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Publications (10 of 128) Show all publications
Attelind, S., Eriksson, N., Sundstroem, A., Wadelius, M. & Hallberg, P. (2023). Identification of risk factors for adverse drug reactions in a pharmacovigilance database. Pharmacoepidemiology and Drug Safety, 32(12), 1431-1438
Open this publication in new window or tab >>Identification of risk factors for adverse drug reactions in a pharmacovigilance database
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2023 (English)In: Pharmacoepidemiology and Drug Safety, ISSN 1053-8569, E-ISSN 1099-1557, Vol. 32, no 12, p. 1431-1438Article in journal (Refereed) Published
Abstract [en]

Introduction In addition to identifying new safety signals, pharmacovigilance databases could be used to identify potential risk factors for adverse drug reactions (ADRs).Objective To evaluate whether data mining in a pharmacovigilance database can be used to identify known and possible novel risk factors for ADRs, for use in pharmacovigilance practice.Method Exploratory data mining was performed within the Swedish national database of spontaneously reported ADRs. Bleeding associated with direct oral anticoagulants (DOACs)-rivaroxaban, apixaban, edoxaban, and dabigatran-was used as a test model. We compared demographics, drug treatment, and clinical features between cases with bleeding (N = 965) and controls who had experienced other serious ADRs to DOACs (N = 511). Statistical analysis was performed by unadjusted and age adjusted logistic regression models, and the random forest based machine-learning method Boruta.Results In the logistic regression, 13 factors were significantly more common among cases of bleeding compared with controls. Eleven were labelled or previously proposed risk factors. Cardiac arrhythmia (e.g., atrial fibrillation), hypertension, mental impairment disorders (e.g., dementia), renal and urinary tract procedures, gastrointestinal ulceration and perforation, and interacting drugs remained significant after adjustment for age. In the Boruta analysis, high age, arrhythmia, hypertension, cardiac failure, thromboembolism, and pharmacodynamically interacting drugs had a larger than random association with the outcome. High age, cardiac arrhythmia, hypertension, cardiac failure, and pharmacodynamically interacting drugs had odds ratios for bleeding above one, while thromboembolism had an odds ratio below one.Conclusions We demonstrated that data mining within a pharmacovigilance database identifies known risk factors for DOAC bleeding, and potential risk factors such as dementia and atrial fibrillation. We propose that the method could be used in pharmacovigilance for identification of potential ADR risk factors that merit further evaluation.

Place, publisher, year, edition, pages
John Wiley & Sons, 2023
Keywords
anticoagulant-induced bleedings, direct oral anticoagulants, pharmacovigilance database, risk factors, suspected adverse drug reactions
National Category
Cardiac and Cardiovascular Systems Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-522417 (URN)10.1002/pds.5679 (DOI)001049818600001 ()37580910 (PubMedID)
Funder
Swedish Heart Lung Foundation, 20200777EU, Horizon 2020
Available from: 2024-02-13 Created: 2024-02-13 Last updated: 2024-02-13Bibliographically approved
Ollila, H. M., Sharon, E., Lin, L., Sinnott-Armstrong, N., Ambati, A., Yogeshwar, S. M., . . . Mignot, E. J. (2023). Narcolepsy risk loci outline role of T cell autoimmunity and infectious triggers in narcolepsy. Nature Communications, 14, Article ID 2709.
Open this publication in new window or tab >>Narcolepsy risk loci outline role of T cell autoimmunity and infectious triggers in narcolepsy
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2023 (English)In: Nature Communications, E-ISSN 2041-1723, Vol. 14, article id 2709Article in journal (Refereed) Published
Abstract [en]

Narcolepsy type 1 (NT1) is caused by a loss of hypocretin/orexin transmission. Risk factors include pandemic 2009 H1N1 influenza A infection and immunization with Pandemrix (R). Here, we dissect disease mechanisms and interactions with environmental triggers in a multi-ethnic sample of 6,073 cases and 84,856 controls. We fine-mapped GWAS signals within HLA (DQ0602, DQB1*03:01 and DPB1*04:02) and discovered seven novel associations (CD207, NAB1, IKZF4-ERBB3, CTSC, DENND1B, SIRPG, PRF1). Significant signals at TRA and DQB1*06:02 loci were found in 245 vaccination-related cases, who also shared polygenic risk. T cell receptor associations in NT1 modulated TRAJ*24, TRAJ*28 and TRBV*4-2 chain-usage. Partitioned heritability and immune cell enrichment analyses found genetic signals to be driven by dendritic and helper T cells. Lastly comorbidity analysis using data from FinnGen, suggests shared effects between NT1 and other autoimmune diseases. NT1 genetic variants shape autoimmunity and response to environmental triggers, including influenza A infection and immunization with Pandemrix (R).

