Evidence map›Paper›PMID 23498310›Full record

ArticleAnnals of vascular surgery2013

Inflammatory "adiposopathy" in major amputation patients.

Christine R Mauro, Binh T Nguyen, Peng Yu, Ming Tao, Ian Gao, Michael A Seidman, Louis L Nguyen, C Keith Ozaki

Registry-linked trialAbstract read
In one paragraph

Article in Annals of vascular surgery, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05457881 (Short-Term Endogenous Hydrogen Sulfide Upregulation For Vein Graft Disease), which is not on this map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT05457881 nawithdrawnnot on this mapstarted 2024, after this paper: background citation

Short-Term Endogenous Hydrogen Sulfide Upregulation For Vein Graft Disease

TypeinterventionalSponsorBrigham and Women's HospitalRan2024 to 2029Enrolled0ConditionsVascular Diseases, SurgeryArmsScandi-Shake
3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Trial
  2. Article
  3. Adipose tissue: a neglected organ in the response to severe trauma?Cellular and molecular life sciences : CMLS · 2022
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Diversity of lipid mediators in human adipose tissue depots.American journal of physiology. Cell physiology · 2013
    Article
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Christine R MauroDepartment of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Binh T Nguyen
Peng Yu
Ming Tao
Ian Gao
Michael A Seidman
Louis L Nguyen
C Keith Ozaki

Funding

HARVARD-LONGWOOD RESEARCH TRAINING IN VASCULAR SURGERYT32HL007734 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FERRAN, CHRISTIANE, LOGERFO, FRANK W · 1993 to 2023
$10.5M
Cytokine Driven Mechanisms of Vein Graft FailureR01HL079135 · NHLBI · UNIVERSITY OF FLORIDA · PI OZAKI, C KEITH · 2005 to 2009
$1.8M
NHLBI NIH HHS 1R01HL079135-06S1NHLBI NIH HHS R01 HL079135NHLBI NIH HHS R01HL079135NHLBI NIH HHS T32 HL007734
6 · The paper itself

Abstract

backgroundMuch has been made of obesity's health impact, largely founded on data regarding patient weight and circulating adipose-derived mediator levels. Paradoxically, a "healthy obese" state exists, but substantial knowledge gaps also exist regarding human adipose-phenotype determinants. Surgical major amputation (AMP) patients are the "sickest-of-the-sick." Conversely, elective knee replacement (TKR) is reserved for patients who expect continued health and longevity. To delineate human adipose biology variability and clinical determinants, we studied fresh subcutaneous adipose from AMP patients, using TKR patients as controls. We hypothesized that AMP patients would display a pro-inflammatory adipokine signature, and that certain clinical conditions (diabetes, hypertension, hyperlipidemia, high BMI, uremia) would independently drive elevated adipose inflammation.

methodsAMP (n = 29) and TKR (n = 20) adipose tissue samples and clinical data were collected prospectively, and protein was isolated and analyzed for 8 adipose-related mediators. Statistical analyses included Wilcoxon's rank sum test, Fisher's exact test, and multiple linear regression modeling of clinical parameter predictors of mediator expression.

resultsInterleukin-(IL)-6, IL-8, leptin, resistin, and PAI-1 were differentially expressed (up to 200-fold) between AMP/TKR cohorts. Key clinical parameters that associated with protein levels of adipose phenotype included age, gender, hypertension, hyperlipidemia, congestive heart failure, cerebrovascular disease, renal disease, and warfarin, statin, and insulin use. BMI failed to be predictive.

conclusionsAMP patients display adiposopathy with a pro-inflammatory adipose phenotypic signature compared with TKR controls. BMI fails to predict phenotype, yet other clinical conditions, such as age, hyperlipidemia, and renal insufficiency, do drive adipokine expression. Understanding human adipose phenotypic determinants stands as a fundamental priority when future studies dissect the interplay between adipose biology and surgical diseases/outcomes.

Indexed as

Amputation, SurgicalAgedAge FactorsArthroplasty, Replacement, KneeCardiovascular DiseasesCase-Control StudiesChronic DiseaseComorbidityCytokinesDiabetes MellitusElective Surgical ProceduresFemaleHumansInflammationInflammation MediatorsInterleukin-6CXCL8 protein, humanCytokinesIL6 protein, humanInflammation MediatorsInterleukin-6Interleukin-8LeptinPlasminogen Activator Inhibitor 1ResistinRETN protein, humanSERPINE1 protein, human

Identifiers

PMID23498310
PMCPMC3603344

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.