small proportion of patients have a progressive liver injury, which histologically consists of centrizonal necrosis (Figure?3) and perivenular fibrosis, affecting the areas in which hypoxia may be most prevalent. The severity of centrizonal necrosis can be assessed using plasma isocitrate dehydrogenase levels in plasma, offering a convenient method for grading the hepatic injury. 62 The clinical presentation of this type of injury is usually that of a self?limiting hepatitis; however, there are a few case reports of thyrotoxic patients presenting with fulminant hepatic failure. 63 The precipitation of the clinical presentation is generally attributable to the onset of cardiac failure, often precipitated by arrhythmias. 63 Cholestatic injury An elevated serum alkaline phosphatase is seen in 64% of patients with thyrotoxicosis. 64 However this is not necessarily liver?specific, as it can originate from bone and/or liver. It is therefore important to look at elevations in ??glutamyl transpeptidase (17%) and bilirubin (5%) as an indicator of cholestasis. 64 In patients with cholestatic injury, the histological features are similar to the non?specific changes seen in hepatitic injury. However, in addition there appears to be centri?lobular intrahepatocytic cholestasis (Figure?4). 65 Jaundice is uncommon but when it occurs, complications of thyrotoxicosis (cardiac failure/sepsis) or intrinsic liver disease need to be excluded. It is difficult to establish which features seen in thyrotoxic liver injury are from tissue thyroid status alone, and which are in combination with complications such as cardiac failure, malnutrition and sepsis. It is probably impractical to try and separate the causes out, as