dc.contributor.author |
Wadelius, Mia |
dc.contributor.author |
Eriksson, Niclas |
dc.contributor.author |
Kreutz, Reinhold |
dc.contributor.author |
Bondon-Guitton, Emmanuelle |
dc.contributor.author |
Ibáñez, Luisa |
dc.contributor.author |
Carvajal, Alfonso |
dc.contributor.author |
Lucena, M. Isabel |
dc.contributor.author |
Sancho Ponce, Esther |
dc.contributor.author |
Molokhia, Mariam |
dc.contributor.author |
Martin Martinez, Javier |
dc.contributor.author |
Axelsson, Tomas |
dc.contributor.author |
Kohnke, Hugo |
dc.contributor.author |
Yue, Qun-Ying |
dc.contributor.author |
Magnusson, Patrik K. E. |
dc.contributor.author |
Bengtsson, Mats |
dc.contributor.author |
Hallberg, Pär |
dc.contributor.author |
Universitat Autònoma de Barcelona |
dc.date |
2018 |
dc.identifier |
https://ddd.uab.cat/record/190166 |
dc.identifier |
urn:10.1002/cpt.805 |
dc.identifier |
urn:oai:ddd.uab.cat:190166 |
dc.identifier |
urn:pmid:28762467 |
dc.identifier |
urn:pmcid:PMC5947520 |
dc.identifier |
urn:pmc-uid:5947520 |
dc.identifier |
urn:articleid:15326535v103n5p843 |
dc.identifier |
urn:scopus_id:85030456898 |
dc.identifier |
urn:wos_id:000430118300025 |
dc.identifier |
urn:altmetric_id:23342192 |
dc.identifier |
urn:recercauab:ARE-90572 |
dc.identifier |
urn:oai:egreta.uab.cat:publications/fc6fe707-84d4-4033-908d-21c37b4c3b3e |
dc.identifier |
urn:oai:pubmedcentral.nih.gov:5947520 |
dc.format |
application/pdf |
dc.language |
eng |
dc.publisher |
|
dc.relation |
Instituto de Salud Carlos III FIS10-02632 |
dc.relation |
Instituto de Salud Carlos III FIS12-00378 |
dc.relation |
Clinical Pharmacology and Therapeutics ; Vol. 103, núm. 5 (May 2018), p. 843-853 |
dc.rights |
open access |
dc.rights |
Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, sempre que no sigui amb finalitats comercials, i sempre que es reconegui l'autoria de l'obra original. |
dc.rights |
https://creativecommons.org/licenses/by-nc/4.0/ |
dc.title |
Sulfasalazine-induced agranulocytosis is associated with the human leukocyte antigen locus |
dc.type |
Article |
dc.description.abstract |
Agranulocytosis is a serious, although rare, adverse reaction to sulfasalazine, which is used to treat inflammatory joint and bowel disease. We performed a genome-wide association study comprising 9,380,034 polymorphisms and 180 HLA alleles in 36 cases of sulfasalazine-induced agranulocytosis and 5,170 population controls. Sulfasalazine-induced agranulocytosis was significantly associated with the HLA region on chromosome 6. The top hit (rs9266634) was located close to HLA-B, odds ratio (OR) 5.36 (95% confidence interval (CI) (2.97, 9.69) P = 2.55 × 10 −8). We HLA-sequenced a second cohort consisting of 40 cases and 142 treated controls, and confirmed significant associations with HLA-B*08:01, OR = 2.25 (95% CI (1.02, 4.97) P = 0.0439), in particular the HLA-B*08:01 haplotype HLA-DQB1*02:01-DRB1*03:01-B*08:01-C*07:01, OR = 3.79 (95% CI (1.63, 8.80) P = 0.0019), and with HLA-A*31:01, OR = 4.81 (95% CI (1.52, 15.26) P = 0.0077). The number needed to test for HLA-B*08:01 and HLA-A*31:01 to avoid one case was estimated to be 1,500. We suggest that intensified monitoring or alternative treatment should be considered for known carriers of HLA-B*08:01 or HLA-A*31:01. |