5 research outputs found
Herb-Induced Liver Injury in the Berlin Case-Control Surveillance Study
Herb-induced liver injury (HILI) has recently attracted attention due to
increasing reports of hepatotoxicity associated with use of phytotherapeutics.
Here, we present data on HILI from the Berlin Case-Control Surveillance Study.
The study was initiated in 2000 to investigate the serious toxicity of drugs
including herbal medicines. Potential cases of liver injury were ascertained
in more than 180 Departments of all 51 Berlin hospitals from October 2002 to
December 2011. Drug or herb intake was assessed through a standardized face-
to-face interview. Drug or herbal aetiology was assessed based on the updated
Council for International Organizations of Medical Sciences scale. In ten of
all 198 cases of hepatotoxicity included in the study, herbal aetiology was
assessed as probable (once ayurvedic herb) or possible (Valeriana five times,
Mentha piperita once, Pelargonium sidoides once, Hypericum perforatum once,
Eucalyptus globulus once). Mean age was 56.4 Ā± 9.7 years, and the predominant
pattern of liver injury was hepatocellular. No cases of acute liver failure or
death were observed. This case series corroborates known risks for ayurvedic
herbs, supports the suspected association between Valeriana use and liver
injury, and indicates a hepatotoxic potential for herbs such as Pelargonium
sidoides, Hypericum perforatum or Mentha piperita that were rarely associated
with liver injury before. However, given that possible causality does not
prove clinical significance, further studies in this field are needed
Drugāinduced liver injury: results from the hospitalābased Berlin CaseāControl Surveillance Study
AIM: Drugāinduced liver injury (DILI) is often responsible for acute liver failure, drug withdrawal, boxed warnings or drug nonāapproval. Therefore, we conducted a caseācontrol study to determine the hepatotoxic risk of a wide range of drugs. METHODS: The Berlin CaseāControl Surveillance Study FAKOS included all 51 Berlin hospitals in a hospital network. Between 2002 and 2011, 198 patients with acute idiopathic hepatitis, 377 inpatient controls and 708 outpatient controls were ascertained. Case patients were thoroughly validated using anamnestic, clinical, laboratory and histological data. Drug exposure was obtained in a faceātoāface interview. A possible drug aetiology was assessed in individual patients by applying the updated Council for International Organizations of Medical Sciences (CIOMS) scale. Drug risks were further quantified [odds ratios (OR) with 95% confidence intervals (CI)] in a caseācontrol design with unconditional logistic regression analysis. Drug intake in the last 28 days before index date was considered for the analysis. RESULTS: The study corroborated hepatotoxic risks for a number of drugs, including phenprocoumon (OR 3.3, 95% CI 1.5, 6.7), amiodarone (OR 5.5, 95% CI 1.3, 21.2), clozapine (OR 34.6, 95% CI 2.8, 824.9) and flupirtine (OR 40.2, 95% CI 5.5, 856.9). Increased risks were also suggested for less commonly reported substances such as angiotensin II receptor blockers, atypical antipsychotics and for biperiden, a drug never before reported to be hepatotoxic. CONCLUSIONS: Our study identified a large number of drugs as possible causes of hepatotoxicity. The observed risk for seldom reported substances highlights the need for further postāauthorization safety studies not exclusively focusing on drugs already labelled as potentially hepatotoxic