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Alcohol and chronic HBV, HCV infection on iron status
207
Virul hepatitis: clinical aspects
ALCOHOL AND CHRONIC HBV, HCV INFECTION ON IRON STATUS
A. Fonseca. D. Neto National Institute of Health and Regional Alcoholism Treatment Center, Lisbon, Portugal J. Peneda,
Chronic alcohol consumption and chronic HBV, HCV infections tendency promoting iron overload. What happens at iron status levels with abstinence? In 55 iqtients for alcoholism treatment we studied the iron status (iron serum, transferrin and % saturation, ferritin, AXIS and CDT for abnormal transferrin) at initial treatment (TO) and after 4 weeks of controled abstinence (Tl) with(A) and without(B) virus infection (25 and 30 patients). Results: FGA index (h4athurin,l996 Hepatology) at TO score: < 6 64.2%; ~8 - 97.5%; > 9 - 2.5%. A group (TO-Tl): serum iron 118.8f72.7 - 122.7f60.7; transferrin 287.2i61.7 - 301.2k77.5; %tf32.4&22.3 - 35.1f18.8; ferritin 730.3f1300 - 383.3f 450.4; AXIS 5.8f3.8 - 3.9f1.9; CDT 21.6f10.9 - 16.9f7.7. The differences are not significative(NS). B group (TO-Tl): serom iron 140.4f67.3 - 102f34.8, ~0.01; Tf 314.6ti8.1 - 306.4f58.9, NS; %Tf 35.4f18.3 - 27.M1.4, NS; ferritin 407f449.9 - 193.4i214.7, 60.05; AXIS 6.9k44.3- 3.3f1.3, pcO.01; CDT 30.1f14.5 - 12.6f3.9, p
I COW086 I
The effect of interferon-alpha (IFN) therapy on serum level of procollagen III peptid (PIIIP) was examined in 23 treatment periods of 18 patients suffering from chronic viral hepatitis (type B: 1, type D: 4, type C: 13). The dose of IFN was 9 MU every second day in type B, 10 and 5 MU thrice a week in type D and C hepatitis. The duration of therapy was 6 months in type B, 18 and 12 months in type D and C hepatitis. Complete response (transaminase levels became normal, markers of viral replication were absent at the end of the therapy and during the 6 months of the follow up) occured in 10 (group I.), partial response (transaminase levels decreased more than SO%, markers of viral replication remained positive) was observed in 10 cases (group II.) and non-responder were 3 patients. Serum PIIIP level decreased significantly in the group I. at the end of the therapy (p
(
HGV RNA IN ACUTE NON A-C HEPATITIS P. Grabarczvk. ‘W Krvczka. E. Broier. J. Medvliska. ‘J. Institute of Haematology and Blood Transfusion, Warsaw. ‘Department of Infectious Diseases of Provincial General Klelce, Poland.
CHANGES IN SERUM PROCOLLAGEN III PEPTID LEVELS DURING INTERFERON THERAPY FOR CHRONIC VIRAL HEPATITIS G.Horvath. H.Osztroaodcz Gv.Tolvai. G. Stotz*. K.David Central Hospital of the Ministry of the Interior, 1st Dept. Med., Dept. of Pathology*, Budapest, Hungary
Kublcka Poland. Hospital,
AIM: To estimate the role of HGV in patients with non A-C acute hepatitis. Material and methods: We’ve analysed data of 44 consecutive patients with acute hepatitis (serologically non A-C]. The control group consisted of 71 health blood donors (ED]. Obstructive jaundice, autoimmune hepatitis and alcoholic liver disease were excluded in all pts. Sera of all pts. were tested for HGV RNA HCV RNA and HGV RNA by RT PCR method. Results: was detected in serum of one BD Cl ,4%]. All ED were negative for HCV RNA. HGV was the only infective agent in 7 of 44 (15,9%) patients, and in coexistence with HC virus was present in 6 of 44 (13,6%] patients. In 12/44 (27,2%) pte. there was only HCV RNA present and in remaining 19 143,2%) patients neither HCV nor HGV were detected. No significant differences in the course of acute non A-C hepatitis were found between pts. HGVRNA-positive and HGVRNA-negative. No differences were also found in the course of acute hepatitis C with and without HGVRNA In the serum. Conclusions: In our study HGV was detected in 26,9% (7/26] of patients with acute non A-C hepatitis. On the basis of our observations we can conclude that the course of hepatitis non A-C with HGV present doesn’t have any characteristic clinical signs.
