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R Moreno-Otero

Publications and source records attributed to R Moreno-Otero.

At least 19 recordsLinked to original sources
PubMed1998

Inducible nitric oxide synthase expression in chronic viral hepatitis. Evidence for a virus-induced gene upregulation.

Increased nitric oxide (NO) production may contribute to the pathological changes featuring in some inflammatory diseases, but the role of NO in chronic viral hepatitis is still unknown. We compared the inducible NO synthase (NOS2) expression in the liver of patients with chronic viral hepatitis with that of both nonviral liver disease and histologically normal liver. NOS2 expression was assessed by immunohistochemical and in situ hybridization studies of liver biopsy sections. An intense hepatocellular NOS2 reactivity was detected in chronic viral hepatitis, whereas it was weakly or not observed in nonviral liver disease or normal liver, respectively. In addition, we determined whether the hepatitis B virus (HBV) might regulate the synthesis of this enzyme. NOS2 mRNA and protein levels as well as enzyme activity were assessed in cytokine-stimulated HBV-transfected and untransfected hepatoma cells. Transfection with either HBV genome or HBV X gene resulted in induction of NOS2 mRNA expression, and the maximal induction of this transcript and NO production was observed in cytokine-stimulated HBV-transfected cells. These results indicate that hepatotropic viral infections are able to upregulate the NOS2 gene expression in human hepatocytes, suggesting that NO may mediate important pathogenic events in the course of chronic viral hepatitis.

Cells, Cultured↗
PubMed1997

Immunohistochemical evidence of immunopathogenetic mechanisms in chronic hepatitis C recurrence after liver transplantation.

Viremia and genotype are implicated in a rapid course of posttransplant hepatitis C virus (HCV) infection recurrence, but the role played by host immune reactions has not yet been evaluated. We correlated the degree of liver injury with the intrahepatic expression of molecules involved in immune response. The study included 32 biopsies of 30 liver transplant recipients. Recurrence of viremia was detected by Amplicor assay. Genotype was tested by Inno-Lipa. Cryostat sections were assessed by immunohistochemistry, using a wide panel of monoclonal antibodies. Correlations between histological-immunohistochemical semiquantitative evaluation and levels of viremia were performed. In severe hepatic inflammation, high numbers of activated cytotoxic T cells were found, along with marked hepatocellular expression of beta 2-microglobulin (beta 2-MG) and intercellular adhesion molecules. Likewise, a strong vascular adhesion molecule expression was observed mainly in those areas that were more inflamed. A striking endoglin reactivity was detected in enlarged portal tracts, and the presence of neoformed microvessels was also noteworthy. By contrast, in mild hepatic inflammation only a few activated T cells were detected, together with a weaker reactivity for all molecules studied. The level of viremia did not correlate with the degree of liver damage. The severe forms of post-transplant HCV infection recurrence are associated with a marked and aberrant intrahepatic expression of molecules involved in antigen recognition, and intercellular and vascular adhesion, decisive in regulating the recruitment and activation of cytotoxic T lymphocytes.

Adult↗
PubMed1997

Hepatitis C virus infection detected by viral RNA analysis in porphyria cutanea tarda.

The high prevalence (62%) of anti-HCV in patients with porphyria cutanea tarda (PCT) found in a recent study prompted us to speculate that hepatitis C virus (HCV) infection could contribute to liver damage in this disease. The relationship between a positive serologic test and infectivity remains elusive, as anti-HCV false-positive reactivity has been described in some patients with chronic liver disease. Hence, it needs to be established if HCV infection plays a role in the pathogenesis of liver injury, or anti-HCV positivity may be an epiphenomenon in PCT patients. The aim of this study was to evaluate the existence of true HCV infection by verifying the presence of serum viral RNA in patients with PCT. HCV RNA was studied in sera from 36 patients with clinical and biochemical features of PCT using a polymerase chain reaction technique. Additionally, 26 patients with chronic alcoholic liver disease and 29 patients with different dermatological lesions but with no liver disease were studied as control groups. HCV RNA was positive in 29 of 36 patients (80.5%) with anti-HCV positive PCT. For alcoholic liver disease and dermatological disease controls the values for HCV RNA were 11.5% and 3.4%, respectively. HCV infection was found to be significantly higher in patients with PCT than in controls (P < 0.001), demonstrating that most subjects with clinically expressed PCT have true HCV infection. These data support the hypothesis that liver damage in some patients with PCT may be attributed to prolonged HCV infection, suggesting that treatment for chronic hepatitis C could be indicated.