Place, publisher, year, edition, pages
Springer Nature, 2023
National Category
Immunology in the medical area Neurosciences
Identifiers
urn:nbn:se:uu:diva-507041 (URN)10.1038/s41467-023-36120-z (DOI)000994445900002 ()37188663 (PubMedID)
Funder
Swedish Medical Products Agency
Available from: 2023-07-04 Created: 2023-07-04 Last updated: 2023-07-04Bibliographically approved
McMillin, G. A., Wadelius, M. & Pratt, V. M. (2022). Chapter 73: Pharmacogenetics (7ed.). In: Rifai, Nader (Ed.), Tietz Textbook of Laboratory Medicine, 7th Edition: . Amsterdam: Elsevier
Open this publication in new window or tab >>Chapter 73: Pharmacogenetics
2022 (English)In: Tietz Textbook of Laboratory Medicine, 7th Edition / [ed] Rifai, Nader, Amsterdam: Elsevier, 2022, 7Chapter in book (Refereed)
Place, publisher, year, edition, pages
Amsterdam: Elsevier, 2022 Edition: 7
Series
 Tietz Textbook of Laboratory Medicine
National Category
Clinical Laboratory Medicine
Research subject
Clinical Pharmacology
Identifiers
urn:nbn:se:uu:diva-462658 (URN)9780323775724 (ISBN)
Available from: 2021-12-29 Created: 2021-12-29 Last updated: 2022-11-01Bibliographically approved
Attelind, S., Hallberg, P., Wadelius, M., Hamberg, A.-K., Siegbahn, A., Granger, C. B., . . . Eriksson, N. (2022). Genetic determinants of apixaban plasma levels and their relationship to bleeding and thromboembolic events. Frontiers in Genetics, 13, Article ID 982955.
Open this publication in new window or tab >>Genetic determinants of apixaban plasma levels and their relationship to bleeding and thromboembolic events
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2022 (English)In: Frontiers in Genetics, E-ISSN 1664-8021, Vol. 13, article id 982955Article in journal (Refereed) Published
Abstract [en]

Apixaban is a direct oral anticoagulant, a factor Xa inhibitor, used for the prevention of ischemic stroke in patients with atrial fibrillation. Despite using recommended dosing a few patients might still experience bleeding or lack of efficacy that might be related to inappropriate drug exposure. We conducted a genome-wide association study using data from 1,325 participants in the pivotal phase three trial of apixaban with the aim to identify genetic factors affecting the pharmacokinetics of apixaban. A candidate gene analysis was also performed for pre-specified variants in ABCB1, ABCG2, CYP3A4, CYP3A5, and SULT1A1, with a subsequent analysis of all available polymorphisms within the candidate genes. Significant findings were further evaluated to assess a potential association with clinical outcome such as bleeding or thromboembolic events. No variant was consistently associated with an altered apixaban exposure on a genome-wide level. The candidate gene analyses showed a statistically significant association with a well-known variant in the drug transporter gene ABCG2 (c.421G > T, rs2231142). Patients carrying this variant had a higher exposure to apixaban [area under the curve (AUC), beta = 151 (95% CI 59-243), p = 0.001]. On average, heterozygotes displayed a 5% increase of AUC and homozygotes a 17% increase of AUC, compared with homozygotes for the wild-type allele. Bleeding or thromboembolic events were not significantly associated with ABCG2 rs2231142. This large genome-wide study demonstrates that genetic variation in the drug transporter gene ABCG2 is associated with the pharmacokinetics of apixaban. However, the influence of this finding on drug exposure was small, and further studies are needed to better understand whether it is of relevance for ischemic and bleeding events.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2022
Keywords
factor Xa inhibitors, apixaban, atrial fibrillation, genome-wide association study, pharmacokinetics, pharmacogenetics, drug-related side effects and adverse reactions
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-486690 (URN)10.3389/fgene.2022.982955 (DOI)000861877900001 ()36186466 (PubMedID)
Funder
Swedish Foundation for Strategic Research, RB13-0197Swedish Heart Lung Foundation, 20200777The Swedish Brain Foundation, FO 2020-0234The Swedish Stroke AssociationErik, Karin och Gösta Selanders Foundation
Available from: 2022-10-17 Created: 2022-10-17 Last updated: 2023-02-23Bibliographically approved
Cavalli, M., Eriksson, N., Karlsson Sundbaum, J., Wallenberg, M., Kohnke, H., Baecklund, E., . . . Wadelius, M. (2022). Genome-wide association study of liver enzyme elevation in an extended cohort of rheumatoid arthritis patients starting low-dose methotrexate. Pharmacogenomics (London), 23(15), 813-820
Open this publication in new window or tab >>Genome-wide association study of liver enzyme elevation in an extended cohort of rheumatoid arthritis patients starting low-dose methotrexate
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2022 (English)In: Pharmacogenomics (London), ISSN 1462-2416, E-ISSN 1744-8042, Vol. 23, no 15, p. 813-820Article in journal (Refereed) Published
Abstract [en]

