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Introduction: The plasma levels of the cytokine interleukin-6 (IL-6) have been reported to be associated with risk of chronic kidney disease (CKD) and erythropoietin (EPO) responsiveness. The G/C promoter polymorphism of IL-6 is associated with expression and levels of IL-6, so it may confer increased risk to CKD and modulate EPO responsiveness. Objectives: This study aimed to examine the association of IL-6 G/C polymorphism with risk of CKD and EPO hyporesponsiveness. Patients and Methods: A total of 40 haemodialysis patients on EPO therapy, and 30 age- and sexmatched apparently healthy volunteers as a control group were recruited for this study. Blood samples were collected from each participant and used for complete blood count (CBC) using automated haematology analyser and molecular analysis of IL-6 -174 G/C polymorphism using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The results showed that IL-6 GG genotype is the most frequent in patients (82.5%) followed by GC genotype (17.5%), while all subjects of the control group were found to have GG genotype only. There was a statistically significant association between the polymorphism and end-stage CKD (P = 0.02). Only 10% of the patients were found to achieve the target haemoglobin level. Although all of them had GG genotype, no association was found between the polymorphism and the achievement of target haemoglobin level (P = 0.16). Conclusion: IL-6 G/C polymorphism is significantly associated with CKD, but not with EPO responsiveness in haemodialysis patients. [ABSTRACT FROM AUTHOR]

Context: Sickle cell anemia (SCA) is a group of hemoglobin disorders in which the sickle β-globin gene is inherited. It is associated with many complications; most of them are related to thrombotic events. Aim: This study aimed to investigate the association between angiotensin converting enzyme (ACE) insertion/deletion polymorphism and complications of SCA. Settings and Design: A case-control study was conducted in Khartoum state. Subjects and Methods: A total of 50 patients with SCA and 40 healthy volunteers as a control group were enrolled in this study. Three milliliters of ethylenediamine tetraacetic acid anticoagulated blood were collected from each subject, DNA was extracted by salting-out method, and target DNA regions of the ACE gene were amplified using allele-specific polymerase chain reaction. Statistical Analysis Used: Data of this study was analyzed by Statistical Package for Social Sciences. Frequency of qualitative variables was calculated, and correlation was tested by Chi-square test. Regression was used to investigate the association between the polymorphism and complications of SCA. Results: The frequencies of the DD, ID, and II genotypes were 42%, 50%, and 8%, respectively, for patients, whereas in the control group, it was 80% for DD genotype and 20% for ID, while II genotype was totally absent. The regression analysis showed no statistically significant association between the disease complications and each of the ACE polymorphic genotypes. Conclusion: No statistically significant association was found between ACE polymorphism and complications of SCA. [ABSTRACT FROM AUTHOR]

Background: Genetic polymorphisms of platelet glycoprotein IIIa ( GPIIIa gene) have been investigated intensively in several thrombotic diseases, but their role in cardiovascular diseases remains controversial. This study aimed to investigate the association between platelet glycoprotein IIIa PlA1/PlA2 polymorphism and susceptibility to myocardial infarction in non-diabetics., Methods: A total of 200 participants were recruited for the study, 100 non-diabetic patients with myocardial infarction and 100 apparently healthy volunteers as a control group. GPIIIa PlA1/PlA2 polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism., Results: The distribution of GPIIIa PlA1/PlA2 polymorphic genotypes among the study groups was significantly different (P value = 0.00). The PlA1/PlA2 and PlA2/PlA2 genotypes were more frequent in the patients with myocardial infarction while the genotype PlA1/PlA1 was more prevalent in the control group. There was a statistically significant association between the PlA1/PlA1 genotype and reduced risk of both ST-segment elevation myocardial infarction (odds ratio (OR) = 0.19; 95% confidence interval (CI): 0.09 - 0.34, P value = 0.00) and non-ST-segment elevation myocardial infarction (OR = 0.21; 95% CI: 0.09 - 0.45, P value = 0.00). The genotype PlA1/PlA2 was found to be associated with an increased risk of both types of myocardial infarction (OR = 6.0; 95% CI: 2.61 - 13.8, P value = 0.00 for ST-segment elevation myocardial infarction and OR = 6.65; 95% CI: 2.69 - 16.45, P value = 0.00 for non- ST-segment elevation myocardial infarction. In the patients carrying the PlA1/PlA2 genotype, the risk of ST-segment elevation myocardial infarction was increased to about 14 folds in the presence of family history (OR: 13.57, 95% CI: 1.42 - 130.03, P value = 0.02), and the risk of non-ST-segment elevation myocardial infarction increased to about 18 folds in the smokers carrying the genotype PlA2/PlA2 (OR: 17.63, 95% CI: 0.96 - 324.70, P value = 0.05)., Conclusions: The GPIII PlA1/PlA1 genotype is associated with a reduced risk of ST-segment elevation and non-ST-segment elevation myocardial infarction, while PlA1/PlA2 is associated with an increased risk of both types of myocardial infarction., Competing Interests: The authors declare that there is no conflict of interest., (Copyright 2024, Mohamed Ahmed et al.)

Background: Thrombosis plays a crucial role in the morbidity and mortality of coronavirus disease-19 (COVID-19). About one-third of COVID-19 patients experience a thrombotic event, most commonly pulmonary embolism. Based on published data, the mechanism of thrombosis in COVID-19 patients seems to be multi-factorial., Methods: In this article, we reviewed the publsihed data concerning with thrombosis in COVID-19 and summarized the predisposing factors and the mechanisms behind COVID-19 related thrombosis., Results: Inflammatory response to SARS-CoV-2 and the consequent hyperviscosity thought to cause endothelial damage and initiate coagulation. Furthermore, inflammation promotes platelet activation and exerts a pathogenic effect on endothelial cells. The presence of anticardiolipin and anti-β2-glycoprotein antibodies in some patients with COVID-19 suggests that SARS-CoV-2, like many other viral infections, induces the formation of antiphospholipid antibodies, which provoke hypercoagulability. Thrombophilic mutations, mainly factor V Leiden and prothrombin G20201A mutations, can be a contributing factor in the development of thrombosis in COVID-19 patients, and they are associated with increased disease severity and pulmonary embolism. However, the research concerning with the association of thrombophilic mutations with COVID-19 related thrombosis showed conflict results., Conclusion: The mechanism of thrombosis in COVID-19 patients seems to be multifactorial. Endothelial damage, antiphospholipid antibodies, inflammation, hyperviscosity, and thrombophilic mutations are the main factors that predispose COVID-19 patients to. thrombosis., Competing Interests: There are no conflicts of interest., (© 2022 Elshazali Widaa Ali, Ibrahim Khedir Ibrahim.)