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LINKED CONTENT: This article is linked to Kuo et al papers. To view these articles, visit https://doi.org/10.1111/apt.17637 and https://doi.org/10.1111/apt.17677 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Kaur et al papers. To view these articles, visit https://doi.org/10.1111/apt.18202 and https://doi.org/10.1111/apt.18238 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Kuo et al papers. To view these articles, visit https://doi.org/10.1111/apt.17637 and https://doi.org/10.1111/apt.17742 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Idalsoaga et al papers. To view these articles, visit https://doi.org/10.1111/apt.18193 and https://doi.org/10.1111/apt.18220 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Eunice et al papers. To view these articles, visit https://doi.org/10.1111/apt.17914 and https://doi.org/10.1111/apt.17951 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Dominik et al paper. To view this article, visit https://doi.org/10.1111/apt.17945 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Higuchi et al papers. To view these articles, visit https://doi.org/10.1111/apt.16745 and https://doi.org/10.1111/apt.16792 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Thiele et al papers. To view these articles, visit https://doi.org/10.1111/apt.16567 and https://doi.org/10.1111/apt.16633 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Thiele et al papers. To view these articles, visit https://doi.org/10.1111/apt.16567 and https://doi.org/10.1111/apt.16672 [ABSTRACT FROM AUTHOR]

Summary: Background: Direct‐acting anti‐viral therapy (DAA) has transformed hepatitis C virus (HCV) care, particularly in patients with decompensated cirrhosis. However, their impact on hepatocellular carcinoma (HCC) remains unclear. Aim: To use a national registry of patients with advanced liver disease to explore the relationship between DAA therapy and HCC. Methods: All patients with de novo HCC post DAA therapy were frequency matched with patients who did not develop HCC. Demographic, clinical and laboratory data were obtained. Cross‐sectional imaging and multidisciplinary team reports were reviewed for dates of HCC diagnosis and HCC progression. Patients were categorised by treatment outcome and time of HCC development. Data were examined by multivariable analysis and Kaplan‐Meier estimation. Results: Eighty patients with HCC were compared with 165 patients without HCC, treated between June 2014 and September 2015. Mean follow‐up from start of DAA therapy was 32.4 months. Twenty‐eight patients were diagnosed with early HCC (within 6 months of therapy) and 52 presented late. Baseline nonmalignant lesions (HR: 1.99), thrombocytopaenia (HR: 1.59) and diabetes (HR: 1.68) increased likelihood of HCC. Response to therapy was reduced in patients who developed liver cancer (SVR in patients with HCC = 54/80 (68%), SVR in patients without HCC = 143/165 (87%), P < 0.001, OR: 3.13, 95% CI: 1.64‐5.99). We found no difference between tumour size, progression or survival between viraemic and nonviraemic patients. Conclusion: There is no alteration in prognosis or cancer progression following HCC development after HCV treatment. However, baseline nonmalignant liver lesions, diabetes and thrombocytopaenia increase the risk of HCC, and HCC is associated with a decreased SVR rate. Linked Content This article is linked to Hollande and Pol paper. To view this article, visit https://doi.org/10.1111/apt.15328. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Tan et al paper. To view this article, visit https://doi.org/10.1111/apt.17914 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Hey et al paper. To view this article, visit https://doi.org/10.1111/apt.17917 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Tong et al papers. To view these articles, visit https://doi.org/10.1111/apt.17263 and https://doi.org/10.1111/apt.17320 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Tong et al papers. To view these articles, visit https://doi.org/10.1111/apt.17263 and https://doi.org/10.1111/apt.17319 [ABSTRACT FROM AUTHOR]

Linked Content This article is linked to Wong and Coenen et al and Hooymans papers. To view these articles visit https://doi.org/10.1111/apt.13879 and https://doi.org/10.1111/apt.13955. [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Tsung et al paper. To view this article, visit https://doi.org/10.1111/apt.15413. [ABSTRACT FROM AUTHOR]

