Hyperammonemia during total parenteral nutrition in children

Serial blood ammonia (NH3) determinations in 19 low birth weight (LBW) infants, 14 term neonates and 12 children receiving total parenteral nutrition (TPN) have shown that 73% of patients had one or more elevated NH3 values (greater than 150 micrograms/dl). The mean blood NH3 was 220 +/- 13 micrograms/dl in LBW infants, 180 +/- 9 micrograms/dl in 10 infants, and 140 +/- 7 micrograms/dl in children. All of these values are significantly higher than normal (p less than 0.001). There was no difference in incidence or mean blood ammonia concentration between patients receiving casein hydrolysate and those receiving a crystalline amino acid solution. Only four patients were symptomatic and several infants remained fully alert despite blood NH3 concentration in excess of 400 micrograms/dl. One infant who had sustained hyperammonemia was given another amino acid source (Travasol) containing 1.2 mmol/dl of arginine; blood NH3 promptly fell to the normal range. However, six of seven additional infants had hyperammonemia while receiving Travasol (mean = 184 micrograms/dl). Hyperammonemia is common during TPN in children, often is not recognized clinically, and occurs with equal frequency in infants and older children. The high levels observed in LBW infants may be due to hepatic immaturity. Blood NH3 concentration should be monitored frequently during TPN. Persistent hyperammonemia should be treated by decreasing protein content of the infusate. The role of supplemental arginine is unclear.     

Effects of high carnitine supplementation on substrate utilization in low-birth-weight infants receiving total parenteral nutrition

Parenterally fed preterm neonates are known to be at risk for carnitine deficiency. We studied substrate utilization in low-birth-weight infants receiving total parenteral nutrition (TPN) with (A) and without (B) supplementation of 48 mg carnitine.kg-1.d-1 on days 4-7 (birth weights 1334 +/- 282 vs 1318 +/- 248 g, gestational age 32 +/- 2 vs 32 +/- 2 wk, A vs B, respectively). TPN consisted of 11 g glucose.kg-1.d-1 and 2.4 g.kg-1.d-1 of both protein and fat. Plasma carnitine concentrations at day 7 were for free carnitine 11.8 +/- 5.0 vs 164 +/- 56 mumol/L and for acyl carnitine 3.8 +/- 2.0 vs 33.9 +/- 15.4 mumol/L, respectively. Indirect calorimetry at day 7 showed a higher fat oxidation (0.21, -0.31 to +0.60 vs 1.18, 0.70 to 1.95 g. kg-1.d-1, respectively, P less than 0.02, median and interquartile range) in group B and a higher protein oxidation (0.37, 0.30-0.43 vs 0.63, 0.53-0.88 g.kg-1.d-1, P less than 0.001). The time to regain birth weight was also higher in group B (7, 5.5-9 vs 9, 7-14 d, P less than 0.05). Carnitine supplementation and calorie intake were the best explanatory variables for metabolic rate (R2 = 0.45, P less than 0.002). We conclude that carnitine supplementation of TPN in this dosage does not seem advisable.     

Total parenteral nutrition in very low birth weight infants with Travasol 10% blend C

Ten very low birth weight (VLBW) infants (birth weight: 994 +/- 66 g, gestational age: 27 +/- 0.5 wk) requiring total parenteral nutrition (TPN) were studied in order to evaluate their metabolic response to the amino acid solution Travasol 10% blend C. These patients received the solution at a constant rate, providing 2.61 +/- 0.02 g/kg/day of amino acids and 76 +/- 1 kcal/kg/day. Plasma amino acids analysis was performed after 4.6 +/- 0.3 day of infusion and compared to values reported previously with Travasol blend B. The new solution (blend C) showed a significantly lower (p less than 0.001) glycinemia (485 +/- 24 vs 993 +/- 69 mumol/liter), methioninemia (39 +/- 2 vs 114 +/- 12 mumol/liter) and phenylalaninemia (67 +/- 3 vs 92 +/- 5 mumol/liter) related to the lower intake of these amino acids. Despite the provision of 47.5 mmol/liter of serine with blend C no changes in plasma level (182 +/- 15 vs 196 +/- 41 mumol/liter) were noted. The increased molar arginine/glycine ratio (blend C: 0.48 vs blend B 0.22) could have contributed to keep ammoniemia within normal levels (55.1 +/- 4.2 mumol/liter). Wide variations in insulin response (9.9 to 26.4 microU/ml) allowed for a correlation between its plasma concentration and those of sensitive amino acids, underlining its role in protein metabolism. Despite the immaturity of the study population no short-term metabolic imbalance has been encountered with the Travasol blend C solution.     

