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Long-term effects of bariatric surgery in patients with obesity and chromosome 16 p11.2 microdeletion

Kristensson, Felipe M. (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine
Andersson-Assarsson, Johanna C., 1974 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine
Kanerva, Noora (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine
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Peltonen, M. (författare)
Carlsson, Björn, 1958 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine
Carlsson, Lena M S, 1957 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine
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 (creator_code:org_t)
Elsevier BV, 2017
2017
Engelska.
Ingår i: Surgery for Obesity and Related Diseases. - : Elsevier BV. - 1550-7289. ; 13:8, s. 1321-1326
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • Background: Chromosome 16 p11.2 microdeletion is associated with early-onset obesity. Information is limited about the effect of bariatric surgery in patients with genetic obesity. Objective: To examine the effects of bariatric surgery in obese patients with chromosome 16 p11.2 microdeletion. Methods: The Swedish Obese Subjects study is a prospective study with 2010 participants receiving bariatric surgery. DNA was available for 1843 participants. Multiplex ligation-dependent probe amplification was used to identify 16 p11.2 microdeletion carriers. Follow-up time was 10 years. In carriers and noncarriers, follow-up rate was 86% and 82%, respectively, at 10 years. Results: Nine carriers of the chromosome 16 p11.2 microdeletion (9/1843, .49%) were found. At baseline, most risk factors were similar; however, carriers had higher body mass index (BMI), insulin levels, and systolic blood pressure compared to noncarriers. At the 1 -year examination, the percent excess BMI lost (%EBMIL) in carriers and noncarriers was 71.9 and 62.2, respectively; P = .031 (37.9 and 30.6 kg). This was followed by partial weight regain in both groups, and after 10 years %BBMIL was 25.5 and 41.5 (15.7 and 21.3 kg), respectively (P = .377). Changes in risk factors were similar in the carriers and noncarriers. Two carriers who had type 2 diabetes at baseline were both in remission at 2 -year follow-up but relapsed at 10 -year follow-up. Perceived health status was similar in carriers and noncarriers during follow-up (overall P = .198). Conclusions: Despite a small sample size, our results indicate that bariatric surgery is a treatment option for obese patients with chromosome 16 p11.2 microdeletion. (Surg Obes Relat Dis 2017;13:1321-1326.) (C) 2017 American Society for Metabolic and Bariatric Surgery. All rights reserved.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kirurgi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Surgery (hsv//eng)

Nyckelord

Obesity
Bariatric surgery
Chromosome 16 p11.2 microdeletion
health-care needs
developmental-disabilities
children

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