Biomedical subjects

M W Fried

Publications and source records attributed to M W Fried.

At least 19 recordsLinked to original sources

PubMed1999

Sequence heterogeneity within three different regions of the hepatitis G virus genome.

Two sets of primers derived from the 5'-terminal region and the NS5 region of the hepatitis G virus (HGV) genome were used to amplify PCR fragments from serum specimens obtained from different parts of the world. All PCR fragments from the 5'-terminal region (5'-PCR, n = 56) and from the NS5 region (NS5-PCR, n = 85) were sequenced and compared to corresponding published HGV sequences. The range of nucleotide sequence similarity varied from 74 and 78% to 100% for 5'-PCR and NS5-PCR fragments, respectively. Additionally, five overlapping PCR fragments comprising an approximately 2.0-kb structural region of the HGV genome were sequenced from each of five sera obtained from three United States residents. These sequences were compared to 20 published sequences comprising the same region of the HGV genome. Nucleotide and deduced amino acid sequences obtained from different individuals were homologous from 82.9 to 93. 6% and from 90.4 to 99.0%, respectively. Sequences obtained from follow-up specimens were almost identical. Comparative analysis of deduced amino acid sequences of the HGV structural proteins and hepatitis C virus (HCV) structural proteins combined with an analysis of predicted secondary structures and hydrophobic profiles allowed prediction of processing sites within the HGV structural proteins. A phylogenetic sequence analysis performed on the 2.0-kb structural region supports the existence of three previously identified HGV genetic groups. However, phylogenetic analysis performed on only small DNA fragments yielded inconsistent genetic grouping and failed to confirm the existence of genetic groups. Thus, in contrast to HCV where almost any region can be used for genotyping, only large or carefully selected genome fragments can be used to identify consistent HGV genetic groups.

5' Untranslated Regions↗

PubMed1999

A pilot study of rimantadine for patients with chronic hepatitis C unresponsive to interferon therapy.

OBJECTIVE: Therapeutic options are limited for chronic hepatitis C patients who have not responded to a course of interferon therapy. Recently, a 6-month course of amantadine was shown to result in a sustained virological response in chronic hepatitis C patients who were unresponsive to interferon therapy. The aim of this study was to evaluate the effect of rimantadine on chronic hepatitis C patients who had not responded to interferon therapy. METHODS: This was an open label trial involving 17 patients who were treated with rimantadine 100 mg b.i.d. for 6 months. Changes in serum aminotransferase activities and HCV-RNA levels were determined. RESULTS: Mean alanine aminotransferase activities and HCV RNA levels did not change significantly during therapy. HCV RNA remained detectable in all patients throughout therapy. Neurologic symptoms (headaches, nervousness, and dizziness) developed in 29% of patients. A total of 12% of patients required dose reduction after 12 wk of therapy because of dizziness. CONCLUSION: Rimantadine has no significant antiviral activity against HCV.

Adult↗

PubMed1998

Is vaccination against hepatitis B infection indicated in patients waiting for or after orthotopic liver transplantation?

It is a common practice to immunize patients against hepatitis B infection while they are waiting for liver transplantation, but the efficacy of this practice is unclear. This is a retrospective analysis of the antibody response to 20 microg of a recombinant hepatitis B vaccine in patients waiting for and after liver transplantation. The response to vaccination was measured 1-3 months after completion of the vaccination series. The risk of acquiring hepatitis B virus after liver transplant was determined by reviewing the results of tests for hepatitis B infection in 171 patients who underwent transplantation for non-hepatitis B diseases and who had not been vaccinated. Fifty-seven patients awaiting transplantation were eligible for the study, and a response to vaccination was observed in only 9 (16%). Patients with cholestatic liver disease had a significantly higher response (6 of 14; 43%) compared with noncholestatic liver disease (3 of 43; 7%; P = .004). Forty-five liver transplant recipients were immunized against hepatitis B after transplantation, and only 3 (6.7%) developed an antibody response. The frequency of posttransplant hepatitis B infection in the 171 patients who were not immunized and who lacked any evidence of hepatitis B infection pretransplantation was 4 of 171 (2.3%). The response rate to immunization with a recombinant hepatitis B vaccine in patients with chronic liver disease who are waiting for a liver transplant and after transplantation is poor. Given the poor response to vaccination and the low risk of acquiring hepatitis B virus after transplantation, centers need to reconsider the routine use of the hepatitis B virus vaccine in patients awaiting liver transplantation.

