The Prognostic Value of Different Levels of Cortisol and High-Sensitivity C-Reactive Protein in Early Acute Pancreatitis.

BACKGROUND: Acute pancreatitis (AP) ranges in severity from mild to severe with high mortality. Severe AP, similar to other critical illnesses, is associated with changes in cortisol level. Early increase of high-sensitivity C-reactive protein (hs-CRP) as an inflammatory marker could be an indicator of AP progression. We aimed to assess the level of cortisol and hs-CRP on initial diagnosis of AP and identify their prognostic value. METHODS: This case-control study included patients with AP and a control group of healthy subjects. Laboratory tests such as liver profile, kidney functions, blood picture, lactate dehydrogenase, blood glucose, and lipogram were evaluated, the severity of AP was determined, the duration of hospitalization, complications, and outcomes were identified, and the serum levels of cortisol and hs-CRP were assessed. RESULTS: There were 90 patients with AP and 60 controls with a higher percent of females in both groups. Serum cortisol and hs-CRP were significantly higher in AP relative to controls and were higher in severe AP relative to mild AP. Significant positive correlation was present between high cortisol and severity of AP (r = 0.520 and p<0.001) and negatively with pancreatic necrosis (r= - 0.303 and p = 0.007) and morality (r= - 0.432, p = 0.005) while hs-CRP did not show significant correlation. CONCLUSIONS: Different levels of serum cortisol in early AP should be considered on initial diagnosis. High cortisol level was a good prognostic indicator for AP with low mortality. This could have further implications on the appropriate initiation of steroid therapy to prevent necrotizing pancreatitis and lower the mortality. Meanwhile, hs-CRP has a low prognostic value in early AP.

Antimicrobial Resistance and Comparative Genome Analysis of Klebsiella pneumoniae Strains Isolated in Egypt.

Klebsiella pneumoniae is an important human pathogen in both developing and industrialised countries that can causes a variety of human infections, such as pneumonia, urinary tract infections and bacteremia. Like many Gram-negative bacteria, it is becoming resistant to many frontline antibiotics, such as carbapenem and cephalosporin antibiotics. In Egypt, K. pneumoniae is increasingly recognised as an emerging pathogen, with high levels of antibiotic resistance. However, few Egyptian K. pneumoniae strains have been sequenced and characterised. Hence, here, we present the genome sequence of a multidrug resistant K. pneumoniae strain, KPE16, which was isolated from a child in Assiut, Egypt. We report that it carries multiple antimicrobial resistance genes, including a blaNDM-1 carbapenemase and extended spectrum ß-lactamase genes (i.e., blaSHV-40, blaTEM-1B, blaOXA-9 and blaCTX-M-15). By comparing this strain with other Egyptian isolates, we identified common plasmids, resistance genes and virulence determinants. Our analysis suggests that some of the resistance plasmids that we have identified are circulating in K. pneumoniae strains in Egypt, and are likely a source of antibiotic resistance throughout the world.

Antimicrobial resistance and gene regulation in Enteroaggregative Escherichia coli from Egyptian children with diarrhoea: Similarities and differences.

Enteroaggregative Escherichia coli (EAEC) is a common diarrhoeagenic human pathogen, isolated from patients in both developing and industrialized countries, that is becoming increasingly resistant to many frontline antibiotics. In this study, we screened 50 E. coli strains from children presenting with diarrhea at the outpatients clinic of Assiut University Children's Hospital, Egypt. We show that all of these isolates were resistant to multiple classes of antibiotics and identified two as being typical EAEC strains. Using whole genome sequencing, we determined that both isolates carried, amongst others, blaCTX-M and blaTEM antibiotic resistance genes, as well as many classical EAEC virulence determinants, including the transcriptional regulator, AggR. We demonstrate that the expression of these virulence determinants is dependent on AggR, including aar, which encodes for a repressor of AggR, Aar. Since biofilm formation is the hallmark of EAEC infection, we examined the effect of Aar overexpression on both biofilm formation and AggR-dependent gene expression. We show that whilst Aar has a minimal effect on AggR-dependent transcription it is able to completely disrupt biofilm formation, suggesting that Aar affects these two processes differently. Taken together, our results suggest a model for the induction of virulence gene expression in EAEC that may explain the ubiquity of EAEC in both sick and healthy individuals.

Impact of the etiology and Vitamin D receptor TaqI rs731236 gene polymorphism on the severity of acute pancreatitis.