Linked Content This article is linked to Shen et al and Kim and Kim papers. To view these articles, visit https://doi.org/10.1111/apt.15298 and https://doi.org/10.1111/apt.15364. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Higuchi et al papers. To view these articles, visit https://doi.org/10.1111/apt.16745 and https://doi.org/10.1111/apt.16774 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Lazarus et al papers. To view these articles, visit https://doi.org/10.1111/apt.16720 and https://doi.org/10.1111/apt.16750 [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Lazarus et al papers. To view these articles, visit https://doi.org/10.1111/apt.16720 and https://doi.org/10.1111/apt.16768 [ABSTRACT FROM AUTHOR]

Summary: Background: Epidemiological data suggest that coffee has a dose‐dependent protective effect on liver‐related mortality. Aim: To estimate the potential impact of increased per capita coffee consumption on global liver‐related mortality. Methods: Using the Global Burden of Disease 2016 dataset (adults > 15 years), we modelled the impact of increased per capita coffee consumption on liver‐related mortality in 2016 for 194 countries using published risk ratios for >2 cups coffee/ day (RR 0.54, 95% CI 0.42‐0.69) and ≥4 cups/ day (RR 0.29, 95% CI 0.17‐0.50), adjusted for confounders and tested model assumptions using sensitivity analyses. Results: Worldwide, there were an estimated 1,240,201 (95% CI 118 4300‐1 354 410) adult liver‐related deaths in 2016. Median global liver mortality rate in 2016 was 15 deaths/ 100 000 population/ year (all ages, both genders; IQR 11‐21 deaths per 100 000). If all countries with per capita coffee intake ≤2 cups/ day increased to >2 cups/ day, the predicted total number of liver‐related deaths would have been 630 947 in 2016 (95% CI 629 693‐631 861) with 452 861 (95% CI 451 948‐454 116) deaths averted (PPR 7.8 liver‐related deaths/ 100 000/ year). If per capita consumption was ≥ 4 cups/ day, the predicted number of liver‐related deaths in 2016 would have been 360 523 (95% CI 359 825‐361 992) with 723 287 (95% CI 721 817‐723 984) deaths averted (PPR 12.1 liver‐related deaths/100 000/year). Conclusion: Increasing per capita coffee consumption to > 2 cups per day on a population level has the potential to avert hundreds of thousands of liver‐related deaths annually if the impact of coffee on liver‐related mortality is confirmed in clinical trials. [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Viuff et al paper. To view this article, visit https://doi.org/10.1111/apt.16277 [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Chon et al paper. To view this article, visit https://doi.org/10.1111/apt.16267 [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Ponziani et al paper. To view this article, visit https://doi.org/10.1111/apt.15996 [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Huang et al and Packer and Bangash papers. To view these articles, visit https://doi.org/10.1111/apt.15962 and https://doi.org/10.1111/apt.16014 [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Huang et al papers. To view these articles, visit https://doi.org/10.1111/apt.15962 and https://doi.org/10.1111/apt.16046 [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Mederacke et al and Huang and Chuang papers. To view these articles, visit https://doi.org/10.1111/apt.15722 and https://doi.org/10.1111/apt.15788. [ABSTRACT FROM AUTHOR]