Zinc, copper, manganese, and iron balance of parenterally fed very low birth weight preterm infants receiving a trace element supplement

To evaluate a pediatric trace element supplement (Ped-El, Pharmacia) 18 metabolic balance studies were completed in 13 infants (mean birth weight 909 +/- 67 g, x +/- SEM; mean gestational age 27.2 +/- 1 weeks) who received total parenteral nutrition. The supplement supplied 40 micrograms/kg/day of zinc resulting in negative retention of 226 micrograms/kg/day. Copper infused at 20 micrograms/kg/day led to a positive retention of 8 micrograms/kg/day and an increase in serum Cu (p less than 0.05) not related to Cu intakes. Manganese infused at 40 micrograms/kg/day was nearly all retained (88 +/- 16% retention). Iron infused at 120 micrograms/kg/day led to a positive retention of 93 micrograms/kg/day. Although plasma ferritin and percent transferrin saturation were elevated, only plasma Fe values were correlated with Fe intake. This trace element supplement does not appear suitable for very low birth weight preterm infants.     

Concurrent administration of albumin with total parenteral nutrition in sick newborn infants.

The effects of concurrent administration of albumin with total parenteral nutrition were studied in 12 premature newborns (birth weight 1.26 +/- 0.1 kg [mean +/- SEM] and gestational age 30 +/- 0.8 weeks [mean +/- SEM]) compared with a control group of 12 premature newborns (birth weight 1.17 +/- 0.2 kg and gestational age 29 +/- 0.1 weeks) who received total parenteral nutrition. All newborns had a plasma albumin level below 3 g/dL and were in cardiorespiratory distress requiring assisted ventilation. Albumin supplementation of total parenteral nutrition resulted in a sustained increase in serum albumin concentration as well as increased mean arterial blood pressures in the study group. Slow albumin infusion had no observed effect on the severity of respiratory distress. Study group infants regained birth weight earlier than control group infants. These data suggest that the concurrent administration of albumin may be clinically beneficial in critically ill newborn infants.     

Response of preterm infants to aluminum in parenteral nutrition

Twenty-five preterm infants with birth weights (BW) 540 to 2280 g (20 with birth weight less than 1500 g) and gestational ages 24 to 37 weeks, were studied to determine the response to 2 levels of aluminum (Al) loading from currently unavoidable contamination of various components of parenteral nutrition (PN) solution. High Al loading group (H) received solutions with measured Al content of 306 +/- 16 micrograms/liter and low A1 loading group (L) received solutions with 144 +/- 16 micrograms A1/liter. Urine Al:Creatinine (Al:Cr) ratios (micrograms:mg) became elevated and significantly higher in H (1.6 +/- 0.38 vs 0.5 +/- 0.1, p less than 0.05) at the third sampling point (mean 19 days). Serum Al concentrations were highest at onset in both groups and stabilized with study but remained consistently higher than the normal median of 18 micrograms/liter. Calculated urine Al excretion were consistently low and were 34 +/- 6% vs 28 +/- 5% in the H and L groups, respectively. One infant in the L group who died 39 days after termination of above study showed the presence of A1 in bone trabeculae and the presence of excessive unmineralized osteoid along the trabeculae. We conclude that small preterm infants are able to increase urine Al excretion with increased Al load. However urine Al excretion is incomplete with bone deposition of Al and persistently elevated serum Al concentrations.     

