Incidence of Post-Transfusion Hepatitis before and after Screening for Hepatitis C Virus Antibody

To evaluate the effectiveness of screening test for antibody to hepatitis C virus (anti-HCV), the incidence of acute post-transfusion HCV infection in patients who underwent cardiovascular surgery and received blood transfusion was studied. All patients were followed prospectively with serum biochemistry tests and viral hepatitis markers before and periodically for at least 6 months after cardiovascular surgery. None of them had history of liver disease and none tested positive for anti-HCV prior to blood transfusion. Before blood donors were screened for anti-HCV with a second-generation HCV diagnostic kit, 28 (12.4%) of 226 patients or 0.49% of 5,690 unit transfusion had seroconverted to anti-HCV during a 6-month follow-up. The incidence of post-transfusion hepatitis (PTH) C in 91 patients who had received 1–12 units transfusion was significantly lower than in 135 patients who had received more than 12 units transfusion (6.6 vs. 16.3%, p<0.05). However, none of the 87 transfused patients, since anti-HCV screening in July 1992, developed PTH C (p<0.05). The result demonstrates that screening for anti-HCV by a more sensitive second-generation HCV diagnostic assay may protect the patients studied from PTH C. It further provides a firm argument for the necessity of a nation-wide blood donor screening.     

Prospective controlled study of post-transfusion hepatitis after cardiac surgery in a large referral hospital in India.

We studied the risk of post-transfusion hepatitis (PTH) in recipients of blood collected from voluntary donors screened for HBsAg. Two hundred and fifty patients without any previous history of liver disease or transfusion were followed up for 12 months subsequent to cardiac surgery. Thirty-five of them had closed-heart surgery without receiving transfusion and served as controls. The remaining 215 patients received single-point transfusions (mean 4 +/- 2.4 units). None of the controls and 15 (6.9%) blood recipients developed PTH. Three (20%) patients had hepatitis-B-virus-induced hepatitis while the remainder (80%) had non A, non B (NANB) hepatitis. The number of units of blood transfused and surrogate markers for development of PTH (donor alanine aminotransferase, anti-HBc and anti-HBs antibody) were not associated with the occurrence of PTH (p greater than 0.05). Nine (60%) of the 15 patients developing PTH were asymptomatic. All the patients recovered from the PTH, except one who died of fulminant hepatitis. At the end of 1 year of follow-up, none of the patients had evidence of chronic hepatitis. Only three (25%) of the patients with NANB-PTH developed anti-hepatitis C virus (HCV) antibody during the follow-up. We conclude that the incidence of PTH in India is similar to other parts of the world and NANB virus was the major cause of the PTH. The absence of chronicity and lack of seroconversion to anti-HCV antibody in the majority of the patients after 1 year of follow-up may suggest the possibility of a NANB virus other than HCV as the major cause of PTH in India.     

Antibody to Hepatitis-C-Virus-Related Proteins in Sera from Alanine-Aminotransferase-Screened Blood Donors and Prospectively Studied Recipients

Abstract. A prospective study of posttransfusion non-A, non-B hepatitis was conducted in Malmö, Sweden, in 1984–1985, in which donors were alanine aminotransferase (ALT) screened but not ALT selected. Among 741 patients studied at 0, 6, and 12 weeks after transfusion, 13 developed non-A, non-B hepatitis, and these were further followed up. Stored sera from the 13 hepatitis patients and their 123 donors were tested for anti-hepatitis C virus (HCV) by ELISA and, if positive, analyzed by recombinant immunoblot assay (RIBA). All ALT-elevated blood units (n = 301) and a similar number of ALT-normal units were also tested. Only 4/13 patients with non-A, non-B hepatitis seroconverted to anti-HCV, all with ALT peaks >10 times the upper normal. All seroconversions occurred within 5 months after transfusion and could be confirmed by RIBA. Hepatitis C in recipients occurred both after transfusion of blood that was strongly positive, weakly positive, and/or negative for anti-HCV by ELISA. In donors grouped by ALT levels, the anti-HCV prevalence varied between 0.4 (normal ALT) and 14% (ALT elevated ≥ 2 times). Of the total of 9 donor units positive by ELISA, only 5 were confirmed by RIBA. Of the 5 recipients of the RIBA-positive blood units, 3 went into hepatitis, 1 remained normal at 10.5 weeks, and 1 showed a slight, transient ALT elevation at week 12. The recipients of ELISA-positive but RIBA-negative blood remained healthy.     

