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Drug-induced liver injury: case reportA 53-year-old woman developed drug-induced liver injury (DILI) during treatment with empagliflozin for type 2 diabetes mellitus (T2DM).The woman, who had T2DM, nonalcoholic fatty liver disease (NAFLD) and hyperlipidaemia, was referred to a gastroenterology clinic due to elevated liver enzymes. Four weeks prior to this presentation, she had started receiving empagliflozin 10mg daily [route not stated] for T2DM. Her concomitant medications included atorvastatin and metformin. It was noted that, one week prior to this presentation (3 weeks after initiation of empagliflozin), elevated liver enzymes were detected (aspartate transaminase 190 IU/L, alanine transaminase 209 IU/L, total bilirubin 0.5 mg/dL, alkaline phosphatase 162 IU/L and international normalised ratio 0.9), indicating a liver injury. Two months prior to this presentation, her liver enzymes were noted to be within the normal limits. At the presentation, her physical examination was found to be normal. Also, the serological markers for acute viral hepatitis were noted to be negative. Ferritin, iron saturation, immunoglobulin and α-1-antitrypsin were found to be within the normal limits, and antibody testing (antimitochondrial antibody, antinuclear antibody and anti-smooth antibody) was also found to be negative. Abdominal CT scan revealed fatty infiltration of the liver. Based on the investigations and clinical presentation, a diagnosis of DILI secondary to empagliflozin was suspected.The woman's therapy with empagliflozin was therefore discontinued. Four weeks after discontinuation of empagliflozin, her laboratory tests showed an improvement in the liver enzymes, which was consistent with the diagnosis of empagliflozin-induced liver injury.
Drug-induced liver injury: case reportA 53-year-old woman developed drug-induced liver injury (DILI) during treatment with empagliflozin for type 2 diabetes mellitus (T2DM).The woman, who had T2DM, nonalcoholic fatty liver disease (NAFLD) and hyperlipidaemia, was referred to a gastroenterology clinic due to elevated liver enzymes. Four weeks prior to this presentation, she had started receiving empagliflozin 10mg daily [route not stated] for T2DM. Her concomitant medications included atorvastatin and metformin. It was noted that, one week prior to this presentation (3 weeks after initiation of empagliflozin), elevated liver enzymes were detected (aspartate transaminase 190 IU/L, alanine transaminase 209 IU/L, total bilirubin 0.5 mg/dL, alkaline phosphatase 162 IU/L and international normalised ratio 0.9), indicating a liver injury. Two months prior to this presentation, her liver enzymes were noted to be within the normal limits. At the presentation, her physical examination was found to be normal. Also, the serological markers for acute viral hepatitis were noted to be negative. Ferritin, iron saturation, immunoglobulin and α-1-antitrypsin were found to be within the normal limits, and antibody testing (antimitochondrial antibody, antinuclear antibody and anti-smooth antibody) was also found to be negative. Abdominal CT scan revealed fatty infiltration of the liver. Based on the investigations and clinical presentation, a diagnosis of DILI secondary to empagliflozin was suspected.The woman's therapy with empagliflozin was therefore discontinued. Four weeks after discontinuation of empagliflozin, her laboratory tests showed an improvement in the liver enzymes, which was consistent with the diagnosis of empagliflozin-induced liver injury.
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