Serum cholesterol and low-density lipoprotein cholesterol levels as predictors of response to interferon therapy for chronic hepatitis C.
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Antiviral Agents↗
Biomedical subjects
G Y Minuk
Publications and source records attributed to G Y Minuk.
The effects of various organ preservation solutions on hepatocyte membrane potentials, intracellular calcium concentrations, and outcome following liver transplantation.
BACKGROUND: Hepatocyte membrane potential differences (PDs) may be altered by the preservation solutions used in liver transplantation. Such alterations could impact on the survival of the donor liver, extent of biochemical injury, and flux of important ionic compounds. The purpose of the present study was to document these outcomes in the presence of four different preservation solutions. METHODS: Livers of adult male Sprague-Dawley rats (N = 3 to 4 per group) were impaled with intracellular microelectrodes prior to and at various time periods for 6 hours following complete hepatic resection. Just prior to resection, each liver was perfused with preservation solutions associated with high (normal saline [NS]), moderate (Euro-Collins [EC]), and low (University of Wisconsin solution [UW]) risks of reperfusion injury. RESULTS: Baseline (in situ) PDs were similar in all groups (-37 +/- 4 mV, mean +/- SD). Ten minutes postresection, hepatic PDs were as follows: NS, -23.8 +/- 3.5 mV; EC, -11.4 +/- 0.4 mV; and UW, -8.7 +/- 0.3 mV (P <0.01 for all groups). Maximum depolarization occurred at 6 hours postresection (NS, -8.1 +/- 1.1 mV; EC, -7.7 +/- 1.3 mV; and UW, -8.6 +/- 1.0 mV). To determine whether these changes are of pathophysiologic importance, the NS solution was modified (addition of 0.1% ethanol) to achieve similar PD changes as those observed with UW. Liver transplants were then performed where the donor livers had been perfused and preserved for 6 hours with either NS or the modified NS (MNS) solution. Posttransplant (10 day) survival was 1 of 6 (17%) in the NS group and 4 of 6 (67%) in the MNS group (P <0.05). Regarding the effects of PD changes on ionic flux, intracellular calcium levels were documented for up to 4 hours by fluorescence video microscopy using Fura-2 in isolated hepatocytes exposed to NS, UW, and MNS solutions. Intracellular calcium levels were similar in all solutions at each time point studied. CONCLUSIONS: The results of this study indicate that hepatocytes undergo prompt and marked depolarization following hepatic resection, and the extent of the depolarization correlates with survival following transplantation.
Adenosine↗
Effect of preoperative interventions on outcome following liver resection in a rat model of cirrhosis.
BACKGROUND/AIMS: High morbidity and mortality rates in cirrhotic patients undergoing resections for hepatocellular malignancies underscore the need for identifying a therapy that will decrease fibrosis or enhance hepatic regenerative activity in the perioperative period. Thus, in the present study, 104 carbon tetrachloride-induced cirrhotic rats received either saline (untreated cirrhotic controls) or one of the following agents that have been reported to decrease hepatic fibrosis or increase hepatic regeneration; pentoxifylline, ciprofloxacin or a traditional Chinese herbal remedy (TCHR). Twelve additional rats served as healthy, non-cirrhotic controls. METHODS: Treatments were administered daily by gavage for 4 weeks followed by a 70% partial hepatectomy. Hepatic fibrosis was documented at the time of surgery by computer-assisted quantitation of collagen content. Liver function and hepatic regenerative activity were documented 24 h post partial hepatectomy by serum bilirubin determinations and a combination of 3[H]-Thymidine incorporation into hepatic DNA and proliferating cell nuclear antigen (PCNA) quantitation, respectively. RESULTS: Compared to untreated cirrhotic controls (8.1 +/- 0.7%), fibrosis was significantly reduced in the pentoxifylline- and ciprofloxacin-treated groups (4.6 +/- 0.2%, p<0.005 and 5.5 +/- 0.6%, p<0.05) but unchanged in the TCHR-treated group (6.6 +/- 11.0%). Post-operatively, total serum bilirubin levels were lower in the pentoxifylline (1.40 +/- 0.15 mg/dl,p<0.01) and ciprofloxacin (1.87 +/- 0.25 mg/dl, p<0.05)-treated groups, but unchanged in the TCHR group (2.20 +/- 0.45 mg/dl), when compared to untreated cirrhotic controls (3.00 +/- 0.37 mg/dl). Hepatic regenerative activity was also significantly improved in the pentoxifylline-treated group (17.8 +/- 2.2 versus 9.9 +/- 1.9 DPM/microg DNA in untreated cirrhotic controls, p<0.05), but unchanged in the ciprofloxacin (16.1 +/- 1.8 DPM/microg DNA) and TCHR (10.9 +/- 1.2 DPM/microg DNA)-treated groups. PCNA protein determinations were in keeping with the 3[H]-Thymidine results CONCLUSIONS: Pre-operative pentoxifylline holds promise as a useful therapeutic intervention for patients with cirrhosis requiring hepatic resection.