Prospective controlled study of posttransfusion hepatitis after cardiac surgery in a large referral hospital in India

ABSTRACT— We studied the risk of post-transfusion hepatitis (PTH) in recipients of blood collected from voluntary donors screened for HBsAg. Two hundred and fifty patients without any previous history of liver disease or transfusion were followed up for 12 months subsequent to cardiac surgery. Thirty-five of them had closed-heart surgery without receiving transfusion and served as controls. The remaining 215 patients received single-point transfusions (mean 4 ± 2.4 units). None of the controls and 15 (6.9%) blood recipients developed PTH. Three (20%) patients had hepatitis-B-virus-induced hepatitis while the remainder (80%) had non A, non B (NANB) hepatitis. The number of units of blood transfused and surrogate markers for development of PTH (donor alanine aminotransferase, anti-HBc and anti-HBs antibody) were not associated with the occurrence of PTH (p>0.05). Nine (60%) of the 15 patients developing PTH were asymptomatic. All the patients recovered from the PTH, except one who died of fulminant hepatitis. At the end of 1 year of follow-up, none of the patients had evidence of chronic hepatitis. Only three (25%) of the patients with NANB-PTH developed anti-hepatitis C virus (HCV) antibody during the follow-up. We conclude that the incidence of PTH in India is similar to other parts of the world and NANB virus was the major cause of the PTH. The absence of chronicity and lack of seroconversion to anti-HCV antibody in the majority of the patients after 1 year of follow-up may suggest the possibility of a NANB virus other than HCV as the major cause of PTH in India.     

Anti-HCV in post-transfusion hepatitis: deductions from a prospective study

Stored sera from 52 patients who developed post-transfusion hepatitis (PTH) during a prospective study of PTH in Toronto in 1984/85, sera from 111 donors whose blood was transfused into these patients and sera from 50 patients with chronic active hepatitis with a remote history of blood transfusion were tested for anti-HCV. In patients with PTH seroconversion occurred relatively early. Ten converted in less than 14 weeks after transfusion. Only three of the 34 patients (9%) whose hepatitis resolved developed anti-HCV compared to 11 of 18 (61%) whose hepatitis became chronic. Patients who seroconverted had higher alanine aminotransferase (ALT) values during the phase of acute hepatitis than those who did not seroconvert. Most of the patients who developed PTH received blood that was negative for anti-HCV. Four donors whose blood was positive for anti-HCV transmitted hepatitis. Three of the patients developed anti-HCV and chronic hepatitis. One of the recipients did not seroconvert and the hepatitis resolved. Forty-two of the 50 patients (84%) with chronic hepatitis and a remote history of blood transfusion were positive for anti-HCV. We conclude that anti-HCV-positive donors may transmit hepatitis C; that if anti-HCV is diagnostic of hepatitis C, most cases of acute PTH are either not due to hepatitis C or may represent cases of hepatitis C in which the anti-HCV test was undetectable. On the other hand, most cases of PTH which progress to chronic hepatitis are caused by HCV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improved Serodiagnosis of Posttransfusion Hepatitis C Virus Infection by a Second-Generation Immunoassay Based on Multiple Recombinant Antigens

