ABSTRACT
Background EBV was the first human virus directly implicated in carcinogenesis. Since its discovery it has been considered as a major player in the development of a wide range of cancers. Recent studies have concluded EBV itself or infected cell clones might promote replication of the HCV
EBNAl is responsible for supporting HCV replication, suggesting that EBV may be involved in the development of hepatocellular carcinoma [HCC] The detection of EBV gene products in HCC additionally supports this assumption
Methods Methods This study was carried out on cases divided into three groups:-Group I included 15 very low cone, of EBV [IgG] with both negative HCC and HCV RNA patients, Group 2 included 15 moderate cone, of EBV [IgG] with positive HCC and negative HCV RNA patients and Group 3 included 15 high cone, of EBV [IgG] with both positive HCC and HCV RNA patients Reverse transcription PCR [RT-PCR] was performed to detect HCV RNA
Immunohistochemistry was performed to detect EBV[IgG].. The positive ratios were compared between HCC group and control group
Results Our retrospective study determines serum level of hepatitis C, Epstien - Barr [IgG] and Alpha feto protein and to correlate their serum levels with each other in the patient of hepatocellular carcinoma assessed by histopathological staging of liver biopsy. HCV level increased significantly with progression of Serum level ofEBV[IgG] and AFP had no statistical significant change with EBV[IgG]
Conclusion: The existence of EBV infection in HCC tissues suggests that EBV may be involved in the hepatocellular carcinogenesis in Egypt. HCV infection may be a major cause of HCC. There is correlation between EBV and HCV in the development of HCC. EBV enhancement the replication of HCV
ABSTRACT
Background: the induction of apoptosis for the virus-infected cells is an important host defense mechanism against invading pathogens. Activated T cells express Fas receptor; virus-infected hepatocytes bear the receptor as well. Both immune mediated reaction and cytopathic effects of HCV may be involved in pathogenesis. The apoptosis in immune or non-immune tissue and the mechanism of liver damage in chronic HCV infection remains uncertain
Aim: to assess the relationship between serum concentrations of adhesion and apoptotic-related soluble structures in patients affected by Hepatitis C Virus [HCV]. Investigate serum levels of soluble Fas antigen [sFas], soluble intercellular adhesion molecules-1 [sICAM-1]; study their roles in pathogenesis and liver cell damage in chronic hepatitis C patients
Patients and methods: sixty chronic hepatitis C patients [78.33% male vs. 22.66% female] and twenty controls recruited, they were positive for anti-HCV, and HCV-RNA by quantitative PCR. Liver biopsies were fixed and examination. Patients were classified into Group A [n=23] Chronic Hepatitis C minimal activity [0-3], Group B [n=19] mild activity [4 -8], and Group C [n=13] moderate and severe activity [9-13, and >13] depending on Histological Activity Index [HAI] score, then, assessment of hepatic [periportal, intra-lobular and total] was done. Patients were categorized into cirrhotic group [n=18] and non-cirrhotic group [n=42]. Tissue Fas [tFas] was assessed using anti-Fas antibody. Serum Soluble Fas [sFas] and [sICAM-1] were measured using EIA kits
Result: sFas was significantly increased in patients subgroups compared to controls [p<0.001] and in comparing cirrhotic to no cirrhotic [p<0.01]. tFas showed rising significance with disease activity [p<0.01].Both studied parameters of Fas were not correlated with ALT level [r=0.04, 0.03]. sICAM-1 revealed significant correlation of albumin levels in Group B [mild activity], with sFas antigen in non-cirrhotic patients group correlation not yet reach significance. No correlation was found between viral load, Fas parameters and sICAM [r=0.19, 0.16 and 0.21] respectively, while correlated with HAI [r=0.91, 0.96] respectively, expect in patients group A of [minimal activity]. In addition, sFas correlated significantly with tFas expect group A
Conclusion: Fas studied parameters can reflect severity of liver inflammation and play a crucial role in HCV infection. Equally, Soluble Fas and sICAM-1may serve as serological indicator of active inflammation. Strategies to prevent Fas-mediated apoptosis during inflammation might offer exciting therapeutic potential
ABSTRACT
Background: a growing body of evidence indicates that many trace elements an play important role in a number of carcinogenic processes that proceed through various mechanisms. Trace elements are involved in chronic liver diseases because these elements may have a direct hepatic toxicity or may be decreased as a consequence of the impaired liver functions. Hepatitis infection may alter serum content of several trace elements e.g. Iron, Cupper, Manganese and Zinc. This alteration may play a role on ongoing liver fibro genesis. Serum metal levels, such as cupper [Cu], zinc [Zn], iron [Fe] and manganese [Mn] have been reported to be highly sensitive in the diagnosis of some diseases
Aim of work to evaluate the level of some trace metals in HCV and HCC patients, also correlating their levels with HCC tumor size
Patients and methods: sixty liver disease patients and fifteen healthy subjects served as a healthy control group. Patients were classified into Group A [n=20] chronic hepatitis C virus infection [compensated], Group B [n=20] patients [un compensated HCV], and Group C [n=20] patients diagnosed as hepatocellular carcinoma. After verbal consent, all patients detection of subjected to full history taking, clinical examination, and routine laboratory testing, in addition to viral hepatitis markers for the presence of HCV-Ab by linked immune sorbent assay [ELISA], the presence of HCV-RNA by PCR, alpha-fetoprotein, abdominal ultrasonography and estimation of serum minerals [Fe, Cu, Mn, and Zn] using atomic absorption spectrophotometry