Aim: A follow-up genome-wide association study (GWAS) in an extended cohort of rheumatoid arthritis (RA) patients starting low-dose methotrexate (MTX) treatment was performed to identify further genetic variants associated with alanine aminotransferase (ALT) elevation. Patients & methods: A GWAS was performed on 346 RA patients. Two outcomes within the first 6 months of MTX treatment were assessed: ALT >1.5-times the upper level of normal (ULN) and maximum level of ALT. Results: SPATA9 (rs72783407) was significantly associated with maximum level of ALT (p = 2.58 x 10(-8)) and PLCG2 (rs60427389) was tentatively associated with ALT >1.5 x ULN. Conclusion: Associations with SNPs in genes related to male fertility (SPATA9) and inflammatory processes (PLCG2) were identified.

Place, publisher, year, edition, pages
Future Medicine Ltd, 2022
Keywords
adverse reactions, drug-related side effects, genome-wide association study, hepatotoxicity, methotrexate, pharmacogenetics, rheumatoid arthritis
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:uu:diva-491220 (URN)10.2217/pgs-2022-0074 (DOI)000850598700001 ()36070248 (PubMedID)
Funder
Swedish Research Council, 521-2011-2440Swedish Research Council, 521-2014-3370Swedish Research Council, 2018-03307Swedish Heart Lung Foundation, 20120557Swedish Heart Lung Foundation, 20140291Swedish Heart Lung Foundation, 20170711
Available from: 2022-12-20 Created: 2022-12-20 Last updated: 2022-12-20Bibliographically approved
Ås, J., Bertulyte, I., Eriksson, N., Magnusson, P. K. E., Wadelius, M. & Hallberg, P. (2022). HLA variants associated with azathioprine-induced pancreatitis in patients with Crohn's disease. Clinical and Translational Science, 15(5), 1249-1256, Article ID 13244.
Open this publication in new window or tab >>HLA variants associated with azathioprine-induced pancreatitis in patients with Crohn's disease
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2022 (English)In: Clinical and Translational Science, ISSN 1752-8054, E-ISSN 1752-8062, Vol. 15, no 5, p. 1249-1256, article id 13244Article in journal (Refereed) Published
Abstract [en]

The immunosuppressant drug azathioprine is associated with a 4% risk of acute pancreatitis in patients with inflammatory bowel disease (IBD). Studies have demonstrated an increased risk in carriers of HLA-DQA1*02:01 and HLA-DRB1*07:01. We investigated whether these human leukocyte antigen (HLA) types were associated with azathioprine-induced pancreatitis also in Swedish patients with IBD, and whether the type of disease affected the association. Nineteen individuals with IBD who developed acute pancreatitis after initiation of azathioprine were genotyped and compared with a population control cohort (n = 4891) and a control group matched for disease (n = 81). HLA-DQA1*02:01 and HLA-DRB1*07:01 were in full linkage disequilibrium, and were significantly associated with acute pancreatitis both when cases were compared with population controls (OR 3.97 [95% CI 1.57-9.97], p = 0.0035) and matched controls (OR 3.55 [95% CI 1.23-10.98], p = 0.0275). In a disease-specific analysis, the correlation was positive in patients with Crohn's disease versus matched controls (OR 9.27 [95% CI 1.86-46.19], p = 0.0066), but not in those with ulcerative colitis versus matched controls (OR 0.69 [95% CI 0.07-6.74], p = 0.749). In patients with Crohn's disease, we estimated the conditional risk of carriers of HLA-DQA1*02:01-HLA-DRB1*07:01 to 7.3%, and the conditional risk of a non-carrier to 2.2%. We conclude that HLA-DQA1*02:01-HLA-DRB1*07:01 is a marker for increased risk of acute pancreatitis in individuals of Swedish genetic origin, treated with azathioprine for Crohn's disease.