Animals↗
Increased GABAergic activity inhibits alpha-fetoprotein mRNA expression and the proliferative activity of the HepG2 human hepatocellular carcinoma cell line.
BACKGROUND/AIMS: Gamma aminobutyric acid (GABA) is a potent inhibitory neurotransmitter with growth regulatory properties. Recent data indicate that increased GABAergic activity inhibits hepatocyte proliferation in regenerating livers. In the present study, we aimed to investigate whether GABA inhibits the growth of malignant hepatocytes. METHODS: Increasing concentrations of muscimol (0.05-50 microM), a specific GABA(A) receptor agonist, were added to HepG2 human hepatocellular carcinoma cells and alpha-fetoprotein (AFP) and albumin mRNA expression were determined for varying periods of time (maximum 24 h) thereafter. Cell proliferation was also documented after 48 h of exposure to muscimol. RESULTS: Muscimol significantly (p<0.0001) decreased AFP mRNA expression (maximum decrease: 65% below baseline values) without affecting albumin mRNA expression. However, the effect on AFP mRNA was transient (maximum duration: 3-6 h) and not associated with changes in cell proliferation. Because preliminary data indicate that GABA(A) receptor activity is markedly downregulated in malignant hepatocytes, transfection studies were performed wherein HepG2 cells were cotransfected with GABA(A) receptor beta2 and beta2 subunit genes in a pCDM8 expression vector or vector alone followed by re-exposure to either muscimol (5 betaM) or saline. In this series of experiments, in addition to AFP mRNA inhibition being as extensive and more prolonged (maximum duration: 6-12 h) in muscimol-treated, GABA(A) receptor-transfected cells, proliferative activity was also significantly inhibited when compared to saline-treated GABA(A) receptor-transfected controls (p<0.01) and muscimol-treated cells transfected with vector alone (p<0.005). CONCLUSION: The results of this study indicate that increased GABAergic activity inhibits AFP mRNA expression and cell proliferation in this malignant hepatocyte cell line.
Albumins↗
Pre-core mutant infections in the Canadian Inuit.
BACKGROUND/AIMS: Previous cross-sectional data suggested that chronic hepatitis B viral (HBV) infections in the Canadian Inuit were inactive. The aim of this study was to confirm these findings and document the prevalence of the subsequently described "pre-core mutant" variant of HBV in this population. METHODS: We obtained sera from residents of five remote Canadian Inuit communities. Residents were selected if they were known to be hepatitis B surface antigen (HBsAg) positive or had a history of liver disease. HBV serology, HBV-DNA, and pre-core mutant testing were performed by commercially available assays, polymerase chain reaction (PCR) and direct sequencing of the viral genome, respectively. RESULTS: Sera were obtained from 176/266 (66%) of selected individuals. Thirty-eight (22%) were HBsAg positive and 16 (9.1%) anti-HBs positive. Of HBsAg positive carriers 25/38 (66%) were male as compared to 68/138 (49%) of the remaining individuals (p<0.05). Of 37 HBsAg positive carriers, none were HBeAg positive, 36 (97%) anti-HBe positive and one (3%) HBeAg and anti-HBe negative. Liver enzyme and function tests were normal in all cases. 30/37 (81%) HBsAg positive carriers were HBV-DNA positive and 26/30 (87%) were pre-core mutant positive. CONCLUSION: The majority of HBV infections in community-based Canadian Inuit are inactive and the prevalence of pre-core mutant infections is the highest reported to date.
Adult↗
The expression of insulin-like growth factor binding proteins in human hepatocellular carcinoma.