Adult↗

PubMed1998

Treatment of hepatocellular carcinoma: medical options.

Nonsurgical therapy provides some benefit to patients with advanced hepatocellular carcinoma, although surgical options, including transplantation, remain the only chance for cure. Careful patient selection is required; patients with small nodular tumors may be considered for PEI therapy, whereas patients with larger tumors may be considered for TACE. Regardless of the treatment modality, the likelihood of survival is usually directly associated with the degree of hepatic dysfunction. Randomized, controlled trials of these treatment modalities are limited in number and design; therefore, it is difficult to assess their true impact on patient survival and quality of life. Secondary chemoprophylaxis against recurrent disease with vitamin A analogues is a promising adjunctive measure to both surgical and nonsurgical treatments for hepatocellular carcinoma.

Antineoplastic Agents↗

PubMed1997

Hepatitis G virus co-infection in liver transplantation recipients with chronic hepatitis C and nonviral chronic liver disease.

Hepatitis G virus (HGV) is a newly described RNA virus that is parenterally transmitted and has been found frequently in patients with chronic hepatitis C infection. To determine the impact of hepatitis G virus co-infection on morbidity and mortality following liver transplantation, we measured HGV RNA by polymerase chain reaction in pre and posttransplantation sera from a cohort of patients transplanted for chronic hepatitis C and a control group of patients transplanted for nonviral causes who were negative for hepatitis C virus (HCV) RNA in serum. The overall prevalence rate of HGV RNA in transplanted patients with chronic hepatitis C was 20.7%. HGV infection was present before transplantation in 13% while it appeared to have been acquired at the time of transplantation in 7.4%. Mean serum alanine aminotransferase activity, hepatic histological activity, and patient and graft survival were similar between HGV-positive and HGV-negative patients. The prevalence rate of HGV RNA in transplanted controls was 64% (P < .01) with a significantly higher rate of acquisition of HGV infection following transplantation (53%, P < .001) when compared with patients with chronic hepatitis C. Mean serum alanine aminotransferase activity was significantly lower in the control patients with HGV infection alone following transplantation than in patients co-infected with hepatitis C (37 +/- 9 vs. 70 +/- 33 U/L, P < .01). Thus, HGV is frequently found in transplantation patients co-infected with hepatitis C although it appears to have minimal clinical impact. In patients transplanted for nonviral causes of end-stage liver disease, a high rate of hepatitis G acquisition at the time of transplantation may occur but does not appear to predispose to chronic hepatitis.

Adult↗

PubMed1997

Assessment of monoethylglycinexylidide as measure of liver function for patients with chronic viral hepatitis.

The liver metabolizes lidocaine by oxidative deethylation to form monoethylglycinexylidide (MEGX), an analyte proposed as an index of liver function. We determined MEGX and lidocaine serum concentrations with the TDx (Abbott Laboratories) at baseline and 15, 30, 60, and 90 min after the intravenous administration of lidocaine (1 mg/kg), analyzing specimens from 12 apparently healthy volunteers and 40 patients with chronic viral hepatitis diagnosed by liver biopsy and serum tests. The patients were grouped on the basis of the histology activity index. The following laboratory tests were performed on serum specimens from all subjects: albumin (ALB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, total bilirubin, and prothrombin time. The results showed no significant difference among the four groups for the concentrations of MEGX, lidocaine, and lidocaine/MEGX at the four time points. However, the concentrations of ALB, ALT, AST, AST/ALT, and prothrombin time were substantially different among the four groups. Thus, we conclude that assay of MEGX in our patients with chronic viral hepatitis did not contribute to the assessment of liver function when compared with apparently healthy volunteers and traditional tests of liver function.

Adult↗

PubMed1996

Transjugular intrahepatic portosystemic shunt for the management of severe venoocclusive disease following bone marrow transplantation.

