Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 박성수 | - |
dc.date.accessioned | 2018-04-25T23:06:08Z | - |
dc.date.available | 2018-04-25T23:06:08Z | - |
dc.date.issued | 2012-05 | - |
dc.identifier.citation | Liver international : official journal of the International Association for the Study of the Liver, v.32, no.5[2012], pp.809 - 814 | en_US |
dc.identifier.issn | 1478-3223 | - |
dc.identifier.uri | http://onlinelibrary.wiley.com/doi/abs/10.1111/j.1478-3231.2011.02697.x | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/70598 | - |
dc.description.abstract | Background: While the mechanisms underlying the development of druginduced liver injury are not clear, there is evidence to suggest that tumor necrosis factor-a (TNF-a) plays an important role in drug-or drug metabolite- induced immune responses. We hypothesized that polymorphisms in the TNF-a gene are associated with anti-tuberculosis drug (ATD)-induced hepatitis. Methods: Patients who suffered from ATD-induced hepatitis were enrolled in the study. ATD-induced hepatitis was defined as an increase in liver transaminase levels that were more than three times the upper limit of normal. ATD-tolerant patients were used as a control. Patients were treated with first line ATD therapies including isoniazid, rifampicin, ethambutol, and pyrazinamide. We compared the genotype frequencies of the TNF-a polymorphism -308G/ A in 77 patients with ATD-induced hepatitis and 229 ATD-tolerant patients. Results: The frequency of carrying the variant allele (AG or AA) was significantly higher in patients with ATD-induced hepatitis compared with ATD-tolerant patients [26.0% vs. 15.3%, P = 0.034, OR (95% CI) = 1.94 (1.04-3.64)] and the frequency of the A allele was significantly different between the two groups [0.143 vs. 0.079, P = 0.018, OR (95% CI) = 1.95 (1.11-3.44)]. Conclusion: These results reveal that the TNF-a genetic polymorphism -308G/ A is significantly associated with ATD-induced hepatitis. This genetic variant may be a risk factor for ATD-induced hepatitis in individuals from Korea. | en_US |
dc.description.sponsorship | This study was supported by a grant fro m the KoreaHealth 21 R&D project, Ministry for Health and We l-fare, Republic of Korea (A111218-11-PG01). Theauthors thank Eun-S oon Shin, PhD for assistance in thestatistic al analyses.Conflicts of interest statement: None of the authorshave any conflicts of interest to declare in relation tothis work. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Oxford, UK :Blackwell Munksgaard | en_US |
dc.subject | antituberculosis drugs | en_US |
dc.subject | genetic polymorphism | en_US |
dc.subject | hepatitis | en_US |
dc.subject | tumour necrosis factor-a | en_US |
dc.title | TNF-alpha genetic polymorphism -308G/A and antituberculosis drug-induced hepatitis | en_US |
dc.title.alternative | A and antituberculosis drug-induced hepatitis | en_US |
dc.type | Article | en_US |
dc.relation.no | 5 | - |
dc.relation.volume | 32 | - |
dc.identifier.doi | 10.1111/j.1478-3231.2011.02697.x | - |
dc.relation.page | 809-814 | - |
dc.relation.journal | LIVER INTERNATIONAL | - |
dc.contributor.googleauthor | Park, Sung Soo | - |
dc.contributor.googleauthor | Kim, Sang‐Heon | - |
dc.contributor.googleauthor | Kim, Sang‐Hoon | - |
dc.contributor.googleauthor | Yoon, Ho Joo | - |
dc.contributor.googleauthor | Shin, Dong Ho | - |
dc.contributor.googleauthor | Kim, Youn‐Seup | - |
dc.contributor.googleauthor | Park, Jae‐Seuk | - |
dc.contributor.googleauthor | Jee, Young‐Koo | - |
dc.relation.code | 2012211589 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | parkss | - |
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