Primary biliary cholangitis associated with drug-induced liver injury and alcoholic liver fibrosis: A case report. Issue 37 (September 2018)

• Record Type: Journal Article
• Authors: Sun, Yu; Shao, Chen; Qu, Hao; Zuo, Gang; Jing, Tao; Wan, Taihu; Ji, Shangwei
• Other Names: NA. section editor.
• Is Part Of: Medicine. Volume 97:Issue 37(2018)
• Publication Date: 2018-09
• Subjects: alcoholic liver fibrosis -- drug-induced liver injury (DILI) -- primary biliary cholangitis (PBC); Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Geneeskunde; Medicine; Periodicals; Periodicals; 610.5
• DOI: 10.1097/MD.0000000000012395
• Languages: English
• ISSNs: 0025-7974

Abstract

Abstract: Rationale: Primary biliary cholangitis (PBC) is a liver autoimmune disease. If this disease is associated with other liver injury factors, both misdiagnosis and missed diagnosis will easily occur. Therefore, detailed disease history collection and related laboratory examination should be performed on patients with liver injury for unidentified causes. When necessary, liver biopsy should be performed to confirm the histopathological diagnosis. Patient concerns: The subject patient was a 63-year-old Chinese male with chronic liver injury who had a drinking history of about 30 years and drank 500 g daily on average and began to take health products and dietary supplements (multivitamins) since June 2014. Diagnoses: Drug-induced liver injury (DILI) and alcoholic fatty liver disease (AFLD) were initially considered because the patient had a history of using health products (HP) and dietary supplements (DS) and drinking alcohol. However, he was subsequently considered with PBC based on the findings of anti-mitochondrial antibody positivity and elevated immunoglobulin level. Obstructive jaundice and space-occupying lesion in the liver were excluded by imaging examinations. Liver biopsy was performed to confirm the reasons for liver injury. Histopathological examination was conducted, and the patient was diagnosed with PBC associated with DILI and alcoholic liver fibrosis. Interventions: Ursodeoxycholic acid, glycyrrhizic acid, and methylprednisolone (small dose) were used to treat the patient. Outcomes: After 2 months, the serum levels of ALT, AST, AKP, GGT, and globulin returned to normal. After 4 months, the patient showed liver injury once again (an increase in ALT, AST, AKP, GGT and GLB) caused by repaglinide administration due to hyperglycemia. Ursodeoxycholic acid and methylprednisolone replaced the repaglinide administration. After 3 weeks, the levels of ALT, AST, AKP, GGT, and GLB returned to normal again. Lessons: The correct knowledge on PBC and early-stage recognition and diagnosis should be emphasized. When other causes of the liver injury cannot be excluded, liver biopsy is suggested. Histopathological change can be used to further clarify the reasons for liver injury and the principal contradiction as well as to guide the theraputic regimen.