Posttransfusion hepatitis C virus infection in children

Ni, Yen‐Hsuan; Chang, Mei–Hwei; Lue, Hung-Chi; Hsu, Hong–Yuan; Wang, Shuo-Meng; Chen, Pei‐Jer; Chen, Ding‐Shinn

doi:10.1016/s0022-3476(05)81359-9

Cited by 51 publications

(25 citation statements)

References 24 publications

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“…Viral clearance rates after transfusion acquired HCV also vary, from 14 to 55% in previous studies (Table 2). 7,8 , 15,16 As differences in age at transfusion may be important in viral clearance, we can only compare our results with the study by O’Riordan et al. , which reported a clearance rate of 42% in a small cohort ( n = 12) of neonatal transfusion acquired HCV infection 8 .…”

Section: Discussionmentioning

confidence: 72%

Long‐term outcome of vertically acquired and post‐transfusion hepatitis C infection in children

Rerksuppaphol

Hardikar

Dore

2004

J of Gastro and Hepatol

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Section: Discussionmentioning

confidence: 72%

Long‐term outcome of vertically acquired and post‐transfusion hepatitis C infection in children

Rerksuppaphol

Hardikar

Dore

2004

J of Gastro and Hepatol

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“…[16][17][18][19] The course of hepatitis C infection in our patients, who were treated for cancer in childhood, does not seem to differ much from the outcome of infected patients who were not treated for neoplastic diseases but who also acquired hepatitis C perinatally or during childhood. [20][21][22][23][24][25][26] As far as we can see, no single risk factor played a significant role in worsening the course of hepatitis.…”

Section: Discussionmentioning

confidence: 77%

HCV Infection in Very-Long-Term Survivors After Cancer Chemotherapy and Bone Marrow Transplantation

Fioredda¹,

Gigliotti²,

Haupt³

et al. 2005

Journal of Pediatric Hematology/Oncology

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The long-term evolution of hepatitis C virus (HCV) infection in oncologic and/or transplanted patients is still unknown. Patients treated for cancer are different from the general HCV-infected population because of the immunosuppression and the hepatotoxic treatments, which act as co-factors of liver damage. Recently it was observed that antimetabolites play a role in accelerating the process of hepatic fibrosis. The aims of this retrospective study were to describe the clinical course of chronic hepatitis C acquired during anticancer treatment in a group of patients referred to a single center, and to correlate the course of hepatic disease to the type of treatment they received. Among the 17 children who underwent very long follow-up (range 10-18.5 years), the authors identified a group with more active hepatic cytolysis through the serial observation of mean ALT values, HCV RNA determination, and histologic data when available. During follow-up, none of them developed hepatic failure, cirrhosis, or hepatocarcinoma. No single risk factor, such as exposure to antimetabolites, alkylating agents, or other chemotherapy, radiotherapy to the abdomen, exposure to other hepatotoxic drugs, appearance of vaso-occlusive disease, acute and/or chronic graft-versus-host disease, or length of immunosuppression, correlated with a worse course of hepatitis. No definitive conclusions can be drawn. However, multivariate analysis of hepatic risk factors in larger cohorts of patients will be able to provide us with more precise information about the clinical outcome of chronic hepatitis in survivors.

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“…In the children with non-A to E hepatitis, HBsAg was checked by RIA (Abbot Laboratories, North Chicago, IL) and anti-HCV was assayed by a commercially available second generation ELISA (Hepatitis C II; Abbott Laboratories). HCV RNA and HGV RNA were detected by RT-PCR, and serum anti-HEV was detected by EIA as those described previously [Ni et al, 1994;Chen et al, 1997;Lai et al, 1997].…”

Section: Subjectsmentioning

confidence: 99%

TT virus infection in healthy children, children after blood transfusion, and children with non‐A to E hepatitis or other liver diseases in Taiwan

Hsu

Chen

et al. 2002

Journal of Medical Virology

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Serum samples from healthy and diseased children were studied for the presence of TTV DNA by nested PCR using primer sets generated from N-22 region and from the untranslated region (UTR) of the viral genome. N-22 positive TTV DNA was detectable in 33 (27%) of 122 healthy children, 47 (73.4%) of 64 polytransfused thalassemic children, 37 (46.3%) of 80 children who received transfusion during cardiac surgery, 8 (42.1%) of 19 non-A to E hepatitis, 10 (33.3%) of 30 HBV carrier children, and 5 (15.6%) of 32 infants with biliary atresia. A much higher prevalence of TTV DNA with rates varying from 78-100% in the above study groups was observed using the UTR primers. For children with N-22 positive TTV DNA, biochemical assessment of isolated TTV viremia in thalassemic children or children transfused during surgery showed no convincing association between raised ALT levels and TTV viremia. Coinfection with TTV in chronic HCV-infected or HBV-infected children did not result in higher peak ALT levels during follow-up, suggesting that TTV has no synergistic pathogenic effect. The phylogenetic analysis of the N-22 positive TTV DNA isolates revealed that most isolates from healthy children, children transfused during surgery, and non-A to E fulminant hepatitis children were type 1 TTV. These results indicate that TTV infection in children was significantly associated with transfusion. TTV infection is highly prevalent in early childhood in Taiwan but plays a minimal role in the induction of hepatitis in children.

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Posttransfusion hepatitis C virus infection in children

Cited by 51 publications

References 24 publications

Long‐term outcome of vertically acquired and post‐transfusion hepatitis C infection in children

Long‐term outcome of vertically acquired and post‐transfusion hepatitis C infection in children

HCV Infection in Very-Long-Term Survivors After Cancer Chemotherapy and Bone Marrow Transplantation

TT virus infection in healthy children, children after blood transfusion, and children with non‐A to E hepatitis or other liver diseases in Taiwan

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