Viral hepatitis is the leading cause of liver disease worldwide and can be caused by several agents, including hepatitis A (HAV), B (HBV), and C (HCV) virus. We employed multiplexed protein immune assays to identify biomarker signatures of viral hepatitis in order to define unique and common responses for three different acute viral infections of the liver. We performed multianalyte profiling, measuring the concentrations of 182 serum proteins obtained from acute HAV- (18), HBV- (18), and HCV-infected (28) individuals, recruited as part of a hospital-based surveillance program in Cairo, Egypt. Virus-specific biomarker signatures were identified and validation was performed using a unique patient population. A core signature of 46 plasma proteins was commonly modulated in all three infections, as compared to healthy controls. Principle component analysis (PCA) revealed a host response based upon 34 proteins, which could distinguish HCV patients from HAV- and HBV-infected individuals or healthy controls. When HAV and HBV groups were compared directly, 34 differentially expressed serum proteins allowed the separation of these two patient groups. A validation study was performed on an additional 111 patients, confirming the relevance of our initial findings, and defining the 17 analytes that reproducibly segregated the patient populations.This combined discovery and biomarker validation approach revealed a previously unrecognized virus-specific induction of host proteins. The identification of hepatitis virus specific signatures provides a foundation for functional studies and the identification of potential correlates of viral clearance.
Numerous immune cells are involved in developing multiple sclerosis (MS). Monocytes are believed to be the first to enter the brain and initiate inflammation. The role of monocyte subtypes in MS needs to be better understood. Objective: The current study aims to investigate the presence of different subsets of monocytes in relapsing-remitting MS (RRMS) Egyptian patients and their correlation with disease activity.
The aim of this study was to evaluate the metabolic effects of 12-week honey consumption on patients suffering from type 1 diabetes mellitus (DM). This was a randomized crossover clinical trial done in the National Institute for Diabetes and Endocrinology, Cairo, Egypt. Twenty patients of both sexes aged 4–18 years with type 1 DM and HbA1C<10% participated in the study. They were randomized into two equal groups (intervention to control and control to intervention). The dietary intervention was 12-week honey consumption in a dose of 0.5 mL/kg body weight per day. The main outcome measures were serum glucose, lipids, and C-peptide, and anthropometric measurements. None of participants were lost in follow-up. The intervention resulted in significant decreases in subscapular skin fold thickness (SSFT; P=.002), fasting serum glucose (FSG; P=.001), total cholesterol (P=.0001), serum triglycerides (TG; P=.0001), and low-density lipoprotein (P=.0009), and significant increases in fasting C-peptide (FCP; P=.0004) and 2-h postprandial C-peptide (PCP; P=.002). As possible long-term effects of honey after its withdrawal, statistically significant reductions in midarm circumference (P=.000), triceps skin fold thickness (P=.006), SSFT (P=.003), FSG (P=.005), 2-h postprandial serum glucose (P=.000), TG (P=.003), and HbA1C (P=.043), and significant increases in FCP (P=.002) and PCP (P=.003) were observed. This small clinical trial suggests that long-term consumption of honey might have positive effects on the metabolic derangements of type 1 DM.
Abstract Background Diversity of risk factors, namely, vitamin D and lipid panel abnormalities, are connected to multiple sclerosis (MS) etiology and may possess an influential role on disease course. In a cross-sectional study, we correlated the demographic, clinical and radiological characteristics of 111 relapsing–remitting MS (RRMS) patients with their serum levels of vitamin D and lipid profile to evaluate the consequences of their abnormalities on disease activity and/or its progression. Results In the study group, the mean serum level of vitamin D was 18.93 ± 9.85 ng/mL, over 80% had insufficient level ( < 30 ng/mL) and significantly lower in females ( P = 0.011). Insufficient vitamin D significantly associated with high relapse frequency ( P = 0.005). Measurement the direction of this association showed that each 1 ng/mL increase in vitamin D was correlated with both decrease in annualized relapse rate (ARR) of 0.02 relapse/year ( P = 0.017) and with decrease in number of relapses during last 2 years of 0.02 relapse ( P = 0.045). Analysis of serum lipid panel showed a direct link between higher levels of TC and LDL to increased total number of relapses ( P < 0.001 and 0.003, respectively) and EDSS ( P = 0.001 and 0.022), also between higher TG and EDSS ( P = 0.001). This link became indirect between HDL and both total number of relapse and EDSS ( P = 0.001 and 0.001). Radiologically, positively linked confluent brain lesion to elevated TC and TG levels ( P = 0.001 and 0.002, respectively) and cord lesions to elevated TC ( P = 0.007). Longer disease duration positively associated with all lipids-related variables. As a direct effect on lipid metabolism, each 1 ng/mL increase in vitamin D was associated with reduction in serum TC of 1.48 mg/dL ( P = 0.002) and rise in HDL of 0.35 mg/dL ( P = 0.028). Conclusions Management of vitamin D insufficiency may decrease risk of higher ARR and the same for dyslipidemia in reduction of disability and confluent brain T2 lesion. Increasing vitamin D was positively correlated with HDL but negatively with TC.