BACKGROUND/PURPOSE: This work aimed to assess the impact of different etiologies of acute pancreatitis (AP) and vitamin D receptor (VDR) TaqI rs731236 gene polymorphism on the severity of AP. METHODS: This case-control study included 70 patients with AP and 40 healthy controls. Etiologies of AP were identified by imaging, ANA, cytomegalovirus (CMV) IgM, coxsackie B virus IgM, and IgG4. Genotyping of VDR TaqI rs731236 polymorphism, Laboratory tests and severity scores using Ranson, BISAP, Atlanta and APACHE II scores were determined. RESULTS: The age in AP patients was 36.03 ± 10.76, and females were 85.7%. The etiologies of AP were as follows: biliary (51.4%), coxsackievirus (22.9%), autoimmune (14.3%), post-ERCP (8.6%) and 2.9% were idiopathic. The TT genotype of VDR polymorphism was significantly more common in AP than control (P = .001) and allele T dominated in AP group (OR = 2; 95% CI: 0.665-5.64). Most cases showed low severity scores with significant differences among etiologies and VDR genotypes. Biliary pancreatitis showed highest percentages of severe AP. However, etiologies and VDR polymorphism were not predictors of severity. CONCLUSION: Etiology of AP could have impact on the disease severity. VDR gene polymorphism increases the risk of AP. Neither the etiology nor VDR gene polymorphism could predict AP severity.

IP-10 Levels in Patients Infected with HBV Predicts The Response to Treatment with Entecavir.

Interferon--inducible protein-10 (IP-10), is an inflammatory cytokine produced by different subsets of the immune cells and induces chemotaxis, apoptosis, growth of cells and angiostasis after binding to its receptor CXCR3. Inflammatory disorders, involving infectious diseases, immune dysfunction, and tumour growth have been linked to changes in CXCL10 levels. We aimed to investigate serum levels of IP-10 in chronic HBV infected patients undergoing treatment with entecavir and possible correlation with response to therapy. A total of 53 chronic HBV infected patients and 25 healthy controls were enrolled in this study. Patients included 20 with cirrhosis and 33 non-cirrhotic individuals. All patients received 0.5 mg/day entecavir and serum IP-10 level was determined by ELISA at baseline and at week 24 of treatment. mRNA expression of CXCR3 of PBMC was assessed by real-time polymerase chain reaction (RT-PCR). Response to therapy was achieved in 27/33 (81.8%) non-cirrhotic and 14/20 (70%) cirrhotic patients. Mean serum IP-10 levels was higher in patients than healthy controls, and cirrhotic patients had higher IP-10 than non-cirrhotic patients (520 vs 293.5 pg/ml; P<0.005). Response to treatment was associated with decreased IP-10 levels. Before treatment, the mean level in non-cirrhotic patients was 235±54 pg/ml, which decreased to 95±34 pg/ml (P<0.005) at week 24 of treatment. Similarly, in the cirrhotic group, IP-10 decreased from 458±42 pg/ml to 354±25 pg/ml (P <0.05) after 24 weeks of treatment. On the other hand, no change in IP-10 levels was observed for patients who did not respond to treatment. Interestingly, IP-10 levels correlated with PBMC's expression of CXCR3 mRNA (r= 0.448, P = 0.004), ALT level (r=0.273, P =0.048), liver fibrosis score 4 (FIB-4) (r=0.664, P = 0.01) and HBV DNA level (r=0.762, P =0.0001). In conclusion; IP10 may be used to predict response to therapy in HBV-infected patients.

Regulatory T Cells, IL10 and IL6 in HCV Related Hepatocellular Carcinoma after Transarterial Chemoembolization (TACE).

Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. Tumors can recruit and promote the expansion of regulatory T cells (Tregs) to suppress antitumor immune responses for survival and progression. Furthermore, there is a strong evidence for the potential roles of cytokines in promoting HCC carcinogenesis and progression. We aimed to evaluate the frequency of Treg cells and serum levels of IL6 and IL10 before and after transarterial chemoembolization (TACE). We carried out a cross-sectional study at Assiut University hospitals that included 34 HCC patients and 10 matched apparently healthy controls. Peripheral Treg frequency was evaluated by Flow cytometry. IL6 and IL10 serum levels were evaluated by ELISA before and after TACE. HCC patients had a significantly higher level of IL6 and IL10 when compared to the control group (P=0.0002, P < 0.0001), respectively. However, after treatment, there was an elevation in the levels of IL6 and IL10 followed by a decrease to the baseline levels. Patients with large tumors (≥5 cm) showed higher levels of both IL 6 and IL 10 than those with smaller tumors. Moreover, HCC patients showed a higher frequency of Treg cells in comparison to the controls (P=0.002). No significant correlation was observed between the frequency of Treg cells and IL10 before and after treatment (r=0.38, P=0.30). In conclusion, HCC patients have significantly higher levels of IL 6, IL 10 and a higher percentage of Tregs than control individuals. Treg levels are altered after chemoembolization. IL 6 have a potential in reflecting the patient's condition after treatment, thus, can help in monitoring therapy.

