Total Parenteral Nutrition Patients Research Articles

Family caregivers' perceptions of important knowledge and skills needed for managing total parenteral nutrition in the home

The purpose of this study was to describe the perceived knowledge and skills learning needs of 20 family caregivers, who assist the Total Parenteral Nutrition (TPN) patient with care at home. Family caregivers were surveyed concerning perceived educational needs. Nurses that provided the education were also surveyed about the content taught and other health care personnel involved in teaching. Frequencies from responses to caregiver and nurse questionnaires indicate caregivers felt information the nurses had taught them was important but that emotional social information should be expanded. Knowles' androgogy framework was used to interpret the implications of these data for practice.

Serious renal impairment is associated with long-term parenteral nutrition.

Thirty-three current long-term total parenteral nutrition (TPN) patients (13 men, 20 women) aged 21 to 79 years were prospectively studied to evaluate their change in glomerular filtration rate since beginning TPN. Creatinine clearance (CrCl) from the subject's initial home TPN clinic visit and at present were estimated from standard formulas and compared. The CrCl in 12 patients who had received home TPN for > 10 years was estimated retrospectively on a yearly basis. The estimated CrCl as an accurate measure of glomerular filtration rate was confirmed by measuring plasma indium-111 diethylenetriamine pentaacetic acid clearance. The mean daily intravenous protein intake and days during which nephrotoxic medications were used and number of bacteremic/fungemic episodes were determined for each subject. CrCl declined by 3.5 +/- 6.3% per year (p = .004). Twenty-nine of 33 patients had decreases of 0.6% to 15.4% per year. Tubular function, as determined by the tubular reabsorption of phosphate, was impaired in 52% of the subjects. The intravenous protein load averaged 1.28 +/- 0.32 g/kg per day, nephrotoxic drug use averaged 3.4 +/- 4.0% of all days on home TPN, and each patient averaged 2.3 episodes of bacteremia or fungemia since home TPN was started (0.5 +/- 0.5 episodes per year). When all factors were assessed simultaneously, nephrotoxic drug use, episodes of bacteremia/fungemia, and age accounted for approximately 46% of the variability in CrCl. When bacteremia/fungemia was expressed as a yearly rate, nephrotoxic drug use assumed no role in the glomerular filtration rate determination; infection rate and age alone accounted for 53% of the CrCl variability. We describe a profound decrease in renal function associated with long-term TPN, most of which is largely unexplained.

Small intestinal mucosa changes, including epithelial cell proliferative activity, of children receiving total parenteral nutrition (TPN).

We examined the small intestinal histology disaccharidase activities as well as the incorporation of [3H]thymidine into DNA of biopsies maintained in organ culture from seven children (ages 9 months to 5 years) receiving total parenteral nutrition (TPN). Three children suffered from inflammatory bowel disease and received TPN for one month (short term). Four required long-term TPN (> 9 months) for short-bowel syndrome. DNA was extracted from the samples following serial precipitation with perchloric acid. Results were compared to those from 22 age-matched children investigated for abdominal pain or chronic diarrhea. Short-term TPN resulted in slightly lower lactase, sucrase, and palatinase activities that were not statistically different from controls. Long-term TPN resulted in focal mild villus atrophy and a decrease in disaccharidase activity in two patients. Biopsies from long-term TPN patients incorporated less thymidine compared to those of controls (P < 0.001) when data was expressed per total biopsy (3.6 +/- 1.1 vs. 8.4 +/- 1.1 fmol) or per milligram of tissue (1.0 +/- 0.12 vs 2.7 +/- 0.7 fmol). The above data are in general agreement with the hypoplastic effect of TPN in animals. However, in children, much longer periods of TPN are required to realize the changes.

Lecithin increases plasma free choline and decreases hepatic steatosis in long-term total parenteral nutrition patients.

