scholarly journals The role of IL-4 gene polymorphism in HCV-related hepatocellular carcinoma in Egyptian patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mohy-Eldin Abd-Elfattah ◽  
Mary Naguib ◽  
Mohammed Elkheer ◽  
Eman Abdelsameea ◽  
Ali Nada

Abstract Background Interleukin-4 (IL-4), a pleiotropic anti-inflammatory cytokine, is produced mainly by activated T helper 2 (Th2). Hepatocellular carcinoma (HCC) is a typical inflammation-related cancer. Alterations influencing IL-4 expression may disturb immune response and may be associated with HCC risk. We aimed to verify role of IL4 gene polymorphism (IL-4-589C/T (rs2243250)) in HCV-related hepatocellular carcinoma in Egyptian patients. IL-4-589C/T (rs2243250) polymorphism was examined in 50 patients with HCC on top of HCV, 40 patients with HCV-induced liver cirrhosis, and 30 healthy controls using the polymerase chain reaction- restriction fragment length polymorphism method. Results Overall IL-4 gene polymorphism (IL-4-589C/T (rs2243250)) showed significant difference between hepatocellular carcinoma group versus liver cirrhosis and healthy control groups. TT homozygous genotype was more prevalent in HCC group (24%) versus (5%) in liver cirrhosis and (3.3%) in control. TT homozygous genotype had 10 times more risk of hepatocellular carcinoma versus healthy control group and 6.33 times more risk versus cirrhotic patients group (p value = 0.018 and 0.016 respectively). Conclusion IL-4-589C/T (rs2243250) polymorphism, TT homozygous genetic model, may be a risk factor in HCV-related HCC in Egyptian patients.

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Nehal Atef elshabrawy ◽  
Hussein Sheashaa ◽  
Adel L Abdelsalam ◽  
Ahmed Mohammed Abd El Wahab

Abstract Background and Aims There are six IL-17-family ligands [IL-17A, IL-17B, IL-17C, IL-17D, IL-17E (IL-25) and IL-17F]. Interleukin-17A (IL-17A) also commonly called IL-17, is produced by the T helper17 (Th17) subset of CD4+ T cells.Interleukin-17 and other Th17 cytokines are linked to the pathogenesis of diverse autoimmune and inflammatory diseases. IL-17A is detected in synovial fluids and synovium from RA patients and induces proinflammatory cytokine production from synoviocytes, also expression of IL-17A was higher in SLE patients and its level positively correlated with the severity of lupus nephritis, because of its contribution to increasing anti-double-stranded DNA (dsDNA) antibody production in SLE. The aim of the present study is to determine the IL-17A gene polymorphism (rs2275913 G>A) frequency in patients with SLE and lupus nephritis, and to determine the association of this polymorphism with the disease activity. Method This cross-sectional, observational, case control study was carried out on 50 females patients, with their age ranged from 15 to 50 years (mean 25.67±9.29 years) with SLE attending Mansoura University Hospital .A control group of 50 healthy females of matched age were also included. The patient group was subdivided into patients with and those without lupus Nephritis (35 and 15 patients, respectively). Lupus nephritis was confirmed by renal biopsy. All patients were subjected to a thorough clinical evaluation and routine laboratory tests. SLEDAI score was calculated for all patients to determine the degree of lupus activity. DNA extraction was performed for all patients as well as controls, One SNPs of IL-17A (rs2275913G>A) was genotyped utilizing PCR- RFLP technique. Results The frequency of rs2275913 A allele was significantly higher in SLE patients than the control group (34.0% vs. 21.0%, respectively; p=0.04, OR =1.9, 95%CI =1.03-3.65). While G allele was significantly higher in control group, (P=0.04)). Moreover, AA genotype was significantly higher in the SLE patients than in the control group (8.0% vs. 0.0%, respectively; p=0.036) and associated with higher SLEDAI, ANA, and anti-dsDNA antibodies titer, (P=0.03, P=.039, P=0.047 respectively).on the other hand there was no significant difference in GG and GA genotypes in the SLE patients versus the control group. The frequency of both genotype GA and AA was higher in the SLE patients than the controls (60% vs. 42%, respectivley; OR=2.07, CI-95%=0.9-5.59); although the difference was not statistically significant (P= 0.07).Although A allele was numerically higher in lupus nephritis group versus non nephritis group(37.0% vs 27.0%, respectively), the Analysis of the frequency of IL-17A rs2275913 alleles and genotypes showed no statistical differences between the two groups. Moreover there was no statistical significance between different genotypes in cases of nephritis regard lupus nephritis class (P=0.9) and no statistical significance between different genotypes (GG-GA-AA) regarding activity indices (AI) or chronicity indices (CI) in lupus nephritis group (P=0.18, P=0.56 respectively). Conclusion We suggest that there was a significant association between IL-17A rs2275913 G>A polymorphism and SLE, as A allele and AA genotype were increased in SLE patients, lupus nephritis especially those with high activity