Summary: Background: No prospective diagnostic studies have directly compared widespread non‐invasive liver tests in patients with type 2 diabetes (T2D) using the intention‐to‐diagnose method for each of the three main histological features of metabolic dysfunction associated steatotic liver disease ‐ namely fibrosis, metabolic dysfunction‐associated steatohepatitis (MASH), and steatosis. Aims: To compare the performance of nine tests using the intention‐to‐diagnose rather than the standard method, which would exclude non‐evaluable participants Methods: Biopsy was used as the reference with predetermined cut‐offs, advanced fibrosis being the main endpoint. The Nash‐FibroTest panel including FibroTest‐T2D, SteatoTest‐T2D and MashTest‐T2D was optimised for type 2 diabetes. FibroTest‐T2D was compared to vibration‐controlled transient elastography stiffness (VCTE), two‐dimensional shear‐wave elastography stiffness (TD‐SWE), and Fibrosis‐4 blood test. NashTest‐T2D was compared to aspartate aminotransferase. SteatoTest‐T2D was compared to the controlled attenuation parameter and the hepatorenal gradient. Results: Among 402 cases, non‐evaluable tests were 6.7% for VCTE, 4.0% for hepatorenal gradient, 3.2% for controlled attenuation parameter, 1.5% for TD‐SWE, 1.2% for NashTest‐T2D, and 0.02% for Fibrosis‐4, aspartate aminotransferase and SteatoTest‐T2D. The VCTE AUROC for advanced fibrosis was over‐estimated by 6% (0.83 [95% CI: 0.78–0.87]) by standard analysis compared to intention‐to‐diagnose (0.77 [0.72–0.81] p = 0.008). The AUROCs for advanced fibrosis did not differ significantly in intention‐to‐diagnose between FibroTest‐T2D (0.77; 95% CI: 0.73–0.82), VCTE (0.77; 95% CI: 0.72–0.81) and TD‐SWE(0.78; 0.74–0.83) but were all higher than the Fibrosis‐4 score (0.70; 95% CI all differences ≥7%; p ≤ 0.03). For MASH, MashTest‐T2D had a higher AUROC (0.76; 95% CI: 0.70–0.80) than aspartate aminotransferase (0.72; 95% CI: 0.66–0.77; p = 0.035). For steatosis, AUROCs did not differ significantly between SteatoTest‐T2D, controlled attenuation parameter and hepatorenal gradient. Conclusions: In intention‐to‐diagnose analysis, FibroTest‐T2D, TD‐SWE and VCTE performed similarly for staging fibrosis, and out‐performed Fibrosis‐4 in outpatients with type 2 diabetes. The standard analysis over‐estimated VCTE performance. ClinicalTrial.gov: NCT03634098. [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Shen et al and Dong and Cai papers. To view these articles, visit https://doi.org/10.1111/apt.15298 and https://doi.org/10.1111/apt.15410. [ABSTRACT FROM AUTHOR]

Linked Content This article is linked to Shen et al and Shen and Fan papers. To view these articles, visit https://doi.org/10.1111/apt.15298 and https://doi.org/10.1111/apt.15387. [ABSTRACT FROM AUTHOR]

Linked Content This article is linked to Wong and Coenen et al and Fraser papers. To view these articles visit https://doi.org/10.1111/apt.13879 and https://doi.org/10.1111/apt.13942. [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Shen et al and Shen and Fan papers. To view these articles, visit https://doi.org/10.1111/apt.15298 and https://doi.org/10.1111/apt.15422. [ABSTRACT FROM AUTHOR]

Linked Content This article is linked to Buzzetti et al and Buzzetti and Tsochatzis papers. To view these articles, visit https://doi.org/10.1111/apt.15219 and https://doi.org/10.1111/apt.15385. [ABSTRACT FROM AUTHOR]

Summary: Background: Previous studies suggested increased mortality in patients with hepatorenal syndrome type 1 (HRS1) and advanced acute‐on‐chronic liver failure (ACLF). Aim: To assess mortality and respiratory failure (RF) in patients with HRS1 and ACLF treated with terlipressin. Methods: In the CONFIRM study, we randomised 299 patients with HRS1 2:1 to terlipressin or placebo, both with albumin. At enrolment, all patients were assessed for organ failure (OF) using a validated ACLF grading system. Post hoc analyses assessed the effects of terlipressin vs. placebo on the incidence of RF and 90‐day mortality. Results: The incidence of RF with terlipressin (n = 200) was 9.4% in patients with grades 1–2 ACLF, and 30% with grade 3 ACLF (p = 0.0002); no such difference was observed in placebo‐treated patients (n = 99) (6.2% grades 1–2 vs. 0% grade 3 ACLF, p > 0.05). RF incidence between terlipressin and placebo in patients with grade 3 ACLF was significant (p = 0.01). Baseline predictors of RF with terlipressin were INR (p = 0.011), mean arterial pressure (p = 0.037), and SpO2 (p = 0.014). Prior albumin as a continuous variable was not a predictor of RF. 90‐day survival between terlipressin and placebo arms was similar for grades 1–2 ACLF (55.5% and 56.6%, respectively), but lower for grade 3 ACLF (27.55% vs. 50.0%) (p = 0.122), mainly related to RF. Conclusion: Terlipressin should be used with caution in patients with HRS1 and grade 3 ACLF. Patients with hypoxaemia are at increased risk of RF and mortality. [ABSTRACT FROM AUTHOR]

