Evidence map›Paper›PMID 40316706›Full record

Observational studyScientific reports2025

Impact of Amerindian ancestry on clinical outcomes in Crohn's disease and ulcerative colitis in a Latino population.

Tamara Pérez-Jeldres, María Leonor Bustamante, Danilo Alvares, Manuel Alvarez-Lobos, Lajos Kalmer, Lorena Azocar, Roberto Segovia Melero, Gabriel Ascui, Nataly Aguilar, Ricardo Estela and 11 more

Abstract readObservational Study
In one paragraph

Observational study in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. 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

21 authors.

Tamara Pérez-JeldresDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile. tamaperez@hotmail.com.
María Leonor BustamanteFaculty of Medicine- ICBM, Universidad de Chile, Santiago, Chile.
Danilo AlvaresMRC Biostatistics Unit, University of Cambridge, Cambridge, UK.
Manuel Alvarez-LobosDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Lajos KalmerMRC Toxicology Unit, University of Cambridge, Cambridge, UK.
Lorena AzocarDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Roberto Segovia MeleroDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Gabriel AscuiLa Jolla Institute for Immunology, San Diego, CA, USA.
Nataly AguilarDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Ricardo EstelaDepartment of Gastroenterology, Hospital San Borja Arriarán, Santa Rosa 1234, Santiago, Chile.
Cristian Hernández-RochaDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Roberto CandiaDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Mauricio GonzálezDepartment of Gastroenterology, Hospital San Borja Arriarán, Santa Rosa 1234, Santiago, Chile.
Verónica SilvaDepartment of Gastroenterology, Hospital San Borja Arriarán, Santa Rosa 1234, Santiago, Chile.
Andrés De La VegaDepartment of Gastroenterology, Hospital San Borja Arriarán, Santa Rosa 1234, Santiago, Chile.
Elizabeth ArriagadaDepartment of Gastroenterology, Hospital San Borja Arriarán, Santa Rosa 1234, Santiago, Chile.
Carolina A SerranoDepartamento de Gastroenterología y Nutrición, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
Carolina Pávez-OvalleDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Carol Moraga QuinterosComputational Biology Laboratory(CBL), Instituto de Ciencias de la Ingeniería, Universidad de O'Higgins, Rancagua, Chile.
Juan Francisco MiquelDepartment of Gastroenterology, School of Medicine, Pontificia Universidad Católica de Chile, Marcoleta 367, Santiago, Chile.
Di Genova AlexComputational Biology Laboratory(CBL), Instituto de Ciencias de la Ingeniería, Universidad de O'Higgins, Rancagua, Chile.

Funding

Agencia Nacional de Investigación y Desarrollo Fondecyt Regular [Grant 1211344]Agencia Nacional de Investigación y Desarrollo Grant 1221029 and SA77210017.Agencia Nacional de Investigación y Desarrollo Project Fondecyt Initiation [Grant Number 11220147UK Research and Innovation [Grant number MC_UU_00002/5]
6 · The paper itself

Abstract

Research in Inflammatory Bowel Disease (IBD) assessing the genetic structure and its association with IBD phenotypes is needed, especially in IBD-underrepresented populations such as the South American IBD population. Aim. We examine the correlation between Amerindian ancestry and IBD phenotypes within a South American cohort and investigate the association between previously identified IBD risk variants and phenotypes. We assessed the ancestral structure (IBD = 291, Controls = 51) to examine the association between Amerindian ancestry (AMR) and IBD variables. Additionally, we analyzed the influence of known IBD genetic risk factors on disease outcomes. We used Chi-square and Fisher's tests to analyze the relationship between phenotypes and ancestry proportions, calculating odds ratios (OR) and confidence intervals (CI). Logistic regression examined genetic variants associations with IBD outcomes, and classification models for predicting prolonged remission were developed using decision tree and random forest techniques. The median distribution of global ancestry was 58% European, 39% Amerindian, and 3% African. There were no significant differences in IBD risk based on ancestry proportion between cases and controls. In Ulcerative colitis (UC), patients with a high Amerindian Ancestry Proportion (HAAP) were significantly linked to increased chances of resective surgery (OR = 4.27, CI = 1.41-12.94, p = 0.01), pouch formation (OR = 7.47, CI = 1.86-30.1, p = 0.003), and IBD reactivation during COVID-19 infection (OR = 5.16, CI = 1.61-6.53, p = 0.005). Whereas, in the Crohn's Disease (CD) group, the median Amerindian ancestry proportion was lower in the group with perianal disease (33.5% versus 39.5%, P value = 0.03). CD patients with High Amerindian Ancestry proportion had lower risk for surgery (OR = 0.17, CI = 0.03-0.83, P value = 0.02). Our study highlights the impact of Amerindian ancestry on IBD phenotypes, suggesting a role for genetic and ancestral factors in disease phenotype. Further investigation is needed to unravel the underlying mechanisms driving these associations.

Indexed as

Colitis, UlcerativeCrohn DiseaseHispanic or LatinoIndians, South AmericanAdultChileFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedPhenotypePolymorphism, Single NucleotideRisk FactorsWhite PeopleAncestryInflammatory bowel diseaseSouth America

Identifiers

PMID40316706
PMCPMC12048483

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Registered trials

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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.