Hypocupremia in patients receiving total parenteral nutrition

Although hypocupremia is a well-known consequence of long-term total parenteral nutrition (TPN), its incidence as well as the duration of TPN necessary to induce it are still unsettled. The purpose of this study is to review the changes in serum copper level in 25 patients receiving TPN for a period longer than 2 wk (mean duration 6 wk) at the Istituto Nazionale Tumori of Milan and to evaluate the possible relationship of cupremia with the basic disease. Main indications for TPN included enterocutaneous fistulas (11 patients), cancer cachexia (10 patients), radiation enteropathy (two patients), and severe postoperative stricture following esophagogastric resection (two patients). Mean value of serum copper at the beginning of the study was 143 micrograms/100 ml (normal value 65-165 micrograms/100 ml), and the regression analysis showed a mean fall of 5.64 micrograms/100 ml/wk. Hypocupremia occurred in four patients (three with intestinal fistulas and one with radiation obstructive enteritis) at 5th, 6th, 9th, and 6th wk of TPN, respectively. No patient with cancer cachexia developed hypocupremia. No patient with hypocupremia had clinical evidence of a copper deficiency syndrome. We conclude that 1) hypocupremia does not occur within the first month of TPN; 2) its incidence is about 16% in patients intravenously fed for period longer than 2 wk; 3) it is more frequent in patients with enterocutaneous fistulas, whereas it never occurs in patients with cancer cachexia, and 4) it is not necessarily associated to a clinicometabolic syndrome of copper deficiency. Finally, the "nutritional" meaning of serum copper should be questioned in cancer patients since it could represent a "tumor marker."     

Hyperalimentation-associated neonatal cholestasis: effect of oral gentamicin

The effect of oral gentamicin on the incidence of parenteral nutrition-associated cholestasis in preterm infants less than 1500 g birth weight was assessed retrospectively. Of 24 patients on parenteral nutrition for more than 10 days, 12 infants who received oral gentamicin (group I) for prophylaxis against neonatal necrotizing enterocolitis were compared to 12 infants who did not (group II). Both mean and peak direct bilirubin levels were significantly higher in group II. The increase in both mean and peak direct bilirubin levels after initiation of total parenteral nutrition (TPN) was significant in group II only. The incidence of cholestasis was significantly higher in group II than in group I. These results suggest that oral gentamicin may have a protective effect against parenteral nutrition-associated cholestasis in the newborn preterm infant.     

Neonatal metabolic acidosis: effect of chloride from normal saline flushes

Metabolic Acidosis is a reported complication of total parenteral nutrition (TPN). A large number of infants receiving TPN in an NICU were noted to have metabolic acidosis. We evaluated the effect of lowering the chloride intake on the incidence of metabolic acidosis in low birth weight (LBW) infants on TPN. Standard TPN solutions were adjusted to provide about 2-3 mEq/kg/day chloride instead of 5-7 mEq/kg/day provided previously. Most infants on TPN received approximately another 1-3 mEq/kg/day from intravenous and arterial line flushes with normal saline. Ten infants who had been on the original TPN solutions were compared to 10 infants who were on the revised TPN solutions. Serum pH, bicarbonate, and base deficit were used to measure acidosis. Medical records were reviewed for the number of days the infants had abnormal values. Serum chloride levels were also recorded. While similar in gestational age, birth weight, age during study period, days on TPN, and days on orally supplemented parenteral nutrition, the group with higher chloride intake had significantly more days of metabolic acidosis. They also had significantly higher serum chlorides. It is concluded that a total chloride load in excess of 6 mEq/kg/day in LBW infants receiving TPN is associated with more metabolic acidosis. Also, if saline is used for clearing of intravenous and arterial lines, standard TPN solutions should be formulated with consideration of the total chloride load.     

Plasma choline in normal newborns, infants, toddlers, and in very-low-birth-weight neonates requiring total parenteral nutrition

