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      Call for Papers: Current Management of Duodenal Neoplasia

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      About Digestion: 3.0 Impact Factor I 7.9 CiteScore I 0.891 Scimago Journal & Country Rank (SJR)

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      Possible Development of Burn-Out Nonalcoholic Steatohepatitis under Long-Term Steroid Use

      case-report

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A 74-year-old man, who lived alone, was found in an unconscious state in his house by a neighbor after mail accumulated in his mailbox. He had asthma and nephrotic syndrome, which had been treated by prednisolone (10 mg) for more than 10 years, and steroid-induced DM. He had been obese since his 20s and had never drunk or smoked in his life. On arrival, he was obese and in a coma and shock state with respiratory failure. He therefore underwent rapid fluid resuscitation, tracheal intubation, mechanical ventilation, with cardiopressor treatment. Whole body computed tomography revealed atrophic liver and excess visceral fat. The clinical diagnosis was septic shock, acute respiratory failure, renal failure with hyperkalemia, cerebral ischemia, liver cirrhosis, rhabdomyolysis, DM, and upper gastrointestinal bleeding. On day 3, his circulation, respiratory function, and consciousness stabilized, and he was extubated. Further studies led to a diagnosis of burn-out nonalcoholic steatohepatitis (NASH). His condition was complicated by adrenal insufficiency, pulmonary embolism, lower extremity motor weakness, and left leg phlegmon during hospitalization. He was transferred to another hospital for rehabilitation on day 34 after the improvement of phlegmon. The present case showed the potential for NASH to develop in individuals with long-term steroid use. The further accumulation and analysis of cases is required to determine whether this possibility is correct or not.

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          Most cited references29

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          The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD.

          Patients with nonalcoholic fatty liver disease (NAFLD) and advanced liver fibrosis are at the highest risk for progressing to end-stage liver disease. We constructed and validated a scoring system consisting of routinely measured and readily available clinical and laboratory data to separate NAFLD patients with and without advanced fibrosis. A total of 733 patients with NAFLD confirmed by liver biopsy were divided into 2 groups to construct (n = 480) and validate (n = 253) a scoring system. Routine demographic, clinical, and laboratory variables were analyzed by multivariate modeling to predict presence or absence of advanced fibrosis. Age, hyperglycemia, body mass index, platelet count, albumin, and AST/ALT ratio were independent indicators of advanced liver fibrosis. A scoring system with these 6 variables had an area under the receiver operating characteristic curve of 0.88 and 0.82 in the estimation and validation groups, respectively. By applying the low cutoff score (-1.455), advanced fibrosis could be excluded with high accuracy (negative predictive value of 93% and 88% in the estimation and validation groups, respectively). By applying the high cutoff score (0.676), the presence of advanced fibrosis could be diagnosed with high accuracy (positive predictive value of 90% and 82% in the estimation and validation groups, respectively). By applying this model, a liver biopsy would have been avoided in 549 (75%) of the 733 patients, with correct prediction in 496 (90%). a simple scoring system accurately separates patients with NAFLD with and without advanced fibrosis, rendering liver biopsy for identification of advanced fibrosis unnecessary in a substantial proportion of patients.
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            Genetics and epigenetics of NAFLD and NASH: Clinical impact.

            Non-alcoholic fatty liver disease (NAFLD) is now recognised as the most common liver disease worldwide. It encompasses a broad spectrum of conditions, from simple steatosis, through non-alcoholic steatohepatitis, to fibrosis and ultimately cirrhosis and hepatocellular carcinoma. A hallmark of NAFLD is the substantial inter-patient variation in disease progression. NAFLD is considered a complex disease trait such that interactions between the environment and a susceptible polygenic host background determine disease phenotype and influence progression. Recent years have witnessed multiple genome-wide association and large candidate gene studies, which have enriched our understanding of the genetic basis of NAFLD. Notably, the I148M PNPLA3 variant has been identified as the major common genetic determinant of NAFLD. Variants with moderate effect size in TM6SF2, MBOAT7 and GCKR have also been shown to have a significant contribution. The premise for this review is to discuss the status of research into important genetic and epigenetic modifiers of NAFLD progression. The potential to translate the accumulating wealth of genetic data into the design of novel therapeutics and the clinical implementation of diagnostic/prognostic biomarkers will be explored. Finally, personalised medicine and the opportunities for future research and challenges in the immediate post genetics era will be illustrated and discussed.
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              11β-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess.

              The adverse metabolic effects of prescribed and endogenous glucocorticoid (GC) excess, Cushing syndrome, create a significant health burden. We found that tissue regeneration of GCs by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), rather than circulating delivery, is critical to developing the phenotype of GC excess; 11β-HSD1 KO mice with circulating GC excess are protected from the glucose intolerance, hyperinsulinemia, hepatic steatosis, adiposity, hypertension, myopathy, and dermal atrophy of Cushing syndrome. Whereas liver-specific 11β-HSD1 KO mice developed a full Cushingoid phenotype, adipose-specific 11β-HSD1 KO mice were protected from hepatic steatosis and circulating fatty acid excess. These data challenge our current view of GC action, demonstrating 11β-HSD1, particularly in adipose tissue, is key to the development of the adverse metabolic profile associated with circulating GC excess, offering 11β-HSD1 inhibition as a previously unidentified approach to treat Cushing syndrome.
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                Author and article information

                Journal
                Case Rep Gastroenterol
                Case Rep Gastroenterol
                CRG
                Case Reports in Gastroenterology
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )
                1662-0631
                Sep-Dec 2022
                19 September 2022
                19 September 2022
                : 16
                : 3
                : 557-562
                Affiliations
                Department of Acute Critical Care Medicine, Shizuoka Hospital, Juntendo University, Izunokuni, Japan
                Author notes
                Article
                crg-0016-0557
                10.1159/000526570
                9941765
                ae8a4258-9754-4456-b156-ffcf7aa86b2d
                Copyright © 2022 by The Author(s). Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-4.0 International License (CC BY-NC) (http://www.karger.com/Services/OpenAccessLicense). Usage and distribution for commercial purposes requires written permission.

                History
                : 31 May 2022
                : 5 August 2022
                : 2022
                Page count
                Figures: 1, Tables: 1, References: 15, Pages: 6
                Funding
                This work was supported in part by a Grant-in-Aid for Special Research in Subsidies for ordinary expenses of private schools from The Promotion and Mutual Aid Corporation for Private Schools of Japan. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Case Report

                Gastroenterology & Hepatology
                nonalcoholic steatohepatitis,steroid,complication
                Gastroenterology & Hepatology
                nonalcoholic steatohepatitis, steroid, complication

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