Hepatic venoocclusive disease (VOD) is a common, life-threatening complication of bone marrow transplantation (BMT). Portal hypertension is usually present and accounts for many of the clinical manifestations of this syndrome. We describe the results of transjugular intrahepatic portosystemic shunt (TIPS) for the management of VOD after BMT TIPS was performed in six patients with histologically confirmed VOD who had progressive jaundice and ascites. Portal hypertension was improved by TIPS in all patients (mean portal pressure gradient before TIPS, 20.2 +/- 4.6 vs. 6.7 +/- 1.9 mm Hg post-TIPS, P < .004). Three patients who underwent TIPS late in the course of VOD did not demonstrate any clinical improvement after TIPS and expired within 2 weeks of the procedure. The remaining three patients had less advanced disease and demonstrated decreases in serum bilirubin, improvement in coagulopathy, and decreased ascites after TIPS. Two patients subsequently expired, one with persistent histological changes of VOD. The lone survivor continues to do well with resolution of ascites, jaundice, and coagulopathy as of her last outpatient visit. TIPS was an effective method for portal decompression in patients with VOD after BMT, and was associated with clinical improvement in some patients. However, these effects may be transient and may not improve overall survival.

Adult↗

PubMed1996

Therapy of chronic viral hepatitis.

Interferon alpha is effective therapy for patients with chronic hepatitis B and hepatitis C. Only 20% to 40% of patients, however, have a sustained benefit from therapy. For the majority of patients with these diseases, alternative forms of therapy are needed. Nucleoside analogues appear to be extremely promising for the treatment of chronic hepatitis B and will undoubtedly play a major role in the management of this disease. For chronic hepatitis C, prolonged therapy with interferon, improved patient selection, and combined therapy with multiple agents such as ribavirin may lead to an improved therapeutic response.

Antiviral Agents↗

PubMed1995

Ribavirin as therapy for chronic hepatitis C. A randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To evaluate ribavirin, an oral antiviral agent, as therapy for chronic hepatitis C. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Clinical Center of the National Institutes of Health, a tertiary referral research hospital. PATIENTS: 29 patients with chronic hepatitis C who received oral ribavirin (600 mg twice daily) for 12 months and 29 controls with chronic hepatitis C who received placebo for 12 months. MEASUREMENTS: Effects of therapy were evaluated by measuring serum aminotransferase and hepatitis C virus (HCV) RNA levels before, during, and for 6 months after therapy and by histologic examination of liver specimens before and at the end of treatment. RESULTS: Patients treated with ribavirin had a prompt decrease in serum aminotransferase levels (54% overall) compared with levels before treatment and levels in controls (5% decrease). Serum aminotransferase levels became normal or nearly normal in 10 patients treated with ribavirin (35% [95% CI, 18% to 54%]) but in no controls (0% [CI, 0% to 12%]). Aminotransferase levels remained normal in only 2 patients after ribavirin therapy was discontinued (7% [CI, 1% to 23%]). Serum HCV RNA levels did not change during or after therapy. Liver biopsy specimens showed a decrease in hepatic inflammation and necrosis among ribavirin-treated patients whose aminotransferase levels became normal. CONCLUSIONS: Ribavirin has beneficial effects on serum aminotransferase levels and histologic findings in the liver in patients with chronic hepatitis C, but these effects are not accompanied by changes in HCV RNA levels and are not sustained when ribavirin therapy is discontinued. Thus, ribavirin alone for periods as long as 12 months is unlikely to be of value as therapy for chronic hepatitis C.

Administration, Oral↗

PubMed1995

Hepatic failure and lactic acidosis due to fialuridine (FIAU), an investigational nucleoside analogue for chronic hepatitis B.

BACKGROUND: We describe severe and unexpected multisystem toxicity that occurred during a study of the antiviral nucleoside analogue fialuridine (1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-iodouracil, or FIAU) as therapy for chronic hepatitis B virus infection. METHODS: Fifteen patients with chronic hepatitis B were randomly assigned to receive fialuridine at a dose of either 0.10 or 0.25 mg per kilogram of body weight per day for 24 weeks and were monitored every 1 to 2 weeks by means of a physical examination, blood tests, and testing for hepatitis B virus markers. RESULTS: During the 13th week lactic acidosis and liver failure suddenly developed in one patient. The study was terminated on an emergency basis, and all treatment with fialuridine was discontinued. Seven patients were found to have severe hepatotoxicity, with progressive lactic acidosis, worsening jaundice, and deteriorating hepatic synthetic function despite the discontinuation of fialuridine. Three other patients had mild hepatotoxicity. Several patients also had pancreatitis, neuropathy, or myopathy. Of the seven patients with severe hepatotoxicity, five died and two survived after liver transplantation. Histologic analysis of liver tissue revealed marked accumulation of microvesicular and macrovesicular fat, with minimal necrosis of hepatocytes or architectural changes. Electron microscopy showed abnormal mitochondria and the accumulation of fat in hepatocytes. CONCLUSIONS: In patients with chronic hepatitis B, treatment with fialuridine induced a severe toxic reaction characterized by hepatic failure, lactic acidosis, pancreatitis, neuropathy, and myopathy. This toxic reaction was probably caused by widespread mitochondrial damage and may occur infrequently with other nucleoside analogues.