Insulin-like growth factors (IGF), IGF receptors and IGF binding proteins (IGFBPs) play an important role in cell growth and differentiation. The liver is the major source of IGF-1 and at least two IGFBPs (IGFBP-1 and IGFBP-3). IGFBPs most often serve to attenuate the effects of IGF at the receptor level and thereby limit IGF-induced cell growth and differentiation. Although changes in IGFBP expression have been described during controlled liver growth such as hepatic regeneration following partial hepatectomy, there is limited knowledge of IGFBPs gene expression in uncontrolled growth or hepatocellular carcinoma. In the present study, we employed Northern blotting techniques to document the expression of IGFBP-1, 3 and 4 in normal human livers, cirrhotic and hepatocellular carcinoma tissues. The results revealed no differences in IGFBP-1, 3 and 4 mRNA levels between normal and cirrhotic tissues. However, the expression of all three IGFBPs mRNA were significantly down regulated in hepatocellular carcinoma tissues. These findings are in keeping with IGFBPs playing an important inhibitory role in the development and/or growth of hepatocellular carcinoma in humans.
Blotting, Northern↗
The effects of acute ethanol exposure on inhibitors of hepatic regenerative activity in the rat.
The purpose of this study was to identify the mechanism(s) whereby acute ethanol exposure inhibits hepatic regenerative activity in the rat. Adult, male, Sprague-Dawley rats (200-250 g) were randomized to receive either ethanol (1 g/kg i.p. q 4 h) or an equal volume of saline (controls) for 24 h beginning 1 h prior to a 70% partial hepatectomy (PHx). At 0, 3, 6, 12 and 24 h post-PHx, rats were sacrificed (N = 4-6/group), and the expression of the following genes associated with inhibition of hepatocyte proliferation were documented; p53, p21, transforming growth factor-beta1 (TGF-beta1) and gamma aminobutyric acid transport protein (GABA-TP). Inhibition of hepatic regenerative activity was confirmed by 3H-thymidine incorporation into hepatic DNA at 24 h post-PHx. The results of the study revealed that in ethanol-treated rats, DNA synthesis was inhibited by 37% when compared to saline-treated controls (p < 0.01). Regarding suppressor gene expression, both p21 and TGF-beta1 mRNA expression in ethanol-treated rats were similar to those obtained in saline-treated controls. Although p53 mRNA expression differed in the two groups, in the ethanol-treated group, p53 mRNA expression was decreased rather than increased (relative to controls) at 24 h post-PHx, a finding not in keeping with inhibition of DNA synthesis. GABA-TP mRNA was strongly expressed prior to PHx in both ethanol- and saline-treated rats. Following PHx, GABA-TP mRNA expression decreased in both groups but remained low in the saline-treated group while returning to pre-PHx values in ethanol-treated rats. In summary, the results of this study indicate that the inhibitory effects of ethanol on hepatic regeneration are not associated with significant or the appropriate changes in mRNA expression of the p53, p21 or TGF-beta1 suppressor genes. On the other hand, transcriptional changes in GABA-TP gene expression post-PHx are in keeping with an inhibitory effect of GABA on hepatic regeneration.
Animals↗
GABA and hepatocellular carcinoma.
Data derived from models of hepatic regeneration indicate that transient, reciprocal changes in polyamines, potent growth promoters, and gamma aminobutyric acid (GABA), an amino acid neurotransmitter with growth inhibitory properties, play important roles in enhancing and inhibiting respectively regulated hepatocyte proliferation. Based on these findings and supportive data derived from studies of human carcinoma tissues and malignant cell lines we propose that permanent increases in polyamine and decreases in GABAergic activity act in concert to contribute to the pathogenesis of hepatocellular carcinoma.
Animals↗
Light ethanol consumption enhances liver regeneration after partial hepatectomy in rats.
BACKGROUND & AIMS: The effects of "social drinking" on the liver have yet to be fully documented. The aim of this study was to document the effects of daily light, moderate, and heavy ethanol exposure on hepatic regenerative activity in the rat. METHODS: Adult male Sprague-Dawley rats underwent daily gavages with 1.0 (light), 2. 0 (moderate), or 4.0 (heavy) g/kg of ethanol or tap water (controls) for 30 days before 70% partial hepatectomy (PHx). Hepatic regenerative activity was then documented on days 1, 3, 5, and 7 after PHx. RESULTS: Compared with controls, restitution of liver mass, [(3)H]thymidine incorporation, and proliferating cell nuclear antigen expression were decreased in the heavy (-10%, -60%, and -36%, respectively), unchanged in the moderate (-4%, -8%, and -16%, respectively), and increased in the light (+6%, +38%, and +29%, respectively) ethanol groups. Messenger RNA differential display of resected livers at PHx identified a band present only in the light ethanol group that encodes a unique 47-kilodalton protein with growth-promoting features designated light ethanol-induced stimulatory protein. CONCLUSIONS: The results indicate that light ethanol consumption enhances hepatic regenerative activity after PHx in rats. Further studies are required to determine the mechanism involved and whether social drinking has beneficial or adverse effects on the natural history of acute or chronic liver disease in humans.
