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IgM antibodies to hepatitis C virus in chronic active hepatitis C in NW Greece. Solution or more questions?
Correspondence
IglM antibodiesto hepatitis C virus in chronic active hepatitis C in NW Greece. Solution or more questions? To the Editor:
It is well known that approximately 50% of patients with hepatitis C virus (HCV) infection may progress to chronicity, fluctuating from chronic non-specific reactive, persistent or active hepatitis to cirrhosis. Many studies have already shown that about 50% of patients with chronic active hepatitis C have a biochemical and/or histological response to treatment with recombinant interferon alpha (1,2). However, relapse has been observed in approximately half of the responders after suspending the therapy (1,2). Camps et al. (3) reported that low y-glutamyltransferase acticity, absence of obesity and absence of cirrhosis can predict the response of chronic hepatitis C to interferon alpha. In addition, it has been reported that IgM antibodies to HCV may be an early predictor (when IgM deletion is observed) of successful treatment of the disease (4,5). So far, Brillanti et al. (4,6), Tassopoulos et al. (5) and Quiroga et al. (7) have found frequencies of IgM antibodies to HCV as high as 82%, 90%, 40.8% and 5 l%, respectively, although the exact antigenic IgM response was different (to the Cic+s and to the structural core antigen of HCV). Furthermore, Brillanti et al. (6) suggested that since polymerase chain reaction (PCR) is not available in many laboratories, the presence of serum IgM antibody to HCV might be used as a marker of active hepatitis C, independently of the duration of HCV infection. Our experience is not similar to these previous reports. In fact, only 2 out of 17 patients (11.7%, 95% CI: 14.6%36.40/o) with well-defined (based on clinical, laboratory and histological evaluation) chronic active C hepatitis (CAH), who received recombinant interferon-a2b (Intron-A, Schering, Kelinworth, New Jersey, 3MU, subcutaneously, thrice weekly for 6 months), had detectable IgM antibody to HCV core antigen (anti-HCcore IgM, Abbott GmbH Diagnostica, Wiesbaden-Delkenheim, Germany) with a serum sample OD/mean OD of negative control more than 3.0. Fourteen of the 17 patients (82.4%, 95% CI: 56.6?&96.2%) responded to therapy, but 9114 (64.3%, 95% CI: 38.3%85.8%) relapsed within 3 to 5 months after the end of therapy. The response (5/17) was not associated with the presence of anti-HCcore IgM before the initiating of therapy (Fisher’s exact test, p=NS). Although one of the two patients who were reactive for the anti-HCcore IgM lost his reactivity during treatment, this was not accompanied by a sustained response, and relapse was observed 3 months after suspending the therapy. Like Quiroga et al. (7), we believe that testing for HCV-RNA sequences by PCR is a better laboratory marker to distinguish viremic from non-viremic patients with CAH than IgM anti-HCV testing. We did not find any statistical significance in the detection of IgM antiHCV testing. Although we have so far investigated only a small number of patients, we could not suggest that when the anti-HCcore IgM antibody is present and subsequently disappears during therapy, patients could have a sustained response. Perhaps, in this subgroup of patients with chronic hepatitis C (small in our region, possibly reflecting the particular differences of our population in general) (8,9) the deletion of anti-HCcore IgM antibody may be of some slight utility as in our study (transient response), but no general conclusions
can be derived. Nevertheless, the question(s) remain(s): what about the others? George N. Dalekos, Eleftheria Zervou’ and Epameinondas V Tsianos Department of Internal Medicine (Hepato-Gastroenteroiogy School of Medicine and ‘Blood Bank of the University loannina, Greece
Division). Hospital of