Choline deficiency is associated with hepatic abnormalities in adult volunteers and patients administered total parenteral nutrition (TPN). Preliminary investigation has suggested that plasma-free choline concentration (PFCh) is greater in neonatal animals, including humans, than in adults. The aims of this study were to determine the normal PFCh and phospholipid-bound choline concentration (PPLBCh) for newborns, infants, and toddlers and to determine the change during TPN. We also sought to determine the degree of fetal choline extraction, the relation between maternal and newborn plasma choline concentrations, and the relation between plasma choline status and normal newborn length, weight, and gestational age. Blood samples were obtained from 104 full-term newborns in two centers (Ben Taub and Maimonides), 25 mothers, 21 normal infants aged 20.3 +/- 11.8 wk, 12 normal infants aged 62.4 +/- 3.9 wk, and 14 preterm infants (gestational age = 28.9 +/- 2.2 wk) who required TPN. The vein PFChs were 28.1 +/- 13.0 nmol/mL (Ben Taub) and 68.1 +/- 16.9 nmol/mL (Maimonides). The artery PFChs were 27.1 +/- 13.0 nmol/mL (Ben Taub) and 57.9 +/- 11.6 nmol/mL (Maimonides). The vein PPLChs were 1004.7 +/- 246.6 nmol/mL (Ben Taub) and 1121.2 +/- 289.6 nmol/mL (Maimonides). The artery PPLChs were 1065.7 +/- 469.3 nmol/mL (Ben Taub) and 1106.9 +/- 285.8 nmol/mL (Maimonides). The vein-minus-artery differences for PFCh were 1.0 +/- 9.7 nmol/mL (Ben Taub) and 10.2 +/- 10.9 nmol/mL (Maimonides). The vein-minus-artery differences for PPLCh were -51.9 +/- 398.2 nmol/mL (Ben Taub General Hospital, Houston, Texas) and 14.4 +/- 254.3 nmol/mL (Maimonides, New York, New York). Maternal venous PFCh was 8.4 +/- 3.1 nmol/mL. Maternal venous PPLCh was 2592.1 +/- 584.0 nmol/mL (range = 1227.8-3729.0). Maternal venous PFCh correlated with newborn arterial PFCh (r = 0.53, P < 0.05) but not with newborn venous PFCh. No correlation was seen between maternal venous and newborn PPLCh. No significant differences were seen in PPLCh or choline extraction in Ben Taub versus Maimonides patients, although PFCh was significantly greater in the newborns from Maimonides (P < 0.05). The mean venous PFCh and PPLCh in the preterm infants before beginning TPN was 21.2 +/- 6.3 and 1366.8 +/- 339.1 nmol/mL, respectively. Just before initiation of tube feeding (4.0 +/- 2.7 d after TPN had been started), mean venous PFCh and PPLCh was 18.4 +/- 5.3 and 2251.8 +/- 686.9 nmol/mL, respectively. When TPN was discontinued and tube feeding increased to goal, after 10.8 +/- 10.4 d, venous PFCh and PPLCh was 22.6 +/- 8.7 and 2072.5 +/- 540.6 nmol/mL, respectively. Venous PFCh and PPLCh was 13.4 +/- 2.5 and 1827.5 +/- 327.0 nmol/mL, respectively in the older infant group. In conclusion, newborn PFCh is significantly greater than PFCh in adults but falls to adult levels within the first year of life. Low maternal PFCh may be associated with low newborn PFCh. Normal newborn plasma choline status has no bearing on intrauterine growth, although the role of maternal choline deficiency in underweight newborns is unknown. Newborn PPLCh is substantially below that of adults, which suggests its use in membrane synthesis during growth.     

Preterm birth affects the intestinal response to parenteral and enteral nutrition in newborn pigs

Maturation of gastrointestinal (GI) function in neonates is stimulated by enteral nutrition, whereas parenteral nutrition induces GI atrophy and malfunction. We investigated whether preterm birth alters the GI responses to parenteral and enteral nutrition. Pigs were delivered either preterm (107 d gestation) or at term (115 d gestation) and fed total parenteral nutrition (TPN) or enteral sow's milk (ENT) for 6 d after birth. Immaturity of the preterm pigs was documented by reduced blood pH, oxygen saturation and neutrophil granulocyte function, impaired intestinal immunoglobulin G uptake from colostrum, and altered relative weights of visceral organs (small intestine, liver, spleen, pancreas, and adrenals). For both ages at delivery, increases occurred in pancreatic weight (30-75%) and amylase activity (0.5- to 13-fold) after birth, but much more in ENT than in TPN pigs (P < 0.05). Six days of TPN feeding was associated with reduced intestinal weight for both delivery groups (60% of values in ENT, P < 0.001), but only in term TPN pigs was the weight lower than at birth (-20%, P < 0.05). Likewise, it was only in term TPN pigs that intestinal maltase activity increased, compared with ENT, and the absorption of glucose and proline decreased. Only in preterm pigs did TPN feeding increase lactase activity (+50% compared with ENT, P < 0.05). For both delivery ages, the mRNA of lactase-phloridzin hydrolase and sodium-coupled glucose transporter 1 (SGLT-1) were increased in TPN, compared with ENT. In conclusion, the trophic effect of enteral vs. parenteral nutrition on the GI tract is also present after preterm birth, but the postnatal maturation of many GI functions is modified, compared with term birth. The effects of nutritional regimen on the maturation of the gut epithelium in neonates depend on gestational age at birth.     