Several investigators, including the authors, have demonstrated that patients receiving long‐term total parenteral nutrition (TPN) have low plasma choline levels.1–3 In the present study, 15 patients who were receiving home TPN were randomly chosen from a group of long‐term TPN patients found to have low levels of plasma free choline on initial screening.3The patients received TPN for 7.0 ± 1.1 years (range, 1.5 to 12.5 years). Their TPN consisted of 2 to 3 liters of 15% to 25% dextrose solution with 3.5% to 4.25% amino acids, electrolytes, trace elements, and vitamins. Patients received 20.1 ± 2.2 kcal/kg per day actual body weight. Parenteral lipid supplied was 22 ± 5% of daily intravenous caloric intake (Intralipid 20%, Kabi‐Vitrum, Alameda, CA).Patients received either lecithin supplementation (20 g/12 hours in 2.5 tablespoons of soybean oil‐based liquid) or placebo (2.5 tablespoons of oil) for 6 weeks in a double‐blind fashion. Patients were evaluated at baseline and at 2 and 6 weeks. Laboratory measurements included plasma and red blood cell free choline, plasma and red blood cell phospholipid‐bound choline, transaminases, alkaline phosphatase, bilirubin, cholesterol, high and low density lipoproteins, carnitine (total and free), and methionine. Free and phospholipid‐bound choline levels were measured in bottles of Intralipid. Liver imaging was carried out by computed tomography (CT) scanning. Limited noncontrast CT scans of the liver and spleen were performed at 120 kV, 120 mA with a 3.0‐second scan time. Multiple representative sections were examined and a mean CT number in Hounsfield units was determined by two methods, determination of the mean absolute liver CT number and the liver spleen differential, obtained by subtracting the average spleen CT number from the average liver CT number to correct for interscan variability. Data were analyzed statistically by comparing percent changes in blood tests at 2 and 6 weeks and absolute changes in Hounsfield units.The full 6‐week study was completed in 10 of the 15 patients. Eight of 15 subjects had fatty livers at baseline. Lecithin supplementation led to an increase in plasma free choline of 53.4% ± 15.4% at 2 weeks (p &lt;.04), whereas the placebo group had no change at 2 weeks. A significant (p &lt;.02) decrease in liver fat, indicated by the change in Hounsfield units was seen at 2 weeks in the lecithin‐supplemented group (7.5 ± 1.7 units). No significant changes were seen in the placebo group.The authors concluded that hepatic steatosis in many patients receiving long‐term TPN is caused by plasma free choline deficiency and may be reversed with lecithin supplementation.

Lecithin increases plasma free choline and decreases hepatic steatosis in long-term total parenteral nutrition patients

Plasma-free choline levels have previously been found below normal in patients receiving long term parenteral nutrition (TPN). In a group of 15 patients receiving home TPN who had low plasma free choline levels (6.3 ± 0.8 mmol/L), we found 50% had hepatic steatosis. These patients were given oral lecithin or placebo in a double-blind randomized trial for 6 weeks. Lecithin supplementation led to an increase in plasma free choline of 53.4% ± 15.4% at 2 weeks (P = 0.04), which continued at 6 weeks. The placebo group had no change in plasma-free choline at 2 weeks, but a significant decrease of 25.4% ± 7.1% (P = 0.01) at 6 weeks. A significant and progressive decrease in hepatic fat was indicated by increased liver-spleen CT Hounsfield units at 2 and 6 weeks (7.5 ± 1.7 units, P = 0.02; 13.8 ± 3.5 units, P = 0.03) in the lecithin supplemental group. Nonsignificant changes were seen in the placebo group. It was concluded that hepatic steatosis in many patients receiving long term TPN is caused by plasma-free choline deficiency and may be reversed with lecithin supplementation. Choline is a conditionally essential nutrient in this population.

Lecithin increases plasma free choline and decreases hepatic steatosis in long-term total parenteral nutrition patients

Plasma-free choline levels have previously been found below normal in patients receiving long term parenteral nutrition (TPN). In a group of 15 patients receiving home TPN who had low plasma free choline levels (6.3 +/- 0.8 mmol/L), we found 50% had hepatic steatosis. These patients were given oral lecithin or placebo in a double-blind randomized trial for 6 weeks. Lecithin supplementation led to an increase in plasma free choline of 53.4% +/- 15.4% at 2 weeks (P = 0.04), which continued at 6 weeks. The placebo group had no change in plasma-free choline at 2 weeks, but a significant decrease of 25.4% +/- 7.1% (P = 0.01) at 6 weeks. A significant and progressive decrease in hepatic fat was indicated by increased liver-spleen CT Hounsfield units at 2 and 6 weeks (7.5 +/- 1.7 units, P = 0.02; 13.8 +/- 3.5 units, P = 0.03) in the lecithin supplemental group. Nonsignificant changes were seen in the placebo group. It was concluded that hepatic steatosis in many patients receiving long term TPN is caused by plasma-free choline deficiency and may be reversed with lecithin supplementation. Choline is a conditionally essential nutrient in this population. (Gastroenterology 1992 Apr;102(4 Pt 1):1363-70)

