Exploratory Study of Autoantibody Profiling in Drug‐Induced Liver Injury with an Autoimmune Phenotype
Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from de novo autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI‐DILI by profiling serum autoantibodies. Autoantibod...
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| Published in | Hepatology communications Vol. 4; no. 11; pp. 1651 - 1663 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Wolters Kluwer Health Medical Research, Lippincott Williams & Wilkins
01.11.2020
John Wiley and Sons Inc Wolters Kluwer Health/LWW |
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| Abstract | Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from de novo autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI‐DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI‐DILI (n = 65), DILI controls (n = 67), de novo AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI‐DILI, samples were also collected 6 months after presentation. AI‐DILI and de novo AIH had similar anti‐neutrophil antibody and anti‐smooth muscle antibody prevalence. Compared to HCs, de novo AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI‐DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing de novo AIH to AI‐DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in de novo AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI‐DILI and de novo AIH were common; however, AI‐DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin‐related AI‐DILI showing a higher number of increased IgM autoantibodies. AI‐DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79‐0.95) to distinguish de novo AIH from AI‐DILI. Conclusion: The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI‐DILI from de novo AIH. |
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| AbstractList | Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from
de novo
autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI‐DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI‐DILI (n = 65), DILI controls (n = 67),
de novo
AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI‐DILI, samples were also collected 6 months after presentation. AI‐DILI and
de novo
AIH had similar anti‐neutrophil antibody and anti‐smooth muscle antibody prevalence. Compared to HCs,
de novo
AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI‐DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing
de novo
AIH to AI‐DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in
de novo
AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI‐DILI and
de novo
AIH were common; however, AI‐DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin‐related AI‐DILI showing a higher number of increased IgM autoantibodies. AI‐DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79‐0.95) to distinguish
de novo
AIH from AI‐DILI.
Conclusion:
The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI‐DILI from
de novo
AIH. Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from de novo autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI‐DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI‐DILI (n = 65), DILI controls (n = 67), de novo AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI‐DILI, samples were also collected 6 months after presentation. AI‐DILI and de novo AIH had similar anti‐neutrophil antibody and anti‐smooth muscle antibody prevalence. Compared to HCs, de novo AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI‐DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing de novo AIH to AI‐DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in de novo AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI‐DILI and de novo AIH were common; however, AI‐DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin‐related AI‐DILI showing a higher number of increased IgM autoantibodies. AI‐DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79‐0.95) to distinguish de novo AIH from AI‐DILI. Conclusion: The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI‐DILI from de novo AIH. Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from de novo autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI‐DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI‐DILI (n = 65), DILI controls (n = 67), de novo AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI‐DILI, samples were also collected 6 months after presentation. AI‐DILI and de novo AIH had similar anti‐neutrophil antibody and anti‐smooth muscle antibody prevalence. Compared to HCs, de novo AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI‐DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing de novo AIH to AI‐DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in de novo AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI‐DILI and de novo AIH were common; however, AI‐DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin‐related AI‐DILI showing a higher number of increased IgM autoantibodies. AI‐DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79‐0.95) to distinguish de novo AIH from AI‐DILI. Conclusion: The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI‐DILI from de novo AIH. Drug-induced liver injury (DILI) sometimes presents with an autoimmune hepatitis-like phenotype (AI-DILI), and it is challenging to distinguish it from autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI-DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI-DILI (n = 65), DILI controls (n = 67), AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI-DILI, samples were also collected 6 months after presentation. AI-DILI and AIH had similar anti-neutrophil antibody and anti-smooth muscle antibody prevalence. Compared to HCs, AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI-DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing AIH to AI-DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI-DILI and AIH were common; however, AI-DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin-related AI-DILI showing a higher number of increased IgM autoantibodies. AI-DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79-0.95) to distinguish AIH from AI-DILI. The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI-DILI from AIH. Drug-induced liver injury (DILI) sometimes presents with an autoimmune hepatitis-like phenotype (AI-DILI), and it is challenging to distinguish it from de novo autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI-DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI-DILI (n = 65), DILI controls (n = 67), de novo AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI-DILI, samples were also collected 6 months after presentation. AI-DILI and de novo AIH had similar anti-neutrophil antibody and anti-smooth muscle antibody prevalence. Compared to HCs, de novo AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI-DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing de novo AIH to AI-DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in de novo AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI-DILI and de novo AIH were common; however, AI-DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin-related AI-DILI showing a higher number of increased IgM autoantibodies. AI-DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79-0.95) to distinguish de novo AIH from AI-DILI. Conclusion: The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI-DILI from de novo AIH.Drug-induced liver injury (DILI) sometimes presents with an autoimmune hepatitis-like phenotype (AI-DILI), and it is challenging to distinguish it from de novo autoimmune hepatitis (AIH). We conducted a study to identify autoantibodies unique to AI-DILI by profiling serum autoantibodies. Autoantibodies were quantified using an autoantigen array containing 94 autoantigens from four groups: AI-DILI (n = 65), DILI controls (n = 67), de novo AIH (n = 17), and healthy controls (HCs; n = 30). In 37 patients with AI-DILI, samples were also collected 6 months after presentation. AI-DILI and de novo AIH had similar anti-neutrophil antibody and anti-smooth muscle antibody prevalence. Compared to HCs, de novo AIH had an increase in many immunoglobulin G (IgG; 35 [46.1%]) and IgM (51 [70%]) autoantibodies, whereas AI-DILI had an increase of IgM (40 [54.8%]) but not IgG autoantibodies. DILI controls had a similar IgG and IgM profile compared to HCs. Comparing de novo AIH to AI-DILI identified 18 (23.7%) elevated IgG but only one (1.4%) IgM autoantibodies, indicating the unique IgG autoantibody profile in de novo AIH. Compared to DILI and HCs, increased IgM autoantibodies in AI-DILI and de novo AIH were common; however, AI-DILI induced by different drugs showed different frequencies of IgM autoantibodies, with nitrofurantoin-related AI-DILI showing a higher number of increased IgM autoantibodies. AI-DILI autoantibody levels at diagnosis and at 6 months showed a significant decline in 37 IgM autoantibodies. A model with highly correlated IgG and IgM was fitted into multivariate logistic regression and revealed an area under the curve of 0.87 (95% confidence interval, 0.79-0.95) to distinguish de novo AIH from AI-DILI. Conclusion: The unique IgG and IgM autoantibody signature appears to be a promising biomarker for distinguishing AI-DILI from de novo AIH. |
| Author | Zhu, Chengsong Lammert, Craig Chalasani, Naga Raman, Indu Eckert, George Li, Quan‐Zhen Lian, Yun |
| AuthorAffiliation | 1 Department of Medicine Indiana University School of Medicine Indianapolis IN USA 2 Department of Immunology and Internal Medicine Genomics and Microarray Core University of Texas Southwestern Dallas TX USA |
| AuthorAffiliation_xml | – name: 2 Department of Immunology and Internal Medicine Genomics and Microarray Core University of Texas Southwestern Dallas TX USA – name: 1 Department of Medicine Indiana University School of Medicine Indianapolis IN USA |
| Author_xml | – sequence: 1 givenname: Craig orcidid: 0000-0003-3809-640X surname: Lammert fullname: Lammert, Craig organization: Indiana University School of Medicine – sequence: 2 givenname: Chengsong surname: Zhu fullname: Zhu, Chengsong organization: University of Texas Southwestern – sequence: 3 givenname: Yun surname: Lian fullname: Lian, Yun organization: University of Texas Southwestern – sequence: 4 givenname: Indu surname: Raman fullname: Raman, Indu organization: University of Texas Southwestern – sequence: 5 givenname: George surname: Eckert fullname: Eckert, George organization: Indiana University School of Medicine – sequence: 6 givenname: Quan‐Zhen surname: Li fullname: Li, Quan‐Zhen email: Quan.li@utsouthwestern.edu organization: University of Texas Southwestern – sequence: 7 givenname: Naga orcidid: 0000-0003-4082-3178 surname: Chalasani fullname: Chalasani, Naga email: nchalasa@iu.edu organization: Indiana University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33163835$$D View this record in MEDLINE/PubMed |
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| Copyright | 2020 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of the American Association for the Study of Liver Diseases. 2020. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Notes | These authors contributed equally to this work. Potential conflict of interest: Dr. Chalasani consults for NuSirt, AbbVie, Allergan, Madrigal, Genentech, Foresite, Galectin, and Zydus; he has received grant support from Intercept and Exact Sciences. The other authors have nothing to report. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| Snippet | Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from de novo... Drug‐induced liver injury (DILI) sometimes presents with an autoimmune hepatitis‐like phenotype (AI‐DILI), and it is challenging to distinguish it from de novo... Drug-induced liver injury (DILI) sometimes presents with an autoimmune hepatitis-like phenotype (AI-DILI), and it is challenging to distinguish it from... Drug-induced liver injury (DILI) sometimes presents with an autoimmune hepatitis-like phenotype (AI-DILI), and it is challenging to distinguish it from de novo... |
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| SubjectTerms | Antibiotics Antibodies Antigens Biomarkers Causality Hepatitis Immunoglobulins Laboratories Liver Lupus Neutrophils Noise Original Phosphatase Principal components analysis Rheumatoid arthritis Smooth muscle Statistical analysis |
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| Title | Exploratory Study of Autoantibody Profiling in Drug‐Induced Liver Injury with an Autoimmune Phenotype |
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