Female↗
PubMed1996

Thyroid autoimmune disorders in patients with chronic hepatitis C before and during interferon-alpha therapy.

BACKGROUND AND AIMS: Hepatitis C virus is involved in the induction of autoimmunity and interferon can also induce hepatic and non-hepatic autoimmune reactions. This study assessed the prevalence of thyroid autoantibodies and autoimmune thyroid disorders in patients with chronic hepatitis C before and during interferon therapy. PATIENTS AND METHODS: We studied prospectively 207 patients positive for anti-HCV and viral RNA. One hundred and forty-four of them received a therapeutic trial of one year with interferon-alpha. Free thyroxine, TSH and autoantibodies to thyroglobulin and thyroid microsomes were systematically tested at entry and at weeks 12 and 24 in both untreated and treated patients. RESULTS: Sixteen of the 207 patients (7.7%) had thyroid dysfunction, including positive antithyroid antibodies in 14 (6.7%) and hypothyroidism in 10 (4.8%) prior to interferon therapy. In addition, during pretreatment evaluation one patient developed clinical hyperthyroidism after transient subclinical hypothyroidism and another had subclinical hyperthyroidism. Prevalences of positive antithyroid antibodies and hypothyroidism were significantly higher in women (14.7 and 10.5%, respectively, vs 0% in men, P < 0.01) and were directly associated with increasing age (P < 0.01). The incidence of thyroid dysfunction was also significantly higher in patients with other autoantibodies such as anti-nuclear (ANA) (P < 0.01). A trial with interferon was initiated in 144 patients and 8 of 142 (5.6%) without previous thyroid abnormalities developed thyroid dysfunction, including positive antithyroid antibodies in 7 (4.9%) and hypothyroidism in 4 (2.8%) with a prevalence again significantly higher in women (12.7 and 8.3%, respectively, vs 1% in men, P < 0.01) and also directly related to increasing age (P < 0.01). An association was found between the development of thyroid dysfunction during interferon therapy and the presence of other autoantibodies, including ANA, anti-DNA and anti-Sjögren's antibodies (P < 0.01), as well as with the induction of autoimmune hepatitis and Sjögren's syndrome (P < 0.01 and < 0.05 respectively). Thyroid abnormalities were reversed in all patients when interferon therapy was discontinued. CONCLUSIONS: No significant association was found between chronic hepatitis C and the presence of thyroid autoimmunity in female patients. On the contrary, interferon therapy induced antithyroid autoantibodies and thyroid dysfunction de novo in patients with chronic hepatitis C without pre-existing thyroid abnormalities. Thyroid dysfunction secondary to interferon was reversible after discontinuation of therapy.

Adult↗
PubMed1996

Hepatitis C virus infection in Spanish volunteer blood donors: HCV RNA analysis and liver disease.

OBJECTIVE: To evaluate in a large group of volunteer blood donors the prevalence of antibodies to hepatitis C virus (anti-HCV) and the relation of transaminase (ALT) levels and viraemia to liver damage. DESIGN: A prospective study. SETTING: Transfusion Centre of the Autonomous Community of Madrid and the Liver Unit of the Princesa University Hospital. PATIENTS: From a population of 55,587 volunteer blood donors, 160 seropositive cases were further evaluated for virological and histological assessment. METHODS: Anti-HCV was tested by ELISA-2 and RIBA-2 assays. HCV RNA was analysed by nested PCR. Liver biopsies were obtained in 35 volunteer blood donors with abnormal ALT levels. RESULTS: The prevalence of anti-HCV detected by ELISA-2 was 0.93%. Serum ALT was abnormal in 61 of the 160 volunteers (38.1%). Of these, RIBA-2 was positive in 96.7% and HCV RNA was detectable in 96.1%. Serum ALT was normal in the remaining 99, 70.7% being RIBA-2 negative and 98.3% HCV RNA negative. The majority of biopsies (85.6%) showed chronic hepatitis. CONCLUSION: This study demonstrates that in blood donors screening for anti-HCV, a positive ELISA-2 test, when associated with abnormal ALT levels, is effective in recognizing subjects with active infection detected by HCV RNA and liver disease. Concerning ELISA-2 positive volunteer blood donors with normal ALT, long-term studies are warranted to elucidate whether they are really infected by HCV.