CO6/088
1
PILOT STUDY ON SAFETY AND EFFICACY OF RECOMBINANT ALFA2B INTERFERON (IFN) FOR TREATMENT OF HCV LIVER ran G. Tamam* CIRRHOSIS tL. ‘. M. Greeorutti. F. Zorat. G. Pozzato. Inst. Medicina Clink, University of Tries& *Laboratory of Children Hospital“Burlo Garofolo”, Tries& Italy. To determine the role of IFN treatment in HCV+ hver cirrhosis, we assessed the clinical and biochemical effects of IFN in a group of 30 patients (mean age 59+9) affected by HCV+ compensated cirrhosis without any sign of portal hypertension: esophageal varices were excluded by endoscopy, and ascites and splenomegaly by nltrasonography (portal diameter was under normal limit in each case). The liver biopsy was performed in any case 30 patients affected by HCV+ positive cirrhosis, matched for sex and age (62+7), were used as controls. The patients received 3MU thrice a week of alfa2b IFN for 6 months, while controls did not receive any therapy. In addition to usual liver function tests, liver fibrosis was assessed by serum collagen IV” (CL-IV) determination. In fact, in previous reports (1) we observed a strong correlation between the liver fibrosis (assessed by histology) and CL-IV serum level. Patients were followed for at least 1 year after the suspension of treatment. All patients were HCV-RNA positive. There was no difference behveen controls and and alphatreated patients m prothrombin time, serum albumin, bilirnbin, foetoprotein levels before the therapy as well as at the end of the therapy, and of the follow-up. In treated patients, normalization of ALT occured in 11 cases (36%), but in 6 of them the therapy was interrupted for the presence of serious side effects: nentropenia or tbrombocytopenia or skin lesions.5 cases showed relapse at the end of the treatment, and only 2 patient (6.6%) recovered from HCV with normal ALT and negativity of HCV-RNA, two years after the end of the therapy. Controls and treated patients had comparable CL-IV level before therapy (158+56 vs 167*65 ng/ml respectively) but under IF’N tretment the mean CL-IV level decreased signifmantly in treated patients (87+98), whereas no changes were noticed in controls. Interstingly, even non-responders showed a decrease of CL-IV serum level. After the end of the therapy, CL-IV rose slowly to pm-treatment values This study mdicates that antiviral therapy could be efficacy even in HCV+ liver cirrhosis, though in a very small fraction of patients. lndipendently from inhibition of viral replication, IFN therapy seems to reduce liver fibrosis, therefore, this drug could be able to induce a trend toward a delayed development of portal hypertension. Given the short followup, this study is not able to determine whether IFN may improve the survival of treated patients Further studies with long-term follow-up and longer treatment course are warranted. 1) Mazzoran et al. Eur. J. Gastroenterol Hepatol. 12 (2) 1997
Virul hepatitis: clinical aspects
ALCOHOL AND CHRONIC HBV, HCV INFECTION ON IRON STATUS
A. Fonseca. D. Neto National Institute of Health and Regional Alcoholism Treatment Center, Lisbon, Portugal J. Peneda,
Chronic alcohol consumption and chronic HBV, HCV infections tendency promoting iron overload. What happens at iron status levels with abstinence? In 55 iqtients for alcoholism treatment we studied the iron status (iron serum, transferrin and % saturation, ferritin, AXIS and CDT for abnormal transferrin) at initial treatment (TO) and after 4 weeks of controled abstinence (Tl) with(A) and without(B) virus infection (25 and 30 patients). Results: FGA index (h4athurin,l996 Hepatology) at TO score: < 6 64.2%; ~8 - 97.5%; > 9 - 2.5%. A group (TO-Tl): serum iron 118.8f72.7 - 122.7f60.7; transferrin 287.2i61.7 - 301.2k77.5; %tf32.4&22.3 - 35.1f18.8; ferritin 730.3f1300 - 383.3f 450.4; AXIS 5.8f3.8 - 3.9f1.9; CDT 21.6f10.9 - 16.9f7.7. The differences are not significative(NS). B group (TO-Tl): serom iron 140.4f67.3 - 102f34.8, ~0.01; Tf 314.6ti8.1 - 306.4f58.9, NS; %Tf 35.4f18.3 - 27.M1.4, NS; ferritin 407f449.9 - 193.4i214.7, 60.05; AXIS 6.9k44.3- 3.3f1.3, pcO.01; CDT 30.1f14.5 - 12.6f3.9, p
I COW086 I
The effect of interferon-alpha (IFN) therapy on serum level of procollagen III peptid (PIIIP) was examined in 23 treatment periods of 18 patients suffering from chronic viral hepatitis (type B: 1, type D: 4, type C: 13). The dose of IFN was 9 MU every second day in type B, 10 and 5 MU thrice a week in type D and C hepatitis. The duration of therapy was 6 months in type B, 18 and 12 months in type D and C hepatitis. Complete response (transaminase levels became normal, markers of viral replication were absent at the end of the therapy and during the 6 months of the follow up) occured in 10 (group I.), partial response (transaminase levels decreased more than SO%, markers of viral replication remained positive) was observed in 10 cases (group II.) and non-responder were 3 patients. Serum PIIIP level decreased significantly in the group I. at the end of the therapy (p
(
HGV RNA IN ACUTE NON A-C HEPATITIS P. Grabarczvk. ‘W Krvczka. E. Broier. J. Medvliska. ‘J. Institute of Haematology and Blood Transfusion, Warsaw. ‘Department of Infectious Diseases of Provincial General Klelce, Poland.
