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Article: A Suspected Case of Carbon Monoxide Poisoning Consistent with Fentanyl Toxicity.

Brian Lam, K H / Sobolevsky, Tim / Ahrens, Brian / Song, Lu / Metushi, Imir G

The journal of applied laboratory medicine

2023 Volume 8, Issue 2, Page(s) 413–417

MeSH term(s)	Humans ; Carbon Monoxide Poisoning/diagnosis ; Fentanyl/toxicity
Chemical Substances	Fentanyl (UF599785JZ)
Language	English
Publishing date	2023-01-20
Publishing country	England
Document type	Case Reports ; Journal Article
ISSN	2576-9456
ISSN	2576-9456
DOI	10.1093/jalm/jfac140
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Article: A case of false positive opiate immunoassay results from rifampin (rifampicin) treatment.

Lam, K H Brian / Song, Lu / Buggs, Vincent / Vithlani, Gopal / Metushi, Imir G

Practical laboratory medicine

2023 Volume 37, Page(s) e00334

Abstract: The drug screen test on a 12-year-old male patient was positive for opiates by a kinetic interaction of microparticles in solution (KIMS) immunoassay method on the Roche Cobas C502. The positive opiates result was not confirmed by the liquid ... ...

Abstract	The drug screen test on a 12-year-old male patient was positive for opiates by a kinetic interaction of microparticles in solution (KIMS) immunoassay method on the Roche Cobas C502. The positive opiates result was not confirmed by the liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. A chart review revealed that the patient had tuberculosis and was on rifampin. We spiked rifampin into drug-free urine and tested opiates with the Cobas method. Once again, a positive result was obtained. This case showed that rifampin can still cause false positive opiate results measured with the KIMS method. We want to stress the importance of confirming positive screen results by more specific methods such as LC-MS/MS.
Language	English
Publishing date	2023-08-29
Publishing country	Netherlands
Document type	Case Reports
ZDB-ID	2834973-8
ISSN	2352-5517
ISSN	2352-5517
DOI	10.1016/j.plabm.2023.e00334
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Article ; Online: A case of false positive opiate immunoassay results from rifampin (rifampicin) treatment

K.H. Brian Lam / Lu Song / Vincent Buggs / Gopal Vithlani / Imir G. Metushi

Practical Laboratory Medicine, Vol 37, Iss , Pp e00334- (2023)

2023

Abstract	The drug screen test on a 12-year-old male patient was positive for opiates by a kinetic interaction of microparticles in solution (KIMS) immunoassay method on the Roche Cobas C502. The positive opiates result was not confirmed by the liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. A chart review revealed that the patient had tuberculosis and was on rifampin. We spiked rifampin into drug-free urine and tested opiates with the Cobas method. Once again, a positive result was obtained. This case showed that rifampin can still cause false positive opiate results measured with the KIMS method. We want to stress the importance of confirming positive screen results by more specific methods such as LC-MS/MS.
Keywords	Rifampin ; Opiate ; HPLC ; LC-MS/MS ; False-positive ; Medicine (General) ; R5-920 ; Chemistry ; QD1-999
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: U-47700 Reply.

Schneir, Aaron / Metushi, Imir G / Fitzgerald, Robert L

Clinical toxicology (Philadelphia, Pa.)

2016 Volume 55, Issue 1, Page(s) 73

Language	English
Publishing date	2016-10-17
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	204476-6
ISSN	1556-9519 ; 0009-9309 ; 0731-3810 ; 1556-3650
ISSN (online)	1556-9519
ISSN	0009-9309 ; 0731-3810 ; 1556-3650
DOI	10.1080/15563650.2016.1239108
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Article ; Online: Positive Predictive Value of PCP Immunoassay at UC San Diego Health.

Metushi, Imir G / Fitzgerald, Robert / Pesce, Amadeo

Journal of analytical toxicology

2016 Volume 41, Issue 3, Page(s) 258

MeSH term(s)	Immunoassay ; Retrospective Studies ; Street Drugs
Chemical Substances	Street Drugs
Language	English
Publishing date	2016-12-21
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	752391-9
ISSN	1945-2403 ; 0146-4760
ISSN (online)	1945-2403
ISSN	0146-4760
DOI	10.1093/jat/bkw130
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Article ; Online: Mechanism of isoniazid-induced hepatotoxicity: then and now.