Adolescent↗
PubMed1996

Tonsillectomy and inflammatory bowel disease location.

OBJECTIVE: Epidemiological studies have found an increased frequency of childhood infections and tonsillectomies in patients with inflammatory bowel disease (IBD). The aim of our study was to test whether particular clinical patterns of IBD could be associated with previous tonsillectomy. METHODS: Two hundred and twenty consecutive IBD patients (100 with Crohn's disease (CD) and 120 with ulcerative colitis (UC)) were prospectively assessed and classified into groups according to disease location. In those with a positive history of tonsillectomy, an ear, nose and throat (ENT) examination was carried out to confirm the diagnosis. RESULTS: Eighty-two IBD patients (37%) underwent tonsillectomy in childhood: 47 out of 100 CD patients (47%), and 35 out of 120 UC patients (29%). Disease location in CD patients affected the ileum in 28, and 21 of them were tonsillectomized (tonsillectomy rate of 75%). Thirty-six patients had an ileocolonic location, and 14 of them had had a tonsillectomy (39%). With disease confined to the colon, only 9 out of 29 patients (31%) had undergone previous tonsillectomy. The higher prevalence of tonsillectomy in patients with CD ileitis was statistically significant (P = 0.0034). No significant differences between groups of UC patients according to the extent of the disease were found. CONCLUSION: The ileum is the most prevalent location of disease in CD patients with previous tonsillectomy.

Adult↗
PubMed1995

Vascular adhesion molecule expression in viral chronic hepatitis: evidence of neoangiogenesis in portal tracts.

BACKGROUND/AIMS: T cell-mediated immune reactions could be crucial for hepatocellular damage in viral chronic hepatitis. The aims of this study were to compare the expression of activation and cell adhesion molecules on peripheral blood and intrahepatic lymphocytes from chronic hepatitis C and to analyze the intrahepatic expression of vascular adhesion molecules in viral chronic hepatitis. METHODS: Lymphocytes from patients with chronic hepatitis C were studied by flow cytometry. Intrahepatic expression of vascular adhesion molecules was assessed by immunohistochemistry. RESULTS: Liver-derived T cells showed a high expression of activation and cell adhesion molecules. Interestingly, we observed that vascular cell adhesion molecule 1 was up-regulated on both sinusoidal endothelial and portal dendritic cells. A novel finding was the neoformation of microvessels in inflamed portal tracts. An enhanced expression of endoglin was located on sinusoidal endothelial cells and on portal tracts. CONCLUSIONS: Activated cytotoxic T cells, which showed an up-regulated expression of cell adhesion molecules, composed the majority of intrahepatic lymphocytes in chronic hepatitis C. The expression of vascular cell adhesion molecule 1 on portal dendritic cells and the microvessels neoformation in portal tracts from viral chronic hepatitis could define the main pathway for the recruitment and priming of liver-infiltrating T cells.

Blood Cells↗
PubMed1994

Induction of tumor necrosis factor alpha production by human hepatocytes in chronic viral hepatitis.

Tumor necrosis factor alpha (TNF-alpha) is a multifunctional cytokine that has an important role in the pathogenesis of inflammation, cachexia, and septic shock. Although TNF-alpha is mainly produced by macrophages, there is evidence regarding TNF-alpha production by cells that are not derived from bone marrow. TNF-alpha production by normal and inflamed human liver was assessed at both mRNA and protein levels. Using a wide panel of novel anti-TNF-alpha monoclonal antibodies and a specific polyclonal antiserum, TNF-alpha immunoreactivity was found in hepatocytes from patients chronically infected with either hepatitis B virus (HBV) or hepatitis C virus. Minimal TNF-alpha immunoreactivity was detected in the mononuclear cell infiltrate and Kupffer cells. In situ hybridization experiments using a TNF-alpha RNA probe showed a significant expression of TNF-alpha mRNA in hepatocytes, Kupffer cells, and some infiltrating mononuclear cells. By contrast, TNF-alpha was detected at low levels in liver biopsies from normal individuals or patients with alcoholic liver disease and low expression of TNF-alpha mRNA was observed in these specimens. Transfection of HepG2 hepatoblastoma cells with either HBV genome or HBV X gene resulted in induction of TNF-alpha expression. Our results demonstrate that viral infection induces, both in vivo and in vitro, TNF-alpha production in hepatocytes, and indicate that the HBV X protein may regulate the expression of this cytokine. These findings suggest that TNF-alpha may have an important role in human liver diseases induced by viruses.

