Despite the small sample size, this study suggests that IGF-I plays an important role in the pathogenesis of fibrosis, characteristic of morphoea. Studies on a larger number of patients with morphoea as well as on patients with systemic sclerosis are recommended. Furthermore, therapeutic trials using IGF-I antagonist (octreotide) are highly recommended in patients with morphoea.

Background Persistence of hepatitis C virus (HCV) infection and response to antiviral therapy has been shown to be associated with inappropriate levels of cytokines and microRNAs (miRNAs). miRNA levels have been reported to fluctuate during treatment. Thus they could be useful predictors for responses to treatment among HCV infected patients, thereby reducing ineffective treatments. Aim The current study aimed to investigate the relation between miRNA‐21 expression profiles, transforming growth factor β (TGF‐β) serum levels and response to treatment with the new direct antiviral drugs (sofosbuvir + daclatasvir ± ribavirin), among HCV infected Egyptian patients. Subjects and Methods This prospective study was conducted on 50 HCV infected patients (before and after treatment) and 20 healthy volunteers. miRNA expression profiles were determined by real‐time polymerase chain reaction and TGF‐β1 serum levels were measured by using enzyme‐linked immunosorbent assay. Results There was a significant increase in serum albumin, platelets count and a significant decrease in liver enzymes, serum bilirubin, and prothrombin time after treatment. Significant reduction of viral load among HCV patients after receiving the treatment was reported. Concomitantly, there was an increase in the relative quantity of miRNA‐21 (P = .001*) and serum levels of TGF‐β1 ( P = .337) among HCV patients after receiving treatment. Conclusion Nearly all responders to direct antiviral drugs showed increased levels of both miRNA‐21 and TGF‐β1. This may indicate an interplay between TGF‐β1 and miRNA‐21 during remission or progression of viral infection. Thus miRNA‐21 could be used as promising serum biomarker, for assessment of antiviral treatment efficacy and improvement of fibrosis among chronically infected HCV patients.

Background: The metabolic syndrome (MetS) is a clustering of vascular risk factors that tend to increase the risk of occurrence of diabetes mellitus type 2 (DMT2), cardiovascular and cerebrovascular ischemic events. The aim of the present study is to investigate the association of extracranial and intracranial arterial atherosclerosis as well as silent brain infarction (SBI) with MetS, thereby determining the potential cerebrovascular atherosclerotic risk of MetS in the Egyptian population. Methods: A case control study was conducted on 50 Egyptian subjects with MetS and 30 without with age range from 40-60 years old. All participants were free from cerebrovascular ischemic events [stroke or transient ischemic attack (TIA)]. All participants underwent complete neurological examination, assessment of the diagnostic criteria for MetS, carotid and transcranial duplex ultrasonography (U/S) and brain MRI. Results: Preclinical carotid atherosclerosis (atherosclerotic plaques with <50% stenosis) was associated with MetS (P value = 0.02) that persisted after adjustment for age and other confounders. There was no significant association between increased intima media thickness (IMT) and MetS. There was non-significant association between MetS and intracranial atherosclerotic disease (ICAD) or the degree of intracranial stenosis (ICS). Conversely, there was a highly significant association between MetS and SBI even after adjustment for age and other confounders (P value = 0.001). Conclusion: Metabolic syndrome is an important factor associated with mild to moderate atherosclerosis (<50% stenosis) and silent brain infarcts among asymptomatic individuals. Interventions to reduce MetS are important for prevention of subclinical and clinical cerebral atherosclerotic disease.

Hepatitis C and brucellosis are infectious diseases that occur worldwide, and both are endemic in Egypt. Co-infection with both agents is possible, and this can involve the liver in various ways. In this study, we investigated serum tissue inhibitor metalloproteinase-1 (TIMP-1), viral load, and liver functions in patients co-infected with hepatitis C virus (HCV) before and after brucellosis treatment. Over 3 years, 241 consecutive HCV patients (before interferon therapy was received) with recurrent fever who had occupational contact with animals were tested for brucellosis co-infection by a standard tube agglutination test. In patients with dual infection, viraemia (RT-PCR), TIMP-1 measured by ELISA, and liver functions were assessed and re-evaluated 2 months after brucellosis treatment. The number of patients with HCV/brucellosis co-infection was 32 out of 241 (13.3%). TIMP-1, viraemia, AST, ALT and bilirubin showed significant decrease (improvement) after brucellosis treatment (p < 0.001) but an insignificant difference (p > 0.05) with regard to serum albumin and prothrombin concentration. The study revealed that brucellosis is an important infection in HCV-infected patients and can aggravate the course of disease, suggesting that early treatment and prevention are important.

Different genetic and environmental factors are implicated in type I diabetes (T1DM) pathogenesis. About 50% of the genetic susceptibility for T1DM is related to human leukocyte antigen (HLA) genes. Other non-HLA genes have variable roles in the destruction of pancreatic β cells. A highly variable gene called endoplasmic reticulum associated with antigen processing gene 1(ERAP1) shares in activating autoreactive CD8+ T lymphocytes, peptide trimming, and subsequent pancreatic β cells destruction. Local production of inflammatory cytokines within the cells of islets of Langerhans is linked to T1DM progression. Different viral and autoimmune disorders have been linked to genetic variations in type III interferon (IFNλs). This study aimed to determine genetic polymorphisms of interferon lambda 4 (IFNλ4rs 73555604) and endoplasmic reticulum aminopeptidases 1 (ERAP1 rs26618) in Egyptian patients with T1DM. The study recruited 120 patients with T1DM from Kafrelsheikh University Hospital and 100 normal controls who were age and sex matched with the patients’ group. Single-nucleotide polymorphism (SNP) genotyping of ERAP1(rs26618) and IFN-λ-4(rs73555604) was performed using real-time polymerase chain reaction. Patients with CC genotype were less likely to develop T1DM than those with TC and TT genotypes for both genes. In addition, T allele frequency in comparison to C allele frequency was significantly increased in T1DM patients when compared to control group (p<0.001). There were positive correlations between studied SNPs for both genes, fasting and postprandial blood glucose levels which suggest the association of these genes with T1DM occurrence. We concluded that the studied SNPs of ERAP1gene (rs26618) and IFNλ-4 gene(rs73555604) may be associated with T1DM development. In addition, T alleles for both genes could be considered risk alleles while C alleles would be regarded as a protective allele. Patients with TC and TT genotypes would be at a higher risk for T1DM than those carrying CC genotype.