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    ABSTRACT: Syndecan-1 is a trans-membrane heparan sulfate proteoglycan that localizes in epithelial cells and has been shown to be present in normal hepatocytes. It is thought to be involved in processes such as cell growth, differentiation and adhesion. However, the clinical data regarding syndecan-1 in patients with hepatocellular carcinoma (HCC) are scarce and controversial. Therefore, we need to evaluate the effects of HCC on the serum levels of syndecan-1. Thus, 40 patients with HCC and 31 patients with liver cirrhosis were physically examined. Blood samples were taken for measurements of routine markers (sGPT, sGOT, bilirubin, albumin, and α-fetoprotein), as well as serum levels of interleukin (IL)-6 and syndecan-1. Patients with liver cirrhosis showed significant increase in serum IL-6 as compared with HCC patients and the control subjects. Serum level of syndecan-1 was significantly increased in HCC patients as compared with the cirrhotic and control groups. In addition, significant positive correlations between syndecan-1 and serum levels of ALT, AST in HCC patients were found. Moreover, syndecan-1 increased significantly with increasing stage of Barcelona-Clinic Liver Cancer Group diagnostic and treatment strategy. In conclusion, the development of HCC is accompanied by a significant elevation in serum syndecan-1 levels. The increase in serum syndecan-1 may be linked with progression of HCC.
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    ABSTRACT: Background Chronic hepatitis C (CHC) is associated with multiple extrahepatic manifestations, including the recently recognized effect on pulmonary function tests (PFTs) and lung parenchyma. Aim To evaluate changes in PFTs and lung parenchyma in asymptomatic Egyptian patients with a CHC infection. Patients and methods This cross-sectional study included 70 CHC patients. All patients were subjected to a liver biopsy. Fibrosis stage and activity grade were assessed according to the METAVIR scoring system using scale ranges from 0 to 4. All patients were subjected to PFTs, measurement of arterial blood gases, and high-resolution computed tomography (HRCT) of the chest. All smokers, obese (BMIZ30) patients, and patients with known pulmonary disease were excluded. Results An alteration in PFTs was observed in 29 (41.42%) patients out of 70. A restrictive pattern was found in 27 patients (38.57%), in whom forced vital capacity and the total lung capacity values were reduced to less than 80% of the predicted values. Forced expiratory volume in 1 s/forced vital capacity value was more than 70%. Also, HRCT of the chest showed interstitial pulmonary fibrosis (IPF) with either an interstitial or an alveolar pattern with a total score not exceeding 2. These findings correlated significantly with the PFTs results. Also, there was no significant correlation between the presence of a restrictive pattern in PFTs or IPF in HRCT with other parameters in terms of age, BMI, sex, liver fibrosis, activity score, level of viremia, and duration of disease. Conclusion Hepatitis C virus could be a trigger factor for alterations in PFTs and lung parenchyma in the studied asymptomatic Egyptian patients with a CHC genotype 4 infection. HRCT AQ2 could be a sensitive, noninvasive method for the early detection of IPF in these patients.
