Prevalence of Hepatitis C Virus Antibody
2000; King Faisal Specialist Hospital and Research Centre; Volume: 20; Issue: 5-6 Linguagem: Inglês
10.5144/0256-4947.2000.488
ISSN0975-4466
Autores Tópico(s)Liver Disease Diagnosis and Treatment
ResumoLetter to the EditorPrevalence of Hepatitis C Virus Antibody Zakaria M. Al-HawsawiMD Zakaria M. Al-Hawsawi Madina Maternity & Children's Hospital, P.O. Box 6205, Madina, Saudi Arabia Search for more papers by this author Published Online::1 Sep 2000https://doi.org/10.5144/0256-4947.2000.488SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutIntroductionTo the Editor: The prognosis of thalassemia major has improved greatly over the last 20 years, owing to intensive blood transfusion regimens and chelation therapy.1 However, thalassemia patients are at a high risk of posttransfusion hepatitis (PTH). Hepatitis C virus (HCV) is the leading cause of PTH worldwide.2–4 People who are at a high risk of HCV infection are those who receive multiple blood transfusions, especially thalassemia and sickle cell anemia patients.5 Between 50% and 60% of patients develop chronic hepatitis, and almost 30% go on to develop cirrhosis of the liver. Hepatocellular carcinoma may result as a late consequence of the HCV infection.6β-thalassemia and sickle cell disease (SCD) are common in Saudi Arabia. In Madina, the estimated gene frequency of β-thalassemia is 0.100, and the prevalence of sickle cell homozygosity (HbSS) is 0.01.7 The Madina Maternity & Children's Hospital (MMCH) is a 400-bed hospital with a 200-bed pediatric section. It is the main referral hospital for the Madina region and its surrounding villages, and serves approximately 350,000 children. The Thalassemia Center was established in 1992 within the pediatric section to provide comprehensive management of thalassemic patients, which includes regular blood transfusion at three to four weekly intervals. The age limit for admission for pediatric patients is 13 years, however, for thalassemic patients the limit is 18 years. The aim of this study was to identify the prevalence of HCV antibody in 80 patients with thalassemia and SCD on multiple transfusion regimens, who were regularly attending the Thalassemia Center at MMCH for a comprehensive management program.PATIENTS AND METHODSIn January 1998, 80 transfusion patients with β-thalassemia and SCD were screened for HCV antibody and hepatitis B surface antigen (HbSAg). The diagnoses of thalassemia and SCD were confirmed by hemoglobin electrophoresis (Helena Laboratories, Texas, USA). All patients received blood transfusions for a minimum of two years at three to four weekly intervals. None of the patients had a history of alcohol abuse, homosexuality or intravenous drug use. All patients were screened for HCV antibody by using a third-generation enzyme-linked immunosorbent assay (ELISA) (Murex Anti-HCV Version III), which utilizes antigens from the putative core (C structural), protease/helicase (NS3, non-structural), NS4 (non-structural) and replicase (NS5, non-structural) regions of the virus to provide a sensitive diagnostic test. Positive results by ELISA were confirmed by recombinant immunoblot assay (Chiron, RIBA, HCV 2.0 S1A). This is a strip immunoblot assay, which utilizes four recombinant HCV-encoded antigens which are immobilized as individual bands onto test strips. The presence of HbSAg was determined with appropriate commercially available assay Auszyme monoclonal, which is a qualitative, third-generation enzyme immunoassay for the detection of HbSAg in human serum or plasma (Abbott Laboratories, Diagnostic Division, USA). The units of blood were provided by the Central Blood Bank in Madina, which introduced routine screening for HCV antibody using second-generation ELISA, for all blood donors in 1993. All patients routinely received HBV vaccine at the time of diagnosis.RESULTSOf the 80 patients, 32 were seropositive to hepatitis C virus, giving a prevalence rate of 40%, 29 (91%) were thalassemic, and three patients (9%) had sickle cell anemia. Of the 32 seropositive patients, 18 (56%) were Saudis and 14 (44%o) were non-Saudis, and comprised 19 males (59%) and 13 females (41%). Twenty-eight patients (88%) received more than 100 units of blood for transfusion, and 29 patients (91%) received blood transfusions for more than five years. As well, 14 patients (44%) had ALT of 100 IU/L or more (normal 40 IU/L), 24 patients (75%) had serum ferritin of more than 2000 ng/mL, and seven of 14 patients with elevated ALT had serum ferritin of more than 5000 ng/mL.DISCUSSIONThis is the first study from the Madina Region which reports the prevalence of hepatitis C virus antibody among a high-risk group of thalassemia and sickle cell patients. We found a prevalence of 40%, which is similar to other regional studies,8,9 however, it is lower than what has been reported from the Riyadh region by Al Fawaz et al.,10 where a prevalence of 70% was reported. Indeed, the prevalence of anti-HCV positivity ranges from 8.7% to more