Predicting the risk of portal vein thrombosis in patients with liver cirrhosis and hepatocellular carcinoma.

The mechanisms of the hypercoagulable state in cirrhotics with and without hepatocellular carcinoma are incompetently comprehended. Objective: We aimed to explore the plasma Annexin A5/PS + MP ratio in these patients. Higher levels of Annexin A5 and PhosphatidylSerine bearing microparticles have been observed in cases of inflammation and increased coagulation but there are no studies which explore if there is an association between them and PVT in cirrhotics with and without HCC. So, our goal is to estimate their role in predicting PVT within HCV cirrhotics with and without HCC. 91 HCV cirrhotics with and without HCC and 20 healthy people (controls) were enlisted. Cirrhotics with and without HCC who developed PVT displayed higher levels of PS + MPs and lower Annexin A5/PS + MPs ratio (38.73 ± 1.92) and (0.00238 ± 0.00047) than cirrhotics who didn't develop PVT (22.19 ± 10.58) and (0.00451 ± 0.0023) (P < 0.001). Among the tested factors, lower Annexin A5/PS + MPs ratio show higher performance in predicting PVT in total cirrhotics, AUC, 0.919 followed by PS + MPs level, 0.876, Portal flow velocity, 0.842, Plasma Annexin A5 level, 0.509. In our hypothesis, As phosphatidylserine exposure increase due to increased level of circulating microparticles in cirrhotics with and without HCC, anenxin-A5 may be secreted by platelets and endothelial cells into the circulation as a physiological response to inactivate the elevated levels of PS bearing MPs produced in these patients but the increase in anenxin-A5 level isn't equivalent to the increase in PS bearing MPs levels. The equilibrium between plasma annexin A5 and PS bearing MPs levels is defected.

Determination of liver fibrosis stages in Egyptian chronic hepatitis B patients by a noninvasive tool

Background/aim: Hepatitis B virus (HBV) infection is the leading cause of liver fibrosis (LF). The prognosis and management of patients with chronic hepatitis B virus depend on the amount and progression of liver fibrosis. Angiopoietin-like protein 2 (Angptl2) is not only a chronic inflammatory mediator, but also a tissue-remodeling factor. The aim of this study is to explore the predictive value of Angptl2 in different fibrosis stages in patients chronically infected with HBV. Materials and methods: Eighty patients with chronic HBV infection undergoing Fibroscan were included. Serum concentrations of Angptl2 were detected using a commercial ELISA kit. Results: Angptl2 levels were significantly associated with liver fibrosis stages (P = 0.02). The area under the curve (AUC) of Angptl2 for distinguishing patients who showed significant fibrosis (F2­F4) was70.2%. Angptl2 with fibrosis-4 (FIB-4) and Angptl2 with AST/platelets ratio (APRI) performed best with an AUC of 92.5%. Conclusion: In patients with chronic HBV infection, Angptl2 level represents a potential biomarker independently associated with fibrosis stages. The combination of Angptl2 with FIB-4 or Angptl2 with APRI performed better than the existing models for diagnosing significant fibrosis.

Micro-RNA-96 and interleukin-10 are independent biomarkers for multiple sclerosis activity.

BACKGROUND: Micro-RNAs (miRNAs) are evolving as biological markers for multiple sclerosis (MS) both in activity and remission. miR-96 is associated with remission, however, the exact mechanism through which it contributes to the anti-inflammatory pathway is not clear. OBJECTIVE: To study the expression of miR-96 and IL-10 (anti-inflammatory mediator) in relapsing remitting (RR) MS. SUBJECTS AND METHODS: A case control study including 32 RRMS patients from Kasr Al-Ainy MS clinic, Cairo University, Egypt, and 26 healthy controls (HC). Assessment of serum IL-10 by ELISA, and miR-96 via real time PCR was done during relapse and remission in patients, and in HC. RESULTS: IL-10 was higher in RRMS patients during remission and in HC compared with relapse (P ˂ 0.001). miR-96 expression was higher in RRMS patients during remission compared with relapse and HC, and was higher in HC than in relapse (P ˂ 0.001). IL-10 level in remission correlated positively with disease duration (r = 0.41; P = 0.02). Otherwise, no correlation was found between IL-10 and relapse number or EDSS (P>0.05). miR-96 in relapse negatively correlated with EDSS in relapse (r=-0.47; P=0.007), but no correlation was found with disease duration or relapse number, whereas, miR-96 in remission did not correlate with any clinical parameters (P>0.05). No correlation was found between IL-10 and miR-96 either in relapse or remission (P>0.05). CONCLUSION: IL-10 and miR-96 are associated with MS quiescence, however, the lack of a significant correlation between them implicates that the influence of miR-96 may be exhibited through some pathway other than IL-10.

Micro-RNA 18b and interleukin 17A profiles in relapsing remitting multiple sclerosis.

BACKGROUND: The involvement of micro RNAs (miRNAs) in multiple sclerosis (MS) has been recently explored. Up-regulated miRNAs may play critical roles in MS pathogenesis and may be used as a signature for MS. Besides, the role of inflammatory cytokines has been long established with recent focus on interleukin-17 (IL-17). OBJECTIVE: To evaluate the level of expression miR-18b in relation to IL-17A in relapsing remitting (RR) MS patients during relapse and remission SUBJECTS AND METHODS: Twenty-eight RRMS patients and 26 age and sex matched control subjects were included. Serum miR-18b was assessed by quantitative real-time PCR, and serum level of IL-17A was measured by ELISA. RESULTS: Serum miR-18b expression was higher in relapse compared with remission and with controls (24.8 ±â€¯21.91 vs 2.49 ±â€¯0.97 vs 1 ±â€¯0.36 respectively; P < 0.001). Serum IL-17Awas higher in MS patients during relapse than during remission and controls (8.49 ±â€¯1.26 vs 5.78 ±â€¯2.27 vs 4.18 ±â€¯2.13, respectively; P < 0.001). No correlations existed between miR-18 and IL-17 in MS patients during relapse (r = 0.35; P = 0.22) or remission (r = 0.340; P = 0.234). CONCLUSION: Upregulation of miR-18 during relapse in patients with RRMS points to a possible contribution to the pathogenesis of the inflammatory process in MS. The lack of a significant correlation between upregulated miR-18 and IL-17A implicates that the influence of miR-18 may be exhibited via another inflammatory pathway.