Acidosis, Lactic↗

PubMed1995

Idiopathic CD4+ T-lymphocytopenia in HIV seronegative men with hemophilia and sex partners of HIV seropositive men. Multicenter Hemophilia Cohort Study.

Persons with hemophilia or other HIV-1 risk factors may be more likely to have idiopathic CD4+ T-lymphocytopenia (ICL). We determined the frequency of ICL in prospectively followed cohorts of HIV-1 seronegative hemophilic men and seronegative female sex partners of HIV-1 infected hemophilic men, and examined factors potentially associated with ICL. Seven of 304 (2.3%) seronegative hemophilic men and one of 160 (0.6%) female partners met the ICL definition, but the condition resolved for two of the men and for the sole female partner. All five men with persistent ICL had lymphocytopenia (< 1,200 total lymphocytes/microliters) and < 300 total CD4+ lymphocytes/microliters; only one had a low CD4+ percentage. On the most recent measurement, 14.5% of the 304 seronegative hemophilic men had lymphocytopenia. Compared with matched hemophilic controls, men with persistent ICL more often had a history of liver disease (3/5 cases, 0/21 controls, P = 0.007) or splenomegaly (3/5 cases, 4/21 controls; P = 0.04), but not severe hemophilia, greater clotting factor concentrate exposure, high alanine aminotransferase levels, hepatitis B virus antigenemia, or detectable hepatitis C virus RNA in plasma. All five cases and 20/21 controls had antibodies to hepatitis C virus present in their serum. In this cohort of hemophilic men, ICL was related to lymphocytopenia associated with liver disease rather than selective loss of CD4+ lymphocytes.

Acquired Immunodeficiency Syndrome↗

PubMed1995

Long-term outcome of hepatitis B virus-related glomerulonephritis after therapy with interferon alfa.

BACKGROUND & AIMS: Glomerulonephritis is an uncommon complication of chronic hepatitis B virus (HBV) infection in adults. A high percentage of patients seem to have short-term response to interferon therapy with improvement of proteinuria. The aim of this study was to assess the long-term response of patients with HBV-related glomerulonephritis to interferon alfa therapy. METHODS: All patients with chronic hepatitis B and glomerulonephritis who were treated with interferon alfa at the National Institutes of Health between 1985 and 1993 were assessed. RESULTS: Of the 15 patients treated, 8 (53%) had a long-term serological response with sustained loss of serum hepatitis B e antigen and HBV DNA. After 1-7 years of follow-up, all 8 responders have normal serum aminotransferase levels and 5 are hepatitis B surface antigen negative. Seven of the responders also showed a gradual but marked improvement in proteinuria. In contrast, the 7 nonresponders continued to have evidence of active renal disease and 1 required long-term dialysis therapy. All 8 responders had membranous glomerulonephritis, whereas 4 of 7 nonresponders had membranoproliferative glomerulonephritis. CONCLUSIONS: Interferon alfa therapy resulted in long-term remission in liver disease in 8 of 15 patients with chronic hepatitis B and glomerulonephritis. This response was accompanied by significant improvement in markers of renal disease in the majority of patients.

Adult↗

PubMed1995

Therapy of hepatitis C.

In acute hepatitis C, the efficacy of alpha interferon has not been definitively demonstrated. However, several small trials have suggested that interferon may decrease the chronicity rate of acute hepatitis C. In view of the high rate of chronic infection resulting from acute hepatitis C, it is warranted to treat patients during the acute phase of illness if they continue to have HCV RNA detectable in serum for 1 month after the onset of symptoms. The regimen of alpha interferon therapy should be 3 mu three times weekly for 24 weeks. In chronic hepatitis C, therapy with 3-5 mu of alpha interferon three times weekly for 24-48 weeks will induce a temporary remission in disease with loss of HCV RNA from serum, fall of aminotransferases into the normal range, and improvement in liver histology in 50% of patients, and a sustained remission persisting after therapy is stopped in 15% to 20% of patients. Younger patients with a short duration of disease, without cirrhosis, and with lower levels of HCV RNA in serum are the most likely to respond. Unfortunately, there are no completely reliable means of predicting which patients will derive long-term benefits from the use of interferon. Interferon remains the only approved therapy for chronic hepatitis C, although the low rate of sustained remissions and the incidence of side effects mandate a search for ways to improve the efficacy of interferon, as well as to find new, more potent agents for the treatment of this disease.

