Evidence map›Paper›PMID 33727573›Full record

Trial reportScientific reports2021

Analysis of the frequency of single nucleotide polymorphisms in cytokine genes in patients with New Onset Diabetes After Transplant.

Mohamed Jahromi, Torki Al-Otaibi, Osama Ashry Gheith, Nashwa Farouk Othman, Tarek Mahmoud, Parasad Nair, Medhat A-Halim, Parul Aggarwal, Grace Messenger, Philip Chu and 2 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Scientific reports, 2021. 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
0.2field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

12 authors at 6 institutions in 5 countries.

Mohamed JahromiClinical Research, Medical Division, Dasman Diabetes Institute, Kuwait City, Kuwait. mjahromi@yahoo.com.
Torki Al-OtaibiNephrology Department, Hamad Al-Essa Organ Transplantation Center, Kuwait City, Kuwait.
Osama Ashry GheithNephrology Department, Hamad Al-Essa Organ Transplantation Center, Kuwait City, Kuwait.
Nashwa Farouk OthmanCommunity department, Faculty of Nursing, Manoura University, Mansoura, Egypt.
Tarek MahmoudNephrology Department, Hamad Al-Essa Organ Transplantation Center, Kuwait City, Kuwait.
Parasad NairNephrology Department, Hamad Al-Essa Organ Transplantation Center, Kuwait City, Kuwait.
Medhat A-HalimNephrology Department, Hamad Al-Essa Organ Transplantation Center, Kuwait City, Kuwait.
Parul AggarwalVontz Center, University of Cincinnati, Cincinnati, USA.
Grace MessengerPodiatry Department, Dasman Diabetes Institute, Kuwait City, Kuwait.
Philip ChuSehatek Awal, Manama, Bahrain.
Sacha A De SerresCHU de Québec - Université Laval, Quebec, QC, Canada.
Jamil R AzziKidney Division, Transplantation Research Center, Harvard Medical School, Brigham and Women's Hospital, Boston, USA.
Dasman Diabetes Institute · KWBahrain Center for Strategic International and Energy Studies · BHBrigham and Women's Hospital · USMansoura University · EGUniversité Laval · CAUniversity of Cincinnati · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

New Onset Diabetes After Transplantation (NODAT) is a serious metabolic complication. While β-cell dysfunction is considered the main contributing factor in the development of NODAT, the precise pathogenesis is not well understood. Cytokines are thought to be involved in the inflammation of islet β-cells in diabetes; however, few studies have investigated this hypothesis in NODAT. A total of 309 kidney transplant recipients (KTRs) were included in this study. An association between kidney transplants, and the development of diabetes after transplant (NODAT) was investigated. Comparison was made between KTRs who develop diabetes (NODAT cases) or did not develop diabetes (control), using key cytokines, IL-6 G (- 174)C, macrophage mediator; IL-4 C (- 490)T, T helper (Th)-2 cytokine profile initiator; Th-1 cytokine profile initiator interferon-γ T (+ 874) A gene and TGF β1 C (+ 869) T gene polymorphisms were investigated. The genes were amplified using well-established polymerase chain reaction (PCR) techniques in our laboratory. Compared to the AA and AT genotypes of interferon gamma (IFNG), there was a strong association between the TT genotype of IFNG and NODAT kidney transplant recipients (KTRs) versus non-NODAT KTRs (p = 0.005). The AA genotype of IFNG was found to be predominant in the control group (p = 0.004). Also, significant variations of IL6 G (- 174) C, IL-4 C (- 590) T, interferon-γ T (+ 874) A gene and transforming growth factor β1 C (+ 869) T may contribute to NODAT. Our data is consistent with theTh-1/T-reg pathway of immunity. Further larger pan Arab studies are required to confirm our findings.

Indexed as

Diabetes MellitusKidney TransplantationPolymorphism, Single NucleotideAdultCytokinesFemaleHumansMaleMiddle AgedCytokines

Identifiers

PMID33727573
PMCPMC7966742
OpenAlexW3138601058

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.