than 70%, and also differs even in similar geographic areas.11 The majority of our patients (91%) were thalassemic, a result which is similar to other studies.10,12 Thalassemic patients are at a greater risk of exposure to HCV because of their life-long requirement of blood transfusion until bone marrow transplantation is done, a procedure which is not commonly available in most developing countries. The three patients with sickle cell anemia had stroke and were on chronic blood transfusion.Approximately 88% of our patients received more than 100 units of packed red blood cell transfusion and 91% received blood transfusion for more than five years. Only 44% had raised ALT, which shows that this marker is not reliable for predicting HCV infection, as other studies have also confirmed.10,13,14Approximately 75% of the patients had elevated serum ferritin, and 50% of those with raised ALT had significant elevation of serum ferritin, which probably suggests that both iron overloading and hepatitis C infection contributed to liver damage in our thalassemic patients, whose compliance with desferrioxamine therapy was less than optimum.Liver biopsy was not done in our patients. It is an essential investigation for assessing the degree and type of liver damage in chronic hepatitis before starting α-interferon therapy. Recent reports indicate that α-interferon induces a sustained virologic and biochemical remission of hepatitis in β-thalassemic patients with chronic HCV infection and non-advanced liver disease. Moreover, it can be used in children and young adults with chronic hepatitis C disease and thalassemia major.15,16In conclusion, it seems that in the treatment of chronic hepatitis C infection with α-interferon, one should use direct assay for hepatitis C virus ribonucleic acid by polymerase chain reaction in both serum and liver biopsy, in order to define subgroups of patients who may benefit from this treatment and to monitor the response of treatment. Until a vaccine against HCV becomes available, preventive measures such as blood donor screening using advanced techniques for detecting HCV infection before transfusion and strict infection control measures are crucial for the control of the spread of HCV among these high-risk patients.ARTICLE REFERENCES:1. Cao A, Gabutti V, Masera G, et al.A short guide to the management of thalassemia. In: Sirchia G, Zanella A, editors. Thalassemia today: the Mediterranean experience. 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"Incidence and frequency of hemoglobinopathies and thalassemia in the northwest sector of Saudi Arabia" . Saudi Med J. 1985; 6:149–62. Google Scholar8. Al-Mahroos FT, Ebrahim A. "Prevalence of hepatitis B, hepatitis C and human immune deficiency virus markers among patients with hereditary haemolytic anaemias" . Ann Trop Paediatr. 1995; 15:121–8. Google Scholar9. Al-Fuzae L, Aboolbacker KC, Al-Saleh Q. "Beta-thalassemia major in Kuwait" . J Trop Paediatr. 1998; 44:311–2. Google Scholar10. Al Fawaz I, Ramia S. "Decline in hepatitis B infection in sickle cell anemia and beta-thalassemia major" . Arch Dis Child. 1993; 69:594–6. Google Scholar11. Locasciulli A, Monguzzi W, Tornotti G, Bianco P, Masera G. "Hepatitis C virus infection and liver disease in children with thalassemia" . Bone Marrow Transplant. 1993; 12:18–20. Google Scholar12. Al Fawaz I, Al-Rasheed S, Al-Mugeiren M, Al-Salloum A, Al-Sohaibani M, Ramia S. "Hepatitis E virus infection in patients from Saudi Arabia with sickle cell anemia and beta-thalassemia major. Possible transmission by blood transfusion" . J Viral Hepat. 1996; 3:203–5. Google Scholar13. Ayoola EA, Huraib S, Arif M, et al. "Prevalence and significance of antibodies to hepatitis C virus among Saudi hemodialysis patients" . J Med Virol. 1991; 35:155–9. Google Scholar14. Willems M, Tong G, Moshage H, et al. "Surrogate markers are not useful for identification of HCV carriers in chronic haemodialysis patients" . J Med Virol. 1991; 35:303–6. Google Scholar15. Di-Marco VLO, Iocono O, Almasio P, et al. "Long-term efficacy of alpha-interferon in beta thalassemics with chronic hepatitis C" . Blood. 1997; 90:2207–12. Google Scholar16. Marcellini M, Kondili LA, et al. "High-dosage alpha interferon for treatment of children and young adults with chronic hepatitis C disease" . Pediatr Infect Dis J. 1997; 16:1049–53. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 20, Issue 5-6September-November 2000 Metrics History Published online1 September 2000 ACKNOWLEDGEMENTSWe would like to express our thanks to the Hospital Director, Dr. Abdulla Allam, for his help and support, to the Laboratory Department for their cooperation, and to Mrs. Aisha Khan and Mrs. Awatif Abdulaziz, staff nurses at the Thalassemia Center, for the collection of medical data. We also thank Dr. Ghulam Nabi for his critical review, and Miss Darna Sarail Alie for the secretarial work.InformationCopyright © 2000, Annals of Saudi MedicinePDF download
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