Background: Amyotrophic lateral sclerosis is a progressive devastating neurodegenerative disorder.It is characterized by both upper and lower motor neuron degeneration, leading to progressive skeletal muscle atrophy, paralysis, and consequent death.The pathogenesis of ALS and the risk factors are still not fully understood.Yet, metabolic abnormalities and nutritional factors have been recently the focus of interest among the various aspects of consideration.Vitamin A metabolite; Retinoic acid plays an important role in motor neuron development and neurite regeneration and its only carrier protein is retinol-binding protein 4. Aim of the work: This study aimed to measure the serum level of retinol-binding protein4 (RBP4) and to investigate the association between the clinical aspects of ALS and serum retinolbinding protein 4 (RBP4) concentration as a potential biomarker for vitamin A metabolism in ALS patients.Subjects and methods: This is a case-control study performed in the neuromuscular unit, Neurology Department, Ain-Shams University hospital.The study period was one year.Forty ALS patients were recruited and matched with forty healthy controls of matched age and sex.A Quantitative determination of human retinol-binding protein 4 concentrations in serum was assayed by Quantikine ELISA kit (2017 R & D Systems, inc.).Results: Serum RBP4 level was statistically non significantly higher among the control group versus the ALS group. Conclusion:Serum RBP4 concentration was found to be lower although statistically nonsignificant in ALS patients than in the controls group, further studies are needed.
The aim of this work was to assess eotaxin 1 level in exhaled breath condensate of exacerbated and stable COPD patients in relation to normal subjects. There were 16 COPD patients (during infective exacerbation), 16 stable COPD patients and 20 healthy volunteers as controls matched with them in age, sex and smoking history. EBC was collected and concentration of eotaxin 1 was measured by using Human Eotaxin 1 ELISA Kits. The mean eotaxin 1 concentration in exhaled breath condensate of studied groups was 962.5 ± 150 pg/ml in the exacerbated COPD group, 427.8 ± 186.6 pg/ml in the stable group and 89.2 ± 47.5 pg/ml in the control group. Age, smoking, FVC, FEV1, and FEV1/FVC, showed no significant correlation with eotaxin 1 levels among all the studied groups. Eotaxin 1 levels in exhaled breath condensate of COPD patients during infective exacerbation was significantly higher than in stable COPD patients and both groups showed significant higher levels than the control group.
Backgrounds With 10% of the general population aged 15–59 years chronically infected with hepatitis C virus (HCV), Egypt is the country with the highest HCV prevalence worldwide. Healthcare workers (HCWs) are therefore at particularly high risk of HCV infection. Our aim was to study HCV infection risk after occupational blood exposure among HCWs in Cairo. Methodology/Principal Findings The study was conducted in 2008–2010 at Ain Shams University Hospital, Cairo. HCWs reporting an occupational blood exposure at screening, having neither anti-HCV antibodies (anti-HCV) nor HCV RNA, and exposed to a HCV RNA positive patient, were enrolled in a 6-month prospective cohort with follow-up visits at weeks 2, 4, 8, 12 and 24. During follow-up, anti-HCV, HCV RNA and ALT were tested. Among 597 HCWs who reported a blood exposure, anti-HCV prevalence at screening was 7.2%, not different from that of the general population of Cairo after age-standardization (11.6% and 10.4% respectively, p = 0.62). The proportion of HCV viremia among index patients was 37%. Of 73 HCWs exposed to HCV RNA from index patients, nine (12.3%; 95%CI, 5.8–22.1%) presented transient viremia, the majority of which occurred within the first two weeks after exposure. None of the workers presented seroconversion or elevation of ALT. Conclusions/Significance HCWs of a general University hospital in Cairo were exposed to a highly viremic patient population. They experienced frequent occupational blood exposures, particularly in early stages of training. These exposures resulted in transient viremic episodes without established infection. These findings call for further investigation of potential immune protection against HCV persistence in this high risk group.