Preterm birth affects the intestinal response to parenteral and enteral nutrition in newborn pigs

Maturation of gastrointestinal (GI) function in neonates is stimulated by enteral nutrition, whereas parenteral nutrition induces GI atrophy and malfunction. We investigated whether preterm birth alters the GI responses to parenteral and enteral nutrition. Pigs were delivered either preterm (107 d gestation) or at term (115 d gestation) and fed total parenteral nutrition (TPN) or enteral sow's milk (ENT) for 6 d after birth. Immaturity of the preterm pigs was documented by reduced blood pH, oxygen saturation and neutrophil granulocyte function, impaired intestinal immunoglobulin G uptake from colostrum, and altered relative weights of visceral organs (small intestine, liver, spleen, pancreas, and adrenals). For both ages at delivery, increases occurred in pancreatic weight (30-75%) and amylase activity (0.5- to 13-fold) after birth, but much more in ENT than in TPN pigs (P < 0.05). Six days of TPN feeding was associated with reduced intestinal weight for both delivery groups (60% of values in ENT, P < 0.001), but only in term TPN pigs was the weight lower than at birth (-20%, P < 0.05). Likewise, it was only in term TPN pigs that intestinal maltase activity increased, compared with ENT, and the absorption of glucose and proline decreased. Only in preterm pigs did TPN feeding increase lactase activity (+50% compared with ENT, P < 0.05). For both delivery ages, the mRNA of lactase-phloridzin hydrolase and sodium-coupled glucose transporter 1 were increased in TPN, compared with ENT. In conclusion, the trophic effect of enteral vs. parenteral nutrition on the GI tract is also present after preterm birth, but the postnatal maturation of many GI functions is modified, compared with term birth. The effects of nutritional regimen on the maturation of the gut epithelium in neonates depend on gestational age at birth.     

An evaluation of total parenteral nutrition using Vamin and Aminosyn as protein base in critically ill preterm infants

A total of 75 preterm infants with gestation less than 32 wk received total parenteral nutrition (TPN) using Vamin and Aminosyn as protein base lasting more than 20 days. They were monitored for signs of liver dysfunction, cholestatic jaundice, and TPN-induced metabolic bone disease (osteopenia of prematurity). It was observed that severity of TPN-induced cholestasis depends on the duration of TPN and quantity of protein infused. When used as a protein base, Vamin seemed to be superior to Aminosyn. TPN-induced metabolic bone disease was strongly correlated to the duration of TPN. We suggest close monitoring of critically ill preterm infants on TPN for quantity of protein infusate, liver dysfunction, cholestatic jaundice, and TPN-induced metabolic bone disease. Intravenous protein intake should be limited to less than 2.5 g/kg/day in preterm infants with gestation less than 32 wk.     

Serum myoinositol concentrations in premature infants fed human milk, formula for infants, and parenteral nutrition

Myoinositol concentration was studied in serum of 65 neonates and their mothers at the time of birth, in samples of various types of feedings for infants, and in serial serum samples of 15 premature infants receiving human milk, formulas for infants, or parenteral nutrition over a 3-wk period. At birth the serum concentration of myoinositol was greater in neonates than in their mothers (108 +/- 10 vs 52 +/- 6 mumol/L, respectively, means +/- SEM, p less than 0.01). In feedings for infants, the concentrations of myoinositol were significantly greater in human milk than in formulas or parenteral nutrition solutions (1840 +/- 451 vs 420 +/- 110 vs 100 +/- 8 mumol/L, respectively, p less than 0.001). Over a 3-wk period the serum concentration of myoinositol increased in infants receiving human milk but not in those receiving formulas or parenteral nutrition. Serum concentrations of myoinositol in neonates are greater than in adults and are directly influenced by myoinositol intake.     