Folia Medica ◽  
2019 ◽  
Vol 61 (1) ◽  
pp. 69-75
Author(s):  
Serdar Olt ◽  
Orhan Öznas ◽  
Haydar Bağış ◽  
Eda Tahir Turanlı

Abstract Background: Previous studies have shown that chemerin has important roles in the development of obesity, insulin resistance, metabolic syndrome, polycystic ovary syndrome (PCOS) and T2DM. The main goal of our study was to investigate the role of Chemerin rs17173608 gene polymorphism in T2DM (type 2 diabetes mellitus). Materials and methods: 100 patients with T2DM and 50 healthy volunteers were included in the present study. DNA isolation from blood samples was performed with K1820-02 DNA Mini Kit. Chemerin gene polymorphism was detected by Tetra- Amplification Refractory mutation system polymerase chain reaction (T-ARMS-PCR). At the end of T-ARMS-PCR, samples were run using gel electrophoresis. Some samples were validated by sequence analysis. Results: In the genotype analysis, 18.0% of patients had TT genotype and 81.0% of TG genotype was detected. GG genotype was not detected in any patient. Genotype of 1 patient was unidentified. Genotype distribution of healthy control group was 12.0% TT genotype and 88.0% TG genotype. Similar to the T2DM group, the GG genotype was not detected in the control group. There was no statistically significant difference between T2DM group and healthy control group for TG and TT genotypes. Conclusion: To our knowledge, chemerin rs17173608 gene polymorphism has been investigated in T2DM for the first time herein. In the present study, the TT genotype ratios were higher in the T2DM subjects than in healthy subjects. G allele frequency in the T2DM group was lower than that in the control group. However, there was no statistically significant difference between the groups.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ashraf Khalil ◽  
Azza Elsheashaey ◽  
Eman Abdelsameea ◽  
Manar Obada ◽  
F. F. Mohamed Bayomy ◽  
...  

Abstract Background Bile acids are essential organic molecules synthesized from cholesterol in the liver and regarded as indicators of hepatobiliary impairment; however, their role in the pathogenesis of hepatocellular carcinoma (HCC) is still unclear. The study aimed to examine the feasibility of bile acids in distinguishing HCC from post hepatitis C virus liver cirrhosis. A UPLC/MS was used to measure 14 bile acids in patients with noncirrhotic HCV disease (n = 50), cirrhotic HCV disease (n = 50), hepatocellular carcinoma (n = 50), and control group (n = 50). Results The progression of liver cirrhosis to HCC was associated with a significant increase in serum bile acids compared to the normal or the noncirrhotic HCV disease (p < 0.05). The fold changes in bile acids concentrations showed a trend that HCC > cirrhotic HCV disease > noncirrhotic HCV disease. Four conjugated acids GCA, GCDCA, GUDCA, and TCDCA steadily increased across the different groups. ROC curves analysis revealed that these bile acids discriminated noncirrhotic liver patients from HCC (AUC 0.850–0.963), with a weaker potential to distinguish chronic liver cirrhosis from HCC (AUC 0.414–0.638). Conclusion The level of serum bile acid was associated primarily with liver cirrhosis, with little value in predicting the progress of chronic liver cirrhotic disease into hepatocellular carcinoma.