Place, publisher, year, edition, pages
John Wiley & SonsWiley, 2022
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:uu:diva-483675 (URN)10.1111/cts.13244 (DOI)000757960600001 ()35120281 (PubMedID)
Funder
Swedish Research Council, 521-2011-2440Swedish Research Council, 521-2014-3370Swedish Research Council, 20170711Swedish Research Council, 2017-00641Swedish Research Council, 2021-00180Swedish Research Council, 2018-05973Swedish Research Council, 2018-03307Swedish Heart Lung Foundation, 20170711Swedish Heart Lung Foundation, 20120557Swedish Heart Lung Foundation, 20140291Knut and Alice Wallenberg Foundation
Available from: 2022-09-01 Created: 2022-09-01 Last updated: 2024-01-15Bibliographically approved
Cooper-DeHoff, R. M., Niemi, M., Ramsey, L. B., Luzum, J. A., Tarkiainen, E. K., Straka, R. J., . . . Voora, D. (2022). The Clinical Pharmacogenetics Implementation Consortium Guideline for SLCO1B1, ABCG2, and CYP2C9 genotypes and Statin-Associated Musculoskeletal Symptoms. Clinical Pharmacology and Therapeutics, 111(5), 1007-1021
Open this publication in new window or tab >>The Clinical Pharmacogenetics Implementation Consortium Guideline for SLCO1B1, ABCG2, and CYP2C9 genotypes and Statin-Associated Musculoskeletal Symptoms
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2022 (English)In: Clinical Pharmacology and Therapeutics, ISSN 0009-9236, E-ISSN 1532-6535, Vol. 111, no 5, p. 1007-1021Article in journal (Refereed) Published
Abstract [en]

Statins reduce cholesterol, prevent cardiovascular disease, and are among the most commonly prescribed medications in the world. Statin-associated musculoskeletal symptoms (SAMS) impact statin adherence and ultimately can impede the long-term effectiveness of statin therapy. There are several identified pharmacogenetic variants that impact statin disposition and adverse events during statin therapy. SLCO1B1 encodes a transporter (SLCO1B1; alternative names include OATP1B1 or OATP-C) that facilitates the hepatic uptake of all statins. ABCG2 encodes an efflux transporter (BCRP) that modulates the absorption and disposition of rosuvastatin. CYP2C9 encodes a phase I drug metabolizing enzyme responsible for the oxidation of some statins. Genetic variation in each of these genes alters systemic exposure to statins (i.e., simvastatin, rosuvastatin, pravastatin, pitavastatin, atorvastatin, fluvastatin, lovastatin), which can increase the risk for SAMS. We summarize the literature supporting these associations and provide therapeutic recommendations for statins based on SLCO1B1, ABCG2, and CYP2C9 genotype with the goal of improving the overall safety, adherence, and effectiveness of statin therapy. This document replaces the 2012 and 2014 Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for SLCO1B1 and simvastatin-induced myopathy.

Place, publisher, year, edition, pages
John Wiley & Sons, 2022
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-485931 (URN)10.1002/cpt.2557 (DOI)000767481000001 ()35152405 (PubMedID)
Funder
EU, European Research Council, 725249
Available from: 2022-10-03 Created: 2022-10-03 Last updated: 2022-10-03Bibliographically approved
Ghouse, J., Ahlberg, G., Andreasen, L., Banasi, K., Brunak, S., Schwinn, M., . . . Olesen, M. S. (2021). Association of Variants Near the Bradykinin Receptor B2 Gene With Angioedema in Patients Taking ACE Inhibitors. Journal of the American College of Cardiology, 78(7), 696-709
Open this publication in new window or tab >>Association of Variants Near the Bradykinin Receptor B2 Gene With Angioedema in Patients Taking ACE Inhibitors
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2021 (English)In: Journal of the American College of Cardiology, ISSN 0735-1097, E-ISSN 1558-3597, Vol. 78, no 7, p. 696-709Article in journal (Refereed) Published
Abstract [en]

