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      Dapagliflozin-Induced Acute-on-Chronic Liver Injury

      case-report
      Author(s): , MD, PhD 1 , , MD 2 , , MD 3 , , MD 4 , , MD, MSc 4 ,
      Publication date (Electronic):
      Journal: ACG Case Reports Journal
      Publisher: American College of Gastroenterology

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          Abstract

          Sodium-glucose cotransporter 2 inhibitors are a new class of oral hypoglycemic agents, and thus safety data are limited. We present a 48-year-old woman with type 2 diabetes mellitus and Child’s Class A cirrhosis secondary to nonalcoholic steatohepatitis presenting with jaundice and acute cholestatic liver injury. Other than starting dapagliflozin, she reported no medication changes or supplement use. Before treatment, her total bilirubin was 1.2 mg/dL. On admission, her liver values were elevated and liver biopsy was consistent with drug-induced liver injury. This report raises awareness about the potential hepatotoxic effects of dapagliflozin, particularly in patients with chronic liver disease.

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          Discovery of dapagliflozin: a potent, selective renal sodium-dependent glucose cotransporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes.

          Gang Wu, P P Sher, Wei Meng … (2008)
          The C-aryl glucoside 6 (dapagliflozin) was identified as a potent and selective hSGLT2 inhibitor which reduced blood glucose levels in a dose-dependent manner by as much as 55% in hyperglycemic streptozotocin (STZ) rats. These findings, combined with a favorable ADME profile, have prompted clinical evaluation of dapagliflozin for the treatment of type 2 diabetes.
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            Localizations of Na(+)-D-glucose cotransporters SGLT1 and SGLT2 in human kidney and of SGLT1 in human small intestine, liver, lung, and heart.

            Ivana Vrhovac, Daniela Balen Eror, Dirk Klessen … (2015)
            Novel affinity-purified antibodies against human SGLT1 (hSGLT1) and SGLT2 (hSGLT2) were used to localize hSGLT2 in human kidney and hSGLT1 in human kidney, small intestine, liver, lung, and heart. The renal locations of both transporters largely resembled those in rats and mice; hSGLT2 and SGLT1 were localized to the brush border membrane (BBM) of proximal tubule S1/S2 and S3 segments, respectively. Different to rodents, the renal expression of hSGLT1 was absent in thick ascending limb of Henle (TALH) and macula densa, and the expression of both hSGLTs was sex-independent. In small intestinal enterocytes, hSGLT1 was localized to the BBM and subapical vesicles. Performing double labeling with glucagon-like peptide 1 (GLP-1) or glucose-dependent insulinotropic peptide (GIP), hSGLT1 was localized to GLP-1-secreting L cells and GIP-secreting K cells as has been shown in mice. In liver, hSGLT1 was localized to biliary duct cells as has been shown in rats. In lung, hSGLT1 was localized to alveolar epithelial type 2 cells and to bronchiolar Clara cells. Expression of hSGLT1 in Clara cells was verified by double labeling with the Clara cell secretory protein CC10. Double labeling of human heart with aquaporin 1 immunolocalized the hSGLT1 protein in heart capillaries rather than in previously assumed myocyte sarcolemma. The newly identified locations of hSGLT1 implicate several extra renal functions of this transporter, such as fluid absorption in the lung, energy supply to Clara cells, regulation of enteroendocrine cells secretion, and release of glucose from heart capillaries. These functions may be blocked by reversible SGLT1 inhibitors which are under development.
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              Randomized, Double-Blind, Phase 3 Trial of Triple Therapy With Dapagliflozin Add-on to Saxagliptin Plus Metformin in Type 2 Diabetes.

              Chantal Mathieu, Aurelian Emil Ranetti, Danshi Li … (2015)
              To compare the efficacy and safety of treatment with dapagliflozin versus that with placebo add-on to saxagliptin plus metformin in patients whose type 2 diabetes is inadequately controlled with saxagliptin plus metformin treatment.
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                Author and article information

                Journal
                Journal ID (nlm-ta): ACG Case Rep J
                Journal ID (publisher-id): crj
                Title: ACG Case Reports Journal
                Publisher: American College of Gastroenterology
                ISSN (Electronic): 2326-3253
                Publication date Collection: August 2016
                Publication date (Electronic): 7 December 2016
                Volume: 3
                Issue: 4
                Electronic Location Identifier: e169
                Affiliations
                [1 ]Department of Internal Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL
                [2 ]Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL
                [3 ]Division of Endocrinology, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL
                [4 ]Division of Gastroenterology and Hepatology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL
                Author notes
                Correspondence: Lisa B. VanWagner, Northwestern University, Feinberg School of Medicine, 676 N St. Clair, Suite 1900, Chicago, IL 60611 ( lvw@ 123456northwestern.edu ).
                Article
                Publisher ID: crj.2016.142
                DOI: 10.14309/crj.2016.142
                PMC ID: 5171930
                SO-VID: fe03f873-cb22-4f8a-a1fb-d8f560860b8d
                Copyright © Copyright © Levine et al.
                License:

                This is an open-access article. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

                History
                Date received : 9 September 2015
                Date accepted : 29 February 2016
                Categories
                Subject: Case Report
                Subject: Liver

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