检索结果-南通市图书馆

Hepatitis C virus induced insulin resistance impairs response to anti viral therapy

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2012年第3期18卷 212-224页

作者： abdel-rahman el-zayadi Mahmoud Anis Tropical Medicine Department Faculty of Medicine Ain-Shams University and Cairo liver center Tropical Medicine Department Faculty of Medicine Tanta University

Hepatitis C virus (HCV) infection is an important risk factor for insulin resistance (IR). The latter is the pathogenic foundation underlying metabolic syndrome, steatosis and cirrhosis, and possibly hepatocellular carcinoma (HCC). The interplay between genetic and environmental risk factors ultimately leads to the development of IR. Obesity is considered a major risk factor, with dysregulation of levels of secreted adipokines from distended adipose tissue playing a major role in IR. HCV-induced IR may be due to the HCV core protein inducing proteasomal degradation of insulin receptor substrates 1 and 2, blocking intracellular insulin signaling. The latter is mediated by increased levels of both tumour necrosis factor-α (TNF-α) and suppressor of cytokine signaling 3 (SOC-3). IR, through different mechanisms, plays a role in the development of steatosis and its progression to steatohepatitis, cirrhosis and even HCC. In addition, IR has a role in impairing TNF signaling cascade, which in turn blocks STAT-1 translocation and interferon stimulated genes production avoiding the antiviral effect of interferon.

关键词：丙型肝炎病毒胰岛素抵抗病毒诱导抗病毒治疗肿瘤坏死因子胰岛素受体底物反应危险因素

Heavy smoking and liver

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2006年第38期12卷 6098-6101页

作者： abdel-rahman el-zayadi Department of Tropical Medicine Ain Shams University and Director of Cairo Liver Center Cairo Egypt

Smoking causes a variety of adverse effects on organs that have no direct contact with the smoke itself such as the liver. It induces three major adverse effects on the liver: direct or indirect toxic effects, immunological effects and oncogenic effects. Smoking yields chemical substances with cytotoxic potential which increase necroinflammation and fibrosis. In addition, smoking increases the production of pro-inflammatory cytokines (IL-1, IL-6 and TNF-α) that would be involved in liver cell injury. It contributes to the development of secondary polycythemia and in turn to increased red cell mass and turnover which might be a contributing factor to secondary iron overload disease promoting oxidative stress of hepatocytes. Increased red cell mass and turnover are associated with increased purine catabolism which promotes excessive production of uric acid. Smoking affects both cell-mediated and humoral immune responses by blocking lymphocyte proliferation and inducing apoptosis of lymphocytes. Smoking also increases serum and hepatic iron which induce oxidative stress and lipid peroxidation that lead to activation of stellate cells and development of fibrosis. Smoking yields chemicals with oncogenic potential that increase the risk of hepatocellular carcinoma (HCC) in patients with viral hepatitis and are independent of viral infection as well. Tobacco smoking has been associated with supression of p53 (tumour suppressor gene). In addition, smoking causes suppression of T-cell responses and is associated with decreased surveillance for tumour cells. Moreover, it has been reported that heavy smoking affects the sustained virological response to interferon (IFN) therapy in hepatitis C patients which can be improved by repeated phlebotomy. Smoker’s syndrome is a clinico-pathological condition where patients complain of episodes of facial flushing, warmth of the palms and soles of feet, throbbing headache, fullness in the head, dizziness, lethargy, prickling sensation, p

关键词：吸烟肝疾病丙型病毒肝炎肝纤维化

Curse of schistosomiasis on Egyptian liver

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2004年第8期10卷 1079-1081页

作者： abdel-rahman el-zayadi Tropical Medicine Department Ain Shams University and Cairo Liver Center5El-Gergawy StDokkiGizaEgypt

Schistosomiasis is a chronic parasitic disease caused by atrematode blood fluke of the genus schistosoma that belongsto the schistosomatidae family. The ancient Egyptianscontracted the disease more than 4 000 years ago. It wasrecognized through haematuria, the main sign of urinarybilharziasis was recorded in the Kahun papyrus 1900 B.C.' a-a-a-' disease.