Summary: Background: Glucagon‐like peptide‐1 receptor agonists may be a treatment option in patients with non‐alcoholic fatty liver disease (NAFLD). Aims: To investigate the effects of semaglutide on liver stiffness and liver fat in subjects with NAFLD using non‐invasive magnetic resonance imaging (MRI) methods. Methods: This randomised, double‐blind, placebo‐controlled trial enrolled subjects with liver stiffness 2.50‐4.63 kPa by magnetic resonance elastography (MRE) and liver steatosis ≥10% by MRI proton density fat fraction (MRI‐PDFF). The primary endpoint was change from baseline to week 48 in liver stiffness assessed by MRE. Results: Sixty‐seven subjects were randomised to once‐daily subcutaneous semaglutide 0.4 mg (n = 34) or placebo (n = 33). Change from baseline in liver stiffness was not significantly different between semaglutide and placebo at week 48 (estimated treatment ratio 0.96 (95% CI 0.89, 1.03; P = 0.2798); significant differences in liver stiffness were not observed at weeks 24 or 72. Reductions in liver steatosis were significantly greater with semaglutide (estimated treatment ratios: 0.70 [0.59, 0.84], P = 0.0002; 0.47 [0.36, 0.60], P < 0.0001; and 0.50 [0.39, 0.66], P < 0.0001) and more subjects achieved a ≥ 30% reduction in liver fat content with semaglutide at weeks 24, 48 and 72, (all P < 0.001). Decreases in liver enzymes, body weight and HbA1c were also observed with semaglutide. Conclusions: The change in liver stiffness in subjects with NAFLD was not significantly different between semaglutide and placebo. However, semaglutide significantly reduced liver steatosis compared with placebo which, together with improvements in liver enzymes and metabolic parameters, suggests a positive impact on disease activity and metabolic profile. ClinicalTrials.gov identifier: NCT03357380. [ABSTRACT FROM AUTHOR]

Summary: Background: The modified PAGE‐B (mPAGE‐B) and PAGE‐B models reliably predict the risk of developing chronic hepatitis B (CHB)‐related hepatocellular carcinoma (HCC). Aim(s): To investigate whether the addition of liver stiffness (LS) value, assessed using transient elastography, enhanced the predictive accuracies of these models Methods: Patients with CHB who started anti‐viral therapy (AVT) between 2007 and 2017 were enrolled. The training (Yonsei University Hospital) and validation (seven Korean referral institutes) cohorts contained 1211 and 973 patients, respectively. Results: Based on multivariate analysis, older age (hazard ratio [HR] = 1.051, 95% confidence interval [CI] = 1.031‐1.071), male sex (HR = 2.265, 95% CI = 1.463‐3.506), lower platelet count (HR = 0.993, 95% CI = 0.989‐0.997) and greater LS values (HR = 1.015, 95% CI = 1.002‐1.028) were independently associated with an increased risk of HCC development (all P < 0.05). Thus, we developed a modified PAGELS‐B model (maximum score 34) that included age, male sex, platelet count and LS value. The integrated area under the curve of the modified PAGELS model was greater than those of the PAGE‐B and mPAGE‐B models (0.760 vs 0.714 and 0.716, respectively) in the derivation dataset. The cumulative HCC incidence was significantly higher in the high‐risk (modified PAGE‐BLS score ≥ 24) group than in the intermediate‐risk (modified PAGELS‐B score 12‐24) or low‐risk (modified PAGELS‐B score < 12) group (all P < 0.001). Similar results were observed in the validation cohort. Conclusions: The predictive accuracies of the PAGE‐B and mPAGE‐B models were validated in Korean patients with CHB receiving AVT. However, the modified PAGELS‐B model featuring the addition of LS value showed higher predictability than the PAGE‐B and mPAGE‐B models. [ABSTRACT FROM AUTHOR]

