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FII and Perplexing Presentations: What is the Evidence Base for and against Current Guidelines, and What are the Implications for Social Services?
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      Clinical perspectives of isoniazid-induced liver injury ☆

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          Abstract

          Isoniazid (INH) is a synthetic anti-mycobacterial agent used to treat active or latent tuberculosis (TB). INH has been in clinical use for nearly 70 years and remains broadly utilized at the front line of anti-TB treatment. However, the potential for liver damage and even fulminant liver failure during INH-based TB treatment presents a major challenge for TB control programs worldwide. In this review, we discuss the hepatotoxic effects of INH and provide an overview of the mechanisms and their applications in prediction and prevention of INH hepatotoxicity in clinical practice.

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          Targeted tuberculin testing and treatment of latent tuberculosis infection. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. This is a Joint Statement of the American Thoracic Society (ATS) and the Centers for Disease Control and Prevention (CDC). This statement was endorsed by the Council of the Infectious Diseases Society of America. (IDSA), September 1999, and the sections of this statement.

          (2000)
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            An orphan nuclear receptor activated by pregnanes defines a novel steroid signaling pathway.

            Steven Kliewer, John T. Moore, Laura Wade … (1998)
            Steroid hormones exert profound effects on differentiation, development, and homeostasis in higher eukaryotes through interactions with nuclear receptors. We describe a novel orphan nuclear receptor, termed the pregnane X receptor (PXR), that is activated by naturally occurring steroids such as pregnenolone and progesterone, and synthetic glucocorticoids and antiglucocorticoids. PXR exists as two isoforms, PXR.1 and PXR.2, that are differentially activated by steroids. Notably, PXR.1 is efficaciously activated by pregnenolone 16alpha-carbonitrile, a glucocorticoid receptor antagonist that induces the expression of the CYP3A family of steroid hydroxylases and modulates sterol and bile acid biosynthesis in vivo. Our results provide evidence for the existence of a novel steroid hormone signaling pathway with potential implications in the regulation of steroid hormone and sterol homeostasis.
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              The human orphan nuclear receptor PXR is activated by compounds that regulate CYP3A4 gene expression and cause drug interactions.

              J Lehmann, D D McKee, M Watson … (1998)
              The cytochrome P-450 monooxygenase 3A4 (CYP3A4) is responsible for the oxidative metabolism of a wide variety of xenobiotics including an estimated 60% of all clinically used drugs. Although expression of the CYP3A4 gene is known to be induced in response to a variety of compounds, the mechanism underlying this induction, which represents a basis for drug interactions in patients, has remained unclear. We report the identification of a human (h) orphan nuclear receptor, termed the pregnane X receptor (PXR), that binds to a response element in the CYP3A4 promoter and is activated by a range of drugs known to induce CYP3A4 expression. Comparison of hPXR with the recently cloned mouse PXR reveals marked differences in their activation by certain drugs, which may account in part for the species-specific effects of compounds on CYP3A gene expression. These findings provide a molecular explanation for the ability of disparate chemicals to induce CYP3A4 levels and, furthermore, provide a basis for developing in vitro assays to aid in predicting whether drugs will interact in humans.
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                Author and article information

                Contributors
                Xiaochao Ma
                Journal
                Journal ID (nlm-ta): Liver Res
                Journal ID (iso-abbrev): Liver Res
                Title: Liver Research
                Publisher: Third Affiliated Hospital of Sun Yat-sen University
                ISSN (Print): 2096-2878
                ISSN (Electronic): 2542-5684
                Publication date PMC-release: 11 February 2021
                Publication date Collection: June 2021
                Publication date (Electronic): 11 February 2021
                Volume: 5
                Issue: 2
                Pages: 45-52
                Affiliations
                [1]Center for Pharmacogenetics, Department of Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, Pittsburgh, PA, USA
                Author notes
                [∗ ]Corresponding author. mxiaocha@ 123456pitt.edu
                Article
                Publisher Item ID: S2542-5684(21)00004-0
                DOI: 10.1016/j.livres.2021.02.001
                PMC ID: 11791842
                SO-VID: f342e6aa-5eda-4b29-8c57-280b0ffdab1e
                Copyright © © 2021 The Third Affiliated Hospital of Sun Yat-sen University. Publishing Services by Elsevier B. V. on behalf of KeAi Communications Co., Ltd.
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 2 December 2020
                Date revision received : 10 January 2021
                Date accepted : 5 February 2021
                Categories
                Subject: Review Article

                Keywords: hepatotoxicity,liver injury,isoniazid (inh),tuberculosis (tb)
                Data availability:
                Keywords: hepatotoxicity, liver injury, isoniazid (inh), tuberculosis (tb)

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