Metushi, Imir / Uetrecht, Jack / Phillips, Elizabeth

British journal of clinical pharmacology

2016 Volume 81, Issue 6, Page(s) 1030–1036

Abstract: Isoniazid (INH) remains a mainstay for the treatment of tuberculosis despite the fact that it can cause liver failure. Previous mechanistic hypotheses have classified this type of drug-induced liver injury (DILI) as 'metabolic idiosyncrasy' which was ... ...

Abstract	Isoniazid (INH) remains a mainstay for the treatment of tuberculosis despite the fact that it can cause liver failure. Previous mechanistic hypotheses have classified this type of drug-induced liver injury (DILI) as 'metabolic idiosyncrasy' which was thought not to involve an immune response and was mainly due to the bioactivation of the acetylhydrazine metabolite. However, more recent studies support an alternative hypothesis, specifically, that INH itself is directly bioactivated to a reactive metabolite, which in some patients leads to an immune response and liver injury. Furthermore, there appear to be two phenotypes of INH-induced liver injury. Most cases involve mild liver injury, which resolves with immune tolerance, while other cases appear to have a more severe phenotype that is associated with the production of anti-drug/anti-CYP P450 antibodies and can progress to liver failure.
MeSH term(s)	Antitubercular Agents/adverse effects ; Antitubercular Agents/pharmacokinetics ; Biotransformation ; Chemical and Drug Induced Liver Injury ; Humans ; Isoniazid/adverse effects ; Isoniazid/pharmacokinetics
Chemical Substances	Antitubercular Agents ; Isoniazid (V83O1VOZ8L)
Language	English
Publishing date	2016-02-25
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	188974-6
ISSN	1365-2125 ; 0306-5251 ; 0264-3774
ISSN (online)	1365-2125
ISSN	0306-5251 ; 0264-3774
DOI	10.1111/bcp.12885
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Article ; Online: Lack of liver injury in Wistar rats treated with the combination of isoniazid and rifampicin.

Metushi, Imir G / Uetrecht, Jack

Molecular and cellular biochemistry

2013 Volume 387, Issue 1-2, Page(s) 9–17

Abstract: Isoniazid (INH) can cause serious idiosyncratic liver injury. An animal model would greatly facilitate mechanistic studies, but it is essential that the mechanism in the model be similar to the liver injury that can occur in humans. We attempted to ... ...

Abstract	Isoniazid (INH) can cause serious idiosyncratic liver injury. An animal model would greatly facilitate mechanistic studies, but it is essential that the mechanism in the model be similar to the liver injury that can occur in humans. We attempted to replicate a previous study in which Wistar rats treated with INH and rifampicin (RMP) developed liver injury, which was promising because of its delayed onset similar to the liver injury that can occur in humans. Wistar rats were treated with either a high dose of INH (150 mg/kg/day) or a combination of INH and RMP (75 mg/kg/day and 50 mg/kg/day, respectively) for up to 4 weeks. However, we did not observe any liver injury or evidence of an inflammatory infiltrate as had been reported; rather, we observed an increase in CTLA4-positive cells in the cervical lymph nodes as well as a decrease in serum CXCL1 and MCP-1. In short, we were unable to reproduce a previously reported model of delayed onset INH-induced liver injury in Wistar rats.
MeSH term(s)	Alanine Transaminase/blood ; Animals ; Antitubercular Agents/toxicity ; CTLA-4 Antigen/metabolism ; Chemical and Drug Induced Liver Injury/blood ; Chemical and Drug Induced Liver Injury/enzymology ; Chemical and Drug Induced Liver Injury/immunology ; Chemical and Drug Induced Liver Injury/pathology ; Cytokines/blood ; Drug Therapy, Combination ; Glutamate Dehydrogenase/blood ; Interleukin-2 Receptor alpha Subunit/metabolism ; Isoniazid/toxicity ; Lymph Nodes/immunology ; Male ; Neck ; Rats ; Rats, Wistar ; Rifampin/toxicity ; Succinate Dehydrogenase/blood
Chemical Substances	Antitubercular Agents ; CTLA-4 Antigen ; Ctla4 protein, rat ; Cytokines ; Interleukin-2 Receptor alpha Subunit ; Succinate Dehydrogenase (EC 1.3.99.1) ; Glutamate Dehydrogenase (EC 1.4.1.2) ; Alanine Transaminase (EC 2.6.1.2) ; Isoniazid (V83O1VOZ8L) ; Rifampin (VJT6J7R4TR)
Language	English
Publishing date	2013-10-23
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184833-1
ISSN	1573-4919 ; 0300-8177
ISSN (online)	1573-4919
ISSN	0300-8177
DOI	10.1007/s11010-013-1864-7
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Article ; Online: Isoniazid-induced liver injury and immune response in mice.