Platelet Glutathione Peroxidase Activity in Long‐Term Total Parenteral Nutrition With and Without Selenium Supplementation

Selenium (Se) is not routinely included in total parenteral nutrition (TPN) solution; thus, patients receiving long-term TPN may be at risk of Se deficiency, which may cause fatal cardiomyopathy. Platelet glutathione peroxidase (GSH-Px) activity, as well as Se levels and GSH-Px activity in plasma and erythrocytes during prolonged TPN, was measured in six patients with chronic gastrointestinal disease. During the time course of TPN, Se administration was discontinued for 12 weeks, and then resupplemented for another 12 weeks. Before the study period, all Se indices had been maintained within the normal range. After discontinuation of Se supplementation, a significant decrease in platelet GSH-Px activity was observed after 1 week (from 64 +/- 7 [mean +/- SD] to 39 +/- 5 U/g of protein). After resupplementation, it increased after 1 week (from 44 +/- 9 to 65 +/- 10 U/g of protein). Plasma Se indices significantly changed within 3 weeks after withdrawal and reintroduction of Se (Se: from 136 +/- 28 to 75 +/- 14 and from 61 +/- 22 to 125 +/- 33 micrograms/L; GSH-Px: from 236 +/- 50 to 140 +/- 36 and from 128 +/- 32 to 220 +/- 64 U/L). Erythrocyte Se indices showed no significant changes during the study period. The results demonstrate that platelet GSH-Px activity is the most sensitive index of Se status in TPN patients.

Immediate enteral nutrition following multisystem trauma: a decade perspective.

Metabolic support is an integral component of surgical critical care. Although prompt restoration of oxygen availability is clearly essential, the timing, composition, and route of nutritional support may also be decisive factors. The ensuing discussion will focus on: (a) timing of substrate delivery and (b) route of administration based on our clinical investigation over the past decade. The acutely injured patient was selected as a model of ICU hypermetabolism because of relative homogeneity with respect to age, comorbid factors, and stress level. Our first study hypothesis was that early nutritional support would improve outcome in the severely injured, but previously well-nourished patient. During an 18-month period, all patients undergoing laparotomy with a abdominal trauma index (ATI) greater than 15 were randomized to a control or total enteral nutrition (TEN) group. The control patients were given total parenteral nutrition (TPN) after POD 5, whereas the TEN cohort had a needle catheter jejunostomy (NCJ) inserted at laparotomy and received an elemental diet within 12 hours. The control (n = 31) and TEN (n = 32) groups were otherwise comparable with respect to risk stratification. The TEN patients, of course, shared improved nitrogen balance (p less than 0.001), but also had significantly (p less than 0.025) less septic morbidity. Nine (29%) of the controls developed major infections, contrasted to three (9%) of the TEN patients. Acknowledging the benefit of early nutrition, the next issue we addressed was the optimal route of substrate delivery; i.e., TEN vs TPN. The hypothesis was that TEN, compared to TPN, would reduce the injury stress response as reflected by the prioritization of hepatic protein synthesis. TEN given via NCJ and a nutritionally matched TPN solution were administered during the same postoperative period. Indeed, the TEN patients (n = 23) had significantly (p less than 0.05) higher constitutive proteins and lower acute-phase proteins, whereas the TPN patients manifested the opposite protein profile as measured by crossed immunoelectrophoresis. In view of these findings, we continued the study to ascertain clinical impact. Ultimately, 75 patients were randomized, providing groups with equivalent risk factors. Eleven (37%) of the TPN patients developed septic complications compared to five (17%) of the TEN group, and the incidence of major infection was six (20%) following TPN vs one (3%) with TEN. Thus, immediate TEN provided an additional clinical benefit compared to early TPN in these high-risk surgical patients.

Vitamin E Status of Patients Receiving Long‐Term Parenteral Nutrition: Is Vitamin E Supplementation Adequate?

