Table 4.

Preferred documentation as example: clinical characteristics of GC hepatotoxicity.

Characteristics of HILI by GC
Characterization of GC hepatotoxicity as a specific disease entity was feasible and based on high causality levels for GC in 16 patients with liver disease.
Causality for GC was graded highly probable and probable in 4 and 12 patients, respectively.
Among these 16 patients, there was an additional causality for comedicated curcuma graded as possible, for comedicated Lycopodium serratum graded as probable, and for biliary disease graded as possible.
The existence of GC hepatotoxicity has been verified by a positive reexposure test in two patients
Ages of the 16 patients ranged from 32 to 69 years with an average of 54.7 years, and the ratio of females: males was 10: 6.
Comedication with synthetic or herbal drugs and dietary supplements including herbal ones and herbal mixtures was used in the majority of assessable cases.
On average, the patients used 10 mg chelidonine daily with lack of daily overdose in any of the cases.
Treatment duration was 3 weeks to 9 months with an average of 2.4 months.
Latency period until first symptoms was 3 weeks to 4.5 months with an average of 1.7 months, which was considerably shorter than the treatment length.
Jaundice was the most frequently reported symptom, rarely also weakness, anorexia, nausea, vomiting, abdominal pains, dark urine, pale stools, and itching.
High serum activities are found for ALT but not for ALP, suggestive of a hepatocellular type of toxic liver injury in patients with GC hepatotoxicity.
Histology showed predominantly liver cell necrosis and hepatitis.
Outcome was favorable in all 16 patients, with lack of both acute liver failure and requirement of a liver transplant.
In one patient, good prognosis was sustained even after 7 months of continued GC Use despite presence of emerging GC hepatotoxicity.
GC hepatotoxicity usually represents the hepatocellular and idiosyncratic type of liver injury with its metabolic subgroup, characterized as acute clinical course.
The underlying mechanism(s) leading to GC hepatotoxicity as well as possible culprit(s) are still unknown.
In cases of liver disease, causality for GC was verified and creates concern regarding safety of patients and pharmacovigilance considerations.
Due to lack of epidemiologic data, the incidence of GC hepatotoxicity cannot accurately be calculated but appears to be low.

Preferred documentation: The data are based on the cases of 16 patients with GC hepatotoxicity and highly probable or probable causality levels for GC and derived from a previous report (Teschke et al., 2012a). Abbreviations: ALT, alanine aminotransferase; ALP, alkaline phosphatase; GC, Greater Celandine.