Alcohol Drinking↗
Serum aspartate but not alanine aminotransferase levels help to predict the histological features of chronic hepatitis C viral infections in adults.
OBJECTIVES: The aims of this study were to assess the predictive values of age, gender, route of transmission, extent of steatosis, alcohol consumption, and serum aminotransferase values on the histological findings in patients with chronic hepatitis C viral infections. METHODS: We retrospectively reviewed the charts and liver biopsy findings from 79 adult patients with serological evidence of chronic hepatitis C viral infections. RESULTS: The mean (+/- SD) age of the patient population was 43.5 +/- 10.8 yr; 47 patients (60%) were male. The routes of transmission were considered to be parenteral drugs in 44 patients (56%), previous blood transfusions in 25 (32%), and miscellaneous parenteral and nonparenteral routes in 10 (13%). The mean histological activity score of the group as described by Desmet et al. was 3.5 +/- 0.8 (maximum possible score, 18) and the fibrosis score 1.5 +/-0.4 (maximum possible score, 4), indicating relatively mild disease in the majority of cases. The extent of inflammation correlated with fibrosis (r = 0.72). By multivariate stepwise regression analyses, serum aspartate aminotransferase (AST) values emerged as the most important predictive variable of histological activity (r = 0.62). When overall histological activity was further divided into portal inflammation, piecemeal necrosis, and lobular activity, correlations were found between AST values and portal inflammation (r = 0.58) and piecemeal necrosis (r = 0.61) but not lobular activity (r = 0.1). A correlation was also observed between AST values and the extent of hepatic fibrosis (r = 0.64). On the other hand, serum ALT values did not correlate with histological activity but did correlate weakly with the extent of hepatic fibrosis (r = 0.39 and 0.51, respectively). There were no significant correlations between age, gender, route of transmission, steatosis, or alcohol consumption with the extent of histological activity or fibrosis. CONCLUSIONS: Serum AST values correlate well with two of three features of hepatic inflammation and with the extent of hepatic fibrosis. These findings suggest that, among other factors, serum AST values should be considered in decisions regarding the need for liver biopsy and treatment in patients with chronic hepatitis C viral infections.
Adult↗
Research toward safer resection of the cirrhotic liver.
Despite recent advances in hepatic surgery, resection of the cirrhotic liver continues to be fraught with high morbidity and mortality rates. As a result, for many patients requiring resection of HCC the postoperative course is complicated and the probability of cure is diminished by coexisting cirrhosis. In this review, we discuss the characteristics of the cirrhotic liver which make it poorly tolerant of resection and the most common complications that follow such surgery. The main purpose of this paper is to review recent attempts to identify interventions that might be beneficial to cirrhotic patients undergoing resection. These interventions include assessment of liver reserve, advances in surgical technique, and improvement in liver function and regeneration.
Aged↗
Risk of sedation for upper GI endoscopy exacerbating subclinical hepatic encephalopathy in patients with cirrhosis.