Vitamin E status of eight patients receiving total parenteral nutrition (TPN), including 10 IU of all-racemic alpha-tocopheryl acetate daily and Intralipid 20% (500 mL; 12 mg of RRR-alpha- and 92 mg of RRR-gamma-tocopherols) two to three times per week for 69 +/- 45 (mean +/- SD) months was assessed by measuring plasma and adipose tissue tocopherol concentrations. Plasma alpha-tocopherols of TPN patients were similar to controls (17.5 +/- 6.6 mumol/L vs 22.4 +/- 5.1), whereas gamma-tocopherols were significantly reduced (6.0 +/- 3.1 vs 11.2 +/- 3.6, p less than 0.03). The adipose tissue alpha- and gamma-tocopherol/triglycerides (TG) were similar (369 +/- 215 nmol/mmol vs 452 +/- 228, and 125 +/- 102 vs 140 +/- 130, respectively), but cholesterol/TG were increased in the TPN patients (7.8 +/- 2.5 mumol/mmol vs 5.1 +/- 3.5, p less than 0.05), suggesting that adipose tissue was relatively TG-depleted and tocopherol/cholesterol measurements better reflect vitamin E status. The mean alpha-tocopherol/cholesterol ratios were significantly lower in the TPN patients than the controls (55 +/- 36 vs 106 +/- 63, p less than 0.04). Thus, current vitamin E supplementation of TPN patients seems insufficient for maintenance of adequate tissue stores.

The effect on body composition and exercise performance of home parenteral nutrition when given as adjunct to chemotherapy of testicular carcinoma

This study has evaluated whether long-term and permanent total parenteral nutrition (TPN) can protect body composition and exercise capacity during iterated courses of chemotherapy (PVB) in men with testicular carcinoma. Thirty-three men were randomly allocated by means of a computer based algorithm to receive either TPN (at hospital and home) during the entire chemotherapy period or to rely on spontaneous oral intake only. Nutrition status was assessed by measurements of whole body nitrogen (neutron activation), total body potassium, body water, urine creatinine excretion, loco-regional body nutrition indexes (AMC, TSF) and biochemical plasma concentrations (albumin, thyroid hormones). Whole body respiratory gas exchanges were measured during resting, submaximal and maximal exercise. TPN was prescribed on an individual basis in all study patients to cover 150% of their measured caloric need; nitrogen was given as 0.2 g N kg-1 day. All individuals were allowed to eat freely throughout the study. TPN patients were in overall positive energy balance (+850 Kcal day-1), while the control group was in negative balance (-532 Kcal day-1). This led to weight gain in the TPN group (+2.2 +/- 1.0 kg) while the control group lost significant weight (-4.2 +/- 1.1 kg). The average spontaneous oral caloric intake was 1014 +/- 153 Kcal day-1 in the TPN group and 1484 +/- 200 Kcal day-1 in the control group; total protein intake corresponded to 1.5 g protein kg day-1 in the TPN group and 0.7 kg day-1 in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose-tissue fatty acid composition in recipients of long-term total parenteral nutrition (TPN)

Adipose-tissue fatty acid composition was studied in nine patients requiring long-term total parenteral nutrition (TPN). The patients received 17 +/- 8% of total energy as soybean-oil emulsion (Intralipid) and 66 +/- 8% as glucose. Despite low intake of 9c-16:1, 11c-18:1, and 13c-18:1, adipose-tissue concentrations of these monounsaturated fatty acids were higher in the TPN patients than in free-living control subjects (P less than 0.05) and inversely correlated with the percent energy from fat (r = -0.56, P = 0.11; r = -0.64, P = 0.06; r = -0.81, P = 0.008, respectively). This suggests that these fatty acids accumulated from endogenous synthesis from carbohydrate and thus may be markers of the percent fat in the diet. The essential fatty acids, 18:2 and 18:3n-3, positively correlated with the percent energy from fat (r = 0.79, P = 0.01; r = 0.80, P = 0.01, respectively). Linear-regression analysis suggests that normal adipose-tissue stores of 18:2 and 18:3n-3 are maintained when intravenous soybean-oil emulsion provides 11-20% and 4-12%, respectively, of total energy.

Liver Dysfunction Associated with Long‐Term Total Parenteral Nutrition in Patients with Massive Bowel Resection

