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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003944naa a2200673 4500
001oai:prod.swepub.kib.ki.se:137518012
003SwePub
008240913s2017 | |||||||||||000 ||eng|
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1375180122 URI
024a https://doi.org/10.1183/13993003.01354-20172 DOI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Miotto, P4 aut
2451 0a A standardised method for interpreting the association between mutations and phenotypic drug resistance in Mycobacterium tuberculosis
264 c 2017-12-28
264 1b European Respiratory Society (ERS),c 2017
520 a A clear understanding of the genetic basis of antibiotic resistance inMycobacterium tuberculosisis required to accelerate the development of rapid drug susceptibility testing methods based on genetic sequence.Raw genotype–phenotype correlation data were extracted as part of a comprehensive systematic review to develop a standardised analytical approach for interpreting resistance associated mutations for rifampicin, isoniazid, ofloxacin/levofloxacin, moxifloxacin, amikacin, kanamycin, capreomycin, streptomycin, ethionamide/prothionamide and pyrazinamide. Mutation frequencies in resistant and susceptible isolates were calculated, together with novel statistical measures to classify mutations as high, moderate, minimal or indeterminate confidence for predicting resistance.We identified 286 confidence-graded mutations associated with resistance. Compared to phenotypic methods, sensitivity (95% CI) for rifampicin was 90.3% (89.6–90.9%), while for isoniazid it was 78.2% (77.4–79.0%) and their specificities were 96.3% (95.7–96.8%) and 94.4% (93.1–95.5%), respectively. For second-line drugs, sensitivity varied from 67.4% (64.1–70.6%) for capreomycin to 88.2% (85.1–90.9%) for moxifloxacin, with specificity ranging from 90.0% (87.1–92.5%) for moxifloxacin to 99.5% (99.0–99.8%) for amikacin.This study provides a standardised and comprehensive approach for the interpretation of mutations as predictors ofM. tuberculosisdrug-resistant phenotypes. These data have implications for the clinical interpretation of molecular diagnostics and next-generation sequencing as well as efficient individualised therapy for patients with drug-resistant tuberculosis.
700a Tessema, B4 aut
700a Tagliani, E4 aut
700a Chindelevitch, L4 aut
700a Starks, AM4 aut
700a Emerson, C4 aut
700a Hanna, D4 aut
700a Kim, PS4 aut
700a Liwski, R4 aut
700a Zignol, M4 aut
700a Gilpin, C4 aut
700a Niemann, S4 aut
700a Denkinger, CM4 aut
700a Fleming, J4 aut
700a Warren, RM4 aut
700a Crook, D4 aut
700a Posey, J4 aut
700a Gagneux, S4 aut
700a Hoffner, Su Karolinska Institutet4 aut
700a Rodrigues, C4 aut
700a Comas, I4 aut
700a Engelthaler, DM4 aut
700a Murray, M4 aut
700a Alland, D4 aut
700a Rigouts, L4 aut
700a Lange, Cu Karolinska Institutet4 aut
700a Dheda, K4 aut
700a Hasan, R4 aut
700a Ranganathan, UDK4 aut
700a McNerney, R4 aut
700a Ezewudo, M4 aut
700a Cirillo, DM4 aut
700a Schito, M4 aut
700a Koser, CU4 aut
700a Rodwell, TC4 aut
710a Karolinska Institutet4 org
773t The European respiratory journald : European Respiratory Society (ERS)g 50:6q 50:6x 1399-3003x 0903-1936
856u https://erj.ersjournals.com/content/erj/50/6/1701354.full.pdf
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:137518012
8564 8u https://doi.org/10.1183/13993003.01354-2017

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