Serial serum samples from 35 patients with posttransfusion non-A, non-B hepatitis in a prospective study were tested for antibody to hepatitis C virus (HCV) by a multiple recombinant antigen based immunoassay [anti-HCV (2nd); Abbott]. Of them, 23 were positive for anti-C100, and 27 were positive for HCV RNA by polymerase chain reaction. By anti-HCV (2nd), 28 patients were positive, and all except 1 of the 28 patients were positive for HCV RNA. A total of 24 patients, who became HCV RNA positive at the acute stage and who were negative for both anti-C100 and anti-HCV (2nd) before transfusion, were considered to have posttransfusion hepatitis C. The mean time to seroconversion for anti-HCV (2nd) was 7.5 or 12.1 weeks after the onset of hepatitis or the date of transfusion, respectively, and was generally 6 weeks earlier than that detected by anti-C100. However, seroconversion was delayed in 2 hepatitis B surface antigen carriers as compared with anti-C100. The anti-C100 assay detected 20 (83%) and the anti-HCV (2nd) all 24 patients with documented posttransfusion hepatitis C. The second-generation test is, therefore, better than conventional anti-C100 for the early diagnosis of HCV infection.     

Anti-Hepatitis C Virus Screening Will Reduce the Incidence of Post-Transfusion Hepatitis C Also in Low-Risk Areas

The incidence of post-transfusion hepatitis non-A, non-B (PTH-NANB) was prospectively assessed in two areas in the southeast region of Sweden. Patients undergoing hip arthroplasty were studied with blood sampling for alanine aminotransferase analysis before and at 2, 3, and 4 months after transfusion. Of the patients 97% and 82% were transfused and received a mean of 5.5 and 3.4 units in Linköping and Oskarshamn, respectively. None of 38 patients in Oskarshamn but 4 of 144 patients (2.8%) in Linköping contracted PTH-NANB. Two of these four patients developed antibodies against hepatitis C virus (HCV) by the first-generation anti-HCV enzyme-linked immunosorbent assay (ELISA) (C100). The other two patients remained negative by this test. HCV infection was, however, indicated in all four patients by positive second-generation anti-HCV ELISA confirmed by positive second-generation recombinant immunoblot assay (4-RIBA). Three of the patients were positive by polymerase chain reaction (PCR). Serum from one blood donor to the four hepatitis patients (altogether three donors) was found positive by first- and second-generation anti-HCV ELISA and 4-RIBA and was also PCR-positive. Three other blood donors, who did not transmit hepatitis, were anti-HCV ELISA (C100)-positive. This study shows that if anti-HCV ELISA had been available at the start of the trial, all cases of PTH would have been avoided at the expense of only 0.7% transfusion units discarded. Routine anti-HCV ELISA testing of all transfusion units will reduce the incidence of PTH-C even in low-risk areas.     

Antibodies to hepatitis C virus in prospectively followed patients with posttransfusion hepatitis.

In an attempt to investigate the incidence and clinical course of type C viral hepatitis among patients with posttransfusion hepatitis, antibodies to hepatitis C virus (anti-HCV) in sera were measured from 42 prospectively followed cardiovascular surgery patients who developed hepatitis after blood transfusions. Of these, 35 (83.3%) had anti-HCV seroconversion during a 6- to 12-month follow-up period. The mean interval between blood transfusion and onset of active anti-HCV seroconversion was approximately 3 months after the first elevation of serum alanine aminotransferase levels (18.1 vs. 6.4 weeks). There was no correlation between fluctuations in serum alanine aminotransferase levels and anti-HCV titers. Of 26 patients with type C posttransfusion hepatitis who were followed greater than 1 year, 20 (76.9%) continued to have abnormal serum alanine aminotransferase levels. The results indicate that HCV is the major agent of posttransfusion hepatitis in Taiwan. Furthermore, it plays an important role in chronic hepatitis among transfused patients.     

Anti-hepatitis C virus screening will reduce the incidence of post-transfusion hepatitis C also in low-risk areas.