Sixteen patients with massive bowel resection receiving long-term home total parenteral nutrition (HTPN) for 31 to 145 months were reviewed for evidence of liver disease. Patients were divided into three groups: group 1 with duodenocolostomy (n = 3), group 2 with an estimated 15-43 cm residual small bowel (n = 7), and group 3 with an estimated 55-120 cm residual small bowel (n = 6). Two patients in group 1 developed liver cirrhosis; one was diabetic and died of sepsis and liver failure at the 88th month on HTPN; the other died of lung cancer at the 46th month on HTPN. The third patient, followed for 33 months, had transient severe liver function abnormalities associated with a blood transfusion. In groups 2 and 3, only one patient (with a history of probable liver disease before HTPN) developed biopsy-proven cirrhosis at the 60th month of HTPN. All four patients with clinically apparent liver disease developed persistent elevation of serum aspartate aminotransferase (AST) early in HTPN. Four other patients (all in group 3) with abnormal AST values in the early phase of HTPN normalized them later; they did not develop clinical liver disease over a mean follow-up time of 110 months (range, 39-152). None of the remaining eight patients (seven in group 2 and one in group 3) had significant liver function test abnormalities and none developed clinical liver disease over a mean follow-up period of 72 months (range, 39-120).(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced retention of urea-nitrogen in patients on total parenteral nutrition for intestinal failure

Urea, the main end product of human nitrogen metabolism, is either excreted in the urine or salvaged for further metabolic interaction, through the activity of the colonic microflora. In patients on TPN (total parenteral nutrition) the bowel is ‘defunctioned’ insofar as the microflora are deprived of exogenous substrate, and it might be expected that urea salvaging is reduced to low levels. The recovery of labelled urea-nitrogen was measured in 7 patients on TPN and compared with 4 normals. Following a single intravenous dose of 15N15N-urea, urine was collected for 48h and analysed for 15N. In normals the median retention of 15N was 17% (range 13–17) of the dose compared with 38% (24–52) in 5 TPN patients not on antibiotics (p < 0.05). TPN patients on antibiotics retained 11 and 15%. Despite the absence of exogenous substrate, the ‘defunctioned’ bowel of patients on TPN appears more active in hydrolysing urea than in normals, and the hydrolysis is sensitive to the effect of antibiotics.

Tumor cytokinetic response to total parenteral nutrition in patients with head and neck cancers

Refeeding of patients with malignant tumors may induce tumor-cell DNA synthesis. The present study was aimed at evaluating whether induction of altered cell-cycle kinetics could be induced by intravenous total parenteral nutrition (TPN) in tumor biopsies from head and neck cancers. Nine malnourished patients with squamous cell carcinoma in the head-and-neck area were investigated before and after 5-7 d of continuous TPN. Tumor biopsies were taken in both fasted and fed states for determination of 1) ornithine decarboxylase (ODC) activity, which is rate limiting for polyamine synthesis; 2) flow-cytometric-DNA-distribution measurements; and 3) the fraction of proliferating cells expressed as immunohistochemical reactivity with the monoclonal antibody Ki-67. The histopathological differentiation, the fraction of aneuploidic cells, ODC activity, and Ki-67 reactivity were not significantly related to each other, although the number of aneuploidic cells in replicative phases correlated with the number of cells expressing the Ki-67 antigen (r = 0.86, P less than 0.01). Tumor cytokinetics showed no evidence of being changed by TPN administration.

Parenteral Drug Products Containing Aluminum as an Ingredient or a Contaminant: Response to Food and Drug Administration Notice of Intent and Request for Information

Aluminum remains a significant contaminant of total parenteral nutrition (TPN) solutions and may be elevated in bone, urine, and plasma of infants receiving TPN. Aluminum accumulation in tissues of uremic patients and adult TPN patients has been associated with low-turnover bone disease. Furthermore, aluminum has also been linked with encephalopathy and anemia in uremic patients and with hepatic cholestasis in experimental animals. Because of the toxic effects of aluminum, the Food and Drug Administration (FDA) recently published a notice of intent to set an upper limit of 25 micrograms/L for aluminum in large-volume parenterals and to require manufacturers of small-volume parenterals, such as calcium and phosphate salts, to measure aluminum content and note this content on the package label. The ASCN/A.S.P.E.N. Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions supports these intentions and further urges the FDA to require that cumulative aluminum intake in terms of safe, unsafe, and toxic quantities of aluminum per kilogram be made known to physicians and pharmacists preparing the TPN solutions, to ensure that manufacturers use appropriate control procedures in aluminum measurements, and to employ a standard unit of aluminum measurement.