关键词：血吸虫病肝硬化慢性寄生虫病埃及 T淋巴细胞肝炎病毒

Hepatic steatosis:A benign disease or a silent killer

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2008年第26期14卷 4120-4126页

作者： abdel-rahman el-zayadi Tropical Medicine Department Ain Shams University and Cairo Liver CenterGiza12311Egypt

Steatosis is a common feature of many liver diseases,namely non-alcoholic steatohepatitis(NASH) and hepatitis C virus(HCV) infection,but the pathogenic mechanisms *** resistance(IR),a key feature of metabolic syndrome,is crucial for NASH development,associated with many underlying genetically determined or acquired mitochondrial and metabolic defects and culminates to inflammation and progression to *** may have potential implications for new drug *** HCV-related disease,steatosis impacts both fibrosis progression and response to *** in HCV-related disease relates to both viral factors(HCV genotype 3),and host factors(alcohol consumption,overweight,hyperlipidemia,diabetes).Among others,IR is a recognized *** steatosis is reported to be associated with disturbance in the signaling cascade of interferon and downregulation of its ***,hepatic steatosis should not be considered a benign feature,but rather a silent killer.

关键词：丙型肝炎胰岛素抵抗肝纤维化脂肪变性

Hepatocellular carcinoma in Egypt: A single center study over a decade

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

World Journal of Gastroenterology 2005年第33期11卷 5193-5198页

作者： Adbel-rahman el-zayadi Hanaa M Badran Eman MF Barakat Mohy el-Deen Attia Sherine Shawky Mostafa K Mohamed Osaima Selim Ahmed Saeid Department of Tropical Medicine Ain Shams University Cairo Egypt Department of Hepatology National Liver Institute MenoufeyaEgypt Department of Tropical Medicine Ain Shams University Cairo Egypt Department of Hepatology and Gastroenterology Theodor Bilharz Research Institute Cairo Egypt The Social Research Center The American University in Cairo Egypt Department of Community Medicine Ain Shams University CairoEgypt Department of Clinical Pathology Ain Shams University CairoEgypt Cairo Liver Center Giza Egypt

AIM: To identify the trend, possible risk factors and any pattern change of hepatocellular carcinoma (HCC) in Egyptover a ***: All HCC patients attending Cairo Liver Center between January 1993 and December 2002, were enrolledin the study. Diagnosis of HCC was based on histopath ological examination and/or detection of hepatic focal lesions by two imaging techniques plus α-fetoprotein level above 200 ng/mL. The duration of the study was divided into two periods of 5 years each; period Ⅰ (1993-1997) and period Ⅱ (1998-2002). Trend, demographic features of patients (age, gender, and residence), risk factors (HBsAg,HCV-Ab, schistosomiasis and others) and pattern of the focal lesions were compared between the two *** regression model was fitted to calculate the adjusted odds ratios for the potential risk factors. The population attributable risk percentage was calculated to estimate the proportion of HCC attributed to hepatitis B and C viral ***: Over a decade, 1 328 HCC patients out of 22 450 chronic liver disease (CLD) patients were diagnosed with an overall proportion of 5.9%. The annual proportion of HCC showed a significant rising trend from 4.0% in 1993 to 7.2% in 2002 (P = 0.000). A significant increase in male proportion from 82.5% to 87.6% (P = 0.009); M/F from 5:1 to 7:1 and a slight increase of the predominant age group (40-59 years) from 62.6% to 66.8% (P = 0.387)in periods Ⅰ and Ⅱ respectively, reflecting a shift to younger age group. In the bivariate analysis, HCC was significantly higher in rural residents, patients with history of schistosomiasis and/or blood transfusion. Yet, after adjustment, these variables did not have a significant risk for development of HCC. There was a significant decline of HBsAg from 38.6% to 20.5% (P = 0.000), and a slight increase of HCV-Ab from 85.6% to 87.9% in periods Ⅰ and Ⅱ respectively. HBV conferred a higher risk to develop HCC more than HCV in period Ⅰ (OR 1.9 vs 1.6) and period

关键词：成年人年龄分发变老癌,肝细胞埃及女性人发生肝瘤男性中年风险因素性别分发