BACKGROUND: The risk of exacerbating subclinical hepatic encephalopathy associated with the administration of sedative drugs in patients with cirrhosis undergoing diagnostic upper gastrointestinal (GI) endoscopy for portal hypertension remains to be determined. METHODS: Ten adult patients with cirrhosis completed number connection tests before sedation for endoscopy and at discharge from the endoscopy unit 2 hours post-procedure. Control patients consisted of five patients with cirrhosis undergoing the same procedure for the same indication who did not receive sedation and 12 patients with no evidence of liver disease who received sedation before diagnostic endoscopy for a variety of GI complaints. The control populations were age, gender, education level, and, in the case of patients with cirrhosis, Child Pugh s score matched to the patients with cirrhosis who received sedation. RESULTS: The mean (+/- SEM) age of patients with cirrhosis who received sedation was 59.6 +/- 3.8 years. Seven of the ten (70%) were men. Their mean Child Pugh s score was 7.2 +/- 1.5. Nine of the ten (90%) had abnormal baseline number connection tests results (mean for the group 52.3 +/- 6.7 seconds) the extent of which correlated with Child Pugh s scores (p < 0.005). Individually, the baseline number connection tests results were normal in one (10%), mild in six (60%), moderate in one (10%), and severe in two (20%). After the procedure (before discharge) the mean number connection tests result was 61.5 +/- 7.9 seconds (p = 0.01 when compared with baseline). The results were now normal in none (0%), mild in four (40%), moderate in four (40%), and severe in two (20%). Pre- and post-procedure number connection tests results did not change in the non-sedated cirrhotic or sedated non-liver disease control patients. CONCLUSIONS: The results of this study indicate that (1) the majority of patients with cirrhosis and suspected portal hypertension have evidence of subclinical hepatic encephalopathy, (2) the extent of encephalopathy correlates with the Child Pugh's score, (3) sedation with midazolam for upper GI endoscopy exacerbates the encephalopathy, and (4) this adverse effect is still evident 2 hours after the procedure.
Adult↗
Regulation of transforming growth factor-beta1 gene expression and cell proliferation in human hepatocellular carcinoma cells (PLC/PRF/5) by tamoxifen.
Hepatocellular carcinoma (HCC) is a common, potentially lethal tumor in human patients. Because the serum levels of transforming growth factor-beta1 (TGF-beta1) correlate with outcome in patients with HCC and because TGFbeta1 mRNA expression is increased in HCC tissues, it raises the possibility that TGF-beta1 may be of importance in the development, growth, and metastases of HCC. Tamoxifen has been used for the treatment of human HCC. However, clinical trials have produced conflicting results. To further delineate whether tamoxifen may be of benefit in altering the course of HCC, we documented the effects of 4-hydroxytamoxifen and 17beta-estradiol on TGF-beta1 mRNA and protein levels and cell proliferation in a human HCC cell line. PLC/PRF/5 cells were treated with carrier (controls), 4-hydroxytamoxifen, 17beta-estradiol, or TGF-beta1. 4-Hydroxytamoxifen and 17beta-estradiol decreased TGF-beta1 mRNA and protein levels in a time- and dose-dependent manner. TGF-beta1 significantly inhibited PLC/PRF/5 cell proliferation, whereas both 4-hydroxytamoxifen and 17beta-estradiol stimulated PLC/PRF/5 cell proliferation. The stimulatory effects of 4-hydroxytamoxifen on PLC/PRF/5 cell proliferation raise concerns regarding its use in the treatment of HCC in human patients and suggest that 4-hydroxytamoxifen may have no beneficial effects in some patients with HCC.
Carcinoma, Hepatocellular↗
Altered transmembrane ionic flux in hepatocytes isolated from cirrhotic rats.
BACKGROUND/AIMS: Although cirrhosis is known to be associated with many hepatocyte abnormalities, there is no well-established model to study the cellular drug uptake process independent of hemodynamic effects. The purpose of the present study was to test the following hypothesis: hepatocytes isolated from cirrhotic animals may be used as a model to study the cellular abnormalities associated with cirrhosis. Our hypothesis was tested by comparing the membrane potential (PD) of hepatocytes in anesthetized healthy and cirrhotic animals, and the PD and [3H]palmitic acid clearance rate of hepatocytes isolated from healthy and cirrhotic animals. METHODS: Mild to moderate cirrhosis was induced in female Sprague-Dawley rats by CCl4 administration. PD was recorded in anesthetized animals using intracellular microelectrodes. Hepatocytes from those livers were subsequently isolated by collagenase perfusion for further determinations of PD and [3H]palmitic acid uptake. RESULTS: The mean (+/-SEM) hepatocyte PD from intact rat livers was 38+/-1 mV (control) and -32+/-1 mV (cirrhosis; n=6/group, p<0.01). The PD (mean+/-SEM) in isolated hepatocytes was -21+/-1 mV (control) and -15+/-1 mV (cirrhosis, n=13/group, p<0.01). The clearance rate of [3H]palmitic acid was lower in hepatocytes isolated from cirrhotic animals (26%) than in those isolated from healthy control animals (p<0.01). CONCLUSION: The results of this study indicate that hepatocytes isolated from cirrhotic animals may be used to study the cellular abnormalities associated with cirrhosis.