Metushi, Imir G / Uetrecht, Jack

Journal of immunotoxicology

2013 Volume 11, Issue 4, Page(s) 383–392

Abstract: Isoniazid (INH) is associated with one of the highest incidences of idiosyncratic drug-induced liver failure of any commonly prescribed drug. The mechanism of this liver injury remains uncertain, and a valid animal model would greatly facilitate ... ...

Abstract	Isoniazid (INH) is associated with one of the highest incidences of idiosyncratic drug-induced liver failure of any commonly prescribed drug. The mechanism of this liver injury remains uncertain, and a valid animal model would greatly facilitate mechanistic studies. Most studies of INH-induced liver toxicity have been acute studies performed in rats with high doses of the drug, and this is very different from the idiosyncratic liver injury that occurs in humans. It has previously been demonstrated that covalent binding of INH in the liver of mice is greater than in rats and more like that in humans. Therefore, mice should be a better species in which to develop an animal model of INH-induced liver injury. Treatment of Cbl-b(-/-) and PD1(-/-) mice, which have impaired immune tolerance, resulted in greater injury than their C57BL/6 background, but not liver failure. This suggested that the injury was mediated by the adaptive immune system; however, Rag(-/-) mice, which do not have competent T- and B-cells, sustained more liver injury than C57BL/6 wild-type mice. This suggested that the adaptive immune system also played a protective role. INH treatment also led to a decrease in the inflammatory cytokines IL-1α and IL-12, which suggests that the drug may have immunosuppressive properties. In short, a mouse model was developed of INH-induced liver injury in which the immune system appears to play a both protective and pathogenic role, but this study was unable to develop a model of INH-induced liver failure.
MeSH term(s)	Adaptive Immunity/drug effects ; Adaptive Immunity/genetics ; Adaptor Proteins, Signal Transducing/genetics ; Animals ; Antitubercular Agents/administration & dosage ; Antitubercular Agents/adverse effects ; Chemical and Drug Induced Liver Injury/immunology ; Disease Models, Animal ; Humans ; Immune Tolerance/drug effects ; Immune Tolerance/genetics ; Immunity, Innate/drug effects ; Immunity, Innate/genetics ; Interleukin-1/metabolism ; Interleukin-12/metabolism ; Isoniazid/administration & dosage ; Isoniazid/adverse effects ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Programmed Cell Death 1 Receptor/genetics ; Proto-Oncogene Proteins c-cbl/genetics ; Rats
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antitubercular Agents ; Cblb protein, mouse ; Interleukin-1 ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Interleukin-12 (187348-17-0) ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27) ; Isoniazid (V83O1VOZ8L)
Language	English
Publishing date	2013-12-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205064-4
ISSN	1547-6901 ; 1547-691X
ISSN (online)	1547-6901
ISSN	1547-691X
DOI	10.3109/1547691X.2013.860644
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Article ; Online: Hepatic effects of aminoglutethimide: a model aromatic amine.

Ng, Winnie / Metushi, Imir G / Uetrecht, Jack

Journal of immunotoxicology

2015 Volume 12, Issue 1, Page(s) 24–32

Abstract: Primary aromatic amine drugs are structural alerts in drug development because of their association with a high incidence of idiosyncratic drug reactions (IDRs). If biomarkers could be found that predict IDR risk, it would have a major impact on drug ... ...