BACKGROUND Angioedema is a rare but potentially life-threatening adverse reaction associated with angiotensinconverting enzyme (ACE) inhibitors. Identification of potential genetic factors related to this adverse event may help identify at-risk patients. OBJECTIVES The aim of this study was to identify genetic factors associated with ACE inhibitor-associated angioedema. METHODS A genomewide association study involving patients of European descent, all taking ACE inhibitors, was conducted in a discovery cohort (Copenhagen Hospital Biobank), and associations were confirmed in a replication cohort (Swedegene). Cases were defined as subjects with angioedema events and filled prescriptions for ACE inhibitors #180 days before the events. Control subjects were defined as those with continuous treatment with ACE inhibitors without any history of angioedema. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed for angioedema risk using logistic mixed model regression analysis. Summary statistics from the discovery and replication cohorts were analyzed using a fixed-effects meta-analysis model. RESULTS The discovery cohort consisted of 462 cases and 53,391 ACE inhibitor-treated control subjects. The replication cohort consisted of 142 cases and 1,345 ACE inhibitor-treated control subjects. In the discovery cohort, 1 locus, residing at chromosome 14q32.2, was identified that associated with angioedema at the genomewide significance level of P <5 x 10-8. The lead variant at this locus, rs34485356, is an intergenic variant located 60 kb upstream of BDKRB2 (OR: 1.62; 95% CI: 1.38 to 1.90; P = 4.3 x 10-9). This variant was validated in our replication cohort with a similar direction and effect size (OR: 1.60; 95% CI: 1.13 to 2.25; P = 7.2 x 10-3). We found that carriers of the risk allele had significantly lower systolic (-0.46 mm Hg per T allele; 95% CI:-0.83 to-0.10; P = 0.013) and diastolic (-0.26 mm Hg per T allele; 95% CI:-0.46 to-0.05; P = 0.013) blood pressure. CONCLUSIONS In this genomewide association study involving individuals treated with ACE inhibitors, we found that common variants located in close proximity to the bradykinin receptor B2 gene were associated with increased risk for ACE inhibitor-related angioedema. 

Place, publisher, year, edition, pages
ElsevierElsevier BV, 2021
Keywords
ACE inhibitors, ADR, angioedema, bradykinin, adverse drug&nbsp, reaction, bradykinin&nbsp, receptor B < sub > 2 <, sub >
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:uu:diva-451732 (URN)10.1016/j.jacc.2021.05.054 (DOI)000684836000008 ()34384552 (PubMedID)
Funder
NordForskSwedish Research Council, 521-2011-2440Swedish Research Council, 521-2014-3370Swedish Research Council, 2018-03307Swedish Heart Lung Foundation, 20120557Swedish Heart Lung Foundation, 20140291Swedish Heart Lung Foundation, 20170711Swedish Research Council, 2017-00641
Available from: 2021-08-31 Created: 2021-08-31 Last updated: 2024-01-15Bibliographically approved
Eliasson, E. & Wadelius, M. (2021). Farmakogenomik – individuell anpassning av läkemedel och dos: [Pharmacogenomics - a cornerstone of Precision Medicine. Genomic Medicine Sweden analyses genotypes associated with serious drug toxicity or therapeutic failure]. Läkartidningen, 118, Article ID 20176.
Open this publication in new window or tab >>Farmakogenomik – individuell anpassning av läkemedel och dos: [Pharmacogenomics - a cornerstone of Precision Medicine. Genomic Medicine Sweden analyses genotypes associated with serious drug toxicity or therapeutic failure]
2021 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 118, article id 20176Article, review/survey (Refereed) Published
Abstract [en]

Serious adverse drug reactions, drug intolerance, and lack of effect are major problems in healthcare. Pharmacogenomics is the part of precision medicine that aims to develop predictive risk markers in this respect and establish such testing in clinical practice. The nation-wide project Genomic Medicine Sweden (GMS) is undertaking large-scale sequencing to predict risk of drug toxicity and lack of efficacy in malignant diseases. The aim is to facilitate an improved, individualized treatment with increased patient safety. In addition to accurate genotyping, other technical or infrastructure-related aspects need to be considered for a successful implementation in healthcare, for example electronic accessibility and visibility of pharmacogenomic data of long-standing relevance for an individual's ongoing and future drug treatment.