Antibodies, Monoclonal↗
PubMed1994

Defective proliferation and regulatory function of CD4+ T cells bearing Leu-8 homing receptor in primary biliary cirrhosis. Phorbol myristate acetate enhances T-cell function.

The majority of circulating CD4+ T cells express the Leu-8 peripheral lymph node homing receptor, and these cells have previously been shown to have suppressor-inducer and suppressor function. In the present study, it was found that CD4+, Leu-8+ T cells from patients with primary biliary cirrhosis (PBC) have a significantly (P < 0.01) lower proliferative response when stimulated with phytohemagglutinin (PHA), concanavalin A (Con A), or pokeweed mitogen (PWM) compared to normal controls. The proliferative response of CD4+, Leu-8- T cells was similar in patients and controls. However, the proliferative responses of CD4+, Leu-8+ from patients with PBC was normal when cells were stimulated with PHA, Con A, anti-CD3 monoclonal antibody, or ionomycin in combination with phorbol myristate acetate (PMA). CD4+ T cells from patients with PBC mediated normal helper function for PWM-stimulated immunoglobulin synthesis at high T/B ratios and their regulatory function was similar to that of normal CD4+ T cells that had been irradiated to inactivate their suppressor activity. When CD4+ T cells from patients with PBC were precultured with the combination of Con A and PMA, they mediated potent inhibitory activity similar to that of normal CD4+ T cells. Thus, CD4+, Leu-8+ T cells from patients with PBC have a defect of proliferation and suppressor function that is reversed by coculture with PMA. This finding suggests that impairment of a PMA-inducible lymphocyte activation pathway contributes to abnormal lymphocyte function in PBC.

Adult↗
PubMed1994

Reduced numbers of CD8+ T cells and B cell-expression of Leu-8 antigen in peripheral blood of patients with primary biliary cirrhosis.

The presence of Leu-8 antigen, the human homologue of the murine MEL-14 peripheral lymph node homing receptor, defines subsets of peripheral blood mononuclear cells (PBMC) with different functions. Since it has been suggested that abnormal function of Leu-8 subsets may contribute to the immunopathogenesis of primary biliary cirrhosis (PBC), this study was undertaken to define whether abnormal expression of the Leu-8 antigen occurs in this disease. We studied 25 PBC patients, 12 with other chronic liver diseases, and 21 normal controls. PBMC were tested by direct immunofluorescence using monoclonal antibodies and flow cytometry. In PBC the proportion of PBMC that were CD4+ was normal; in contrast, the proportion that were CD8+ was decreased (p < 0.01). A negative correlation was found between absolute numbers of CD8+ T cells and total serum bilirubin levels (r = -0.50, p < 0.05). The distribution of Leu-8 antigen on T cells was normal; however, the proportion of PBMC that were B cells was increased (p < 0.01) and the fraction of these that were Leu-8 negative was also increased (p < 0.01). The expression of antigens of activation on B cells was similar to that for normal controls. These findings suggest that in peripheral blood of PBC patients reduced numbers of T cells may occur due to a selective intrahepatic sequestration of CD8+ T cells, and that the decreased expression of Leu-8 antigen by B cells may be associated with their participation in autoimmune processes.

Adult↗
PubMed1993

Hepatitis C virus antibodies and liver disease in patients with porphyria cutanea tarda.

The recent identification of the hepatitis C virus and development of assays to detect antibodies to hepatitis C virus has allowed assessment of the prevalence of hepatitis C virus infection in patients with a variety of liver and other diseases. The aim of this study was to investigate the prevalence of hepatitis C virus antibodies and severity of liver injury in patients with porphyria cutanea tarda. Sixty-two patients were studied. Serum samples were analyzed for liver function parameters and markers of hepatitis B virus infection. Frozen serum samples from 34 patients with porphyria cutanea tarda, obtained when patients were seen at the hospital for the first time, were analyzed for hepatitis C virus antibodies with enzyme-linked immunosorbent assays (first- and second-generation) and a recombinant immunoblot assay. As controls, serum samples from 19,788 blood donors, 40 patients with alcoholic liver disease and 138 hospitalized patients without liver disease were also tested for hepatitis C virus antibodies. Liver biopsy was performed in 42 porphyria cutanea tarda patients. Specimens were evaluated for steatosis, siderosis, fibrosis, severity of inflammation and the presence of cirrhosis. In addition, the degree of necroinflammatory change and fibrosis were quantitated with the histologic activity index described by Knodell et al. The prevalence of hepatitis C virus antibodies in patients with porphyria cutanea tarda (62%) was higher than that in blood donors (0.79%), patients with alcoholic liver disease (17.5%) or hospitalized patients without liver disease (5.8%).(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1993

Down-regulation of intercellular adhesion molecule 1 on hepatocytes in viral chronic hepatitis treated with interferon alfa-2b.

