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Article: Glycogenic hepatopathy as an unusual etiology of deranged liver function in a patient with type 1 diabetes: A case report

TitleGlycogenic hepatopathy as an unusual etiology of deranged liver function in a patient with type 1 diabetes: A case report
Authors
Keywordsdiabetes mellitus type 1
glycogenic hepatopathy
liver function tests
non-alcoholic fatty liver disease
Issue Date2019
PublisherLippincott, Williams & Wilkins: Various Creative Commons. The Journal's web site is located at http://journals.lww.com/md-journal/pages/default.aspx
Citation
Medicine, 2019, v. 98 n. 17, p. article no. e15296 How to Cite?
AbstractRATIONALE: Deranged liver function is a common finding among patients with diabetes mellitus. We report a case of liver biopsy-proven glycogenic hepatopathy (GH) in a patient with long-standing poorly controlled type 1 diabetes (DM1), presented with recurrent transaminitis. PATIENT CONCERNS: A 28-year-old Chinese woman was noted to have deranged liver function with transaminases elevated to more than 15 times the upper limit of normal. DIAGNOSIS: She had underlying long-standing poorly controlled DM1. Blood tests including hepatitis serology and autoimmune panel were negative. Liver biopsy confirmed the diagnosis of GH, showing an increase in glycogen deposition with intact liver parenchymal architecture, and no inflammation or significant fibrosis. INTERVENTIONS: Her glycemic control was optimized. OUTCOMES: Her transaminase levels normalized upon subsequent follow-up with improved glycemic control. LESSONS: GH is suspected when transaminase flare occurs in patients with poorly controlled DM1, usually with exaggerated hemoglobin A1c levels, especially after drug-induced, viral, autoimmune and metabolic liver diseases are excluded. The gold standard of diagnosis is liver biopsy. When diagnosis of GH is ascertained, the mainstay of treatment is to optimize glycemic control. Typically, the transaminases may become normal within days to months after improvement of glycemic control. Compared to non-alcoholic fatty liver disease, GH is associated with favorable prognosis and runs a benign course, making this differentiation clinically important. Abbreviations: ALT = alanine aminotransferase, AST = aspartate aminotransferase, DM1 = type 1 diabetes, GH = glycogenichepatopathy, HbA1c = haemoglobin A1c, NAFLD = non-alcoholic fatty liver disease, NR = normal range, ULN = upper limit of normal.
Persistent Identifierhttp://hdl.handle.net/10722/273933
ISSN
2019 Impact Factor: 1.552
2015 SCImago Journal Rankings: 0.877

 

DC FieldValueLanguage
dc.contributor.authorLui, D-
dc.contributor.authorWoo, YC-
dc.contributor.authorChow, WS-
dc.contributor.authorLee, CH-
dc.contributor.authorLee, A-
dc.contributor.authorLeung, E-
dc.contributor.authorTan, K-
dc.contributor.authorLam, K-
dc.contributor.authorLam, J-
dc.date.accessioned2019-08-18T14:51:38Z-
dc.date.available2019-08-18T14:51:38Z-
dc.date.issued2019-
dc.identifier.citationMedicine, 2019, v. 98 n. 17, p. article no. e15296-
dc.identifier.issn0025-7974-
dc.identifier.urihttp://hdl.handle.net/10722/273933-
dc.description.abstractRATIONALE: Deranged liver function is a common finding among patients with diabetes mellitus. We report a case of liver biopsy-proven glycogenic hepatopathy (GH) in a patient with long-standing poorly controlled type 1 diabetes (DM1), presented with recurrent transaminitis. PATIENT CONCERNS: A 28-year-old Chinese woman was noted to have deranged liver function with transaminases elevated to more than 15 times the upper limit of normal. DIAGNOSIS: She had underlying long-standing poorly controlled DM1. Blood tests including hepatitis serology and autoimmune panel were negative. Liver biopsy confirmed the diagnosis of GH, showing an increase in glycogen deposition with intact liver parenchymal architecture, and no inflammation or significant fibrosis. INTERVENTIONS: Her glycemic control was optimized. OUTCOMES: Her transaminase levels normalized upon subsequent follow-up with improved glycemic control. LESSONS: GH is suspected when transaminase flare occurs in patients with poorly controlled DM1, usually with exaggerated hemoglobin A1c levels, especially after drug-induced, viral, autoimmune and metabolic liver diseases are excluded. The gold standard of diagnosis is liver biopsy. When diagnosis of GH is ascertained, the mainstay of treatment is to optimize glycemic control. Typically, the transaminases may become normal within days to months after improvement of glycemic control. Compared to non-alcoholic fatty liver disease, GH is associated with favorable prognosis and runs a benign course, making this differentiation clinically important. Abbreviations: ALT = alanine aminotransferase, AST = aspartate aminotransferase, DM1 = type 1 diabetes, GH = glycogenichepatopathy, HbA1c = haemoglobin A1c, NAFLD = non-alcoholic fatty liver disease, NR = normal range, ULN = upper limit of normal.-
dc.languageeng-
dc.publisherLippincott, Williams & Wilkins: Various Creative Commons. The Journal's web site is located at http://journals.lww.com/md-journal/pages/default.aspx-
dc.relation.ispartofMedicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectdiabetes mellitus type 1-
dc.subjectglycogenic hepatopathy-
dc.subjectliver function tests-
dc.subjectnon-alcoholic fatty liver disease-
dc.titleGlycogenic hepatopathy as an unusual etiology of deranged liver function in a patient with type 1 diabetes: A case report-
dc.typeArticle-
dc.identifier.emailWoo, YC: wooyucho@hku.hk-
dc.identifier.emailChow, WS: chowws01@hkucc.hku.hk-
dc.identifier.emailLee, CH: pchlee@hku.hk-
dc.identifier.emailLee, A: achlee@hku.hk-
dc.identifier.emailTan, K: kcbtan@hkucc.hku.hk-
dc.identifier.emailLam, K: ksllam@hku.hk-
dc.identifier.emailLam, J: lamkyj@hku.hk-
dc.identifier.authorityLee, CH=rp02043-
dc.identifier.authorityTan, K=rp00402-
dc.identifier.authorityLam, K=rp00343-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1097/MD.0000000000015296-
dc.identifier.pmid31027093-
dc.identifier.scopuseid_2-s2.0-85065297693-
dc.identifier.hkuros301836-
dc.identifier.volume98-
dc.identifier.issue17-
dc.identifier.spagearticle no. e15296-
dc.identifier.epagearticle no. e15296-
dc.publisher.placeUnited States-

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