Mannose-Binding Lectin Serum Level and Gene Polymorphism in Systemic Lupus Erythematosus Egyptian Patients.

Systemic lupus erythematosus (SLE) is an autoimmune disease in which the complement system plays a role in its pathogenesis. Mannose-binding lectin (MBL) is a serum protein, being a component of innate immune system, it is responsible for lectin pathway of complement activation. The presence of several polymorphisms at the coding regions of the MBL-2 gene, especially single point mutation at codon 54, leads to decreased level and /or functional deficits of MBL, which seems to be a risk factor for occurrence of autoimmune diseases, such as in SLE. So, this study was carried out to determine the role of the serum MBL concentration and the genetic polymorphisms of MBL-2 gene exon 1 codon 54 in Egyptian patients with SLE. Forty-eight SLE patients and 48 matched healthy controls were investigated. MBL serum level was measured by ELISA technique. MBL-2 polymorphism at exon 1 codon 54 was determined by PCR-RFLP. Our results revealed a significant reduction in MBL serum level among SLE patient group in comparison to the control group (P < 0.001). MBL-2 genotyping among SLE patients, revealed the wild type (A/A) in 52.1% and mutant types (A/B, B/B) in 47.9%. While among healthy controls, the wild type was detected in 81.2% and the mutant types in 18.8% with a statistically significant association between this polymorphism and SLE susceptibility (P=0.008). Comparison of MBL serum level among different genotypes within the patient group showed that the mutant allele had a suppressive effect on MBL serum level. In conclusion, carrying MBL-2 exon-1 codon 54 variant allele B was shown to be a risk factor for SLE.

Prevalence of occult hepatitis C virus infection in patients who achieved sustained virologic response to direct-acting antiviral agents.

The reappearance of HCV infection months or years after sustained virologic response (SVR) may be due to the persistence of HCV in tissue cells in spite of being undetected in serum. This situation is known as occult hepatitis C infection (OCI). We aimed to assess the prevalence of OCI in Egyptian patients with chronic hepatitis C (CHC) who achieved SVR after treatment with direct-acting antiviral agents (DAA). We carried out a cross-sectional study at the Advanced Center for Liver Diseases of Zagazig University Hospitals and Al-Ahrar Viral Hepatitis Treatment Center, Sharkia Governorate, Egypt. One hundred and fifty adult patients with CHC, who achieved SVR 12-24 weeks after end of treatment with sofosbuvir/daclatasvir ± ribavirin (139 patients, 92.67%), sofosbuvir/ledipasvir ± ribavirin (eight patients, 5.33%), sofosbuvir/simeprevir (two patients, 1.33%), and ombitasvir/ paritaprevir/ritonavir + ribavirin (one patient, 0.67%), according to the Egyptian National Committee for Control of Viral Hepatitis, were included in the study. We tested these patients for HCV RNA in peripheral blood mononuclear cells (PBMCs) immediately after confirmation of SVR12-24 weeks. Statistical analysis was performed by means of the Shapiro-Wilk test, Mann-Whitney U test, Chi-square test, and Fisher's exact test. Seventeen patients (11.33%) were positive for PBMNCs HCV RNA. The prevalence of OCI was highest in patients treated with simeprevir/sofosbuvir (2/2 patients). There is a substantially high prevalence of OCI after treatment with DAAs. We recommend dual testing for HCV RNA in both serum and PBMCs at the end of treatment of HCV infection with DAAs and during validation of the SVR following the initial response.

Upregulation of microRNA-21 is a poor prognostic marker in patients with childhood B cell acute lymphoblastic leukemia.

OBJECTIVES: Many studies have demonstrated that microRNA-21 (miR-21) is an oncogene and is upregulated in tumor tissue. However, its association with B-cell acute lymphoblastic leukemia (B-ALL) remains poorly understood. METHODS: The expression of miR-21 was detected by real-time quantitative PCR in 75 children with de novo B-ALL as well as in 50 healthy controls. This study was conducted to evaluate the miR-21 as a biomarker for risk assessment, diagnosis and prognosis. RESULTS AND DISCUSSION: Compared with normal controls, miR-21 expression was significantly upregulated in childhood B-ALL patients. Using the receiver operating characteristic curve 3.23 was selected as the cut-off value of miR-21 expression in distinguishing patients from controls. Patients group with High miR-21 expression was significantly associated with those aged <2 and >10 years, lower platelets count, more incidence of CNS infiltration and poorer treatment outcome also, they showed a significantly poorer disease-free survival (DFS) and overall survival (OS) compared to those with low miR-21 expression group. Its expression was an independent prognostic marker according to multivariate analysis. CONCLUSION: This is the first report demonstrating the upregulation of miR-21 in childhood B-ALL, and its association with poor response to induction therapy, shorter DFS and OS. These results suggest that miR-21 upregulation represent an unfavorable prognostic marker in Childhood B-ALL.