BACKGROUND: Intercellular adhesion molecule 1 and lymphocyte function-associated antigen 3 are expressed markedly on hepatocytes in viral chronic hepatitis. The aim of this study was to determine whether treatment induces changes in the intrahepatic expression of adhesion molecules. METHODS: The expression patterns of these molecules were studied in liver tissue from 12 patients with chronic hepatitis B and from 14 patients with chronic hepatitis C before and after treatment with interferon alfa-2b. Immunoperoxidase staining was performed in frozen liver biopsy sections. RESULTS: Partial or complete responses to therapy were achieved in 7 (58%) of 12 patients with chronic hepatitis B and in 10 (71%) of 14 patients with chronic hepatitis C. In the first biopsy specimen, hepatocytes showed a marked expression of intercellular adhesion molecule 1. In the second biopsy specimen obtained from responders, hepatocytes showed no reactivity in 4 patients with chronic hepatitis B and in 5 with chronic hepatitis C. However, its expression did not significantly change among nonresponders. A similar pattern of reactivity for lymphocyte function-associated antigen 3 was observed. CONCLUSIONS: Beneficial effect of interferon alfa-2b appears to be associated with a down-regulation of adhesion molecules on hepatocytes, suggesting that this novel immunomodulatory action of interferon could be important to induce a therapeutic response in viral chronic hepatitis.

Adolescent↗
PubMed1993

Variability in the expression of a beta 2-microglobulin epitope on hepatocytes in chronic type C hepatitis on treatment with interferon.

Cytotoxic CD8+ T lymphocytes recognize viral antigens in the context of human leukocyte antigen class I molecule coexpression by target cells. Analysis of beta 2-microglobulin reactivity is useful in evaluating changes in human leukocyte antigen class I antigen distribution. In this study we analyzed liver biopsy specimens obtained from 15 patients with chronic active hepatitis type C who underwent a clinical trial with recombinant interferon-alpha 2b. We comparatively studied by immunohistochemical analysis the expression of human leukocyte antigen class I antigens in frozen liver samples obtained before entry in the protocol and in specimens taken 8 mo after initiation of treatment. Six normal liver samples were used as controls. For immunohistochemical analysis, a panel of several human leukocyte antigen class I monoclonal antibodies, specific for beta 2-microglobulin or different heavy-chain determinants, was used. In addition, we included a novel monoclonal antibody (HP-1H8), characterized in this report, which is specific for a distinct beta 2-microglobulin epitope. On entry, mean serum ALT was 240 +/- 89 IU/L and mean Knodell's index was 9.9 +/- 2.4, whereas at the time of the second biopsy mean values had diminished to 45 +/- 22 IU/L and 4.7 +/- 3.0, respectively. Liver sections from controls and patients expressed human leukocyte antigen class I light- and heavy-chain determinants in hepatocytes, biliary duct epithelium, sinusoidal lining cells and lymphocytes. Remarkably, the beta 2-microglobulin epitope recognized by the HP-1H8 monoclonal antibody was undetectable on hepatocytes from normal livers but clearly evident on hepatocytes from patients with chronic active hepatitis C before interferon treatment. Positive staining was more intense in areas of piecemeal and lobular necrosis. Double immunostaining with a CD2 monoclonal antibody demonstrated that labeling with HP-1H8 was predominantly associated with T-cell infiltration. Interestingly, the reactivity of HP-1H8 with hepatocytes was diminished or disappeared in specimens obtained during interferon treatment; the pattern of reactivity then resembled that of samples from normal controls. Our data indirectly suggest that, in addition to the increased expression of human leukocyte antigen class I molecules on hepatocytes in viral infections, conformational changes may take place in these antigens. These changes can be revealed by immunostaining with the HP-1H8 monoclonal antibody. Interferon therapy could down-regulate this expression through its effect in reducing the histological activity resulting from the lysis of virus-infected hepatocytes by cytotoxic T cells.

