dc.contributor.author | Wergeland, Ida | |
dc.contributor.author | Pullar, Nadine Durema | |
dc.contributor.author | Assmus, Jörg | |
dc.contributor.author | Ueland, Thor | |
dc.contributor.author | Tonby, Kristian | |
dc.contributor.author | Feruglio, Siri | |
dc.contributor.author | Kvale, Dag | |
dc.contributor.author | Damås, Jan Kristian | |
dc.contributor.author | Aukrust, Pål | |
dc.contributor.author | Mollnes, Tom Eirik | |
dc.contributor.author | Dyrhol-Riise, Anne Ma | |
dc.date.accessioned | 2015-10-26T12:12:55Z | |
dc.date.available | 2015-10-26T12:12:55Z | |
dc.date.issued | 2015-01-15 | |
dc.description.abstract | Objectives: Biomarkers for diagnosis and therapy efficacy in tuberculosis (TB)
are requested. We have studied biomarkers that may differentiate between active and
latent TB infection (LTBI), the influence of HIV infection and changes during anti-TB chemotherapy.
Methods: Thirty-eight plasma cytokines, assessed by multiplex and enzyme immunoassays,
were analyzed in patients with active TB before and during 24 weeks of anti-TB chemotherapy
(n Z 65), from individuals with LTBI (n Z 34) and from QuantiFERON-TB (QFT) negative
controls (n Z 65). The study participants were grouped according to HIV status. Results: Plasma levels of the CXC chemokine IP-10 and soluble TNF receptor type 2 (sTNFr2)
significantly differentiated active TB from the LTBI group, irrespective of HIV status. In the
HIV-infected group the sensitivity and specificity was 100% for IP-10 with a cut-off of
2547 pg/mL. Plasma IP-10 declined gradually during anti-TB chemotherapy (12e24 weeks,
p Z 0.002) to a level comparable to LTBI and QFT negative control groups. sTNFr2 fluctuated
throughout therapy, but was decreased after 12e24 weeks (p Z 0.006).
Conclusions: IP-10 distinguished with high accuracy active TB from LTBI irrespective of HIV
infection and declined during anti-TB chemotherapy. Plasma IP-10 may serve as a diagnostic
biomark | en_US |
dc.identifier.citation | Journal of Infection 70(2015) nr. 4 s. 381-391 | en_US |
dc.identifier.cristinID | FRIDAID 1251308 | |
dc.identifier.doi | 10.1016/j.jinf.2014.12.019 | |
dc.identifier.issn | 0163-4453 | |
dc.identifier.uri | https://hdl.handle.net/10037/8228 | |
dc.identifier.urn | URN:NBN:no-uit_munin_7809 | |
dc.language.iso | eng | en_US |
dc.publisher | Elsevier | en_US |
dc.rights.accessRights | openAccess | |
dc.subject | VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Infeksjonsmedisin: 776 | en_US |
dc.subject | VDP::Medical disciplines: 700::Clinical medical disciplines: 750::Communicable diseases: 776 | en_US |
dc.subject | Cytokines | en_US |
dc.subject | Biomarker | en_US |
dc.subject | IP-10 | en_US |
dc.subject | sTNFr2 | en_US |
dc.subject | Tuberculosis | en_US |
dc.subject | HIV | en_US |
dc.subject | Therapy | en_US |
dc.title | IP-10 differentiates between active and latent tuberculosis irrespective of HIV status and declines during therapy | en_US |
dc.type | Journal article | en_US |
dc.type | Tidsskriftartikkel | en_US |
dc.type | Peer reviewed | en_US |