The incidence of post-transfusion hepatitis non-A, non-B (PTH-NANB) was prospectively assessed in two areas in the southeast region of Sweden. Patients undergoing hip arthroplasty were studied with blood sampling for alanine aminotransferase analysis before and at 2, 3, and 4 months after transfusion. Of the patients 97% and 82% were transfused and received a mean of 5.5 and 3.4 units in Link?ping and Oskarshamn, respectively. None of 38 patients in Oskarshamn but 4 of 144 patients (2.8%) in Link?ping contracted PTH-NANB. Two of these four patients developed antibodies against hepatitis C virus (HCV) by the first-generation anti-HCV enzyme-linked immunosorbent assay (ELISA) (C100). The other two patients remained negative by this test. HCV infection was, however, indicated in all four patients by positive second-generation anti-HCV ELISA confirmed by positive second-generation recombinant immunoblot assay (4-RIBA). Three of the patients were positive by polymerase chain reaction (PCR). Serum from one blood donor to the four hepatitis patients (altogether three donors) was found positive by first- and second-generation anti-HCV ELISA and 4-RIBA and was also PCR-positive. Three other blood donors, who did not transmit hepatitis, were anti-HCV ELISA (C100)-positive. This study shows that if anti-HCV ELISA had been available at the start of the trial, all cases of PTH would have been avoided at the expense of only 0.7% transfusion units discarded. Routine anti-HCV ELISA testing of all transfusion units will reduce the incidence of PTH-C even in low-risk areas.     

Seroepidemiology of hepatitis C virus infection in the Philippines: A preliminary study and comparison with hepatitis B virus infection among blood donors, medical personnel, and patient groups in Davao, Philippines

To determine the seroprevalence of hepatitis C virus in the Philippines and compare it with the seroprevalence of hepatitis B virus infection, HBV and HCV markers in 594 serum samples collected from 392 blood donors, 123 medical and paramedical personnel, and 80 patients (45 liver diseases: 25 acute hepatitis, 9 liver cirrhosis, and 11 hepatocellular carcinoma; 28 hepatitis B carriers, and 7 chronic renal failure patients undergoing dialysis) in Davao, Mindanao Island, Philippines, were examined. HBsAg was determined by RPHA, anti-HBc by HI, anti-HBs by PHA, and HBsAg subtypes, HBeAg, and anti-HBe by EIA. HCV markers determined were anti-HCV (anti-C100-3) by ELISA (Ortho Diagnostic Systems), and anti-HCV core (anti-CP9 and/ or anti-CPIO) also by ELISA. Results showed that 9 (2.2%) blood donors were anti HCV positive; 69 (15.4%) were anti-HCV core positive Nine (2.2%) were HBsAg carriers; 240 (61.3%) were anti-HBs and/or anti-HBc positive (HBsAg carriers excluded from this group). Two of 123 medical and paramedical staff (1.6% ) were anti-HCV positive; 11 (8.1%) were anti-HCV core positive; Eight (6.5%) were HBsAg carriers and 81 (65.8%) anti-HBs and/or anti-HBc positive. Five of 11 (45.4%) hepatocellular carcinoma patients were HBsAg carriers; 2 were anti-HCV core positive. Two of 9 liver cirrhosis patients were antiHCV positive (1 to anti-HCV and the other to anti-HCV core). If anti-HCV positivity means carrier state, then the HCV carrier rate of blood donors in Davao, Philippines is the same as the HBV carrier rate and prospective blood donors should be screened not only for HBV but also for HCV to prevent transfusion-associated hepatitis. Less than 50% of liver cirrhosis and hepatoHCV carcinoma cases have HBV markers and HCV markers but, when present, these markers appear at almost the same frequency; the role of HCV and HBV in the pathogenesis of these 2 diseases in Mindanao should be further investigated.     

