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Long-term luseogliflozin therapy improves histological activity of non-alcoholic steatohepatitis accompanied by type 2 diabetes mellitus

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Abstract

A 60-year-old Japanese woman was referred to our hospital for further examination of persistent liver dysfunction. She had been suffering from type 2 diabetes mellitus since the age of 50 years. Her hemoglobin A1c (HbA1c) value was as high as 7.8% despite treatment with dipeptidyl peptidase-4 inhibitor, metformin, and sulfonylurea. After excluding viral hepatitis, alcohol or drug-induced liver injury, and autoimmune liver diseases, liver histology evidence of macrovesicular steatosis, hepatocyte ballooning, and pericellular fibrosis confirmed a diagnosis of non-alcoholic steatohepatitis (NASH). Luseogliflozin (2.5 mg/day), a sodium–glucose cotransporter 2 inhibitor (SGLT2I), was co-administered to strengthen glycemic control. Liver enzymes and HbA1c gradually improved without any adverse events. A second liver biopsy at 15 months after luseogliflozin commencement revealed improvements in steatosis, fibrosis, and overall histological activity score. This case demonstrates that long-term luseogliflozin may be a good therapeutic option for diabetic NAFLD/NASH patients. The merits of persistent SGLT2I administration for NAFLD/NASH patients warrant validation in future studies.

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Acknowledgements

We appreciate Mr. Trevor Ralph for his English editorial assistance and Mr. Yukihiro Mizusawa and Ms. Yukari Mashimo (Asama Nanroku Komoro Medical Center) for their invaluable instruction of ultrasonography imaging.

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Correspondence to Naoki Tanaka.

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Conflict of interest

Fujimori N, Kimura T, and Tanaka N received a research grant from Taisho Pharmaceutical Co., Ltd. Tanaka N received lecture fees from Taisho Pharmaceutical Co., Ltd.

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Fujimori, N., Tanaka, N., Kimura, T. et al. Long-term luseogliflozin therapy improves histological activity of non-alcoholic steatohepatitis accompanied by type 2 diabetes mellitus. Clin J Gastroenterol 13, 83–89 (2020). https://doi.org/10.1007/s12328-019-01018-1

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