Lactic acidosis complicating liver failure after intravenous fructose.

Abstract

procedure she complained of the sudden onset of pain in the chest, shortness of breath, and haemoptysis. A lung scan showed lage areas of impaired perfusion in both lung fields typical of pulmonary embolism. There were no physical signs in her legs but testing with the ultrasound flow detector showed an impairment of venous flow in the left popliteal and lower femoral vein. Peripheral ascending phlebography was carried out as an emergency procedure and showed extensive recent, non-adherent thrombus in most of the calf veins, the popliteral vein, and lower femoral vein of the left side (see Fig.).It was considered advisable to protect her against a further and CommentThis case shows that thrombus can propagate along a vein very quickly. Within an hour the risk to this patient of developing a massive, as opposed to a minor, pulmonary embolus was seriously increased, because the potential embolus had doubled in size. Anticoagulants had not been given because of the recent episode of haemorrhage from the cerebral artery aneurysm and it may be that they would have prevented the growth of the thrombus. Normally we find at operation that the thrombus fits the phlebogram perfectly, but most of these patients are already anticoagulated with heparin as the first line of treatment of their pulmonary embolus.If thrombus can grow so quickly then the value of any routine screening procedure, such as ultrasound flow detection or the labelled fibrinogen uptake test, in the prophylaxis of sudden massive embolism is open to doubt.This case emphasises the urgency with which any procedure must be carried out when attempting to prevent recurrent pulmonary embolism.

Abnormal Renal Urate Homeostasis in Systemic Disorders

“…Parenteral fructose infusion in man has also been shown to be associated with a decrease in erythrocyte PRPP and ribose-5-phosphate concentrations [47], although no detectable change in erythrocyte ATP concentration was observed such as was postulated to occur [125] and to result in reduced inhibition of AMP degradation. The appreciation of the dangers of intravenous fructose in man, especially in hep atic disease and anoxic states (particularly from lactic acidosis), has led to some restriction of its clinical use [25,124].…”

The Roles of Carbohydrate Response Element Binding Protein in the Relationship between Carbohydrate Intake and Diseases

“…Glucokinase, phosphofructokinase, and liver-type pyruvate kinase are rate-limiting enzymes in glycolysis that slow glucose flux [ 29 ]. In contrast, there are no rate-limiting enzymes in fructolysis, and acute fructose infusion sometimes causes lactic acidosis [ 30 ]. Therefore, fructose is easier to metabolize in the fructolytic and glycolytic pathways ( Figure 2 ).…”

Plasma Lactate and Urate Concentrations following Oral Fructose in Patients with Liver Disease

“…This may result in lactic acidosis [8,9], In con trast, healthy subjects produce a small but measurable rise in plasma lactate concentra tion following oral fructose ingestion [10, 111-Fructose administration, oral or intrave nous, has also been shown to produce a rise in plasma urate concentration [3,12). This rise is due to increased catabolism of adeno sine monophosphate (AMP) by AMP deami nase [13].…”

“…The activity of AMP deaminase is primarily controlled by phosphate or guano-sine-5'-triphosphate which inhibit activity. Following fructose administration hepatic concentrations of phosphate and guanosine-5'-triphosphate fall thus promoting AMP ca tabolism [13], Intravenous infusion of fructose has been reported as producing lactic acidosis in some patients with liver disease [8,9], and the ther apeutic use of intravenous fructose is con traindicated in such patients. It has also been suggested that large amounts of oral fructose may be harmful to these patients [8].…”