References 1. Davis GL, Balart LA, Schiff ER, Lindsay K, Bodenheimer HC, Perrilo RP, et al. Treatment of chronic hepatitis C with recombinant interferon alpha: a multicenter randomized controlled trial. N Engl J Med 1989; 321: 1501-6. 2. DiBisceglie AM, Martin P, Kassianides C, Liskez-Melman M, Murray L, Waggener J, et al. Recombinant interferon alpha therapy for chronic hepatitis C. A randomized doubleblind placebo-controlled trial. N Engl J Med 1989; 321: 150610. S, Garcia-Granero M, Riezu-Boj JI, 3. Camps J, Crisostomo Civeira MP, Prieto J. Prediction of the response of chronic hepatitis C to interferon alpha: a statistical analysis of pretreatment variables. Gut 1993; 34: 1714-7. 4. Brillanti S, Masci C, Ricci P, Miglioli M, Barbara L. Significance of IgM antibody to hepatitis C virus in patients with chronic hepatitis C virus. Hepatology 1992; 15: 998-1001. GV, Karv5. Tassopoulos NC, Hatzakis AE, Papatheodoridis ountzis G, Troonen H, Lennartz L. Early prediction of successful alpha interferon therapy of chronic hepatitis C by core-IgM antibodies to hepatitis C virus. J Hepatol (letter) 1994; 20: 305-6. 6. Brillanti S, Foli M, Perini P, Masci C, Miglioli M, Barbara L. Long-term persistence of IgM antibodies to HCV in chronic hepatitis C. J Hepatol (letter) 1993; 19: 185-7. 7 Quiroga JA, Campillo M, Catillo I, Bartolome J, Porres JC, Carreno V IgM antibody to hepatitis C virus in acute and chronic hepatitis C. Hepatology 1991; 14: 3843. 8. Tsianos EV, Masalas C, Merkouropoulos MH, Dalekos GN, Logan RF Incidence of inflammatory bowel disease in NW Greece. Rarity of Crohn’s disease in an area where ulcerative colitis is common. Gut, 1994; 35: 369-72. 9. Tsianos EV, Dalekos GN, Merkouropoulos MH, Tsatsoulis A, Seferiadis K. Frequency of thyroid dysfunction after recombinant alpha interferon therapy in Greek patients with active chronic hepatitis. Eur J Gastroenterol Hepatol 1994; 6: 547-51.
Hepatitis C virus infection in heterosexual partners of HCV carriers To the Editor:
Transmission of hepatitis C virus (HCV) by sexual practice is controversial (1,2). The prevalence of antibodies against HCV (anti-HCV), by first-generation immunoassays, in regular heterosexual partners of anti-HCV patients is &6.7% (2,3), but few data are available using
newer immunoassays and little is known about the incidence of HCV infection in this group. We have investigated the prevalence and incidence of HCV infection among 148 sexual partners of HCV carriers; they had monogamous heterosexual intercourse with an HCV carrier in the preceding 12
509
IglM antibodiesto hepatitis C virus in chronic active hepatitis C in NW Greece. Solution or more questions? To the Editor:
It is well known that approximately 50% of patients with hepatitis C virus (HCV) infection may progress to chronicity, fluctuating from chronic non-specific reactive, persistent or active hepatitis to cirrhosis. Many studies have already shown that about 50% of patients with chronic active hepatitis C have a biochemical and/or histological response to treatment with recombinant interferon alpha (1,2). However, relapse has been observed in approximately half of the responders after suspending the therapy (1,2). Camps et al. (3) reported that low y-glutamyltransferase acticity, absence of obesity and absence of cirrhosis can predict the response of chronic hepatitis C to interferon alpha. In addition, it has been reported that IgM antibodies to HCV may be an early predictor (when IgM deletion is observed) of successful treatment of the disease (4,5). So far, Brillanti et al. (4,6), Tassopoulos et al. (5) and Quiroga et al. (7) have found frequencies of IgM antibodies to HCV as high as 82%, 90%, 40.8% and 5 l%, respectively, although the exact antigenic IgM response was different (to the Cic+s and to the structural core antigen of HCV). Furthermore, Brillanti et al. (6) suggested that since polymerase chain reaction (PCR) is not available in many laboratories, the presence of serum IgM antibody to HCV might be used as a marker of active hepatitis C, independently of the duration of HCV infection. Our experience is not similar to these previous reports. In fact, only 2 out of 17 patients (11.7%, 95% CI: 14.6%36.40/o) with well-defined (based on clinical, laboratory and histological evaluation) chronic active C hepatitis (CAH), who received recombinant interferon-a2b (Intron-A, Schering, Kelinworth, New Jersey, 3MU, subcutaneously, thrice weekly for 6 months), had detectable IgM antibody to HCV core antigen (anti-HCcore IgM, Abbott GmbH Diagnostica, Wiesbaden-Delkenheim, Germany) with a serum sample OD/mean OD of negative control more than 3.0. Fourteen of the 17 patients (82.4%, 95% CI: 56.6?