For the trace element selenium, in contrast to zinc, iron, copper, chromium, manganese and iodine, there is still no clear official recommendation with regard to routine substitution in artificial nutrition. An overview of the manifestations of selenium deficiency in humans during the period 1979-1995 shows that nutritive deficiencies are exclusively TPN-induced or the result of severe malnutrition. The pathology of TPN-induced selenium deficiency and the analytic assessment of selenium status are described. Patients undergoing long-term parenteral nutrition or suffering from an increased loss of intestinal secretions have to be characterized as being especially at risk for clinical selenium deficiency. The relationship of the serum selenium kinetics in pediatric and adult patients to the depletion of body compartments during the course of short-term and prolonged TPN is discussed. Because of the importance of the selenoproteins, the regularly occurring depletion during selenium-free TPN and the borderline supply of selenium in Germany the routine substitution of selenium in TPN is strongly recommended. The pharmaceutical industry should be encouraged to develop a trace element solution that includes selenium, so that the nutritive requirement of patients on TPN can be satisfied. Adequate intravenous dosage recommendations are based on maintenance of glutathione peroxidase homeostasis. The routine supplementation dosage may not meet the selenium requirements of intensive care patients under conditions of increased metabolic demands on their anti-oxidative system.