Background: Despite numerous recent developments in an evidence-based approach to Premature Rupture of Membranes (PPROM) management, there is no widely accepted set of therapeutic techniques. A model for predicting intra-amniotic inflammatory markers is required to prevent a negative neonatal outcome in pregnant women with PPROM. This model has the potential to enhance pregnancy management and parental counselling for at-risk women. This is supported by the prevalence of bacterial infection in premature birth and its association with intra-amniotic inflammation. Objective: The aim of the current study is to determine whether serum interleukine-6 concentrations predict impeding preterm delivery. Patients and methods: This case control study included women with a singleton pregnancy, who were admitted to Maternity Hospital and diagnosed with PROM at gestational age from 24 week to 36 weeks. Participants were divided into Control Group consisted of 30 women who had at least one normal pregnancy without history of PROM, abortion, still birth, or preterm delivery and Study Group consisted of 30 women at high risk of preterm labor with history of at least one preterm labor or mid-trimester abortion. IL-6 was measured in studied groups. Results: For diagnosis of preterm labor (PTL), the best cutoff point of IL-6 was ≥64.5, with sensitivity 80%, specificity 100% and accuracy 90%. Area under the curve was statistically significant. Conclusion: With strong sensitivity and specificity, maternal blood IL-6 can be utilized as a biomarker to identify impending infection in PPROM patients. This information can also help the doctor modify treatment plans to optimize feto-maternal outcomes.
Hepatitis C virus (HCV) infection causes life threatening disease due to its persistence in the liver, over time leading to cirrhosis and hepatocellular carcinoma. Therapeutic intervention with interferon (INF)-alpha combined with ribavirin is aimed at viral clearance, Interferon and ribavirin might discontinue the virus induced hepatocytes damage, thus slowing down the progress to end-stage liver disease. It has been demonstrated that HCV virion, via major structure envelop (E) protein 2 or EIE2 complex could specifically bind to human CD81 molecule, thereby altering the cellular activities in B cells, T cells and natural killer (NK) cells. CD81, a surface protein belonging to the tetraspanin family, facilitates B-T cell interaction in the process of antigen presentation Evidence has revealed that CD81 on B and T cells substantially enhanced T helper IL-4 secretion and NK-cell CD81 enabled E2-mediated reduction of the IFN-gamma levels Those data suggest that CD81 might activate the pathway leading to a predominant type-2 immune response, and as such be prone to cause a strong antibody production but weak or insufficient cytotoxic activities to clear the.The aim of this work was to investigate the clinical relevance and the possible mechanism of CD81 down-regulation under IFNalpha treatment to detect possible role of CD 81in response to INF therapy of chronic HCV patients. Subjects and Methods: The study included: Group I: 10 healthy subjects. And 60 HCV patients classified into 3 groups: Group II: 20 chronic HCV patients have not received treatment Group IIIa: 20 chronic HCV patients have received treatment responsive to treatment Group IIIb: 20 chronic HCV patients have received treatment not responsive to treatment .the patients were subjected to: (CBC) .liver and kidney function tests and special investigation CD 81, CD19, CD 22. Results: TLC and PLT higher in group I while ALT and AST were significantly higher in group II, while T. bilirubin was significantly higher in group IIIb, Direct bilirubin was significantly higher in group II ,and Alb was significantly higher in group I ,ASMA and ANA more higher in group IIIb, AFP and TSH were significantly higher in group IIIb , there was negative correlation between CD81 and TLC positive correlation between ALT, AST and CD81 were positively correlated to T Bilirubin , D Bilirubin and CD81.There was also significant negative correlation between Albumin and CD81. CD81, CD19, CD22 and Lymphocytes were significantly higher in group IIIb. Conclusion: In conclusion, CD81 down-regulation is a primary host response to interferon-alpha-based therapy and an immunophenotype associated with anti-HCV sustained virological response (SVR)
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