Author(s):  
Zainab A A Al-shamma

  Objective: The objective of this research was to study the possible role of renalase in the controlling blood pressure (BP) in patients with different stages of chronic kidney diseases (CKD) to decrease the incidents of cardiovascular disease in these patients.Methods: The serum levels of renalase were determined by enzyme-linked immune sorbent assay (ELISA) methods in 68 non-diabetic CKD patients in different stages (2–5). Fifty healthy control subjects were included in this study. Renalase high-sensitive C-reactive protein and Cystatin-C were measured by ELISA which is included first incubating the test serum in an antigen-coated polystyrene plate, then enzyme-labeled anti-immunoglobulin is added and the enzyme then remaining in plate after washing provides a measure of the amount of specific antibody in the serum, and in the final step, a substance is added that the enzyme can convert to some detectable signal, most commonly a color change in a chemical substrate.Results: There were a significant difference between serum levels of renalase, in CKD patients stage 5, and CKD patients 2–3 stage than in their healthy control group (p<0.05), in addition to a significant difference in renalase level between CKD stage, 2–3 and stage 5 (p<0.05). There was a significant positive correlation between serum renalase with systolic BP (p<0.05) in CKD patients stage 5. In addition, there was a significant negative correlation between the serum renalase and estimated glomerular filtration rate (p<0.05) in both groups.Conclusions: The main conclusion of the study was the positive significant correlation with systolic BP in CKD patients (stage 5). In addition, the serum renalase levels were elevated according the CKD stage in patients with CKD in different stages (2–5) and it increased with the deterioration of renal function. 


Genetika ◽  
2019 ◽  
Vol 51 (3) ◽  
pp. 1139-1149
Author(s):  
Suzana Cvjeticanin ◽  
Milan Terzic ◽  
Dejan Nikolic

Rheumatoid arthritis (RA) is a chronic synovial inflammatory autoimmune disease with multifactorial origin. With epigenetic and genetic mechanisms playing a role in the development of RA, the aim of our study was to evaluate the anthropogenetic variability in tested individuals that were diagnosed with rheumatoid arthritis, and the possible influence of gender in expression of illness. 100 patients with rheumatoid arthritis (RA) and 100 healthy control individuals were evaluated. For the estimation of the degree of recessive homozygosity, the homozygously recessive characteristics (HRC) test was performed testing 20 HRCs. There was a significant difference in the individual variations of 20 HRCs between the individuals of the control group and patients with RA (SX2=135.191; p<0.001). The mean values of the tested HRCs significantly differed between individuals of the control group and RA group (MV?SDControl group-5.97?2.02, MV?SDRA group-7.34?2.00, p=<0.001). There was a decrease in variability in the RA group versus the control group (VRA group=27.19%; VControl group=33.79%).There was significant difference in the frequencies of HRCs between those with and without RA in males (p<0.023) and in females (p<0.001). Our findings pointed to the higher degree of recessive homozygosity along with decreased variability in RA patients compared to a healthy control group. Therefore, it may be assumed that different genes in different proportions have certain influence in the processes responsible for RA susceptibility and its different degrees of expression.


Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4584
Author(s):  
Yen-Yang Chen ◽  
Chao-Long Chen ◽  
Chih-Che Lin ◽  
Chih-Chi Wang ◽  
Yueh-Wei Liu ◽  
...  

Tumor recurrence is the most common cause of death in hepatocellular carcinoma (HCC) patients who received liver transplantation (LT). Recently, lenvatinib was approved for the systemic treatment of unresectable HCC patients; however, the role of lenvatinib in HCC patients after LT remains unclear. There were 56 patients with recurrent HCC after LT from 2008 to 2018 in our institute, and 10 patients who received lenvatinib were identified. Additionally, to understand the difference in the clinical impact of lenvatinib in the LT and non-LT settings, 25 HCC patients without LT who underwent lenvatinib treatment were identified from our HCC database and regarded as the control group. In the LT group, partial response was 20% and stable disease was 50%, resulting in a disease control rate of 70%; the median progression-free survival (PFS), time to treatment failure (TTF) and overall survival (OS) were 3.7, 3.6 and 16.4 months, respectively. Adverse events (AEs) were predominantly grade 1–2 in severity, and the majority of patients tolerated the side effects. There was no significant difference in PFS/OS, and we observed a similar pattern of AEs between these two groups. Our study confirms the comparable efficacy and safety of lenvatinib in HCC patients with LT and non-LT in clinical practice.


