Introduction
Runzaozhiyang capsules (RZZYC) are commonly used over-the-counter Chinese patent medicines containing Polygonum multiflorum (PM), which have been approved for the urticaria. RZZYC are generally well tolerated and, liver injury associated with its use has not been previously described. A 25-year-old female patient was initially referred to our service due to urticaria, and she was started on levocetirizine (LCZ) oral solution, compound glycyrrhizin (CG) and RZZYC. Hepatic enzymes were normal at that time and there was no prior history of hepatic disease. At two weeks, she had jaundice, generalized rash, pruritus and fatigue. Laboratory investigation revealed aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (T-BILI) and bile acid (BA) were increased to 46 U/L, 80 U/L, 10.12 mg/dL and 197.9 μmol/L, respectively. Hepatitis A, B, and C, CMV, EBV and HSV serologies were all negative. Serum anti-mitochondrial antibody, anti-smooth muscle antibody, anti-nuclear antibody, antidsDNA antibody, anti-neutrophil cytoplasm antibody and anti-liver kidney microsome antibody were all negative. Serum ceruloplasmin, laminin, hyaluronic acid and collagen type IV concentrations were within normal limits. Ferritin, complement C3 and C4 concentrations slightly exceeded normal concentrations. An abdominal CT and cardiac uhrasonography were unremarkable. RZZYC was discontinued on the first day on admission, her rash and pruritus improved and serum transaminase was normalized after one week of treatment. Her bilirubin recovered slowly and jaundice was still apparent, and BA was higher than that on the first day of admission. She was started on dexamethasone (10 mg, qd) from day 9 to 10, and dexamethasone was subsequent tapered over the course of her hospital stay as her clinical condition was improved and she was discharged on day 20. A liver biopsy was performed on day 16, which revealed cholestasis with mild hepatic cell watery degeneration and mild portal inflammation. (Figure 1). She continued on outpatient medications, after four-month follow-up, all liver tests were returned to normal (Table 1). She restarted LCZ oral solution and had normal serum transaminase and bilirubin through six months of follow-up.
Discussion
Based on the patient’s medication history, RZZYC-induced liver injury was considered, which belonged to the category of herb-induced liver injury (HILI) [1]. Laboratory tests fail to meet diagnostic criteria for HILI in our patient, though liver biopsy suggested that the clinical presentations of liver injury is cholestatic injury. The reported special clinical types that could not be confirmed by liver function index were excluded [2]. The reason for the special clinical phenotype may be related to the improvement of liver function index by CG [3], and the genetic differences of body factors, especially immune-related factors. In the presence of liver protectors, RZZYC still caused severe liver damage, suggesting that RZZYC has a strong ability to damage liver. We were unable to locate articles and clinical etiology attributing acute liver injury to RZZYC. The underlying mechanisms of RZZYC-associated acute liver injury with special clinical phenotype are unknown.
Controversial glucocorticoid treatment is empirically used by clinicians to treat hepatic injury, but it has not demonstrated benefits in survival in patients with specific clinical types of drug-induced liver injury [4,5], and it can also increase mortality in patients with poor liver function [6]. Our case showed that glucocorticoid therapy was effective for acute liver injury with special clinical phenotype, but there is still a lack of randomized controlled studies of glucocorticoid therapy in liver injury[6]. Glucocorticoids are not recommended for the treatment of hepatic injury in the absence of clear clinical indications.
Conflict of interest
No potential conflict of interest was reported by the author(s).