Evaluation of prognostic markers in severe drug-induced liver disease

Abstract

AIM:To analyze the outcome of patients with severe drug-induced liver disease (DILD) associated with jaundice classified as hepatocellular, cholestatic or mixed liver injury and to evaluate the validity of Hy's rule and the most important predictors for outcome. METHODS:The Adverse Drug Reaction Advisory Committee was set up in 1997 in our hospital to identify all suspicions of DILD following a structured prospective report form. Liver damage was divided into hepatocellular, cholestatic, and mixed types according to laboratory and histologic criteria when available. Further evaluation of causality assessment was performed. RESULTS:From January 1997 to December 2004, 265 patients were diagnosed with DILD，and 140 (52.8%) of them were female. hepatocellular damage was the most common (72.1%), the incidence of death was 9.9% in patients with hepatocellular damage and 9.5% in patients with cholestatic/mixed damage (P < 0.05). There was no difference in age of dead and recovered patients. The proportion of females and males was similar in recovered and dead patients, no difference was observed in duration of treatment between the two groups. The serum total bilirubin (P < 0.001), direct bilirubin (P < 0.001) and aspartate transaminase (AST) (P = 0.013) values were higher in dead patients than in recovered patients. Chinese herbal medicine was the most frequently prescribed, accounting for 24.2% of the whole series. However, antitubercular drugs (3.4%) were found to be the primary etiological factor for fetal DILD. Factors associated with the development of fulminant hepatic failure were hepatic encephalopathy (OR = 43.66, 95% CI = 8.47-224.95, P < 0.0001), ascite (OR = 28.48, 95% CI = 9.26-87.58, P < 0.0001), jaundice (OR = 11.43, 95% CI = 1.52-85.96, P = 0.003), alcohol abuse (OR = 3.83, 95% CI = 1.26-11.67, P = 0.035) and direct bilirubin (OR = 1.93, 95% CI = 1.25-2.58, P = 0.012). CONCLUSION:Death occurs in 9.8% of patients with DILD. Chinese herbal medicine stands out as the most common drug for DILD. While antitubercular drugs are found to be the primary etiological factor for fetal DILD, hepatic encephalopathy, ascites, jaundice, alcohol abuse and direct bilirubin levels are associated with the death of DILD patients.

Association of Serum Bilirubin with Ischemic Stroke Outcomes

“…3 However, various studies among individuals with general medical conditions including hepatic disease have suggested that Dbil levels may be of better prognostic value than Tbil levels. [19][20][21][22] This study's novel finding of a relation between Dbil and incident stroke severity is lent support by the study's concordance with prior investigations regarding other predictors of initial stroke deficit. We observed that higher admission serum glucose, a history of atrial fibrillation, a history of hypertension, or poor premorbid functional status were all associated with greater initial stroke severity.…”

Pectolinarin and Pectolinarigenin of Cirsium setidens Prevent the Hepatic Injury in Rats Caused by D-Galactosamine via an Antioxidant Mechanism

“…24) During the low cellular energy, intracellular K ϩ ions leak out and Na BuOH fractions), rats were treated with GalN and the extract fractions. GalN injection increased serum AST and ALT activities significantly compared with the untreated group (Table 1), and extract treatment ameliorated this increase in a dose-dependent manner.…”

Biochemical analysis of Cassia fistula aqueous extract and phytochemically synthesized gold nanoparticles as hypoglycemic treatment for diabetes mellitus

“…61 Transaminases mediate the catalysis of amino transfer reactions, and are vital markers of liver injury in clinical diagnostics. 62 Alkaline phosphatase is a hydrolase enzyme located in the cytoplasm, 63 and is responsible for removing phosphate from nucleotides and proteins released due to hepatic cellular damage. Assessment of marker enzyme (aspartate transaminase, alanine transaminase, and alkaline phosphatase) levels in streptozotocin-induced diabetic rats showed an elevation resulting from leakage of enzymes into the bloodstream.…”