    Egyptian Liver Journal. 07/2012;
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    EASL; 04/2012
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    ABSTRACT: 1. HCV could be a trigger factor for alterations in PFTs and lung parenchyma in the studied asymptomatic Egyptian patients with CHC-genotype 4 infection. 2. HCRT and Alveolar–arterial O 2 gradient can be used as sensitive methods for early detection of IPF in those patients. 3. Pegylated interferon may induce worsening of chest disease irrespectively of the patient outcomes. 4. So, screening for pulmonary disease is suggested in CHC patients before starting antiviral therapy 100 patients with CHC genotype 4 78 patients continued the course of treatment till 48 weeks 30 with restrictive PFTs+ positive HRCT 14 patients improved PFTS and HRCT findings 12 SVR 2 NR 16 patients remains with restrictive PFTs+ positive HRCT 14 SVR 2 NR 48 patients with initial normal PFTs and HRCT 35 patients remain with normal PFTs and HRCT 29 SVR 6 NR 13 patients developed restrictive PFTs and positive HRCT findings 11 SVR 2 NR 22 patients were excluded; 18 not achieved EVR and 4 patients stopped at week 24 (1 due interstitial pneumonitis and 3 due to breakthrough) ntroduction I Chronic hepatitis C (CHC) triggers multiple extrahepatic immune-lymphoproliferative disorders which might include 'idiopathic' pulmonary fibrosis. This can be detected by effects on pulmonary function tests (PFTs) ± high resolution computed tomography (HRCT) of the chest. Moreover, interferon therapy alone or in combination with ribavirin has been associated with pulmonary complications. Aim of the work: to evaluate changes in PFTs and HRCT of the chest in asymptomatic Egyptian patients with CHC and the effects of interferon/ribavirin therapy Patients and methods: This prospective cohort included 100 patients with chronic HCV-genotype 4. All patients received on a fixed weekly dose of 180 μg of peginterferon α-2a in combination with ribavirin in dose adjusted to body weight. All patients subjected to PFTs, arterial blood gases (ABGs) and HRCT of the chest before and after treatment. HRCT showed lower lung lobes shows interlobular septal thickening of both sides and minimal ground glass opacity in left side. (before treatment). HRCT showed interlobular septal thickening of both sides and bilateral ground glass opacity and honeycomb appearance 24 weeks after treatment SVR sustained virological response, NR non responder
    APASL; 02/2012
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    ABSTRACT: Syndecan-1 is a trans-membrane heparan sulfate proteoglycan that localizes in epithelial cells and has been shown to be present in normal hepatocytes. It is thought to be involved in processes such as cell growth, differentiation and adhesion. However, the clinical data regarding syndecan-1 in patients with hepatocellular carcinoma (HCC) are scarce and controversial. Therefore, we need to evaluate the effects of HCC on the serum levels of syndecan-1. Thus, 40 patients with HCC and 31 patients with liver cirrhosis were physically examined. Blood samples were taken for measurements of routine markers (sGPT, sGOT, bilirubin, albumin, and α-fetoprotein), as well as serum levels of interleukin (IL)-6 and syndecan-1. Patients with liver cirrhosis showed significant increase in serum IL-6 as compared with HCC patients and the control subjects. Serum level of syndecan-1 was significantly increased in HCC patients as compared with the cirrhotic and control groups. In addition, significant positive correlations between syndecan-1 and serum levels of ALT, AST in HCC patients were found. Moreover, syndecan-1 increased significantly with increasing stage of Barcelona-Clinic Liver Cancer Group diagnostic and treatment strategy. In conclusion, the development of HCC is accompanied by a significant elevation in serum syndecan-1 levels. The increase in serum syndecan-1 may be linked with progression of HCC.
    Scientia Pharmaceutica 01/2011;
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    ABSTRACT: In diabetic retinopathy (DR), abnormalities in vascular and neuronal function are closely related to the local production of inflammatory mediators whose potential source is microglia. A(₂A) adenosine receptor (A(₂A)AR) has been shown to possess anti-inflammatory properties that have not been studied in DR. Here, we evaluate the role of A(₂A)AR and its underlying signaling in retinal complications associated with diabetes. Initial studies in wild-type mice revealed that the treatment with the A(₂A)AR agonist resulted in marked decreases in hyperglycemia-induced retinal cell death and tumor necrosis factor (TNF)-α release. To further assess the role of A(₂A)AR in DR, we studied the effects of A(₂A)AR ablation on diabetes-induced retinal abnormalities. Diabetic A(₂A)AR(-/-) mice had significantly more terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells, TNF-α release, and intercellular adhesion molecule-1 expression compared with diabetic wild-type mice. To explore a potential mechanism by which A(₂A)AR signaling regulates inflammation in DR, we performed additional studies using microglial cells treated with Amadori-glycated albumin, a risk factor in diabetic disorders. The results showed that activation of A(₂A)AR attenuated Amadori-glycated albumin-induced TNF-α release in a cAMP/exchange protein directly activated by cAMP-dependent mechanism and significantly repressed the inflammatory cascade, C-Raf/extracellular signal-regulated kinase (ERK), in activated microglia. Collectively, this work provides pharmacological and genetic evidence for A(₂A)AR signaling as a control point of cell death in DR and suggests that the retinal protective effect of A(2A)AR is mediated by abrogating the inflammatory response that occurs in microglia via interaction with C-Raf/ERK pathway.
    American Journal Of Pathology 01/2011; 178(5):2136-2145. · 4.60 Impact Factor

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