Acute Disease↗

PubMed1995

Preclinical evaluation of AMPLICOR hepatitis C virus test for detection of hepatitis C virus RNA.

We compared a single-enzyme, combined reverse transcription-PCR (RT-PCR; AMPLICOR HCV Test; Roche Molecular Systems, Branchburg, N.J.) with an independent, two-enzyme, standard RT-PCR (SRT-PCR) assay for the detection of hepatitis C virus (HCV) RNA in serum and plasma. Test samples included a proficiency testing panel consisting of 10 undiluted plasma samples, three separate dilution series, and sera from 99 patients with chronic liver disease. The quantity of HCV RNA in each patient serum sample was determined by a branched DNA (bDNA) signal amplification assay (Quantiplex HCV-RNA assay; Chiron, Emeryville, Calif.). There was complete concordance between the results of the RT-PCR assays with the 10 undiluted plasma samples used for proficiency testing (3 positive and 7 negative samples). However, the analytical sensitivity of SRT-PCR was 4- to 10-fold greater than that of the AMPLICOR test in the dilution series. HCV RNA was detected in 44, 45, and 40 of the patient serum samples, by SRT-PCR, the AMPLICOR test, and the bDNA assay, respectively. There was 97% agreement between the results of the RT-PCR assays, with only three discrepancies. Review of the patients' medical records resolved all three discrepancies in favor of the AMPLICOR results (two false-negative SRT-PCR results and one false-positive SRT-PCR result). The quantity of HCV RNA in sera from five (11%) patients with viremia detected by AMPLICOR was below the bDNA assay cutoff (< 3.5 x 10(5) RNA equivalents per ml). AMPLICOR compared favorably with SRT-PCR, with key advantages of speed, ease of use, increased sample throughput, and protection against false-positive results because of amplicon carryover.

Adult↗

PubMed1994

Increasing hepatitis C virus RNA levels in hemophiliacs: relationship to human immunodeficiency virus infection and liver disease. Multicenter Hemophilia Cohort Study.

We have previously observed an increased frequency of liver failure in human immunodeficiency virus (HIV)-infected hemophiliacs. The purpose of this study was to quantitate hepatitis C virus (HCV) RNA levels in serial samples from HIV-seropositive (HIV+) and HIV-seronegative (HIV-) hemophiliacs before and after HIV seroconversion, and to examine the relationship of HCV RNA levels to CD4 cell counts and to hepatic dysfunction over time. HCV RNA levels were measured on serial samples of serum stored frozen from 17 HCV+/HIV+ and 17 HCV+/HIV- subjects matched within 5 years of their birth dates. All were HCV+ before study entry. HCV RNA levels were quantitated by a branched DNA-enhanced label amplification (bDNA) assay. For samples less than the cut off, HCV RNA was measured by the nested polymerase chain reaction. Individual changes over time, clinical groups, and mean values within predetermined time windows were compared with Wilcoxon rank sum tests. Mean HCV RNA levels increased from 2.76 (standard error [SE] 1.33) x 10(5) to 2.84 (SE 1.39) x 10(6) eq/mL during the first 2 years after HIV seroconversion (P = .006). Baseline HCV RNA levels in the pre-HIV seroconversion group were not significantly different from the baseline levels in those who remained HIV (P = .79). Over the entire period of study, HCV RNA levels increased nearly threefold in those who remained HIV- (mean 9.47 [SE 4.78] x 10(5) to 2.81 [SE 1.13] x 10(6)/mL; P = .02). Among those who became HIV+, HCV RNA levels increased 58-fold (mean 2.85 [SE 1.26] x 10(5) to 1.66 [SE 0.57] x 10(7) eq/mL; P = .0001). The rate of increase in HCV RNA levels was eightfold faster for HIV+ subjects than for subjects who remained HIV- (P = .009). HCV RNA levels increased twofold higher in 5 subjects who developed liver failure compared with the 12 who did not (P = .43). HCV RNA levels correlated significantly with CD4 counts (R = -.33, P = .01) and serum aspartate aminotransferase levels (AST) (R = .36, P = .007). We conclude that HCV RNA levels are significantly higher in HIV+ than in HIV- multitransfused hemophiliacs. HCV load increases over time, is enhanced by HIV, and further increases as immune deficiency progresses. HCV RNA levels are directly associated with high AST levels. These findings suggest that HIV-induced immune deficiency may promote increased HCV replication.