Summary: Background: Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection is frequently associated with liver test abnormalities. Aims: To describe the evolution of liver involvement during SARS‐CoV‐2 infection and its effect on clinical course and mortality. Methods: Data of 515 SARS‐CoV‐2‐positive patients were collected at baseline and during follow‐up, last evaluation or death. Stratification based on need for hospitalisation, severe disease and admission to intensive care unit (ICU) was performed. The association between liver test abnormalities (baseline and peak values) and ICU admission or death was also explored. Results: Liver test abnormalities were found in 161 (31.3%) patients. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma glutamyl transferase (GGT) were increased in 20.4%, 19% and 13.6% of patients, respectively. Baseline liver test abnormalities were associated with increased risk of ICU admission (OR 2.19 [95% CI 1.24‐3.89], P = 0.007) but not with mortality (OR 0.84 [95% CI 0.49‐1.41], P = 0.51). Alkaline phosphatase (ALP) peak values were correlated with risk of death (OR 1.007 [95% CI 1.002‐1.01], P = 0.005) along with age, multiple comorbidities, acute respiratory distress syndrome, ICU admission and C‐reactive protein. Alterations of liver tests worsened within 15 days of hospitalisation; however, in patients with the longest median follow‐up, the prevalence of liver test alterations decreased over time, returning to around baseline levels. Conclusions: In SARS‐CoV‐2‐positive patients without pre‐existing severe chronic liver disease, baseline liver test abnormalities are associated with the risk of ICU admission and tend to normalise over time. The ALP peak value may be predictive of a worse prognosis. [ABSTRACT FROM AUTHOR]

Summary: Background: Systemic inflammation is a driving force for the development of hepatic encephalopathy and recent studies demonstrated that elevated Interleukin‐6 (IL‐6) serum levels are associated with the presence of minimal hepatic encephalopathy in patients with liver cirrhosis. Aim: To test the hypothesis that IL‐6 is a suitable marker to identify patients with liver cirrhosis at high risk for the development of overt hepatic encephalopathy. Methods: 201 patients were included into this prospective cohort study and were followed for a mean time of 322 days. Covert hepatic encephalopathy was diagnosed according to the West‐Haven criteria (hepatic encephalopathy grade 1) and with the portosystemic encephalopathy (PSE) test. Results: The cumulative incidence of overt hepatic encephalopathy was higher in patients with IL‐6 levels above the median of 9 pg/mL than in patients with IL‐6 levels at or below the median (35.6% vs 1.9%, P < .001). After adjustment for covert hepatic encephalopathy, history of overt hepatic encephalopathy, C‐reactive protein (CRP) and model for end‐stage liver disease (MELD), IL‐6 levels above the median remained independently associated with the development of overt hepatic encephalopathy. The predictive performance of IL‐6 regarding the development of overt hepatic encephalopathy during the next 180 days (AUROC, 0.931) was numerically higher than that of MELD (AUROC, 0.841) or CRP (AUROC, 0.835). In patients without prior overt hepatic encephalopathy, the predictive performance of IL‐6 (AUROC, 0.966) was even significantly higher than that of MELD (AUROC 0.843) or CRP (AUROC 0.850). The ideal cut‐off for IL‐6 in this setting was 23.5 pg/mL with a sensitivity and specificity of 89.3% and 89.5% respectively. Conclusion: IL‐6 serum levels are closely linked to the development of overt hepatic encephalopathy in patients with liver cirrhosis. [ABSTRACT FROM AUTHOR]