&96.2%) responded to therapy, but 9114 (64.3%, 95% CI: 38.3%85.8%) relapsed within 3 to 5 months after the end of therapy. The response (5/17) was not associated with the presence of anti-HCcore IgM before the initiating of therapy (Fisher’s exact test, p=NS). Although one of the two patients who were reactive for the anti-HCcore IgM lost his reactivity during treatment, this was not accompanied by a sustained response, and relapse was observed 3 months after suspending the therapy. Like Quiroga et al. (7), we believe that testing for HCV-RNA sequences by PCR is a better laboratory marker to distinguish viremic from non-viremic patients with CAH than IgM anti-HCV testing. We did not find any statistical significance in the detection of IgM antiHCV testing. Although we have so far investigated only a small number of patients, we could not suggest that when the anti-HCcore IgM antibody is present and subsequently disappears during therapy, patients could have a sustained response. Perhaps, in this subgroup of patients with chronic hepatitis C (small in our region, possibly reflecting the particular differences of our population in general) (8,9) the deletion of anti-HCcore IgM antibody may be of some slight utility as in our study (transient response), but no general conclusions
can be derived. Nevertheless, the question(s) remain(s): what about the others? George N. Dalekos, Eleftheria Zervou’ and Epameinondas V Tsianos Department of Internal Medicine (Hepato-Gastroenteroiogy School of Medicine and ‘Blood Bank of the University loannina, Greece
Division). Hospital of
References 1. Davis GL, Balart LA, Schiff ER, Lindsay K, Bodenheimer HC, Perrilo RP, et al. Treatment of chronic hepatitis C with recombinant interferon alpha: a multicenter randomized controlled trial. N Engl J Med 1989; 321: 1501-6. 2. DiBisceglie AM, Martin P, Kassianides C, Liskez-Melman M, Murray L, Waggener J, et al. Recombinant interferon alpha therapy for chronic hepatitis C. A randomized doubleblind placebo-controlled trial. N Engl J Med 1989; 321: 150610. S, Garcia-Granero M, Riezu-Boj JI, 3. Camps J, Crisostomo Civeira MP, Prieto J. Prediction of the response of chronic hepatitis C to interferon alpha: a statistical analysis of pretreatment variables. Gut 1993; 34: 1714-7. 4. Brillanti S, Masci C, Ricci P, Miglioli M, Barbara L. Significance of IgM antibody to hepatitis C virus in patients with chronic hepatitis C virus. Hepatology 1992; 15: 998-1001. GV, Karv5. Tassopoulos NC, Hatzakis AE, Papatheodoridis ountzis G, Troonen H, Lennartz L. Early prediction of successful alpha interferon therapy of chronic hepatitis C by core-IgM antibodies to hepatitis C virus. J Hepatol (letter) 1994; 20: 305-6. 6. Brillanti S, Foli M, Perini P, Masci C, Miglioli M, Barbara L. Long-term persistence of IgM antibodies to HCV in chronic hepatitis C. J Hepatol (letter) 1993; 19: 185-7. 7 Quiroga JA, Campillo M, Catillo I, Bartolome J, Porres JC, Carreno V IgM antibody to hepatitis C virus in acute and chronic hepatitis C. Hepatology 1991; 14: 3843. 8. Tsianos EV, Masalas C, Merkouropoulos MH, Dalekos GN, Logan RF Incidence of inflammatory bowel disease in NW Greece. Rarity of Crohn’s disease in an area where ulcerative colitis is common. Gut, 1994; 35: 369-72. 9. Tsianos EV, Dalekos GN, Merkouropoulos MH, Tsatsoulis A, Seferiadis K. Frequency of thyroid dysfunction after recombinant alpha interferon therapy in Greek patients with active chronic hepatitis. Eur J Gastroenterol Hepatol 1994; 6: 547-51.
Hepatitis C virus infection in heterosexual partners of HCV carriers To the Editor:
Transmission of hepatitis C virus (HCV) by sexual practice is controversial (1,2). The prevalence of antibodies against HCV (anti-HCV), by first-generation immunoassays, in regular heterosexual partners of anti-HCV patients is &6.7% (2,3), but few data are available using
newer immunoassays and little is known about the incidence of HCV infection in this group. We have investigated the prevalence and incidence of HCV infection among 148 sexual partners of HCV carriers; they had monogamous heterosexual intercourse with an HCV carrier in the preceding 12
509