective was to determine the benefits and harms associated with weight loss in overweight and obese gout patients.

Following our protocol, we searched four electronic databases and two trial registries. We included longitudinal studies with 10 overweight or obese gout patients, where the effects following weight loss (intentionally or unintentionally) were quantitatively estimated. We specified 11 outcomes for data-extraction. During the process, we realised that the planned meta-analyses were not possible, because the studies were too heterogeneous. Thus, we decided to summarise the results from each study. The internal validity and the quality of evidence were assessed using the ROBINS-I tool5 and the GRADE approach,6 respectively.

We included 10 eligible studies. Only sparse data were available, and the most frequently reported outcomes were SU, achieving SU target (<360 μmol/L), and gout flares. Only one of the included studies was a randomised controlled trial, and four of the studies had no comparison group. Interventions included intentional weight loss from dietary changes with or without increased physical activity, bariatric surgery, and unintentional weight loss from a high protein diet, metformin, and diuretics. Three studies stratified cohorts according to weight change. Follow-up ranged from 4 weeks to 7 years, and mean weight loss ranged from 3–34 kg. In the risk of bias assessment, none of the studies were rated low risk for all seven bias domains, and four of the studies were rated critical risk for the first bias domain (bias due to confounding issues).

At the latest follow-up, the studies reported a change in SU ranging from -168 to +30 μmol/L. For those with SU above target at baseline, between 0 and 60% achieved target SU. Gout flares were reported in different ways, but overall, six out of eight studies reported beneficial effects. For all three outcomes (SU, achieving SU target, and gout flares) dose-response relationships were reported. However, it should be noted, that in the short term, two studies reported a temporary increase in SU and gout flares following bariatric surgery. We rated the quality of evidence for the three outcomes to be low, moderate, and low, respectively, because we downgraded for study types, risk of bias, and upgraded for dose response relationship, and large reported effects. In conclusion, the available evidence indicated beneficial effects of weight loss for overweight and obese gout patients, although short-term, unfavourable effects may occur. Since the current evidence consists of only a few studies (mostly observational) of low methodological quality, there is an urgent need to initiate rigorous randomised controlled trials.

References
Richette P et al. Characteristics and management of gout patients in Europe: data from a large cohort of patients. Eur Rev Med Pharmacol Sci. 2015;19(4):630-9. Wang H et al. Association of Serum Uric Acid with Body Mass Index: A Cross-Sectional Study from Jiangsu Province, China. Iran J Public Health. 2014;43(11):1503-9. Richette P et al. Weight loss, xanthine oxidase and serum urate levels: a prospective, longitudinal study of obese patients. Arthritis Care Res. 2016;68(7):1036-42. Richette P et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis. 2017;76(1):29-42. Sterne JA et al. ROBINS-I: a tool for assessing risk of bias in non-randomised studies of interventions. BMJ. 2016;355:i4919. Guyatt GH et al. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ. 2008;336(7650):924-6.
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