Print ISSN: 0027-1446

Online ISSN: 2309-6217

Main Subjects : Medical Immunology


The Serum Level of Proinflammatory TNF-alpha Cytokine in Cyanotic and Acyanotic Congenital Heart Diseases in Mosul City

Asmaa Zeki Sheetawi; Firas Al-Tae; Ahmed Abdullah Ahmed; Mohammed Essmat Ahmed

Annals of the College of Medicine, Mosul, 2022, Volume 44, Issue 1, Pages 1-9
DOI: 10.33899/mmed.2022.133834.1146

Background:Tumor necrosis factor – alpha (TNF-α)  has been proposed to play an important role  in the etiopathology of congenital heart diseases (CHD) worldwide. However, no previous  study about the role of TNF-α in the pathogenesis of CHDs in Mosul city / Iraq has been reported .
Objectives:1) To evaluate the serum levels of TNF-α cytokine in cyanotic and a cyanotic congenital heart diseases (CHDs and to compare the results with control healthy children in Mosul city 2) To find any association between the level of this pro-inflammatory marker  and other  demographic parameters such as age and gender  3) To test the diagnostic validity of this cytokine for the diagnosis of CHD at different cut-off values.
Patients, materials and methods:A case-control study was conducted in the Department of Microbiology / College of Medicine / University of Mosul over two years and 3 months from April 2019 to July 2021. Twenty nine (29) child with a cyanotic congenital heart diseases and seventeen  (17) child with cyanotic heart diseases were included. Another Thirty one (31) healthy child were also included as a controls. . All patients were collected from Al-Khansa teaching hospital in Mosul city. The serum TNF-α concentration was measured in all participants by using ELISA.
Results: Mean age of children with acyanotic heart diseases (2.7 ± 2.9 years) did not significantly differ from that of cyanotics (2.1 ± 1.9) or healthy controls (3.1 ± 1.7) ,  (P>0.05). The average TNF-α level in acyanotic heart diseases was 321.18 ± 325.71 ng/l compared to 120.63 ± 84.33 ng/l in cyanotics and 119.01 ± 139.71 in healthy controls. TNF- α was significantly elevated in acyanotic heart diseases in comparison to healthy children (P = 0.003). No significant difference was noted between acyaotics and cyanotic heart diseases in regards to TNF- α concentrations (P = 0.07). No age or gender effects were noted on TNF-α concentration in both acyanotic and cyanotic heart diseases (P>0.05). At the best cut-off  value of 124 ng/l  TNF-α had a specificity of  90.32% , sensitivity of 48.28% and accuracy rate of 39% as indicated by AUC-ROC curve .
Conclusion: The current study showed  higher TNF- α in acyanotic (but not in cyanotic)  heart diseases compared to healthy controls. TNF-α had poor diagnostic utility to discriminate between CHD and healthy individuals and  therefore not recommended as valuable biological marker for the diagnosis of CHD.

Interleukin – 6 Serum Level and Single Nucleotide Gene -174 G/C promoter Polymorphism in Patients with Rheumatoid Arthritis / Iraq

Ruba Ahmed Ibrahim; Firas Al-Tae

Annals of the College of Medicine, Mosul, 2021, Volume 43, Issue 2, Pages 164-175
DOI: 10.33899/mmed.2021.131144.1108

Objective: To 1) assess IL-6 levels in the serum of patients with rheumatoid arthritis (RA). 2) study IL-6 promoter -174 G>C “single nucleotide polymorphism (SNP)” as an imminent factor for the disease development. 3) find any relation between the level of serum IL-6 cytokine and other parameters such as age, gender, clinical severity of diseases and “disease activity scores (DAS28)”.
Materials & methods: This research was carried out through a case – control approach at “Ibn – Senna Teaching Hospital” in Mosul city between November 2020 and July 2021. It included 61 RA patients diagnosed according to “ACR / EULAR 2010 criteria” and 50 healthy individuals. IL-6 serum levels were ascertained by ELISA and genotyping of IL-6 promoter was accomplished by “sequence-specific primer-polymerase chain reaction (SSP-PCR)”.
Results: Mean IL-6 level in RA (69.42 ng /l ± 62.99) was elevated in comparison to healthy people (14.66 ng /l ± 23.58), P < 0.001. No age or gender effects on IL-6 concentration were noted. The ideal cut-off of IL-6 for discrimination of RA with best discriminative utility compared to healthy controls was 22.80 ng/l. At this value the IL-6 sensitivity was 91.8%, specificity 82.0% and accuracy rate 73.80%. G/G genotype was the most pervasive genotype in both RA patients and controls (70.5% in RA and 64% in healthy controls). However, it did not seem to be a risk factor for RA development compared to G/C or C/C genotypes “(OR = 1.3438, 95% CI=0.605-2.984,P=0.469)”. The mean IL-6 level in patients with GG genotype was (73.70 ng / l ± 71.09) compared to  (58.37 ng /l ± 37.86) in patients with GC genotype. There was no significant difference in the IL-6 level between patients with GG and patients with GC genotypes (P = 0.2375). Although higher IL-6 mean concentration was reported in severe RA, however, no significant difference was found between patients with mild, moderate and severe RA respectively. No correlation of serum levels of IL-6 with genetic promoter polymorphism, clinical severity of diseases or DAS 28 score were reported. 
Conclusion: The concentration of serum IL-6 was elevated in RA in regard to healthy controls which confirmed its pivotal role in RA pathogenesis. Our data did not support the role of IL-6 promoter -174 G> C polymorphism as a risk factor for RA, nor seem to play a major role in the increase of IL-6 level among our patients with RA.