Evidence map›Paper›PMID 35682458›Full record

ArticleInternational journal of environmental research and public health2022

Hepcidin (rs10421768), Transferrin (rs3811647, rs1049296) and Transferrin Receptor 2 (rs7385804) Gene Polymorphism Might Be Associated with the Origin of Multiple Sclerosis.

Laura Stachowska, Dorota Koziarska, Beata Karakiewicz, Artur Kotwas, Anna Knyszyńska, Marcin Folwarski, Karolina Dec, Ewa Stachowska, Viktoria Hawryłkowicz, Monika Kulaszyńska and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of environmental research and public health, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-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

6 citing papers in PubMed, 6 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 1 country.

Laura StachowskaDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University in Szczecin, Broniewskiego 24, 71-460 Szczecin, Poland.ORCID 0000-0002-3386-8645
Dorota KoziarskaDepartment of Neurology, Pomeranian Medical University in Szczecin, Unii Lubelskiej 1, 72-252 Szczecin, Poland.
Beata KarakiewiczSubdepartment of Social Medicine and Public Health Department of Social Medicine, Pomeranian Medical University in Szczecin, Żołnierska 48, 71-210 Szczecin, Poland.ORCID 0000-0001-6527-7287
Artur KotwasSubdepartment of Social Medicine and Public Health Department of Social Medicine, Pomeranian Medical University in Szczecin, Żołnierska 48, 71-210 Szczecin, Poland.ORCID 0000-0002-6805-4713
Anna KnyszyńskaDepartment of Functional Diagnostics and Physical Medicine, Pomeranian Medical University in Szczecin, 71-210 Szczecin, Poland.ORCID 0000-0003-4030-3527
Marcin FolwarskiDepartment of Clinical Nutrition and Dietetics, Medical University of Gdansk, 80-211 Gdańsk, Poland.ORCID 0000-0002-7301-1689
Karolina DecDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University in Szczecin, Broniewskiego 24, 71-460 Szczecin, Poland.
Ewa StachowskaDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University in Szczecin, Broniewskiego 24, 71-460 Szczecin, Poland.ORCID 0000-0002-4009-1977
Viktoria HawryłkowiczDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University in Szczecin, Broniewskiego 24, 71-460 Szczecin, Poland.
Monika KulaszyńskaDepartment of Biochemical Science, Pomeranian Medical University in Szczecin, Broniewskiego 24, 71-460 Szczecin, Poland.
Joanna Sołek-PastuszkaDepartment of Anaesthesiology and Intensive Therapy, Pomeranian Medical University in Szczecin, Unii Lubelskiej 1, 72-252 Szczecin, Poland.
Karolina Skonieczna-ŻydeckaDepartment of Biochemical Science, Pomeranian Medical University in Szczecin, Broniewskiego 24, 71-460 Szczecin, Poland.ORCID 0000-0002-3430-9079
Pomeranian Medical University · PLGdańsk Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system in which there is a multifocal damage to the nerve tissue. Additionally, the literature emphasizes the excessive accumulation of iron in the central nervous system of patients, which is negatively correlated with their psychophysical fitness. Iron metabolism genes polymorphisms may modulate iron deposition in the body and thus affect the clinical course of MS. We aimed to assess the frequency of HAMP, TFR2, and TF polymorphisms in MS patients and their impact on the clinical course of the disease. The studied polymorphisms were identified by the Real-Time PCR using TaqMan technology. Neurological assessment by means of EDSS scale was conducted. This cross-sectional study included 176 patients, with the mean age of onset of symptoms at 30.6 years. The frequency of alleles of the studied polymorphisms was as follows: (a) HAMP rs10421768: A 75.9% (n = 267), G 24.1% (n = 65), (b) TF rs1049296: C 89.2% (n = 314), T 10.8% (n = 38), (c) TF rs3811647: A 39.8% (n = 140), G 60.2% (n = 212), (d) TFR2 rs7385804: A 59.1% (n = 59.1%), C 40.9% (n = 144). In the codominant inheritance model of TF rs1049269, it was shown that people with the CT genotype scored statistically significantly lower points in the EDSS scale at the time of diagnosis than those with the CC genotype (CC Me = 1.5, CT Me = 1.0 p = 0.0236). In the recessive model of TF inheritance rs3811647, it was noticed that the primary relapses were significantly more frequent in patients with at least one G allele compared with those with the AA genotype (AG + GG = 81.2%, AA = 18.8%, p = 0.0354). In the overdominant model rs7385804 TFR2, it was shown that among patients with the AA genotype, multiple sclerosis occurs significantly more often in relatives in a straight line compared with people with the AC and CC genotypes (AA = 100.0%, AC + CC = 0.0%, p = 0.0437). We concluded that the studied polymorphisms might affect the clinical course of MS.

Indexed as

Multiple SclerosisTransferrinAdultCross-Sectional StudiesGenotypeHepcidinsHumansIronPolymorphism, Single NucleotideReceptors, TransferrinHepcidinsIronReceptors, TransferrinTFR2 protein, humanTransferrinironmultiple sclerosisneurodegenerationpolymorphism

Identifiers

PMID35682458
PMCPMC9180173
OpenAlexW4281674020

What OpenQuestion holds

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LicenceCC BY
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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.