Teaching Case

acute fall of hemoglobin due to anticoagulation for acute exacerbation of coronary diseas followed by CT-scan showing an incidental finding concerning liver density

The 83 year-old woman was admitted to the emergency department for unstable angina due to longstanding ischemic cardiopathy complicated by intermittent auricular fibrillation. Prophylactic treatment by anticoagulation was started and the patient underwent continuous monitoring. Three days later there was an acute decrease of haemoglobin level from 14 mg/dl to 7 mg/dl; therefore - without previous abdominal ultrasound investigation - an abdominal computed tomography was performed in search of haemorrhage due to anticoagulation. Indeed, we detected a retroperitoneal hematoma situated along the right psoas muscle (not shown), but the incidental finding concerning the liver (fig 1a,1b) also attracted our attention.

Amiodarone is an amphilic, iodinated, benzofuran derivative, (1) which has been proved to be highly effective in the treatment of a wide range of cardiac arrhythmias refractory to other medical agents. Since amiodarone is the only antiarrhythmic drug without cardiodepressive effects, steady increase of its widespread use is observed (1,2). Nevertheless, numerous side effects are associated due to its high iodinated compound of 39% of the molecular weight causing a pharmacological half-life of up to 45 days and the accumulation in many tissues, such as the liver parenchyma with one of the most pronounced affinity (2,3). Several molecular mechanisms of tissue toxicity have been described (3), among them phospholipidosis, which accounts for the diffuse hyperattenuation of the liver parenchyma you can see in our reported case: Hepatic density of 102-120 HU was measured on native CT without any significant change after intravenous contrast medium injection. Amiodarone and its metabolites are potent inhibitors of intracellular phospholipases. Their interaction with pospholipides results in enzyme-resistant drug-lipid complexes and progressive intralysosomal accumulation of amiodarone (3). This so-called direct toxicity is related to duration and dosage of therapy, which determine the degree of hepatic hyperattenutation reflecting the amount of iodine-containing amiodarone stored in the liver parenchyma (1,2). In general, discontinuation of treatment is not necessary, since the progressive intrahepatic accumulation of the drug doesn’t go along with clinically evident hepatic dysfunction (4) neither tissue alteration (1). Differential diagnosis of diffuse hepatic hyperattenuation includes iron overload, Wilson’s disease gold deposition and glycogen storage disease. Iron overload consits of reticuloendothelial and parenchymal deposition of iron, the latter also involves additional organs, such as the pancreas, myocardium, endocrine glands, joints and commonly results in liver cirrhosis with associated splenomegaly (5), whereas the spleen is normal in the case described above. There is no macroscopical alteration of hepatic morphology due to Amiodarone deposition, unlike in other storage diseases of the liver known to result in cirrhosis (5). In conclusion long-term amiodarone treatment has to be considered as a differential diagnosis to other diffuse hyperdense hepatopathies detected on abdominal CT in order to avoid unnecessary blood tests in search of possible underlying storage diseases.