Energy expenditure measured by the doubly labeled water method during hyperalimentation of patients with liver cirrhosis

Energy expenditure measured by the doubly labeled water method during hyperalimentation of patients with liver cirrhosis

Postheparin plasma diamine oxidase in health and intestinal disease

In animals, the distribution of the enzyme diamine oxidase is confined, almost exclusively, to the small bowel mucosa. In humans, plasma diamine oxidase is at or below assay detection limits but can be liberated into the circulation from binding sites in the intestine by i.v. heparin. Therefore, the authors wished to see if diamine oxidase could be released by a low and safe dose of heparin (5000 U) and if the resultant area under the concentration-time curve would provide a noninvasive marker of segmental intestinal disease. In 17 control subjects, the mean area under the curve (following administration of 5000 U i.v. heparin) was 35.9 ± 5.0 (SEM) mU · L−1 · 2 h−1; in 6 individuals studied on two separate occasions, postheparin plasma diamine oxidase profiles were reproducible (r = 0.98; p < 0.001). The longitudinal distribution of diamine oxidase in the gastrointestinal tract, measured in 12 gastric, 16 jejunal, 6 ileal, and 18 colonic biopsies, was similar in humans to that found in animals. In patients with normal peroral biopsies, there was a linear relationship between jejunal mucosal and postheparin plasma diamine oxidase activities (r = 0.84; p < 0.01). The areas under the curve in controls were then compared with those in patients with segmental intestinal diseases: 21 with ileal disease with or without colonic Crohn's disease (10 unoperated and 11 with ileal resection), 7 with non-Crohn's ileal resection, 8 with ulcerative colitis, 10 with untreated and 7 with treated celiac disease (6 studied before and after a gluten-free diet), and 5 studied during total parenteral nutrition and again after resumption of oral feeding. The results in the 18 ileectomized patients were subdivided into those with major (arbitrarily >75 cm) and minor (< 75 cm) resections. Areas under the curve were markedly reduced in nonresected Crohn's patients (6.0 ± 1.79 mU · L−1 · 2 h−1; p < 0.001 vs. controls), correlating inversely, in a first-order relationship, with disease activity (r = 0.82; p < 0.001) and returning toward normal in 4 patients achieving disease remission. Low areas under the curve in total parenteral nutrition patients (4.5 ± 0.9; p < 0.001) were also reversible on resumption of oral feeding. However, areas under the curve were not significantly lower in patients with limited ileal resection (≤75 cm), with celiac disease (untreated and treated), or ulcerative colitis than in controls. Postheparin plasma diamine oxidase with the dose of heparin used in this study does not provide a marker of proximally confined celiac disease, but it does provide an index of active ileal Crohn's disease, of extensive ileal resection, and of presumed intestinal mucosal hypoplasia during total parenteral nutrition. Areas under the curve were also reduced in patients with major (11.0 ± 1.6; p < 0.01 vs. controls; p < 0.002 vs. major resections) but not in those with limited (< 75 cm) ileal resections (25.7 ± 2.75; NS).

Fecapentaene excretion: aspects of excretion in newborn infants, children, and adult normal subjects and in adults maintained on total parenteral nutrition

People in developed nations such as the United States and Canada have an increased risk of colon cancer. Fecal mutagens have been detected in the feces of individuals at high risk for colon cancer. We describe a rapid, sensitive, reliable, reproducible high-pressure liquid chromatography (HPLC) method for detecting fecapentaenes, the most active and chief mutagen found in human stool. We found fecapentaene in all the stool samples of adults on typical high-fat, low-fiber Western diets. These fecapentaene concentrations remained largely constant when subjects consumed constant diets. Fecapentaene concentrations were reduced for total-parenteral-nutrition (TPN) patients with severe intestinal malabsorption. This finding with TPN patients may reflect changes in important variables of gut microflora in fecapentaene production. Studies with newborns and children showed that fecapentaenes appeared very early in life but are not present in stool at birth.

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)

Selected ultratrace elements in total parenteral nutrition solutions

Ultratrace elements are potentially essential (eg. boron, molybdenum, nickel, and vanadium) or toxic (eg, aluminum and cadmium) in humans. Long-term total parenteral nutrition (TPN) patients can inadvertently receive significant amounts of ultratrace elements present as contaminants in TPN solutions. We determined the intake of selected ultratrace elements from a standard TPN solution and compared it with the amount reported to be absorbed from food in normal subjects. Contamination of TPN solutions with ultratrace elements was widespread and variable. The daily intakes of Mo, Ni, V. and Cd from this contamination were comparable to the amounts reported to be absorbed through the gastrointestinal tract in normal subjects. Al intake was high; B intake was low, approximately 10% of the amount absorbed by normal subjects. Thus, TPN solutions are contaminated with significant amounts of ultratrace elements. The biological significance of the intravenous infusion of these ultratrace elements is unclear and requires further investigation, particularly in home TPN patients.