Place, publisher, year, edition, pages
Läkartidningen Förlag AB, 2021
National Category
Clinical Laboratory Medicine
Identifiers
urn:nbn:se:uu:diva-462624 (URN)33973222 (PubMedID)
Available from: 2021-12-28 Created: 2021-12-28 Last updated: 2023-05-24Bibliographically approved
Nicoletti, P., Devarbhavi, H., Goel, A., Venkatesan, R., Eapen, C. E., Grove, J. I., . . . Aithal, G. P. (2021). Genetic Risk Factors in Drug-Induced Liver Injury Due to Isoniazid-Containing Antituberculosis Drug Regimens. Clinical Pharmacology and Therapeutics, 109(4), 1125-1135
Open this publication in new window or tab >>Genetic Risk Factors in Drug-Induced Liver Injury Due to Isoniazid-Containing Antituberculosis Drug Regimens
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2021 (English)In: Clinical Pharmacology and Therapeutics, ISSN 0009-9236, E-ISSN 1532-6535, Vol. 109, no 4, p. 1125-1135Article in journal (Refereed) Published
Abstract [en]

Drug-induced liver injury (DILI) is a complication of treatment with antituberculosis (TB) drugs, especially in isoniazid (INH)-containing regimens. To investigate genetic risk factors, we performed a genomewide association study (GWAS) involving anti-TB DILI cases (55 Indian and 70 European) and controls (1,199 Indian and 10,397 European). Most cases were treated with a standard anti-TB drug regimen; all received INH. We imputed single nucleotide polymorphism and HLA genotypes and performed trans-ethnic meta-analysis on GWAS and candidate gene genotypes. GWAS found one significant association (rs117491755) in Europeans only. For HLA, HLA-B*52:01 was significant (meta-analysis odds ratio (OR) 2.67, 95% confidence interval (CI) 1.63-4.37, P = 9.4 × 10-5 ). For N-acetyltransferase 2 (NAT2), NAT2*5 frequency was lower in cases (OR 0.69, 95% CI 0.57-0.83, P = 0.01). NAT2*6 and NAT2*7 were more common, with homozygotes for NAT2*6 and/or NAT2*7 enriched among cases (OR 1.89, 95% CI 0.84-4.22, P = 0.004). We conclude HLA genotype makes a small contribution to TB drug-related DILI and that the NAT2 contribution is complex, but consistent with previous reports when differences in the metabolic effect of NAT2*5 compared with those of NAT2*6 and NAT2*7 are considered.

Place, publisher, year, edition, pages
John Wiley & Sons, 2021
National Category
Pharmacology and Toxicology
Research subject
Pharmacology
Identifiers
urn:nbn:se:uu:diva-431942 (URN)10.1002/cpt.2100 (DOI)000595733400001 ()33135175 (PubMedID)
Funder
Swedish Medical Products AgencySwedish Society of Medicine, 2008-21619Swedish Research Council, 521-2011-2440Swedish Research Council, 521-2014-3370Swedish Research Council, 201700641Swedish Heart Lung Foundation, 20120557
Available from: 2021-01-15 Created: 2021-01-15 Last updated: 2023-07-14Bibliographically approved
Projects
Oral anticoagulant pharmacogenetics in clinical practice [2008-05568_VR]; Uppsala UniversityOral anticoagulant pharmacogenetics in clinical practice [2008-07977_VR]; Uppsala UniversityDetection and use of pharmacogenomic biomarkers for personalised treatment [2011-02440_VR]; Uppsala UniversitySwedegene: a national centre for pharmacogenomic studies of adverse drug reactions [2014-03370_VR]; Uppsala UniversityStrategic initiative in pharmacogenetics: from discovery to implementation [2018-03307_VR]; Uppsala UniversityOptimization of novel oral anticoagulant (NOAC) therapy [20200777_HLF]; Uppsala UniversityThe epidemiology, immunology and genetics of adverse reactions to COVID-19 vaccines [2021-05450_VR]; Uppsala University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-6368-2622

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