Anticore Antibody Screening of Transfused Blood

Aliquots of 130 HB8Ag negative units of blood which were administered to 26 recipients were tested under code for anti-HBc by a solid phase radioimmunoassay technqiue. 14 of the 26 recipients developed posttransfusion hepatitis (PTH), including 6 cases of hepatitis B. Anti-HBc was detected in 7 or 5.3% of 130 donor units. Of the 14 patients acquiring PTH, 6 received a unit of anti-HBc-positive blood. Type B hepatitis occurred in 4 of the 7 anti-HBc recipients, and non-type B hepatitis in 2. Only 1 of 12 recipients who failed to develop PTH had received a unit containing anti-HBc.     

High rate of hepatitis C virus transmission to spouses from hepatitis patients with a history of transfusion

Spouses of hepatitis C virus (HCV)-viremic chronic hepatitis patients were tested for antibodies to the core region-derived synthetic oligopeptides and for antibodies detectable by the second-generation enzyme immunoassay, and HCV RNA was determined in those who were positive for at least one of the above antibodies (anti-HCV). The prevalences of anti-HCV and HCV RNA were both significantly higher in 37 spouses of patients with a history of transfusion than in 55 spouses of patients with no such history: 49% vs. 16% for anti-HCV (P < 0.01) and 41% vs. 5% for HCV RNA (P < 0.05). Anti-HCV was detected in 11 (65%) of 17 spouses who had been married longer than 30 years since the patients received the transfusion, with an incidence significantly higher than in four (20%) of 20 spouses with exposure durations less than 30 years (P < 0.001), and HCV RNA was positive in 11 (65%) of the formers, the incidence being significantly greater than in four (20%) of the latter (P < 0.05). HCV-infected patients, in particular with a history of blood transfusion, are thus possible HCV transmission sources for their spouses, with the risk increasing with the duration of marriage, pointing to a need for follow-up not only for posttransfusion hepatitis C patients, but also for early diagnosis and treatment of their spouses.     

Correlation between Anti-HBc Titers and HBV DNA in Blood Units without Detectable HBsAg

Hepatitis B virus (HBV) DNA was tested for in 294 blood units which had antibody against hepatitis B core antigen (anti-HBc) as the isolated serological marker of HBV infection. After amplification by polymerase chain reaction, HBV DNA was detected in 12 (6.9%) of 175 units that were positive for anti-HBc with hemagglutination inhibition titers greater than or equal to 2(6), significantly more often than in none of 119 units with titers less than or equal to 2(5) (p less than 0.01). These results indicate that the exclusion of blood units with isolated high-titer anti-HBc would be effective for further decreasing the risk of posttransfusion hepatitis B.     

Prevalence of Anti-HCV Antibody in Blood Donors in the Tokyo Area

Prospective studies of posttransfusion hepatitis carried out in the past decade showed that 18.1% of the blood transfusions resulted in non-A non-B hepatitis in Japan. As an approach to the prevention of posttransfusion non-A non-B hepatitis (PTNANB), anti-hepatitis C virus (HCV) positivity was measured in 2,970 blood donations in the Tokyo area, and in 200 children aged between 6 and 15 years. Thirty-four cases were anti-HCV-positive, showing an overall positivity of 1.14%. None of the 200 children younger than 15 years old were positive. Correlation of anti-HCV positivity with the serum ALT levels was observed, but by reducing the accepted ALT levels from 35 Karmen Units (KU) down to 25 KU, it is estimated that 62.5% of the observed PTNANB would still have occurred, and 5.1% of the donated blood could not be used for transfusion. On the other hand, it is estimated that the majority of PTNANB could be prevented, with the loss of 1.14% of donated blood units, using the anti-HCV screening test.     

