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Intravenous essential amino acid therapy.

Dr. Norman N. Yoshimura, McGaw Inc., 2525 McGaw Avenue, PO Box 19791, Irvine, CA 92713-9791 (USA) Dear Sir, In a recent issue, Akpolat et al. [1], practicing at the Hacettepe University in Ankara, Turkey, reported on a case of hyperam-monemic encephalopathy in a renal patient receiving intravenous essential amino acids (EAA; NephrAmine®). Although there are no doubts surrounding the clinical observations and corresponding laboratory findings, this is a serious case of misuse of intravenous EAA. Whether infused with or without energy (the report does not state whether the EAA was infused along with dextrose, electrolytes or other important nutrients required for protein synthesis from amino acids), the infusion of 1,000 cm3 of NephrAmine in 8 h represents a dose 2 times the highest recommended dose for the average 70-kg man. In this case, the 20-year-old woman more than likely weighed less than 70 kg making the overdose even larger. It shoud be pointed out that inappropriate use and overdosing can, as the result of a natural metabolic sequelae, lead to hyperammonemia, and as in the case reported by Akpolat et al. encephalopathy. Discontinuing the overload of intravenous EAA would be expected to reduce serum ammonia and the corresponding encephalopathy as reported by Akpolat et al. Three references are cited by Akpolat et al. [2-4] in which hyperammonemia occurred. All three are case reports of a single patient for a grand total of 3 patients. In all three instances, similar overdosing of intravenous EAA occurred. Overdosing more than likely was the cause of the hyperammonemia. Rapp et al. [2] administered 6.22 g of essential amino acid nitrogen to a 59-year-old woman who more than likely weighed less than 70 kg. This is at least 2 times the recommended dose of 1.6-3.2 g of EAA nitrogen. In this case, the dose was reduced to 2.1 g of nitrogen per day and in 24 h serum ammonia decreased from 192 to 70 μmol/l. The patient was awake and responsive. Grazer et al. [3] administered 42 g of protein (assumed to be amino acids in this case) per day to a 47-year-old woman weighing 40 kg for 11 days before becoming symptomatic with hyperammonemia. The recommended dose of EAA is 0.2-0.4 g/kg/day. In this case, approximately 3 times the recommended dose was used. Lamiell et al. [4] administered a mixture of 1,000 ml of EAA and 750 ml of 70% dextrose to a 77-kg, 70-year-old male patient. Hyperammonemia (and hypophosphatemia) was encountered in a crossover regimen, strongly implicating EAA as the culprit. EAAs were more than likely the cause of the hyperammonemia but only because the dose was again at least twice the typical dose. The authors recognized and acknowledged the overdose and infer that the lack of L-arginine in some EAA-based total parenteral nutrition (TPN) leads to hyperammonemia. Arginine is required for detoxifying ammonia via the Krebs urea cycle but is a dispensable amino acid which can be de novo synthesized by man. The preformed