Bacteriological Monitoring of Inanimate Surfaces and Equipment in Some Referral Hospitals in Assiut City, Egypt.

Hospital-acquired infections represent a serious public health problem in all countries. It is clear that monitoring of the hospital environment is an essential element in the control and a part of the policy for preventing nosocomial infections. It allows a better understanding of the microbial ecology for the purpose of conducting preventive and corrective actions. The aims of this work were to determine the percentage of bacterial contamination of environmental samples and to identify potential nosocomial pathogens isolated from environments of seven referral hospitals from 2009 to 2015. By using the swab technique, 12863 samples were collected. Qualitative and quantitative cultures were performed. The organisms were primarily identified by colony morphology, microscopy of Gram stain, and standard biochemical tests. 25.6% of total samples showed contamination (93% was monomicrobial and 7.0% was polymicrobial). The predominant species was coagulase-negative staphylococcus (CNS) (32%), followed by methicillin-resistant S. aureus (MRSA) (26%) and then K. pneumonia (10.6%). The percentage of contamination varied among the covered hospitals and according to the year of monitoring with highly statistically significant difference (p value < 0.001). Direct contact with environmental surfaces or equipment transmits the majority of nosocomial infection. Major nosocomial pathogens have been identified. Hospital managers and healthcare bodies must be aware of the reality of the concept of environmental bacterial tanks and the need for respect of biocleaning procedures and choice of biocleaning tools.

Serological and Molecular Diagnosis of Occult Hepatitis B Virus Infection in Hepatitis C Chronic Liver Diseases.

Occult Hepatitis B infection (OBI), defined as the presence of serum HBV DNA without detectable HBsAg, can be classified into seropositive OBI [anti-HBc and/or anti-hepatitis B surface (anti- HBs) positive] and seronegative OBI (anti-HBc and anti- HBs negative). We examined the role of anti-HBc as a screening test for OBI in HCV patients with chronic liver diseases and evaluated the possible impact of OBI on liver disease progression. 90 patients with hepatitis C related chronic liver diseases (CLD) and negative for HBsAg were divided into three equal groups; chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). Patients were tested for anti-HBc by ELISA and by PCR for S-gene. Total anti-HBc was found in 26 patients (28.9%). 8 patients (8.9%) had positive serum HBV DNA. Of these, 2 were positive for anti-HBc and 6 negative for anti-HBc. No correlation between OBI and severity of HCV related CLD was observed. In conclusion, as OBI was not associated with total anti-HBc, it is invaluable surrogate marker for OBI detection.

Evaluation of Non Invasive versus Invasive Methods for Diagnosis of Helicobacter pylori Infection among Patients with Gastroduodenal Disorders.

H. pylori, a spiral gram-negative bacterium, is associated with gastroduodenal diseases. All H. pylori diagnostic assays have limitations. Cytotoxin-associated gene A (cag A), a virulence marker, can be identified by PCR. We evaluated H. pylori diagnostic methods, invasive: rapid urease test (RUT), and histopathological examination (HE), and serology as non-invasive method. Positive cases were studied for presence of cag A gene. Upper endoscopies and gastric biopsies were performed on 67 dyspeptic patients for RUT, HE and PCR. Anti H. pyloriIgG were measured by ELISA. Of 67 dyspeptic patients, 23 (34%) had more than one endoscopic finding, 46 (68.7%) were H.pylori positive by HE, and 21(31.3%) were negative with variable grades of mucosal antral neutrophil infiltration. Of the 46 HE positives, PCR detected CagA in 22 (47.8%). Using HE as the gold standard test, the sensitivity of ELISA and RUT was 93.48% and 86.96%, respectively; and the specificity was 85.71% and 47.62%, respectively. In conclusion, IgG detection by ELISA is a suitable screening test for diagnosis of H. pylori associated gastroduodenal diseases. Histopathology should be performed in ELISA negative cases to exclude infection.