Continuous infusion of insulin in hyperglycemic low-birth weight infants receiving parenteral nutrition with and without lipid emulsion

The efficiency of a continuous infusion of insulin in improving glucose tolerance was compared in two groups of very low-birth weight infants (mean +/- SEM birth weights 757 +/- 40 vs 828 +/- 80 g and gestational ages 27.6 +/- 0.7 vs. 27.2 +/- 0.5 weeks) receiving total parenteral nutrition with and without the addition of lipid emulsion to the nutrition regimen. The mean +/- SEM cumulative doses of insulin (0.87 +/- 0.1 vs 1.15 +/- 0.3 U/kg) and hours required to decrease the blood glucose level to 120 mg/dL (9.1 +/- 0.8 vs 9.5 +/- 1.0 hours) were similar. Insulin was delivered with a syringe pump used for other routine purposes in the neonatal intensive care unit. Continuous intravenous insulin infusion is an effective, inexpensive, safe method for maintaining glucose homeostasis in low-birth weight infants who develop hyperglycemia as a consequence of total parenteral nutrition.     

Vitamin D requirement in infants receiving parenteral nutrition

The adequacy of low dose vitamin D (25 IU/dl) parenteral nutrition (PN) solution was studied in 18 infants. All infants had surgical indications for PN. The birth weights were 2810 +/- 135 g and gestational ages 37.4 +/- 0.5 wk (mean +/- SEM). Duration of study ranged from 5 to 175 days. Thirteen infants were studied for up to 6 weeks and five infants for 71 to 175 days. Results showed that studied infants maintained growth along normal percentiles for weight, length, and head circumference. Vitamin D status as indicated by serum 25 hydroxyvitamin D (25 OHD) rose from 15 +/- 1.9 ng/ml to 26 +/- 2.8 ng/ml, mean +/- SEM (p less than 0.001) after 9 days, and remained normal up to 6 months. Five infants with biochemical liver dysfunction also had normal serum 25 OHD concentrations, indicating the hepatic 25 hydroxylation process was not severely impaired. Serum total and ionized calcium, phosphorus, and vitamin D-binding protein concentrations were normal. Serum magnesium was mildly elevated in five infants (2.6 to 3 mg/dl) on one occasion and resolved spontaneously. Serum alkaline phosphatase (AP) concentrations rose above baseline values in 12 of 17 infants, but remained within normal range (less than 400 IU/liter at 30 degrees C). Another infant with markedly elevated AP values died from liver dysfunction. Radiographs of the forearms were normal except for marked demineralization in one infant in spite of normal 25 OHD concentrations. We conclude that 25 IU vitamin D/dl of nutrient infusate is adequate to maintain normal vitamin D status, as indicated by normal serum 25 OHD concentrations in infants receiving PN for as long as 6 months.     

Serum vitamin A and E concentrations in pediatric total parenteral nutrition patients

There is uncertainty as to optimal doses of fat soluble vitamins required by pediatric total parenteral nutrition (TPN) patients. We compared serum vitamin A (A) and E (E) concentrations analyzed by HPLC in chronic (greater than 2 weeks) TPN patients aged 1 month to 12 years to values obtained in out-patient surgery patients of the same age. TPN patients received 1500 micrograms of retinol and 2.5 IU of E as alpha-tocopheryl acetate (2.5 ml LyphoMed Multi Vitamin Concentrate). These doses were 214% of the recommended dose of A and 36% for E. Oral intake was minimal in most patients. The results of our study revealed a mean serum A level for TPN patients (N = 29) of 26.0 +/- 15.0 (SD) micrograms/dl vs 25.0 +/- 10.0 (SD) micrograms/dl in controls (N = 52). Mean serum E was 0.63 +/- 0.24 (SD) mg/dl vs 0.89 +/- 0.31 (SD) mg/dl for TPN patients and controls, respectively. There was no consistent trend related to duration of TPN for 23 patients with serial values. Seven (24%) TPN patients had serum A greater than mean + 2 SD of control (p less than 0.01). No values were less than mean - 2 SD. Infants on TPN had a significantly lower mean serum A (22.3 +/- 10.9 micrograms/dl) than TPN patients greater than 1 year of age (34.1 +/- 16.0 micrograms/dl; p less than 0.001). Fifty-two percent of TPN patients vs 26% of control had serum A less than 20 micrograms/dl (p greater than 0.1). For E, one patient had a high value and two patients low values relative to control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Total parenteral nutrition-associated cholestasis in rats: comparison of different amino acid mixtures