CHANGES IN SERUM PROCOLLAGEN III PEPTID LEVELS DURING INTERFERON THERAPY FOR CHRONIC VIRAL HEPATITIS G.Horvath. H.Osztroaodcz Gv.Tolvai. G. Stotz*. K.David Central Hospital of the Ministry of the Interior, 1st Dept. Med., Dept. of Pathology*, Budapest, Hungary
Kublcka Poland. Hospital,
AIM: To estimate the role of HGV in patients with non A-C acute hepatitis. Material and methods: We’ve analysed data of 44 consecutive patients with acute hepatitis (serologically non A-C]. The control group consisted of 71 health blood donors (ED]. Obstructive jaundice, autoimmune hepatitis and alcoholic liver disease were excluded in all pts. Sera of all pts. were tested for HGV RNA HCV RNA and HGV RNA by RT PCR method. Results: was detected in serum of one BD Cl ,4%]. All ED were negative for HCV RNA. HGV was the only infective agent in 7 of 44 (15,9%) patients, and in coexistence with HC virus was present in 6 of 44 (13,6%] patients. In 12/44 (27,2%) pte. there was only HCV RNA present and in remaining 19 143,2%) patients neither HCV nor HGV were detected. No significant differences in the course of acute non A-C hepatitis were found between pts. HGVRNA-positive and HGVRNA-negative. No differences were also found in the course of acute hepatitis C with and without HGVRNA In the serum. Conclusions: In our study HGV was detected in 26,9% (7/26] of patients with acute non A-C hepatitis. On the basis of our observations we can conclude that the course of hepatitis non A-C with HGV present doesn’t have any characteristic clinical signs.
CO6/088
1
PILOT STUDY ON SAFETY AND EFFICACY OF RECOMBINANT ALFA2B INTERFERON (IFN) FOR TREATMENT OF HCV LIVER ran G. Tamam* CIRRHOSIS tL. ‘. M. Greeorutti. F. Zorat. G. Pozzato. Inst. Medicina Clink, University of Tries& *Laboratory of Children Hospital“Burlo Garofolo”, Tries& Italy. To determine the role of IFN treatment in HCV+ hver cirrhosis, we assessed the clinical and biochemical effects of IFN in a group of 30 patients (mean age 59+9) affected by HCV+ compensated cirrhosis without any sign of portal hypertension: esophageal varices were excluded by endoscopy, and ascites and splenomegaly by nltrasonography (portal diameter was under normal limit in each case). The liver biopsy was performed in any case 30 patients affected by HCV+ positive cirrhosis, matched for sex and age (62+7), were used as controls. The patients received 3MU thrice a week of alfa2b IFN for 6 months, while controls did not receive any therapy. In addition to usual liver function tests, liver fibrosis was assessed by serum collagen IV” (CL-IV) determination. In fact, in previous reports (1) we observed a strong correlation between the liver fibrosis (assessed by histology) and CL-IV serum level. Patients were followed for at least 1 year after the suspension of treatment. All patients were HCV-RNA positive. There was no difference behveen controls and and alphatreated patients m prothrombin time, serum albumin, bilirnbin, foetoprotein levels before the therapy as well as at the end of the therapy, and of the follow-up. In treated patients, normalization of ALT occured in 11 cases (36%), but in 6 of them the therapy was interrupted for the presence of serious side effects: nentropenia or tbrombocytopenia or skin lesions.5 cases showed relapse at the end of the treatment, and only 2 patient (6.6%) recovered from HCV with normal ALT and negativity of HCV-RNA, two years after the end of the therapy. Controls and treated patients had comparable CL-IV level before therapy (158+56 vs 167*65 ng/ml respectively) but under IF’N tretment the mean CL-IV level decreased signifmantly in treated patients (87+98), whereas no changes were noticed in controls. Interstingly, even non-responders showed a decrease of CL-IV serum level. After the end of the therapy, CL-IV rose slowly to pm-treatment values This study mdicates that antiviral therapy could be efficacy even in HCV+ liver cirrhosis, though in a very small fraction of patients. lndipendently from inhibition of viral replication, IFN therapy seems to reduce liver fibrosis, therefore, this drug could be able to induce a trend toward a delayed development of portal hypertension. Given the short followup, this study is not able to determine whether IFN may improve the survival of treated patients Further studies with long-term follow-up and longer treatment course are warranted. 1) Mazzoran et al. Eur. J. Gastroenterol Hepatol. 12 (2) 1997