Evidence map›Paper›PMID 27186170›Full record

ArticleArchives of medical science : AMS2016

Impact of I/D polymorphism of ACE gene on risk of development and course of chronic obstructive pulmonary disease.

Radosław Mlak, Iwona Homa-Mlak, Tomasz Powrózek, Barbara Mackiewicz, Marek Michnar, Paweł Krawczyk, Marcin Dziedzic, Renata Rubinsztajn, Ryszarda Chazan, Janusz Milanowski and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Archives of medical science : AMS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 3 pooled it
2.3field-weighted citation impact, top 12% of its field
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

8 citing papers in PubMed, 3 syntheses or guidelines pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. International journal of chronic obstructive pulmonary disease · 2018
    Pooled it
  3. Pooled it
  4. Article
  5. Archives of medical science : AMS · 2021
    Review
  6. Article
  7. Article
  8. The Impact ofIn vivo (Athens, Greece)
    Review
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

11 authors at 2 institutions in 1 country.

Radosław MlakDepartment of Human Physiology, Medical University of Lublin, Lublin, Poland; Department of Oncology, Medical University of Lublin, Lublin, Poland.
Iwona Homa-MlakDepartment of Human Physiology, Medical University of Lublin, Lublin, Poland; Department of Oncology, Medical University of Lublin, Lublin, Poland.
Tomasz PowrózekDepartment of Oncology, Medical University of Lublin, Lublin, Poland.
Barbara MackiewiczDepartment of Oncology, Medical University of Lublin, Lublin, Poland.
Marek MichnarDepartment of Oncology, Medical University of Lublin, Lublin, Poland.
Paweł KrawczykDepartment of Oncology, Medical University of Lublin, Lublin, Poland.
Marcin DziedzicDepartment of Laboratory Diagnostics, Medical University of Lublin, Lublin, Poland.
Renata RubinsztajnDepartment of Internal Medicine, Pulmonology and Allergology, Medical University of Warsaw, Warsaw, Poland.
Ryszarda ChazanDepartment of Internal Medicine, Pulmonology and Allergology, Medical University of Warsaw, Warsaw, Poland.
Janusz MilanowskiDepartment of Oncology, Medical University of Lublin, Lublin, Poland.
Teresa Małecka-MassalskaDepartment of Human Physiology, Medical University of Lublin, Lublin, Poland.
Medical University of Lublin · PLMedical University of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic obstructive pulmonary disease (COPD) affects more than 10% of the world's population over 40 years of age. The main exogenous risk factor is cigarette smoking; however, only 20% of smokers develop COPD, indicating that some other factors, e.g. genetic, may play an important role in the disease pathogenesis. Recent research indicates that ACE (angiotensin-converting enzyme) may be a susceptibility gene for asthma or COPD. The aim of our study was to determine the influence of I/D (insertion/deletion) polymorphism of the ACE gene (AluYa5, rs4646994) on the risk and course of COPD. MATERIAL AND

methodsWe investigated ACE I/D polymorphism in 206 COPD and 165 healthy Caucasian subjects.

resultsIn the generalized linear model (GLZ) analysis of the influence of selected factors on presence of COPD we found a significant independent effect for male sex (repeatedly increases the risk of COPD, OR = 7.7, p = 0.049), as well as smoking or lower body mass index, but only in combination with older age (OR = 0.96, p = 0.003 and OR = 1.005, p = 0.04 respectively). Interestingly, analysis of factors which may influence the risk of a higher number of exacerbations demonstrated that occurrence of DD genotype, but only in men, is associated with a lower risk (OR = 0.7, p = 0.03) of this complication.

conclusionsWe suggest that ACE may not be a susceptibility gene for the origin of COPD but a disease-modifying gene. Since the impact of I/D polymorphism of the ACE gene on COPD risk is moderate or negligible, other molecular changes, that will help predict the development of this disease, should still be sought.

Indexed as

ACE polymorphismchronic obstructive pulmonary diseaseexacerbationrenin-angiotensin-aldosterone system

Identifiers

PMID27186170
PMCPMC4848351
OpenAlexW2397261178

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.