Abstract	Primary aromatic amine drugs are structural alerts in drug development because of their association with a high incidence of idiosyncratic drug reactions (IDRs). If biomarkers could be found that predict IDR risk, it would have a major impact on drug development. Previous attempts to do this through screening of hepatic gene expression profiles in rodents treated with aromatic amine drugs found limited changes. Of the drugs studied, aminoglutethimide (AMG) induced the most changes, and this led to a more comprehensive study of its effects on the liver. Brown Norway rats treated with AMG for up to 14 days showed only a transient elevation of glutamate dehydrogenase. Pathway-specific PCR arrays found few AMG-induced gene changes associated with an immune response and, of these changes, the majority were involved with innate immunity such as Tlr2, Ticam2, CD14, and C3. AMG treatment also led to significant changes in the apoptosis and mitochondrial panel of genes. It was recently found that AMG does induce significant changes in the bone marrow of rats, and agranulocytosis is a common IDR caused by AMG. In contrast, liver injury is not a common IDR associated with AMG. Therefore, the liver may be able to effectively deal with AMG reactive metabolites, and changes observed in this study may be involved in adaptation. Myeloperoxidase is also known to be able to oxidize aromatic amines to reactive metabolites, and these observations suggest that metabolism outside of the liver may be important for the mechanism of aromatic amine-induced IDRs.
MeSH term(s)	3,3'-Diaminobenzidine/chemistry ; Agranulocytosis/chemically induced ; Agranulocytosis/immunology ; Aminoglutethimide/administration & dosage ; Aminoglutethimide/adverse effects ; Aminoglutethimide/chemistry ; Animals ; Apoptosis/drug effects ; Cells, Cultured ; Complement C3/genetics ; Complement C3/metabolism ; Glutamate Dehydrogenase/metabolism ; Humans ; Immunity, Innate/drug effects ; Lipopolysaccharide Receptors/genetics ; Lipopolysaccharide Receptors/metabolism ; Liver/drug effects ; Liver/immunology ; Male ; Mitochondria/genetics ; Mitochondria/metabolism ; Peroxidase/metabolism ; Rats, Inbred Strains ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/metabolism
Chemical Substances	Complement C3 ; Lipopolysaccharide Receptors ; TLR2 protein, human ; Toll-Like Receptor 2 ; Aminoglutethimide (0O54ZQ14I9) ; 3,3'-Diaminobenzidine (2RV4T6KHQI) ; Peroxidase (EC 1.11.1.7) ; Glutamate Dehydrogenase (EC 1.4.1.2)
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205064-4
ISSN	1547-6901 ; 1547-691X
ISSN (online)	1547-6901
ISSN	1547-691X
DOI	10.3109/1547691X.2013.867912
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Article ; Online: Treatment of PD-1(-/-) mice with amodiaquine and anti-CTLA4 leads to liver injury similar to idiosyncratic liver injury in patients.

Metushi, Imir G / Hayes, M Anthony / Uetrecht, Jack

Hepatology (Baltimore, Md.)

2015 Volume 61, Issue 4, Page(s) 1332–1342

Abstract: Unlabelled: The mechanism of idiosyncratic drug-induced liver injury (IDILI) remains poorly understood, to a large degree because of the lack of a valid animal model. Recently, we reported an animal model in which treatment of female C57BL/6 mice with ... ...

Abstract	Unlabelled: The mechanism of idiosyncratic drug-induced liver injury (IDILI) remains poorly understood, to a large degree because of the lack of a valid animal model. Recently, we reported an animal model in which treatment of female C57BL/6 mice with amodiaquine (AQ) resulted in mild liver injury with a delayed onset and resolution despite continued treatment. Such adaptation is a common outcome in the IDILI caused by drugs that can cause liver failure. We had hypothesized that most IDILI is immune-mediated and adaptation represents immune tolerance. In this study we found that AQ treatment of Cbl-b(-/-) and PD-1(-/-) mice, which have impaired immune tolerance, resulted in a slightly greater injury. Cotreatment of C57BL/6 with AQ and anti-CTLA4 also resulted in a greater increase in ALT than treatment with AQ alone; however, these mice also had an increase in T regulatory (Treg) cells and T helper cells expressing PD-1 and CTLA4. The increase in these cells implies the induction of immune tolerance, and the alanine aminotransferase (ALT) activity in these mice returned to normal despite continued treatment. Cotreatment of PD-1(-/-) mice with anti-CTLA4 antibody and AQ resulted in the greatest increase in ALT (200-300 U/L), and necroinflammatory responses characterized by portal infiltration of lymphocytes with interface hepatitis. The lymphocyte infiltration included T and B cells, and the CD8(+) T cells produced perforin and granzyme. In addition, the ALT activity in PD-1(-/-) mice cotreated with anti-CTLA4 antibody and AQ did not return to normal, as it had in other mice. Conclusion: We report here the first animal model of IDILI that is similar to the IDILI that occurs in humans, and it was accomplished by inhibiting immune tolerance.
MeSH term(s)	Amodiaquine/adverse effects ; Animals ; Antibodies/adverse effects ; CTLA-4 Antigen/immunology ; Chemical and Drug Induced Liver Injury/etiology ; Disease Models, Animal ; Female ; Mice ; Mice, Inbred C57BL
Chemical Substances	Antibodies ; CTLA-4 Antigen ; Amodiaquine (220236ED28)
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.27549
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