Adult↗
PubMed1993

A study of the lactic dehydrogenase isoenzyme patterns in the adenoma--carcinoma sequence of the colon.

In order to determine whether the LDH isoenzyme pattern, measuring the percentages of LDH4-5 (M monomer), might be a marker in the adenoma-carcinoma sequence, 103 adenomas, 8 adenomas with proven malignant degeneration and 27 adenocarcinomas of the large intestine, as well as 12 biopsy samples of colonic mucosa from normal controls, were studied histologically and histochemically. The proportion of M polypeptide was significantly increased in adenomas of larger size (diameter > 2 cm), in adenomas with a larger villous component, and in those with severe dysplasia. The largest proportion of M polypeptide was found in villous adenomas and colloid adenocarcinomas, and might reflect a common origin. These results suggest that the histochemical study of the LDH isoenzymogram might be a useful marker for detecting early malignant degeneration in adenomas of the colon.

Adenocarcinoma↗
PubMed1993

[Effectiveness of endoscopic sclerotherapy in the treatment of bleeding esophageal varices].

92 patients to whom urgent endoscopy and sclerotherapy of esophageal varices was performed are studied retrospectively. After the bleeding episode, elective sclerosis sessions were performed to eradicate varices, to prevent hemorrhagic complications and post-sclerotic stenosis somatostatin, H2 antagonists and sucralfate were administered. The Total number of sessions was 331, with a mean of 3.6 per patient (range 1-10). Immediate hemostasis was achieved in 93% of patients, with an early relapse in 10.4% of them. Hemorrhagic relapse two years following therapy was 35.8%. Mortality was 41%; 8% of the decreased patients belonged to Child's A functional grade, 24% belonged to B; and 68% to C. There was a 44% of complications, but only one death was due to the technique. No patient developed symptomatic stenosis neither hemorrhage secondary to esophageal ulceration. We conclude that endoscopic sclerotherapy is one of the principal therapeutic options in the hemorrhage due to esophageal varices, although new studies are necessary to define the role of somatostatin and H2 antagonists in the prophylaxis of complications.

Adult↗
PubMed1992

Functional analysis of peripheral blood lymphocytes isolated from patients with chronic hepatitis type B.

Cell-mediated immunity, evaluated by lymphocyte proliferation and expression of the activation antigen interleukin-2 receptor in response to mitogens such as phytohemagglutinin and concanavalin-A, has been reported to be defective in chronic hepatitis B virus carriers. However, no definite conclusion on the functional state of T cells from these patients can be drawn. In the present study, we have investigated the expression of a wide set of lymphoid activation molecules as well as the proliferative response of peripheral blood lymphocytes isolated from patients with chronic hepatitis type B after in vitro stimulation with monoclonal antibodies to both the T-cell receptor-CD3 complex and the CD2 molecule, which are the two main T-cell activation pathways. Our findings show that peripheral T lymphocytes from patients with chronic hepatitis type B express the activation antigens 4F2 molecule, interleukin-2 receptor, and activation inducer molecule (AIM) antigen, and proliferate normally after specific stimulation through either the T-cell receptor-CD3 complex or the CD2 molecule. These results suggest that the peripheral blood T cells of patients with chronic hepatitis B are fully operative and functionally competent in vitro.

Adult↗
PubMed1992

Intrahepatic up-regulated expression of extracellular matrix protein receptors in chronic active hepatitis type B.

The aim of the present study was to investigate the differences in expression of beta 1 integrins between normal liver and the inflamed livers of patients with chronic active hepatitis B. Immunohistochemical staining with monoclonal antibodies that specifically recognize the common beta 1 chain and five different alpha subunits has been performed in frozen liver biopsy sections from 10 patients with chronic active hepatitis B and from 4 patients with normal livers. The major findings of our study were de novo expression in liver with chronic active hepatitis B of alpha 2 and alpha 3 subunits on both periportal hepatocytes and on lobular hepatocytes in close proximity to lymphocyte infiltrates. These results indicate the existence of an up-regulatory process in the expression of beta 1 integrins, especially the alpha 2 and alpha 3 subunits, in the inflamed liver tissue from patients with chronic active hepatitis B, suggesting that these integrins could play an important role in the development of liver fibrosis and in regulating intrahepatic lymphocyte migration.

Adolescent↗