L-Isoleucine/L-Leucine/L-Lysine Hydrochloride/L-Methionine/L-Phenylalanine/L-Threonine/L-Tryptophan/L-Valine/L-Histidin Hydrochloride Hydrate

This is a case report on six patients with hyperammonemia that developed while they were receiving total parenteral nutrition (TPN) as a component of renal failure therapy. Clinically, the hyperammonemia presented as mental status changes in all six cases. Four of the six patients with renal failure initially received 400 mL Amiyu in 1400 mL 17% glucose (total = 1800 mL TPN‐A) administered over each 24‐hour period. Two patients had been placed on 400 mL complete amino acid in 1400 mL 17% glucose (total = 1800 mL TPN‐C over each 24‐hour period) prior to therapy with TPN‐A. Approximately 3 weeks after initiation of TPN therapy with TPN‐A, episodes of mental status changes of increasing duration and paroxysms were documented in five of the six patients. In one of the patients receiving TPN‐C prior to TPN‐A therapy, toxicity was clinically evident only 4 days after initiation of TPN‐A. Serum ammonia levels were obtained and found to be elevated in the acute (ie, presenting) stage in all patients. With the discontinuance of TPN‐A, ammonia levels normalized uniformly. Mental status also improved in all cases except for the patient with rapid clinical presentation who died 2 weeks after first evidence of clinical toxicity. In cases 1, 2, and 6, serum amino acid analysis in the acute phase showed reduced levels of ornithine and citrulline, the substrate and product, respectively, of condensation with carbamyl phosphate at its entry into the urea cycle. Moreover, levels of arginine, precursor to ornithine, were found to be elevated. And, in cases 1 and 6, the serum concentration of orotic acid was 40 times and 23 times, respectively, the value expected in a normal healthy adult. This is presumably due to funneling of carbamyl phosphate into an alternate biosynthetic pathway as a result of inadequate ornithine needed as substrate for its entrance into the urea cycle. Thus, the common denominator in the hyperammonemia experienced in these cases appears to be a depletion of ornithine stores, which we hypothesize to have mainly resulted from inhibition of arginosuccinate synthetase by histidine. Consequently, in patients requiring long‐term TPN therapy (>3 weeks in our experience with TPN‐A), it may be necessary to supplement ornithine in addition to arginine. In all such patients, we feel it is necessary to monitor serum ammonia for toxicity or long‐term elevation. (Journal of Parenteral and Enteral Nutrition 17:86–90, 1993)

To assess the effect of growth hormone (GH) on myocardial remodeling in infarcted rats.

This study comprised 24 Wistar rats divided into 3 groups as follows: 1) AMI-GH group--comprising 8 rats that underwent infarction and were treated with GH; 2) AMI group--comprising 8 rats that underwent infarction and received only the diluent of the GH solution; and 3) control group (C group)--comprising 8 rats that underwent simulated infarction. After 30 days, the animals underwent functional study through echocardiography, and the changes in myocardial contractility of the isolated left ventricular (LV) papillary muscle were studied.

The echocardiography identified an increase in the diastolic (C=7.32+/-0.49; AMI=8.50+/-0.73; AMI-GH=9.34+/-0.73; P<0.05) and systolic (C=3.38+/-0.47, AMI=5.16+/-1.24; AMI-GH=5.96+/-1.54; P<0.05) diameters (mm) in the LV of the infarcted animals. The AMI-GH group animals had a lower ejection fraction (%) (C=0.9+/-0.03; AMI=0.76+/-0.12; AMI-GH= 0.72+/- 0.14; P<0.05 for C vs AMI-GH) compared with those in controls. The study of the isolated left ventricular papillary muscle showed that the AMI-GH group had changes (C=1.50+/-0.59; AMI=1.28+/-0.38; AMI-GH=1.98+/-0.41; P<0.05 for C vs AMI-GH) only in the tension at rest (TR - g/mm2) and in the time delta for a 50% decrease in the tension developed (TR50, ms) after stimulation with calcium (C=23.75+/-9.16; AMI=-16.56+/-14.82; AMI-GH=-4.69+/-8.39; P<0.05 for C vs AMI-GH) and in the delta of tension developed (TD, g/mm2) after stimulation with isoproterenol (C=0.99+/-0.17; AMI=0.54+/-0.62; AMI-GH=0.08+/-0.75; P<0.05 for C vs AMI-GH) compared with those in control animals.

The early administration of GH in the experimental infarction model in rats may result in adverse effects on the process of ventricular remodeling.