Posttransfusion Hepatitis Type A

Hollinger, F. Blaine

doi:10.1001/jama.1983.03340170039025

Cited by 124 publications

(21 citation statements)

References 31 publications

(3 reference statements)

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“…Raised ALT levels in apparently healthy individuals have been statistically correlated to at least one of the following: male sex [16][17][18], middle age [16][17][18], over weight [10,16,20], alcohol-drinking habits [18,20] and ongoing gastrointestinal symptoms [19]. The association to male sex and overweight is in congruence with our study.…”

Section: Discussionsupporting

confidence: 88%

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Wejstål¹,

Hansson²,

Lindholm³

et al. 1988

Vox Sanguinis

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Five hundred consecutive healthy blood donors were tested for serum alanine aminotransferase (ALT) and 44 (8.8%) had increased levels. Donors with and without raised ALT were compared in several aspects but only weight (expressed as percentage of ideal body weight) and sex differed significantly (119.1 ± 14.5 and 106.3 ± 12.8%, respectively; p<0.001 and males 97.7 and 77.1%, respectively; p<0.01). The 44 donors with raised ALT were followed up and in 13 out of 15 donors with persistently raised ALT without obvious reason, a liver biopsy was performed. Ten donors had various degrees of liver steatosis, 2 had normal liver morphology and in 1 donor chronic hepatitis could not be ruled out. If ALT screening is introduced as a surrogate test for non-A, non-B hepatitis in Swedish blood donors, we suggest that a correction for overweight must be considered in order to minimize donor loss.

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Section: Discussionsupporting

confidence: 88%

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Wejstål¹,

Hansson²,

Lindholm³

et al. 1988

Vox Sanguinis

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“…Already in 1983, Hollinger et al [44] reported a case of an HAV-contaminated plasma donation with no serological findings. According to experiments in chimpanzees, the virus titre in the viraemic phase is 10 5 infectious viruses/ml [45].…”

Section: Infectious Load Of the Starting Materials And Test Methodsmentioning

confidence: 99%

“…These cases of transmission made it clear that HAV can be transmitted by plasma derivatives. In the early 1980s, there were also some reports of HAV transmission following blood transfusions [40][41][42][43][44]. In the last few years, no suspected cases of HAV transmission associated with the use of blood components have been reported to the PEI.…”

Section: Transmissibilitymentioning

confidence: 99%

Hepatitis A Virus

2001

Transfus Med Hemother

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1 Current Knowledge about the Pathogen 1.1 Characteristics of Hepatitis A Virus The clinical features of hepatitis A have been known for a long time. However, the pathogen (hepatitis A virus (HAV)) was firstly identified in 1973 with the aid of immune electron microscopy [1]. HAV is classified in the family of Picornaviridae , genus Hepatovirus . It is a small, spherical, non-enveloped virus with a diameter of approximately 30 nm. The capsid of the viral particle is made up of 60 copies of the three viral structural proteins VP1–VP3. The genome consists of a single- stranded (+)sense RNA molecule of 7,500 bases in length. The 5'' end of the genome is covalently bound to a small protein (VPg). The genome serves as messenger RNA and can be divided into three regions: a long open-reading frame (ORF) is flanked by the non-coding 5'' region and the non-coding 3'' region. The ORF encodes a polyprotein which is cleaved by proteolysis into the mature viral proteins. Two thirds of the genome code for non-structural proteins with enzymatic and regulatory functions. Translation is controlled by an ‘internal ribosomal entry site’ (IRES) located within the non-coding 5'' region [2]. Only one serotype of HAV has been identified so far. Analysis of HAV genome sequences has revealed 6 genotypes to date [3], with genotype I predominating worldwide. Genotypes IV–VI have only been observed in Old World monkeys. ...

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“…According to the National Centre for Surveilance and Intervention of Greece, the median annual prevalence of acute hepatitis A in Greece for the time 1998-2003 was 1.88 cases/100 000 of population, which is comparable to the hepatitis A prevalence of the Western Europe [5] . Parenteral transmission is extremely rare, but can follow transfusion of blood from a donor who is in the incubation period of the disease [6,7] . The relatively short duration of viremia in acute hepatitis A, together with the moderate titer of HAV viral load in the blood [8] , diminishes the likelihood of transfusing a unit of blood infectious for HAV.…”

Section: Introductionmentioning

confidence: 99%

Prevalence of anti-HAV antibodies in multitransfused patients with beta-thalassemia

Siagris

Kouraklis-Symeonidis²,

Konstantinidou³

et al. 2008

WJG

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AIM:To detect the prevalence of anti-HAV IgG antibodies in adult multitransfused beta-thalassemic patients. METHODS:We studied 182 adult beta-thalassemic patients and 209 controls matched for age and sex from the same geographic area, at the same time. Anti-HAV IgG antibodies, viral markers of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection were evaluated. RESULTS:Anti-HAV IgG antibodies were detected more frequently in thalassemic patients (133/182; 73.1%) than in healthy controls (38/209; 18.2%, P < 0.0005). When we retrospectively evaluated the prevalence of anti-HAV IgG antibodies in 176/182 (96.7%) thalassemic patients, whose medical history was available for the previous ten years, it was found that 83 (47.2%) of them were continuously anti-HAV IgG positive, 16 (9.1%) acquired anti-HAV IgG antibody during the previous ten years, 49 (27.8%) presented anti-HAV positivity intermittently and 28 (15.9%) were anti-HAV negative continuously. CONCLUSION:Multitransfused adult beta-thalassemic patients present higher frequency of anti-HAV IgG a n t i b o d i e s t h a n n o r m a l p o p u l a t i o n o f t h e s a m e geographic area. This difference is difficult to explain, but it can be attributed to the higher vulnerability of thalassemics to HAV infection and to passive transfer of anti-HAV antibodies by blood transfusions.

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Posttransfusion Hepatitis Type A

Cited by 124 publications

References 31 publications

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Hepatitis A Virus

Prevalence of anti-HAV antibodies in multitransfused patients with beta-thalassemia

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