2021 ◽  
pp. 1-7
Author(s):  
Rady Eid El-Araby ◽  
Rabab S. Hamad ◽  
Najla K. Al Abdulsalam ◽  
Ahmed R. Mashaal ◽  
Rady Eid El-Araby

Hepatocellular carcinoma (HCC) remains the main type of liver cancer. Understanding the molecular and immune mechanisms of HCC tumorigenesis are required to develop effective biomarkers. This study is designed to measure the circulating MMP9 and CEBPα to provide a diagnostic and prognostic biomarker for HCV-genotype (4) induced liver cirrhosis and carcinogenesis. This study included one hundred Egyptian patients, divided into two groups 50 patients each. The first group: classified into Chronic Liver Disease (CLD) without cirrhosis (n=25) and CLD with cirrhosis (n=25). The second group: classified into CLD patients with HCC, (n=25), and healthy control (25 volunteers). The expression of MMP9 and CEBPα genes were analysed using Real-Time PCR. Our results showed significant downregulation in MMP9 and CEBPα genes in cirrhotic and HCC patients (p< 0.001 and p<0.001) respectively. There was a significant (p< 0.001) diagnostic capacity between HCC patients against CLD with or without cirrhosis patients. Bioinformatics analysis revealed a relationship between MMP9 and CEBPα genes. In conclusion, the gradual decrease in the expression of MMP9 and CEBPα gene during the progression of the disease recommended use of MMP9 and CEBPα genes as a diagnostic and prognostic biomarker for both cirrhosis and HCC in HCV-genotype (4) patients.


2021 ◽  
Author(s):  
Dilek Karakaya ◽  
Gunes Cakmak Genc ◽  
Sevim Karakas Celik ◽  
Tugba Aktas ◽  
Taner Bayraktaroglu ◽  
...  

Abstract BackgroundHashimoto’s thyroiditis (HT) is the most frequent organ-specific autoimmune disease (AIT), which is called lymphocytic thyroiditis in which T helper-1 lymphocytes mediate the disease. IL-18 is expressed in thyroid follicular cells (TFCs) during HT. The findings of studies aimed at investigating the relationship between IL-18 and HT are highly contradictory. In this study, we aimed to investigate the association between IL-18 gene polymorphism and HT.Methods and ResultsThe study was included 97 patients diagnosed with HT and 86 volunteers in the healthy control group. The IL18-607C/A (rs1946518) ve -137G/C (rs187238) genotypes were determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. No significant difference in the mean ages and gender was observed between the groups (p = 0.763 and p = 0.658, respectively). -137 IL18 CG genotype is higher in HT than controls. The risk of the IL-18 CG genotype for HT patients was more than 2.237 times higher (OR; 2.237 %95 Cl: 1.195–4.187, p = 0.039) compared to that of the G/G genotype. Also, -607 AC genotype is higher in the control group than in the HT group (in individuals with the IL18 CG genotype).ConclusionsAccording to our results, the CG genotype might be a risk factor for HT. Conversely, there is a possibility that the AC genotype also plays a protective role against the condition. However, further studies will contribute to the emergence of new solutions by revealing the molecular and cellular mechanisms of HT.


2021 ◽  
Vol 15 (01) ◽  
pp. 123-130
Author(s):  
Ugur Kahveci ◽  
Seda Ozkan ◽  
Adem Melekoglu ◽  
Eren Usul ◽  
Gulfer Ozturk ◽  
...  

Introduction: The present study aimed to investigate the role of plasma presepsin in the early detection of septic shock and in determining the prognosis and mortality of patients with sepsis. Methodology: The study was conducted in the emergency department between 1 January 2017 and 1 July 2017. A total of 106 patients 18 years of age or older who were diagnosed with sepsis according to the quick sequential organ failure assessment (qSOFA) criteria were included in this prospective study. The patients’ symptoms, vital signs, additional diseases, demographic attributes, laboratory results, Mortality in Emergency Department Sepsis (MEDS) scores, imaging findings and treatments were recorded. Moreover, the patients’ blood samples were collected to measure plasma presepsin, procalcitonin and CRP levels. Results: In total, 55.7% of the patients were female. The median age of the patients was 78 (24–103) years, and their 30-day mortality rate was 67%. The presepsin level was significantly higher in the sepsis group than in the healthy control group (p < 0.001). The presepsin levels did not differ significantly between the sepsis and septic shock groups (p = 0.12). Similarly, the procalcitonin levels did not differ significantly between the sepsis and septic shock groups (p > 0.05). There was no significant difference in the presepsin, procalcitonin and CRP levels between survivor and non-survivor patients (p = 0.74). Conclusions: The plasma presepsin level was found to be ineffective in determining the incidence of septic shock and mortality in patients with sepsis in the emergency department.


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