Evidence map›Paper›PMID 30127557›Full record

ArticleIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion2018

Vitamin D Deficiency and Its Association with Inflammatory Markers, Lipid Profile and Regulatory T-cells in Pediatric Sickle Cell Disease Patients.

Yesim Oztas, Selma Unal, Gulcin Eskandari, Lulufer Tamer, Nuriman Ozgunes

Open access · bronzeAbstract read
In one paragraph

Article in Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
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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

5 authors at 2 institutions in 1 country.

Yesim Oztas1Department of Medical Biochemistry, Medical Faculty, Hacettepe University, Ankara, Turkey.ORCID 0000-0002-8638-9744
Selma Unal2Department of Pediatric Hematology, Medical Faculty, Mersin University, Mersin, Turkey.
Gulcin Eskandari3Department of Medical Biochemistry, Medical Faculty, Mersin University, Mersin, Turkey.
Lulufer Tamer3Department of Medical Biochemistry, Medical Faculty, Mersin University, Mersin, Turkey.
Nuriman Ozgunes1Department of Medical Biochemistry, Medical Faculty, Hacettepe University, Ankara, Turkey.
Mersin Üniversitesi · TRHacettepe University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated vitamin D deficiency in pediatric sickle cell disease patients and its association with selected bone, lipid and inflammatory parameters. The study included 64 patients (33 SS and 31 SB) and 21 carriers (AS). Blood was obtained to assess levels of vitamin D, WBC, CRP, Ca, P, ALP, PTH, triglyceride, total cholesterol, LDL, VLDL, HDL, IL-2, IL-12, TNF-α, IL-4, IL-6, IL-10 and regulatory T cells. The patients were grouped according to their genotype (SS, SB) and vitamin D status (low or normal). Carriers were also grouped as low or normal vitamin D. Laboratory findings were similar between low and normal Vit D groups in SS, SB and AS genotypes except a lower IL-12 in SB-low vitamin D compared SB-normal vitamin D group. Acute chest syndrome was more frequent in SS-low Vit D (63%) compared to SS-normal Vit D (25%), SB-low Vit D (21%) and SB-normal Vit D (33%) (

Indexed as

CytokineGenotypeLipidRegulatory T cellSickle cell diseaseTNF-αVitamin DVLDL

Identifiers

PMID30127557
PMCPMC6081317
OpenAlexW2763901059

What OpenQuestion holds

Textmetadata
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.