Characteristic clinical manifestation |
Acute self-limiting, and a serum aspartate transaminase elevation of aminotransferases or jaundice or both.[17] |
After a typical acute onset, patient become deeply jaundiced and went into hepatic encephalopathy within 4 wk of onset of disease without any past history of chronic liver disease.[18] |
Ranging from asymptomatic elevations in aminotransferases to fulminant hepatic failure with jaundice, profound coagulopathy, hepatic coma, and hypoglycemia.[19] Preeclampsia is present in 50% of cases.[20] |
Usually with signs of pre-eclampsia and thrombocytopenia[21],
65% patients present with abdominal pain. |
Ranging from modest pruritus to intractable itching associated
with jaundice.[22] |
Liver biopsy |
Moderate necrosis |
Severe necrosis |
Minor necrosis[23], involves a microvesicular fatty infiltrative disorder, hepatic vacuolization and pallor in the central zone |
Periportal hemorrhage and fibrin deposition |
Bland cholestasis |
Serum aminotransferases and coagulation abnormalities |
At least fivefold increase of serum aminotransferases |
Serum aminotransferases significantly increase at the onset, then decrease as the necrosis of hepatocytes proceed, reduced coagulation abnormalities |
The aminotransferases are
usually elevated but <1000 U, with longer prothrombin time and low fibrinogen. |
Ranging from 70 U to 6,000 U, with 250 U in average.[21] |
normal GGTP, elevated aminotransferases
(<1000 U)[24], increased serum bile acid level |