Elevated alanine aminotransferase (ALT) in blood donors: an assessment of the main associated conditions and its relationship to the development of hepatitis C.

The determination of aminotranferases levels is very useful in the diagnosis of hepatopathies. In recent years, an elevated serum ALT level in blood donors has been associated with an increased risk of post-transfusion hepatitis (PTH). The purpose of the study was to research the factors associated with elevated ALT levels in a cohort of voluntary blood donors and to evaluate the relationship between increased ALT levels and the development of hepatitis C (HCV) infection. 166 volunteer blood donors with elevated ALT at the time of their first donation were studied. All of the donors were questioned about previous hepatopathies, exposure to hepatitis, exposure to chemicals, use of medication or drugs, sexual behaviour, contact with blood or secretions and their intake of alcohol. Every three months, the serum levels of AST, ALT, alkaline phosphatase, gamma glutamyl transpeptidase, cholesterol, triglyceride and glycemia are assessed over a two year follow-up. The serum thyroid hormone levels as well as the presence of auto-antibodies were also measured. Abdominal ultrasound was performed in all patients with persistently elevated ALT or AST levels. A needle biopsy of liver was performed in 9 donors without definite diagnostic after medical investigation. The presence of anti-HCV antibodies in 116 donors were assayed again the first clinical evaluation. At the end of follow-up period (2 years later) 71 donors were tested again for the presence of anti-HCV antibodies. None of donors resulted positive for hepatitis B or hepatitis C markers during the follow-up. Of the 116 donors, 101 (87%) had persistently elevated ALT serum levels during the follow-up. Obesity and alcoholism were the principal conditions related to elevated ALT serum levels in 91/101 (90.1%) donors. Hypertriglyceridemia, hypercholesterolemia, hypothyroidism and diabetes mellitus also were associated with increased ALT levels. Only 1/101 (0.9%) had mild chronic active non A-G viral hepatitis and 3/101 (2.9%) had liver biopsy with non-specific reactive hepatitis. The determination of ALT levels was not useful to detect donors infected with HCV at donation in Brazil, including the initial seronegative anti-HCV phase.

[1]  JB McCormick,et al.  Hepatitis G virus in Karachi, Pakistan , 1996, The Lancet.

[2]  S. Locarnini,et al.  Prevalence of hepatitis G virus in Queensland blood donors , 1996, The Medical journal of Australia.

[3]  K. Masuko,et al.  Infection with hepatitis GB virus C in patients on maintenance hemodialysis. , 1996, New England Journal of Medicine.

[4]  H. Alter.  The cloning and clinical implications of HGV and HGBV-C. , 1996, The New England journal of medicine.

[5]  R. Charrel,et al.  Hepatitis GB virus C in patients on hemodialysis. , 1996, The New England journal of medicine.

[6]  H. Margolis,et al.  Molecular Cloning and Disease Association of Hepatitis G Virus: A Transfusion-Transmissible Agent , 1996, Science.

[7]  S. Kleinman,et al.  Declining value of alanine aminotransferase in screening of blood donors to prevent posttransfusion hepatitis B and C virus infection. The Retrovirus Epidemiology Donor Study , 1995, Transfusion.

[8]  W. H. Hall,et al.  Infectious disease testing for blood transfusions. NIH Consensus Development Panel on Infectious Disease Testing for Blood Transfusions. , 1995, JAMA.

[9]  A. Keller,et al.  Post‐transfusion hepatitis revisited , 1995, The Medical journal of Australia.

[10]  T. Pilot‐Matias,et al.  Isolation of novel virus-like sequences associated with human hepatitis , 1995, Nature Medicine.

[11]  S. Naik,et al.  Effectiveness of mandatory transmissible diseases screening in Indian blood donors. , 1995, The Indian journal of medical research.

[12]  T. Pilot‐Matias,et al.  Identification of two flavivirus-like genomes in the GB hepatitis agent. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[13]  H. Alter.  TRANSFUSION TRANSMITTED HEPATITIS C AND NON‐A, NON‐B, NON‐C , 1994, Vox sanguinis.

[14]  K. Pendry,et al.  Analysis of Pre‐ and Post‐Donation Haematological Values in Plateletpheresis Donors , 1993, Vox sanguinis.

[15]  B. Vanderborght,et al.  Prevalence of Anti‐Hepatitis C Virus in the Blood Donor Population of Rio de Janeiro , 1993, Vox sanguinis.

[16]  C. A. Souza,et al.  Prevalências do HBsAg, do anti-HBc e do anti-HCV na população de candidatos a doadores de sangue do Hemocentro-Campinas , 1993 .

[17]  L. D. Silva,et al.  Hepatites pós-transfusionais na cidade de Campinas, SP, Brasil: I. Incidência, agentes etiológicos e aspectos clínico-epidemiológicos da hepatite por vírus C , 1993 .

[18]  M A Gerber,et al.  The natural history of community-acquired hepatitis C in the United States. The Sentinel Counties Chronic non-A, non-B Hepatitis Study Team. , 1992, The New England journal of medicine.

[19]  D. Primi,et al.  Direct PCR amplification of HCV RNA from human serum. , 1992, PCR methods and applications.

[20]  M. Houghton,et al.  Elevated serum alanine aminotransferase levels in blood donors: the contribution of hepatitis C virus. , 1991, Annals of internal medicine.

[21]  H. Margolis,et al.  Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection. , 1990, JAMA.

[22]  F. Schaffner,et al.  Effect of weight reduction on hepatic abnormalities in overweight patients. , 1990, Gastroenterology.

[23]  R. Tedder,et al.  Detection of hepatitis C viral sequences in blood donations by "nested" polymerase chain reaction and prediction of infectivity , 1990, The Lancet.

[24]  M. Houghton,et al.  Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome. , 1989, Science.

[25]  Jules L. Dienstag,et al.  An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis , 1989 .

[26]  J. Dienstag,et al.  Evaluation of blood donors with elevated serum alanine aminotransferase levels. , 1987, Annals of internal medicine.

[27]  P. Chomczyński,et al.  Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. , 1987, Analytical biochemistry.

[28]  G. Danan,et al.  Cross hepatotoxicity between tricyclic antidepressants. , 1986, Gut.

[29]  W. V. Miller,et al.  The distribution of serum alanine aminotransferase levels in a blood donor population. , 1982, American journal of epidemiology.

[30]  K. Sherman,et al.  Alanine aminotransferase levels among volunteer blood donors: geographic variation and risk factors. , 1982, The Journal of infectious diseases.

[31]  R. Purcell,et al.  Donor transaminase and recipient hepatitis. Impact on blood transfusion services. , 1981, JAMA.

[32]  R. Kahn,et al.  Serum alanine aminotransferase of donors in relation to the risk of non-A,non-B hepatitis in recipients: the transfusion-transmitted viruses study. , 1981, The New England journal of medicine.

[33]  G. Menghini.  One-second needle biopsy of the liver. , 1958, Gastroenterology.

[34]  T. Pilot‐Matias,et al.  Consensus oligonucleotide primers for the detection of GB virus C in human cryptogenic hepatitis. , 1996, Journal of virological methods.

[35]  L. D. Silva,et al.  Hepatites pós-transfusionais na cidade de Campinas, SP, Brasil: II. Presença dos anticorpos anti-HBc e anti-HCV em candidatos a doadores de sangue e ocorrência de hepatites pós-transfusionais pelo vírus C nos receptores de sangue ou derivados , 1993 .

[36]  R. Hultcrantz,et al.  Liver investigation in 149 asymptomatic patients with moderately elevated activities of serum aminotransferases. , 1986, Scandinavian journal of gastroenterology.