Results: Mn and Cu levels were significant when correlated with the uncompensated HCV patients viral load [r = -0.65 and = 0.51, p < 0.01 and <0.02 respectively]. While in HCC patients, only Zn correlated significantly with viral load [P<0.01]. No correlation was found between HCV viral load and the studied trace elements in HCV compensated patients. Also, in HCC patients, serum Zn correlated significantly with tumor size greater than 5cm. while Cu serum level was significantly correlated with tumor size less than 5cm. in the uncompensated HCV group, iron serum level showed high significance results when correlated with ALT [r =0.563 , p <0.01]. Regarding correlation of liver function tests with studied trace elements in HCC patients group , the ALK showed high significant correlation with serum Cu level [r = 0.640, P<0.046]. Also, T.BIL/D.BIL showed slight correlation with Cu serum level but not yet reach significance [r = 0.583, p < 0.076]
Conclusion trace elements were verified to have an essential role in liver disease. Serum cupper levels were correlated with the viral load whereas, serum Mn levels showed a promising role in protecting HCV uncompensated patients. Zn might be of importance in regulating viral replication and liver carcinogenesis in HCV patients. While serum Zn levels were correlated with the viral load and liver damage in HCC patients. Further studies have to be performed to confirm the relation between trace elements and HCC development
ABSTRACT
Preeclampsia [PE] a major cause of maternal and neonatal mortality and morbidity worldwide in which hypertensive disorders during pregnancy account for 25.7% of maternal deaths. Both maternal and fetal genetic factors may predispose towards pre-eclamptic pregnancy, especially severe forms. However, preeclampsia is thought to be the result of the interplay between important genetic components and environmental influences; still, factors and mechanisms that lead to preeclampsia remain mysterious. Insertion/deletion [I/D] polymorphism of ACE gene has attracted significant attention and has been extensively investigated with its serum activity in a spectrum of cardiovascular phenotypes
Aim to study the potential association of I/D polymorphism of ACE gene in PE Egyptian women that gets us closer to understanding the disease
Patients and Methods: one hundred hypertensive and age-matched normotensive primigravida were recruited from Minufiya university Hospital. Routine investigations were done for PE diagnosis. DNA was extracted from whole blood of patients and healthy controls. All samples were genotyped for ACE I/D polymorphism according to Rigat et al. using amplification and PCR of known allelic variants. ACE genotype was identified and followed by serum concentration of ACE activity for both groups
Results: ACE DD genotype was found in 60% of PE patients while 34% of normotensive subjects [P 0.05], although D allele was higher among cases than controls, but it did not show significance [P > 0.05]. High significance was revealed when comparing the mean total ACE activity in the hypertensive patients [32.74 IU/l] and normotensive subjects [28.06 IU/l] [P <0.001]. The ACE activity in cases and controls carrying DD allele differed significantly [P<0.001]. In contrast the other ACE genotype ID and II did not show significance between cases and controls
Conclusion: these findings might bear implications for precise management of pregnancy in high-risk DD genotype women. Further large scale evaluation was required to provide added marker for risk assessment for PE patients
ABSTRACT
Background: Leptin acts mostly as a signaling factor from adipose tissue to central nervous system regulating food intake. Adiponectin and Resistin produced by adipose cells may have a role in preventing the development of insulin resistance. Polycystic ovary syndrome [PCOS] is characterized by insulin resistance and 50% of women affected are obese
Aim of work: To study adipo-cytokines secretion in women with Polycystic Ovary Syndrome and correlate results with insulin resistance
Subjects and Methods: Thirty-two women with PCOS and matched controls were studied; three adipocytokines were measured compared with controls. Diagnosis of PCOS based on the classic criteria of hyperandrogenism and chronic anovulation. PCOS patients mean age was 26.2+/-1 years and Body Mass Index [BMI] mean was 28.7+/-0.7. years Controls of 20 women mean age 25.1+/-0.7 yrs and mean BMI 28.5+/-0.5. Normal ovulation was assessed by serum progesterone [20nM/l] on days 22-23 of menstrual cycle. Controls and PCOS were subdivided into groups of normal weight [BMI 25]; overweight [BMI 25-30], and obese [BMI 30]. Fasting blood samples used during the follicular phase [08:00-09:00 hr] for measurements of LH, FSH, insulin, glucose, leptin, adiponectin, and resistin using RIAs and EIAs. Insulin resistance was calculated by the quantitative insulin-sensitivity check index [QUICKI]
Results: PCOS women had increased insulin level [19.2 +/- 1.1] [P= 0.01] also a lower QUICKI values than controls [19 +/- 0.5] [P= 0.00], but obese women had a greater degree of insulin resistance. The entire PCOS group had lower levels of adiponectin [8.2 +/- 0.6] [P= 0.05] and higher levels of resistin [6.1 +/- 0.4] [P= 0.05] while leptin levels were not significantly different than controls. Leptin was only significantly higher in the obese group [BMI 30] compared with normal. However, adiponectin correlated only with BMI [r 0.58, P=0.05] but not with insulin [r 0.03] nor with QUICKI [r 0.02], and resistin did not correlate with any of these parameters. Leptin maintains its correlations with BMI, insulin and QUICKI [r=0.72, 0.54 and 0.63, P= 0.01, =0.05 and =0.01 respectively]
Conclusion: Circulating adipo-cytokine levels were different resulting in higher leptin and lower adiponectin, being the most marked change, shows similar levels with no marked change of resistin with increasing BMI. These alterations may due to altered adipose tissue function in women with PCOS, which occurs even with normal BMI