Serum and tissue levels of transforming growth factor-B1 in Egyptian patients with chronic hepatitis C genotype 4: correlation with steatosis, and fibrosis

Activation of hepatic stellate cells [HSC] and transforming growth factor-b [TGF-bl] signaling are one of the important events at the beginning of fibrosis. Steatosis is present in liver biopsy in approximately 50% of patients with hepatitis C and its association with stage of fibrosis has been reported. The aim of this work is to study the relation between TGF-beta 1, steatosis, and fibrosis and hepatitis C genotype 4. We studied 47 patients [33 males, 14 females, mean age 43.46 +/- 13.54 years] with chronic HCV infection. Serum TGF-beta 1 was determined in all participants. Hepatitis C virus RNA was detected in patients' sera by reverse transcriptase-polymerase chain reaction [RT-PCR]. Liver biopsies were taken to evaluate steatosis, fibrosis, and tissue level of TGF-pL. Serurn levels of TGF-B1 [p < 0.001] were significantly higher in chronic hepatitis C patients compared with controls. Aspartate aminotransferase [AST], alanine aminotransferase [ALT] [p < 0.001], were significantly higher in chronic hepatitis C patients compared with controls. There was a significant difference between chronic hepatitis subgroups [as regard degree of steatosis] grading and staging [p< 0.001]. There was a significant correlation between steatosis grading and tissue level of TGF-Bl but not with serum level of TGF-B1. There was a significant correlation between fibrosis staging and tissue level of TGF-B1. Also, serum level of TGF-B1 was significantly correlated with advance of fibrosis. HCV-genotype 4 infection is associated with a significant higher serum level of TGF-B1 than those of normal subjects. We have confirmed that steatosis is associated with increased fibrosis and necroinflammation in chronic HCV biopsies

Active human cytomegalovirus infection in newly diagnosed patients with ulcerative colitis in Tanta University Hospitals

Cytomegalovirus infection is common throughout the world; 40%-100% of adults in different populations are infected by the fourth decade. Early studies suggested that CMV infection initiates some cases of ulcerative colitis [UC], plays a role in UC exacerbation, causes self-limited colitis, and increases the incidence of complications, emergency surgery or death in patients with UC. Thirty-seven patients with first-time diagnosed ulcerative colitis were selected retrospectively and included in this study from attendance Tanta University Hospitals. Patients were classified into two groups, group I ulcerative colitis patients infected with CMV; group II ulcerative colitis patients not infected with CMV Severity of UC was assessed clinically using Montreal classification of severity of ulcerative colitis, colonoscopicaly using Montreal classification of extent of ulcerative colitis. Histologically diagnosis and severity was graded using microscopic scores for the assessment of disease activity in UC. Patients were comparable with controls according to age and sex. Clinical and laboratory parameters showed no statistically significant differences except for reduced serum albumin and hemoglobin in group I [p <0.05]. The highest sensitivity was achieved in immunohistochemistry, while the lowest one was achieved in detection of inclusion bodies in H and E-stained biopsy for detection of infection with CMV in patients with UC As regards assessment of severity in patients with UC with or without CMV infection, no significant differences between both groups were detected. CMV infection in patients with UC may be common and is often underestimated. This has definite clinical significance and therefore should not be ignored

HFE mutations, serum iron indices, and hepatic iron: impact on fibrosis severity and steatosis in patients with chronic hepatitis C genotype 4

Iron overload may cause or contribute to hepatic injuiy and fibrosis. Mutations in tbr HFE gene may influence development or progression of chronic liver disease by increasing iron stores or modulating immune responses. The aim of this work was to assess the influence of HFE mutations and serum and hepatic measures of iron status on fibrosis severity and steatosis in patients with chronic hepatitis C genotype 4. We studied 47 patients [33 males, 14 females, mean age 43.46 +/- 13.54 years] with chronic HCV infection. Serum iron indices were determined in all participants. Hepatitis C virus RMA was detected in patients' sera by reverse transcriptase-polymerase chain reaction [RT-PCR]. Liver biopsies were taken to evaluate steatosis, fibrosis, and hepatic iron depositions. We used the method of polymerase chain reaction-restriction fragment length polymorphism [PCR-RFLP] to analyze the HFE mutations. Twenty-three patients 23/47 [48.936%] had increased serum iron stores and only eleven patients 11/47 [23.40%] had positive hepatic iron stain. There was a significant difference between hepatic steatosis subgroups as regards inflammatory grading and fibrosis staging [p <0.001]. Ferritin level was significantly correlated with fibrosis severity and steatosis grading. Hepatic iron deposition was significantly correlated only with steatosis grading but not with fibrosis severity. Heterozyosity for H63D allele was noted to be five patients 5/47 [10.638%] in CHC patients. Our data demonstrated no significant difference in the prevalence of HFE mutations between the HCV patients with increased serum iron store and others without Also, the same results were noticed in patients with and without hepatic iron deposition. Ferritin level should be better considered as a surrogate marker of severe fibrosis in chronic hepatitis C. The prevalence of HFE mutations associated with hereditary hemochromatosis is not increased in the patients with CHC. The HFE mutations may not contribute to iron accumulation in the CHC patients even when serum iron overload is observed in these patients