Adolescent↗

PubMed1994

Therapy of chronic hepatitis B with a 6-month course of ribavirin.

Ribavirin is a nucleoside analogue with broad spectrum antiviral activity that has been shown to inhibit viral replication in the woodchuck model of hepatitis B virus infection. We studied the effect of ribavirin on viral replication in 18 patients with chronic hepatitis B who were positive for hepatitis B e antigen. Patients were randomized to receive a 24-week course of oral ribavirin at a dose of either 800, 1000, or 1200 mg/kg per day. All patients completed 24 weeks of treatment and an additional 24 weeks of follow up without significant side effects except for mild, reversible hemolytic anemia. Response to ribavirin was similar among all three dosage groups (p > 0.5); hence the data were pooled and analyzed together. Mean hepatitis B virus DNA levels decreased from 162.7 (95% confidence interval, 106 to 219) pg/ml before treatment to its lowest level of 114.3 (95% confidence interval, 53 to 175) pg/ml at week 20 (p < 0.05). Two patients became negative for HBV DNA and lost hepatitis B e antigen. Mean serum alanine aminotransferase activity decreased markedly from 131.1 (95% confidence interval, 84 to 178) U/l before treatment to 62.4 (95% confidence interval, 48 to 77) U/l at the end of 24 weeks of ribavirin (p < 0.05) and became normal in four patients (22%). Aminotransferase levels returned to baseline within 4 weeks once ribavirin was discontinued, while HBV DNA concentrations remained below baseline even at the end of 24 weeks of follow up.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1993

Clinical and serological differentiation of autoimmune and hepatitis C virus-related chronic hepatitis.

Recent reports have focused on the difficulty in differentiating autoimmune hepatitis from chronic hepatitis C due to the high prevalence of anti-HCV in autoimmune hepatitis. The aim of this study was to identify clinical, biochemical, and serological variables that would help distinguish these two diseases. Pretreatment clinical and biochemical variables were compared from 17 patients with steroid-responsive autoimmune chronic active hepatitis and 62 patients with chronic hepatitis C. Serum samples from these patients were tested for autoantibodies and for anti-HCV by first- and second-generation ELISA, recombinant immunoblot assay, and HCV RNA by polymerase chain reaction. Patients with autoimmune hepatitis were more likely to be symptomatic (94% vs 47%, P < 0.005) and jaundiced (76% vs 0%, P < 0.005) at the time of referral. Anti-HCV was found in 53% of patients with autoimmune hepatitis, but only two were positive by immunoblot assay and only one of these had detectable HCV RNA. Antinuclear antibody (ANA) was detected in 21% of patients with chronic hepatitis C, although usually at a lower titer than in autoimmune hepatitis (geometric mean titer = 1:160 vs 1:500, P < 0.003). Patients with chronic hepatitis C who were ANA positive were older than those who were ANA negative, although there were no other differences in clinical or biochemical features between these groups. In particular, there was no difference in response rate to antiviral therapy. Thus, autoantibodies are frequently found in chronic hepatitis C, especially in older subjects, but appear to be clinically insignificant. Anti-HCV is frequently present in autoimmune hepatitis but is rarely confirmed by tests of higher specificity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

A 39-year-old man with chronic hepatitis, elevated serum ferritin values, and a family history of hemochromatosis.

The patient described is a heterozygote for hemochromatosis, and he has chronic hepatitis C. We have hypothesized that, because of chronic viral hepatitis, he could either have an increase in circulating NTBI or he could have up-regulation of hepatocyte TfR expression, perhaps caused by a viral effect on the IRE of TfR mRNA, or a combination of both. Either could result in an increase of his hepatocellular iron uptake, resulting in a redistribution of his total body iron burden (which is in the range seen for HHC heterozygotes) and, in effect, "concentrating" the iron in his liver, thus simulating homozygous HHC. It is likely that there are interrelationships between hepatic iron concentration, hepatocellular iron metabolism, and chronic viral hepatitis. Understanding of these interrelationships may be important in the understanding of some of the fundamental mechanisms of viral growth and replication and hepatocellular injury. A clearer understanding of these interactions is necessary to diagnose the cause of liver disease accurately in patients such as this one.

Adult↗