Evidence map›Paper›PMID 30852808›Full record

ArticleIrish journal of medical science2019

Serum amyloid A levels are associated with polymorphic variants in the serum amyloid A 1 and 2 genes.

Kayleigh Griffiths, Alexander P Maxwell, Rachel V McCarter, Patrick Nicol, Ruth E Hogg, Mark Harbinson, Gareth J McKay

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In one paragraph

Article in Irish journal of medical science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of serum amyloid A in atherosclerosis.Current opinion in lipidology · 2019
    Review
  5. 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

7 authors at 1 institution in 1 country.

Kayleigh GriffithsCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
Alexander P MaxwellCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
Rachel V McCarterCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
Patrick NicolCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
Ruth E HoggCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
Mark HarbinsonCentre for Medical Education, Queen's University Belfast, Belfast, Northern Ireland.
Gareth J McKayCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland. g.j.mckay@qub.ac.uk.ORCID http://orcid.org/0000-0001-8197-6280
Queen's University Belfast · GB

Funding

Medical Research Council MC_PC_15025NI HSC STL/4936/14Royal Victoria Hospital Heart Trust Fund RG14-9
6 · The paper itself

Abstract

backgroundSerum amyloid A (SAA) is secreted by liver hepatocytes in response to increased inflammation whereupon it associates with high-density lipoprotein (HDL) and alters the protein and lipid composition of HDL negating some of its anti-atherogenic properties.

aimsTo identify variants within the SAA gene that may be associated with SAA levels and/or cardiovascular disease (CVD).

methodsWe identified exonic variants within the SAA genes by deoxyribonucleic acid (DNA) Sanger sequencing. We tested the association between SAA variants and serum SAA levels in 246 individuals with and without CVD.

resultsIncreased SAA was associated with rs2468844 (beta [β] = 1.73; confidence intervals [CI], 1.14-1.75; p = 0.01), rs1136747 (β = 1.53 (CI, 1.11-1.73); p = 0.01) and rs149926073 (β = 3.37 (CI, 1.70-4.00); p = 0.02), while rs1136745 was significantly associated with decreased SAA levels (β = 0.70 (CI, 0.53-0.94); p = 0.02). Homozygous individuals with the SAA1.3 haplotype had significantly lower levels of SAA compared with those with SAA1.1 or SAA1.5 (β = 0.43 (CI, 0.22-0.85); p = 0.02) while SAA1.3/1.5 heterozygotes had significantly higher SAA levels compared with those homozygous for SAA1.1 (β = 2.58 (CI, 1.19-5.57); p = 0.02).

conclusionsWe have identified novel genetic variants in the SAA genes associated with SAA levels, a biomarker of inflammation and chronic disease. The utility of SAA as a biomarker for inflammation and chronic disease may be influenced by underlying genetic variation in baseline levels.

Indexed as

AgedBiomarkersCardiovascular DiseasesFemaleHumansInflammationLipidsLipoproteins, HDLMaleMiddle AgedSerum Amyloid A ProteinBiomarkersLipidsLipoproteins, HDLSerum Amyloid A ProteinBiomarkerCardiovascular disease (CVD)Genetic variantsSerum amyloid A (SAA)

Identifiers

PMID30852808
OpenAlexW2922281536

What OpenQuestion holds

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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.