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).