Animals↗
Telomeres, telomerase and HCC: the long and the short of it.
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Animals↗
Effects of acute and chronic ethanol exposure on the hepatic gamma-aminobutyric acid transport system in rats.
Ethanol-induced increases in gamma-aminobutyric (GABA)ergic activity contribute to the impairment in hepatic regeneration associated with alcohol-induced liver disease. To determine the mechanism(s) whereby ethanol increases GABAergic activity in the liver, we documented the effects of acute (5 g/kg x 1) and chronic (36% of total calories over 6 weeks) ethanol exposure as well as exogenous GABA (500 microg/g body weight) administration on GABA transport protein (GABA-TP) mRNA expression in the livers of adult male Sprague-Dawley rats at various times (0-72 h) post 70% partial hepatectomy (PHx). We also documented the in vitro effects of ethanol (30-90 microM) on [3H]-GABA uptake in isolated rat hepatocytes. The results of the study revealed that compared to saline-exposed controls, acute but not chronic ethanol exposure resulted in significant decreases in GABA-TP mRNA expression at 12, 24, and 48 h post PHx (saline exposed, 1.04 +/- 0.06, 1.19 +/- 0.21, and 1.15 +/- 0.05. vs. acute ethanol exposed, 0.80 +/- 0.16, 0.88 +/- 0.09, and 0.86 +/- 0.16 optical density units, p < 0.01, 0.05, and 0.05, respectively). An inhibitory effect was also observed following exogenous GABA administration (GABA-TP mRNA expression at 3 h was approximately 40% that of baseline, p < 0.05). [3H]-GABA uptake in isolated rat hepatocytes in vitro was unaffected by the presence of ethanol. In conclusion, the results of this study indicate that acute but not chronic ethanol exposure and exogenously administrated GABA inhibit hepatic GABA-TP mRNA expression following partial hepatectomy in the rat. These findings suggest that the increased GABAergic activity that occurs in the liver following acute ethanol exposure results from alterations in the hepatic GABA transport system at a transcriptional level.
Animals↗
Effects of acute ethanol exposure on polyamine and gamma-aminobutyric acid metabolism in the regenerating liver.
Recently, it has been suggested that ethanol-induced inhibition of liver regeneration results from decreases in hepatic putrescine levels and/or increases in hepatic gamma-aminobutyric acid (GABA)ergic activity. Because putrescine can be metabolized by diamine (DAO) and monoamine (MAO) oxidases to GABA, we documented the effects of acute ethanol exposure on hepatic MAO or DAO activity following partial hepatectomy (PHx) in rats. We also documented the effects of ethanol on GABA transaminase (GABA-T), the enzyme responsible for GABA metabolism in the liver, and tissue putrescine and GABA levels. Adult, male Sprague-Dawley rats (200-250 g) were treated with either ethanol (3 g/kg) or equal volumes of saline by gastric gavage 1 h prior to a 70% PHx or sham surgery. Rats were then sacrificed (n = 5-7/group) at various times (0-72 h) post-PHx. Enzymatic activity and putrescine/GABA levels were determined by standard isotopic techniques and high-performance liquid chromatography respectively. Hepatic DAO activities in ethanol-treated rats were transiently higher than in saline-treated controls (30% increases at 6 h, p < 0.05). Hepatic MAO and GABA-T activities in acute ethanol-treated rats were essentially identical to saline-treated controls. Although hepatic putrescine levels were similar in ethanol- and saline-treated rats, hepatic GABA levels were approximately three times higher in ethanol-treated rats at 12 and 24 h post-PHx (p < 0.0001). In conclusion, the results of this study indicate that acute ethanol exposure has a limited effect on the enzymatic conversion of putrescine to GABA following partial hepatectomy in the liver. The results also indicate that increased GABAergic inhibition rather than decreased putrescine stimulation is more likely to play a role in ethanol-induced inhibition of hepatic regeneration.
4-Aminobutyrate Transaminase↗
The influence of host factors on the natural history of chronic hepatitis C viral infections.
The natural history of hepatitis C is variable, with some patients progressing rapidly to cirrhosis and others showing no significant fibrosis over many decades. A number of studies have examined the factors that influence disease progression. Age at time of infection, gender, alcohol abuse and, perhaps, route of transmission, appear to have the greatest influence on the natural history of the hepatitis C virus with the possible exception of alcohol, the mechanism whereby these factors influence disease progression has yet to be determined.
Disease Progression↗