Influence of therapy on early development of osteoporosis in male smoker subjects with hypoandrogenism influenced by life style and schistosomal hepatic fibrosis

The study aims to evaluate the multifact outcome of hypoandrogenemia colinked with the impact of oxidative stress induced by glucose intolerance, Schistosomal hepatic fibrosis [SHF] and cumulative smoking influence on bone remodeling and early development of osteoporotic manifestations. The effect on vascular endothelium immune mediated mechanisms and antioxidant capacity were monitored in cases of 30 middle aged selected male cases involving 20 subjects with hypoandrogenemia who were either smokers and subjected to sedentary life style, glucose intolerance and SHF [GI] or without [GII] as well as cases of GI after following 6 months therapy [GIII] compared to controls [GIV]. Monitoring of clinical picture and biochemical assessments of osteoporotic indices [osteocalcin, bone alkaline phosphatase, parathyroid hormone, urinary cyclic AMP], hypoandrogenism [dehydroepiandrosterane sulphate "DHEAS" and testosterone] glycemic determinant [insulin] immunoinflammatory response [interleukein-6 "IL-6", tumor necrosis factor a "TNF-alpha", E-selectin, ceruloplasmin] smoking index [serum cotinine], tolal antioxidant capacity [AOC] and lipid peroxidation product [malonedialdehyde] were done before and after 6 months therapeutic program involving supplement of DHEAS, chromium picolinate, and megavit zinc alongside smoking cessation and physical exercise daily for at least 30 minutes. It was evident that the adjustment of hormonal status and antioxidant potential should be dealt with smoking cessation to maintain physical fitness and to retard the early onset of osteoporosis. the recognition of the profound impact of life style choices on bone health, risk factors of which the most frequent include smoking, hypoandrogenemia and glucose intolerance besides metabolic and immunoinflammatory derangement posed by SHF all of which induce oxidative stress and potentiate the early development of osteoporosis in middle aged male smokers. Cessation of smoking and adopting active life style with at least half hour daily sportive exercise besides supplements with DHEAS, chromium, zinc and multivitamin-mineral supplement for six months had retarded and readjusted osteoprotic manifestations in studied group

Prognostic value of analysis of serum and ascitic fluid levels of intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule-1 [VCAM-1] in patients with spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis [SBP] is a life-threatening complication in patients with liver cirrhosis. Renal failure or multiorgan insufficiency is considered to be the main causes of death in patients with SBP. The aim of this work was the evaluation of serum and ascitic fluid levels of intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule-1 [VCAM-1] in patients with spontaneous bacterial peritonitis. We prospectively studied 18 cirrhotic patients with SBP, 9 cirrhotic ascitic individuals without any evidence of infection as cirrhotic ascitic controls and 10 healthy controls. Serum and ascitic fluid levels of ICAM-1 and VCAM-1 were measured and compared. Serum levels of ICAM-1, and VCAM-1 were significantly increased in cirrhotic ascitic patients, either infected or non-infected, compared with healthy controls. SBP was associated with significantly elevated serum and ascitic levels of ICAM-1, and VCAM-1 compared with non-infected cirrhotic ascitic patients. There was also, a significant increase in serum and ascitic levels of ICAM-1, and VCAM-1 in patients with SBP who developed renal failure. A prognostic significance can be attributed to increased serum and ascitic levels of ICAM-1 and VCAM-1 in patients with SBP as regard development of renal failure