Does hypophosphatemia play a role in acute liver failure?

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Abstract
This is the first record of hypophosphataemia in acute liver failure induced by paracetamol; it occurred in most of the patients and was severe (<0.3 mmol/l) in more than one third. At this level hypophosphataemia produces impaired oxygen transport and tissue hypoxia, abnormal leucocyte function, depressed platelet numbers and function, generalised muscle weakness, and disorder of the central nervous system; these are frequent complications of acute liver failure. The similarity of the effects of liver failure and hypophosphataemia on the central nervous system (irritability, muscle weakness, dysarthria, confusion, and coma) suggests that phosphate depletion may be important in hepatic encephalopathy, and a progressive defect of phosphate metabolism in brain tissue of patients with chronic liver disease was shown recently by nuclear magnetic resonance spectroscopy. The cause of hypophosphataemia in acute liver failure remains unclear. None of the recognised causes of moderate (0.3-0.7 mmol/l) hypophosphataemia correlated with the phosphate concentrations in our patients. The reduced maximum tubular reabsorption of phosphate in two patients suggests an increased loss of renal phosphate, perhaps due to a direct effect of paracetamol, although the correlation between plasma phosphate and creatinine concentrations suggests that renal failure may protect against hypophosphataemia. Because of the serious clinical implications of phosphate imbalance in acute liver failure the homoeostatic mechanisms of bone and renal phosphate reabsorption in this condition need to be studied urgently. Plasma phosphate concentrations should be monitored carefully during infusion of glucose in patients with liver failure.