Hepatitis C virus RNA in peripheral blood mononuclear cells: Comparing acute and chronic hepatitis C virus infection

Hepatitis C virus (HCV) can infect peripheral blood mononuclear cells (PBMC) of patients with chronic HCV infection. No data are available on PBMC testing for HCV RNA in acute hepatitis C. This study investigated the presence of HCV RNA in PBMC of patients with acute posttransfusion hepatitis C, compared with those with chronic HCV infection. Nested polymerase chain reaction (PCR) was applied to detect HCV RNA in 111 and 48 paired samples of serum and PBMC of 11 patients with acute posttransfusion hepatitis C and 48 patients with chronic HCV infection, respectively. In patients with acute posttransfusion hepatitis C, HCV RNA was detected in 17 of 29 (59%) and 67 of 82 (82%) serum samples collected during the incubation period and acute phase, respectively. Meanwhile, of the 48 patients with chronic HCV infection, 41 had serum HCV RNA (85%). HCV RNA was not detected in PBMC samples from incubation period or from acute-phase hepatitis, although it was detected in 12 of the 48 PBMC samples of chronically infected patients (25%) P < .005). Of the 12 PBMC specimens positive for positive-stranded HCV RNA, 6 were also positive for negative-stranded HCV RNA. Among patients with chronic HCV infection, HCV infection of PBMC was not related to age, sex, blood transfusion, serum alanine transaminase (ALT) levels, or serum virus titers. In conclusion, HCV infection of PBMC rarely exists in patients with acute hepatitis C. As HCV infection persists, the incidence of HCV infection of PBMC becomes higher. (Hepatology 1996 May;23(5):977-81)     

Prospective assessment of incidence of fulminant hepatitis in post-transfusion hepatitis: A study of 504 cases

The incidence of posttransfusion hepatitis and “fulminant” hepatitis was investigated by a plan devised at our hospital in December 1982. Of 2959 blood recipients between January 1982 and December 1988, 504 (22.5%) developed posttransfusion hepatitis, with a mean transfusion volume of 10.2 units. Of the 504 cases of posttransfusion hepatitis, “icteric” (T-Bil>2.0 mg/dl) and “overt icteric” hepatitis (T-Bil>5.0 mg-dl) developed in 111 cases (22.0%) and 28 cases (5.6%), respectively. Of the 28 overt icteric hepatitis cases, 13 (2.8%) were thought to be true overt icteric posttransfusion hepatitis because the icterus was caused by other reasons in the other 15 cases (seven neonatal jaundice, four hemolytic anemia, one radiation hepatitis, one halothane-induced hepatitis; two other cases were excluded because chronic liver disease was diagnosed by imaging procedures despite serum ALTs in the normal range before transfusion). The anti-HCV serostatus was investigated in five of the 13 true overt icteric posttransfusion hepatitis patients using blood specimens taken 180 days or more following the onset of posttransfusion hepatitis. Anti-HCV seroconversion occurred in three of the five cases (60%). HCV seroconversions were not seen in the cases in which the icterus was due to other reasons.     

Hepatocellular carcinoma in Sweden: its association with viral hepatitis, especially with hepatitis C viral genotypes

Viral markers of chronic hepatitis were tested for in 95 frozen serum samples from 299 patients from Malm?, Sweden, with hepatocellular carcinoma (HCC), diagnosed between 1977 and 1994. Hepatitis B analysis included anti-HBc, HBsAg and, if anti-HBc positive, HBV DNA. Hepatitis C infection analysis included anti-HCV screening, RIBA, HCV RNA and HCV genotyping. HCV genotyping was also carried out in 9 HCV-viraemic HCC-patients from Gothenburg. HCV genotype distribution in HCC cases was compared with Swedish HCV-infected blood donors. Among the 95 patients from Malm?, 28 (29%) had anti-HBc, but only 5 (5%) were chronic HBV carriers, compared with 16 (17%) with chronic hepatitis C (p = 0.021). HCV-related HCC was more common among immigrants (8/16 vs. 8/79; p < 0.001). Genotyping of 25 HCV-infected cases showed genotype 1a in 6 (24%), genotype 1b in 13 (52%), genotype 2b in 4 (16%), and genotype 3a in 2 (8.0%) patients. Genotype 1b was more common among HCC patients than among blood donors (p < 0.001), but 8 of 13 genotype 1b-infected patients were from countries where genotype 1b is predominant. Among native Swedes there was no difference between the HCV genotypes infecting blood donors and those found in HCC patients.     