Summary: Background: Immune checkpoint inhibitors have revolutionised the oncological landscape in the last few years. Possible applications include the treatment of hepatocellular carcinoma and cholangiocarcinoma. Unfortunately, new immune‐related adverse effects have been associated with the use of these agents and the liver is one of the organs most frequently involved. Aims: To provide a general overview of the potential impact of immune checkpoint inhibitors on the liver Methods: We reviewed the literature and abstracts/presentations on immune checkpoint inhibitors at most relevant hepatology meetings over the last 5 years. Results: The role of immune checkpoint inhibitors has been investigated both for the treatment of viral hepatitis and primary liver cancer. Hepatocellular carcinoma and chronic hepatitis B show the greatest potential for treatment with these drugs in the near future. However, immune‐related adverse events involving the liver are a growing concern related to their widespread use. Conclusions: Immune checkpoint inhibitors represent an exciting new class of drugs with currently limited application in malignant and non‐malignant liver disease. Caution must be exercised on the emergence of potentially severe immune adverse reactions. [ABSTRACT FROM AUTHOR]

Background Magnetic resonance imaging-derived measures of liver fat and volume are emerging as accurate, non-invasive imaging biomarkers in non-alcoholic steatohepatitis ( NASH). Little is known about these measures in relation to histology longitudinally. Aim To examine any relationship between MRI-derived proton-density fat-fraction ( PDFF), total liver volume ( TLV), total liver fat index ( TLFI), vs. histology in a NASH trial. Methods This is a secondary analysis of a 24-week randomised, double-blind, placebo-controlled trial of 50 patients with biopsy-proven NASH randomised to oral ezetimibe 10 mg daily ( n = 25) vs. placebo ( n = 25). Baseline and post-treatment anthropometrics, biochemical profiling, MRI and biopsies were obtained. Results Baseline mean PDFF correlated strongly with TLFI (Spearman's ρ = 0.94, n = 45, P < 0.0001) and had good correlation with TLV ( ρ = 0.57, n = 45, P < 0.0001). Mean TLV correlated strongly with TLFI ( ρ = 0.78, n = 45, P < 0.0001). After 24 weeks, PDFF remained strongly correlated with TLFI ( ρ = 0.94, n = 45, P < 0.0001), maintaining good correlation with TLV ( ρ = 0.51, n = 45, P = 0.0004). TLV remained strongly correlated with TLFI ( ρ = 0.74, n = 45, P < 0.0001). Patients with Grade 1 vs. 3 steatosis had lower PDFF, TLV, and TLFI ( P < 0.0001, P = 0.0003, P < 0.0001 respectively). Regression analysis of changes in MRI- PDFF vs. TLV indicates that 10% reduction in MRI- PDFF predicts 257 mL reduction in TLV. Conclusions The MRI- PDFF and TLV strongly correlated with TLFI. Decreases in steatosis were associated with an improvement in hepatomegaly. Lower values of these measures reflect lower histologic steatosis grades. MRI-derived measures of liver fat and volume may be used as dynamic and more responsive imaging biomarkers in a NASH trial, than histology. [ABSTRACT FROM AUTHOR]

Background: Large proportions of patients use herbal medicinal products, and encouraging data in terms of effectiveness exist for some of these. One aspect, however, which is still largely under-investigated is the question of potential harm. Aim: To review the recent evidence on hepatotoxic events associated with the use of herbal medicinal products. Methods: Systematic literature searches were performed on Medline, Embase, The Cochrane Library, Amed and Ciscom. To identify additional data, searches were conducted by hand in relevant medical journals and in our own files. The screening and selection of articles and the extraction of data were performed independently by the two authors. There were no restrictions regarding the language of publication. In order to be included articles were required to report data on hepatotoxic events associated with the therapeutic use of herbal medicinal products. Results: Single medicinal herbs and combination preparations are associated with hepatotoxic events. Clinically, the spectrum ranges from transient elevations of liver enzyme levels to fulminant liver failure and death. In most instances hepatotoxic herbal constituents are believed to be the cause, while others may be due to herb-drug interactions, contamination and/or adulteration. Conclusions: A number of herbal medicinal products are associated with serious hepatotoxic events. Incidence figures are largely unknown, and in most cases a causal attribution is not established. The challenge for the future is to systematically research this area, educate all parties involved, and minimize patient risk. [ABSTRACT FROM AUTHOR]