Background IBD is a multifactorial disease. Although dysbiosis of commensal bacteria and breakdown of the intestinal barrier are considered as major pathological mechanisms in the development of IBD, other important factors such as genetic aberrations also contribute to its development. Results Our results revealed that serum miR-34a RQ values were significantly lower and serum MACF1 RQ values were significantly higher in IBD patients compared to healthy controls. In addition, serum miR-34a in relation to pathological activity and disease severity in the IBD group revealed a significant difference (p>0.05). Conclusion Serum miR-34a RQ and serum MACF1 RQ value-based biomarker panels can act as a potential biomarker for IBD diagnosis and prognosis.
Risk of hepatitis B virus reactivation (HBVr) in patients with resolved HBV infection receiving immunosuppressive therapy has been a growing concern, particularly in the era of biological and targeted therapies. HBV monitoring versus antiviral prophylaxis against HBVr in those patients remains controversial. The aim of the study was to determine the incidence of HBVr and HBVrelated hepatitis in resolved HBV patients who received immunosuppressive therapy with or without antiviral prophylaxis. This retrospective study included 64 patients with resolved HBV infection who received different regimens of immunosuppressive medications, with moderate risk of HBVr, for variable underlying diseases. Patients who had chronic HBV infection or other viral infections were excluded. Patients who received B-cell depleting therapies were ruled out. They were divided into 2 groups: group 1 included 31 patients who received immunosuppressive therapy without antiviral prophylaxis, and group 2 included 33 patients who received antiviral prophylaxis (entecavir) within 2 weeks of commencing the immunosuppressive therapy. HBVr, HBV-related hepatitis, and HBV-unrelated hepatitis were assessed along a 1-year duration. The overall HBVr incidence was 1.56% (1/64). This patient who had HBVr was seen in group 1. There were no significant differences between the 2 groups regarding the incidence of HBVr, HBV-related hepatitis, HBV-unrelated hepatitis, and immunosuppressive therapy interruption along a 1-year duration. Based on this retrospective study, close monitoring was equal to antiviral prophylaxis regarding the outcome of resolved HBV patients who received moderate risk immunosuppressive therapy. HBV treatment should commence once HBVr is confirmed.
Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies and a leading cause of cancer-related death worldwide. Indeed, we need a novel tumor marker other than AFP for early detection and to improve the outcome. Serum thioredoxin is a promising protein involved in pathogenesis in many malignancies. The study aims to evaluate serum thioredoxin and its gene polymorphism in HCC in cirrhotic patients due to HCV infection. Patients and methods: 350 patients with HCC, 350 patients with chronic liver diseases, and 300 healthy controls were enrolled in our study. Serum thioredoxin level was measured by ELISA and molecular study of thioredoxin domain-containing 5 (TXNDC5) gene polymorphism (rs1225943) polymorphism using real-time polymerase chain reaction by Taqman allele discrimination was done for all subjects. Results: Our study revealed a significant increase in serum thioredoxin levels in patients with HCC compared to chronic liver diseases and healthy controls. Using Receiver operating characteristic (ROC) curve at the area under the curve (AUC) 0.917 and cut-off value of >14.6 U/ml, our overall sensitivity and specificity for HCC group over the other groups were 86 % and 92.15% respectively with 92.2% positive predictive value and 54.9% negative predictive value. The molecular study of TXNDC5 gene polymorphism (rs1225943) polymorphism revealed no significant difference between the studied groups. Conclusion: Serum thioredoxin may be used as a promising tumor marker for HCC. Future researches are needed to assess its use as a single or combined with other markers in the diagnosis and follow-up of the patients after interventions.
Summary Cystic echinococcosis is speculated to exert several immune-evasion strategies involving autoimmune-phenomena. We evaluated the hypothesizes that the prevalence of autoantibodies increases in the sera of CE patients that may evidence the association between the parasite and autoimmune diseases. Sera from 63 subjects at distinct types of CE cyst fertility were investigated for antinuclear antibodies (ANA), and anti-CCP antibodies. Plasma levels and cellular production of IL-17A cytokine were specifically defined as being assumed to prime for autoimmunity. Healthy-controls were age and gender-matched to test sera. ANA expressions inside the surgically removed metacestode and adventitial layer were also assayed. Out of 63 patients, 35 % had fertile highly viable cysts (group-1), 41 % had fertile low viable cysts (group-2) and 24 % had non-fertile cysts (group-3). A four-fold increase in ANA sera-levels was detected in group-1 compared with their controls (p-value 0.001) while anti-CCP levels were of insignificant differences. In group-2 and group-3, no significant differences were detected between ANA and anti-CCP sera-levels in CE patients and their controls. IL-17A sera-levels in group-1 and group- 2 were significantly higher than their healthy-controls while being of insignificant differences in group-3, p-value= 0.300. No association was detected between sera-levels of IL-17A and ANA as well as anti-CCP antibodies. Interestingly, relative IL-17A cellular expression associated positive ANA deposition in the parasite cells and adventitial layer. Collectively, based on the parasite fertility, IL-17A and ANA seemed to be involved in the host immune defenses against CE. There is no association between CE and anti-CCP antibodies.
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