It has been suggested that the quantity of amino acids perfused is a pathogenetic factor in total parenteral nutrition (TPN)-associated hepatotoxicity. However, the effect of the qualitative pattern of amino acid solutions has not been studied. Rats on parenteral nutrition for 5 days received 10.2 g of dextrose and 3.4 g of amino acids daily. Bile flow (microliter/min/g liver protein) after administration of Vamin was 16.2 +/- 0.8, which was similar to that in controls given chow and dextrose iv, but it was significantly higher (p less than 0.001) than those on Travasol (12.3 +/- 0.8). The decrease in bile flow was not related to the large concentrations of alanine and glycine present in Travasol. However, the addition to Travasol of serine present only in Vamin increased bile flow significantly. Bile acid secretion rate, biliary lipid constituents, calcium, sodium, and glucose showed little change. In contrast, alpha-amino nitrogen was increased (p less than 0.05) in Vamin-perfused animals. Steatosis was noted in only a few animals in the Travasol group, and was not associated with an increase in the triglycerides content of the liver. Glycogen and protein content of the livers did not differ. The data show that the composition of amino acid solutions may be a determinant of TPN-induced cholestasis and suggest that the presence of methyl donor amino acids may have a protective effect.     

Intravenous vitamins for very-low-birth-weight infants

Term infants and children appear to adapt to large variations in vitamin intakes. This is supported by the finding of similar blood levels of vitamins despite several-fold differences in intake on a body weight basis. By contrast, the finding of marked elevation of some vitamins and low levels of others seen in very-low-birth-weight (VLBW) infants (less than 1500 g) suggest that this group has less adaptive capacity to high- or low-dose intakes. This indicates that their vitamin intakes need to be more closely aligned with actual needs. This paper reviews previously published data on vitamins A, E, B2, and B6 from VLBW infants receiving total parenteral nutrition (TPN). Vitamin A. VLBW infants are relatively deficient in retinol (R) at birth. During TPN large losses of R onto the delivery sets result in a further decline in stores of R as reflected in a progressive decline in plasma R during TPN. Because of the reported lower incidence of bronchopulmonary dysplasia associated with intramuscular vitamin A treatment, alternative methods of vitamin A delivery during TPN have been suggested. First, the vitamins were mixed with Intralipid (IL) and, second, retinyl palmitate (RP) rather than R was used. There was little in vitro loss of R when mixed with IL, and in vivo treatment resulted in higher blood levels after 1 month of retinol administration in IL than seen previously (21.4 +/- 4.2 vs 14.1 +/- 3.7 micrograms/dl).(ABSTRACT TRUNCATED AT 250 WORDS)     

Fatty acid composition of adipocyte membrane phospholipids and stored triglycerides in infants receiving total parenteral nutrition

Fatty acid (FA) composition of membrane phospholipids (PL) and stored triglycerides (TG) from adipose tissue was studied in eight infants aged 1 to 4 months receiving total parenteral nutrition (TPN) since birth. During this period, essential fatty acid (EFA) intake consisted exclusively of soybean oil emulsion administered by intravenous route (Intralipid 20%) representing 301 +/- 88 mg/kg/24 hr of linoleic acid and 58 +/- 18 mg/kg/24 hr of alpha-linolenic acid, or 2.3 +/- 0.6% and 0.4 +/- 0.1%, respectively, of total energy intake. The results were compared with those of eight control infants of the same age receiving orally a normal milk diet with an intake of 660 +/- 260 mg/kg/24 hr of linoleic acid and 101 +/- 35 mg/kg/24 hr of alpha-linolenic acid, or 4.5 +/- 0.7% and 0.7 +/- 0.3%, respectively, of total energy intake. Although their EFA intake was significantly lower (p less than 0.01) and administered only parenterally, after 1 to 4 months the infants receiving TPN still had a membrane phospholipid FA pattern of adipose tissue which was not significantly different from that of normal children of the same age. In stored adipocyte TG, the percentage of linoleic acid was significantly lower (p less than 0.01) in infants receiving TPN. This is probably of nutritional importance as at this stage of life the child builds up its stores of EFA. The proportion of the other fatty acids in adipocyte TG was not significantly modified.