Incidence, prevalence, and clinical course of hepatitis C following liver transplantation.

Hepatitis C virus (HCV) is the agent responsible for posttransfusion hepatitis. The incidence, timing, and clinical course of HCV positive hepatitis in liver transplant recipients are unknown. Three hundred and seventeen donor-recipient liver transplant pairs were grouped on the basis of their pretransplant HCV antibody status. The biopsy findings were examined. Four distinct groups were identified on the basis of HCV serology: group I, both were negative; group II, donor was negative and recipient was positive; group III, donor was positive and recipient was negative; group IV, both were positive. The prevalence of anti-HCV positivity in recipients was 13.6%. The rate of seroconversion was 9.2%. Histologic hepatitis not ascribable to any specific cause other than non-A, non-B (NANB) hepatitis occurred in 13.8%. The incidence of histologic chronic active hepatitis was 1.6%, and none progressed to cirrhosis. The concordance rate for a positive anti-HCV serology and NANB hepatitis was 2.8%. Of the 35 patients (group II and IV) with positive anti-HCV serology pretransplant, only 17 were positive posttransplantation. Based on these data it can be concluded that posttransplant NANB hepatitis occurred in 13.8% of liver recipients. Twenty percent of these were anti-HCV positive. Progression to histologic chronic active hepatitis occurs over a period of 1-5 years in 1.6% of cases.     

Spectrum of viral hepatitis in thalassemic children receiving multiple blood transfusions.

AIM: To investigate the prevalence of infection with hepatitis viruses in children with thalassemia receiving multiple blood transfusions. METHODS: Sera from 50 children with thalassemia aged 5-15 years (30 boys), who had each received over 80 units of blood, were evaluated for the presence of markers for hepatitis A virus (HAV; IgG and IgM anti-HAV), hepatitis B virus (HBV; HBsAg, and IgG and IgM anti-HBc), hepatitis C virus (HCV; IgG and IgM anti-HCV, and HCV RNA) and hepatitis E virus (HEV; IgG and IgM anti-HEV). IgM anti-hepatitis D virus (HDV) was looked for only in HBsAg or IgM anti-HBc positive sera. RESULTS: No child had evidence of recent HAV or HDV infection. IgG anti-HAV was positive in 12 children. One patient had acute HBV infection. Nine patients were HBsAg-positive. HCV infection was present in 15 cases; six of them were HCV RNA positive, and three had superinfection with hepatitis B. Recent HEV infection was present in 5 cases. CONCLUSION: Thalassemic patients receiving multiple blood transfusions often acquire hepatitis B (20%) and C (30%) infections. Recent hepatitis E infection was documented in 10% in this one-point study.     

IgM antibody response in acute hepatitis C viral infection.

IgM antibody against hepatitis C virus (IgM anti-HCV) was measured in serial samples from 15 transfusion recipients in whom posttransfusion chronic non-A, non-B hepatitis (NANBH) developed and three plasmapheresis donors during acute HCV infection using recombinant proteins derived from three immunodominant regions: core, NS-3, and NS-4 (c100). IgM anti-HCV core was detected in 13 of 15 posttransfusion patients. Nine of these patients had transient, acute-phase IgM anti-HCV core detected coincidentally or earlier than active IgG anti-HCV core response. The average duration of IgM anti-HCV core reactivity was 8.1 +/- 3.7 weeks. One patient lacking an IgM anti-HCV core response had detectable IgM anti-HCV NS-3 during the acute phase. Passive transfer of IgM anti-HCV was not observed in these posttransfusion cases, in contrast to the high frequency observed for IgG anti-HCV. Late IgM anti-HCV was detectable against core, c100, and NS-3 in three, two, and one posttransfusion patients, respectively. These data indicate that IgM anti-HCV core is a useful acute-phase marker in HCV infection.