Author
Andrew Stolz
Other affiliations: United States Department of Veterans Affairs, University of California, Los Angeles, Icahn School of Medicine at Mount Sinai
Bio: Andrew Stolz is an academic researcher from University of Southern California. The author has contributed to research in topics: Liver injury & Bile acid. The author has an hindex of 36, co-authored 76 publications receiving 3805 citations. Previous affiliations of Andrew Stolz include United States Department of Veterans Affairs & University of California, Los Angeles.
Topics: Liver injury, Bile acid, Liver transplantation, Liver biopsy, Medicine
Papers published on a yearly basis
Papers
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TL;DR: In this article, the authors present characteristics and subgroup analyses from the first 1257 patients enrolled in the study, and conclude that there are no differences in outcomes of patients with short vs long latency of DILI.
576 citations
TL;DR: Liver injury from nonbodybuilding H DS is more severe than from bodybuilding HDS or medications, as evidenced by differences in unfavorable outcomes (death and transplantation).
310 citations
National Institutes of Health1, University of Texas Southwestern Medical Center2, University of Michigan3, Carolinas Medical Center4, University of California, San Francisco5, Thomas Jefferson University6, University of Pennsylvania7, Mayo Clinic8, University of Southern California9, Duke University10
TL;DR: An approach for evaluating liver histology in DILI is described and numerous associations between pathological findings and clinical presentations are demonstrated that may serve as a foundation for future studies correlating D ILI pathology with its causality and outcome.
292 citations
TL;DR: Drug-induced injury to the liver can mimic any form of acute or chronic liver disease and agents such as estrogens, chlorpromazine, and monohydroxy bile acids alter the chemical and physical properties of membranes, leading to impaired activity of carriers and pumps for bile acid and electrolytes.
Abstract: Drug-induced injury to the liver can mimic any form of acute or chronic liver disease. Acute injury to the liver frequently is due to the action of cytochrome P450, which breaks down drugs into electrophiles or free radicals; these reactive metabolites can covalently bind to protein and unsaturated fatty acids or induce lipid peroxidation, respectively. These events may impair vital functions of the cell, such as maintenance of calcium homeostasis, leading to death; or hypothetically they may elicit a hypersensitivity reaction directed mainly at the liver. Glutathione and tocopherol play critical roles in cellular defense. Cholestatic disease caused by drugs results from a selective disturbance in bile secretion. Agents such as estrogens, chlorpromazine, and monohydroxy bile acids alter the chemical and physical properties of membranes, leading to impaired activity of carriers and pumps for bile acids and electrolytes. Certain drugs produce chronic liver disease that is pathologically identical to chronic active hepatitis, biliary cirrhosis, or alcoholic liver disease.
222 citations
University of Michigan1, University of North Carolina at Chapel Hill2, Duke University3, University of Pennsylvania4, National Institutes of Health5, University of Texas Southwestern Medical Center6, Indiana University – Purdue University Indianapolis7, University of Southern California8, California Pacific Medical Center9, Mayo Clinic10
TL;DR: The profile of liver injury at presentation, initial severity, patient's race, and medical comorbidities are important determinants of the likelihood of death/transplantation or persistent liver injury within 6 months of DILI onset.
183 citations
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TL;DR: The global prevalence of viral hepatitis remains high, while drug-induced liver injury continues to increase as a major cause of acute hepatitis.
1,799 citations
TL;DR: Some possible reasons for the observed differences between the tocopherols (α-, β-, γ-, and δ-) in relation to their interactions with the important chemical species involved in lipid peroxidation, specifically trace metal ions, singlet oxygen, nitrogen oxides, and antioxidant synergists are highlighted.
Abstract: This article is a review of the fundamental chemistry of the tocopherols and tocotrienols relevant to their antioxidant action. Despite the general agreement that α-tocopherol is the most efficient antioxidant and vitamin E homologuein vivo, there was always a considerable discrepancy in its “absolute” and “relative” antioxidant effectivenessin vitro, especially when compared to γ-tocopherol. Many chemical, physical, biochemical, physicochemical, and other factors seem responsible for the observed discrepancy between the relative antioxidant potencies of the tocopherolsin vivo andin vitro. This paper aims at highlighting some possible reasons for the observed differences between the tocopherols (α-, β-, γ-, and δ-) in relation to their interactions with the important chemical species involved in lipid peroxidation, specifically trace metal ions, singlet oxygen, nitrogen oxides, and antioxidant synergists. Although literature reports related to the chemistry of the tocotrienols are quite meager, they also were included in the discussion in virtue of their structural and functional resemblance to the tocopherols.
1,726 citations
TL;DR: It is demonstrated that FXR/BAR is critical for bile acid and lipid homeostasis by virtue of its role as an intracellular bile Acid sensor.
1,613 citations
TL;DR: Maximal therapeutic efficacy in the treatment of castration-resistant prostate cancer will require novel agents capable of inhibiting intracrine steroidogenic pathways within the prostate tumor microenvironment.
Abstract: Therapy for advanced prostate cancer centers on suppressing systemic androgens and blocking activation of the androgen receptor (AR). Despite anorchid serum androgen levels, nearly all patients develop castration-resistant disease. We hypothesized that ongoing steroidogenesis within prostate tumors and the maintenance of intratumoral androgens may contribute to castration-resistant growth. Using mass spectrometry and quantitative reverse transcription-PCR, we evaluated androgen levels and transcripts encoding steroidogenic enzymes in benign prostate tissue, untreated primary prostate cancer, metastases from patients with castration-resistant prostate cancer, and xenografts derived from castration-resistant metastases. Testosterone levels within metastases from anorchid men [0.74 ng/g; 95% confidence interval (95% CI), 0.59-0.89] were significantly higher than levels within primary prostate cancers from untreated eugonadal men (0.23 ng/g; 95% CI, 0.03-0.44; P < 0.0001). Compared with primary prostate tumors, castration-resistant metastases displayed alterations in genes encoding steroidogenic enzymes, including up-regulated expression of FASN, CYP17A1, HSD3B1, HSD17B3, CYP19A1, and UGT2B17 and down-regulated expression of SRD5A2 (P < 0.001 for all). Prostate cancer xenografts derived from castration-resistant tumors maintained similar intratumoral androgen levels when passaged in castrate compared with eugonadal animals. Metastatic prostate cancers from anorchid men express transcripts encoding androgen-synthesizing enzymes and maintain intratumoral androgens at concentrations capable of activating AR target genes and maintaining tumor cell survival. We conclude that intracrine steroidogenesis may permit tumors to circumvent low levels of circulating androgens. Maximal therapeutic efficacy in the treatment of castration-resistant prostate cancer will require novel agents capable of inhibiting intracrine steroidogenic pathways within the prostate tumor microenvironment.
1,341 citations
TL;DR: The role of these four ABC transporter proteins in protecting tissues from a variety of toxicants is discussed and species variations in substrate specificity and tissue distribution of these transporters are addressed since these properties have implications for in vivo models of toxicity used for drug discovery and development.
1,327 citations