Evidence map›Paper›PMID 33173066›Full record

ArticleScientific reports2020

Single nucleotide polymorphisms in LCAT may contribute to dyslipidaemia in HIV-infected individuals on HAART in a Ghanaian population.

Simon Bannison Bani, Kwabena Owusu Danquah, Christian Obirikorang, William K B A Owiredu, Lawrence Quaye, Edmund Muonir Der, Emmanuel Acheampong, Yussif Adams, Peter Paul M Dapare, Moses Banyeh and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Simon Bannison BaniDepartment of Biomedical Laboratory Sciences, School of Allied Health Sciences, University for Development Studies, Tamale, Ghana.
Kwabena Owusu DanquahDepartment of Medical Diagnostics, Faculty of Allied Health Sciences, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Christian ObirikorangDepartment of Molecular Medicine, School of Medicine and Dentistry, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana. krisobiri@yahoo.com.
William K B A OwireduDepartment of Molecular Medicine, School of Medicine and Dentistry, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Lawrence QuayeDepartment of Biomedical Laboratory Sciences, School of Allied Health Sciences, University for Development Studies, Tamale, Ghana.
Edmund Muonir DerDepartment of Pathology, School of Medicine and Health Sciences, University for Development Studies, Tamale, Ghana.
Emmanuel AcheampongDepartment of Molecular Medicine, School of Medicine and Dentistry, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Yussif AdamsDepartment of Biomedical Laboratory Sciences, School of Allied Health Sciences, University for Development Studies, Tamale, Ghana.
Peter Paul M DapareDepartment of Biomedical Laboratory Sciences, School of Allied Health Sciences, University for Development Studies, Tamale, Ghana.
Moses BanyehDepartment of Biomedical Laboratory Sciences, School of Allied Health Sciences, University for Development Studies, Tamale, Ghana.
Enoch Odame AntoDepartment of Medical Diagnostics, Faculty of Allied Health Sciences, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Samuel Asamoah SakyiDepartment of Molecular Medicine, School of Medicine and Dentistry, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.
Kwame Nkrumah University of Science and Technology · GHUniversity for Development Studies · GH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Highly active antiretroviral therapy (HAART) is known to cause lipid abnormalities such as dyslipidaemia in HIV-infected individuals. Yet, dyslipidaemia may not independently occur as it may be worsened by single nucleotide polymorphisms (SNPs) in lecithin cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL). This case-control study was conducted in three-selected hospitals in the Northern part of Ghana. The study constituted a total of 118 HIV-infected participants aged 19-71 years, who had been on HAART for 6-24 months. Dyslipidaemia was defined based on the NCEP-ATP III criteria. HIV-infected individuals on HAART with dyslipidaemia were classified as cases while those without dyslipidaemia were grouped as controls. Lipid profile was measured using an automatic clinical chemistry analyzer and genomic DNA was extracted for PCR (GeneAmp PCR System 2700). Overall, the prevalence of dyslipidaemia was 39.0% (46/118). High levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and reduced levels of high-density lipoprotein cholesterol (HDL-C) were observed in all cases. A total of 256 selected PCR amplicons comprising 137 LPL (exons 3, 5 and 6) and 119 LCAT (exons 1, 4, and 6) were sequenced in 46 samples (Inqaba Biotech). Six (6) clinically significant SNPs were identified in exons 1 and 4 for LCAT whereas 25 non-clinically significant SNPs were identified for LPL in exons 5 and 6. At position 97 for LCAT exon 1, there was a deletion of the nucleotide, 'A' in 32.5% (13/40) of the sampled population while 67.5% (27/40) of the sample population retained the nucleotide, 'A' which was significantly associated with dyslipidaemic outcomes in the study population (p = 0.0004). A total of 25 SNPs were identified in exons 5 and 6 of LPL; 22 were substitutions, and 3 were insertions. However, none of the 25 SNPs identified in LPL exon 5 and 6 were statistically significant. SNPs in LCAT may independently contribute to dyslipidaemia among Ghanaian HIV-infected individuals on HAART, thus, allowing genetic and/or functional differential diagnosis of dyslipidaemia and creating an opportunity for potentially preventive options.

Indexed as

AdolescentAdultCase-Control StudiesCholesterolCholesterol, HDLCholesterol, LDLDyslipidemiasExonsGhanaHIV InfectionsHumansMiddle AgedPhosphatidylcholine-Sterol O-AcyltransferasePolymerase Chain ReactionPolymorphism, Single NucleotideSequence Analysis, DNACholesterolCholesterol, HDLCholesterol, LDLPhosphatidylcholine-Sterol O-AcyltransferaseTriglycerides

Identifiers

PMID33173066
PMCPMC7655843
OpenAlexW3099062572

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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.