Effects of prolonged, purine-free total parenteral and enteral nutrition on urate homeostasis in man

The influence on human urate homeostasis of prolonged, totally purine-free nutritional support, using total parenteral (TPN) or elemental enteral (EN) nutrition, is not well known. In a prospective study, we measured weekly serum uric acid, renal urate excretion and clearance, together with parameters of hydration, in 58 normally hydrated patients receiving prolonged (15 to 170 days) purine-free TPN (30 patients) or EN (28 patients) for various gastrointestinal disorders. A marked, early and sustained decrease (p less than 0.001) in serum uric acid was observed in TPN (155 +/- 9 mumol/l at day 7 versus 318 +/- 13 mumol/l before nutrition, mean +/- SEM) as well as in EN patients (192 +/- 11 mumol/l at day 7 versus 320 +/- 16 mumol/l before nutrition), together with a significant (p less than 0.01) rise in renal urate clearance. The urate clearance/glomerular filtration rate ratio increased significantly, while there was no significant change in natremia or plasma osmolarity. Serum urate and urate clearance returned to normal within 8 days of refeeding with a normally purine-containing diet. Replacement of TPN by EN or vice versa, or substitution of glucose by fructose resulted in no change in hypouricemia. A 4-day oral supply of purines (125 mg/day) in EN patients was associated with a 53% rise (p less than 0.01) in serum urate. We conclude that prolonged, purine-free TPN and elemental EN are a new cause of marked hypouricemia which is mainly due to increased urate clearance, the mechanism of the latter is still poorly known, but is not related to extracellular volume expansion.     

Selenium status prior to and during one month total parenteral nutrition in gastroenterological patients: A randomised study of two dosages of Se supplementation

13 consecutive adult gastroenterological patients with non-malignant disease who were candidates for total parenteral nutrition (TPN), and who had mild protein-energy malnutrition (82 +/- 3% of ideal body weight, serum albumin 32 +/- 2 g/l, mean +/- SEM) were found to have, prior to TPN, a Selenium level 50% less than controls (p < 0.001) as assayed by Se and glutathione peroxidase (GSHPx) in plasma and erythrocytes. Compared with other trace metals and minerals, eg, Mn, Zn and Cu, depletion of Selenium was the most marked in this population. Patients were randomised to be supplemented with either 100 or 200 mug/d of sodium-selenite, equal to 32 mug (0.4 mumol) or 64 mug (0.8 mumol) of selenium, in two cross-over periods of TPN, each of two weeks. In this short term study, significant increases in the four measurements of Se status (p < 0.05) were seen in all patients, but there was no difference between those receiving the high or low dose of the element. GSHPx in plasma was normalised within 1 month whereas the increase seen in the erythrocyte pool was consistent with a 4-month half-life. Pooled Se values for patients and controls showed logarithmic correlations between Se and GSHPx in erythrocytes (p < 0.001) and plasma (p < 0.01). Changes in GSHPx provided further evidence of Se depletion in our patients. This study suggests that malnourished gastroenterological patients receiving TPN require Se supplements and that 100 mug (0.4 mumol)/d of sodium-selenite is adequate for most patients since there was no additional benefit from the higher dose of 200 mug (0.8 mumol).     

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.     

Serum carnitine levels in bone marrow transplant recipients

This study investigated plasma carnitine levels in patients undergoing allogenic bone marrow transplantation. The patients received fat-based TPN (50% fat, 50% CHO; calorie: nitrogen ratio 125:1) for an average of 33 +/- 7.5 days. TPN was started before transplantation and stopped when patients were able to eat. Caloric needs were estimated using the Harris-Benedict equation; 150% of the estimated BEE was given for the first two weeks after transplantation. The amount of TPN was gradually decreased as patients resumed their oral intake. All patients had low-normal serum carnitine levels before transplantation. There was no significant change in total or free serum carnitine levels during the course of TPN. However, in patients who had symptoms of graft vs. host reaction (GVH), the highest carnitine values during GVH (total 72.3 +/- 6.5 and free 61.2 +/- 12.4 mumol/l) were significantly higher (p < 0.001) than the baseline values (total 27.1 +/- 9.3 and free 24.9 +/- 9.6 mumol/l) or the highest non GVH values after transplantation (total 32.0 +/- 10.7 and free 29.0 +/- 10.7 mumol/l, respectively). The serum triglyceride, total cholesterol, and HDL cholesterol remained within normal range. In conclusion, bone marrow transplant patients receiving fat-based TPN have normal circulating levels of carnitine. GVH reaction caused an increase in the carnitine levels, which was probably due to increased tissue catabolism.     

Decreased serum selenium in alcoholics as related to liver structure and function

Serum selenium was evaluated in relation to hepatic structure and function in 46 alcoholics with diagnostic liver biopsy classified into 4 groups by hepatic histology. Their serum selenium concentration varied from 12 to 88 micrograms/l and was lower (p less than 0.001) in all groups of alcoholics, ie patients with normal liver (53.0 +/- 20.7 micrograms/l, mean +/- SD), fatty liver (55.8 +/- 21.2 micrograms/l), alcoholic hepatitis (46.0 +/- 14.1 micrograms/l), and cirrhosis (41.1 +/- 12.8 micrograms/l), than in 25 healthy controls (88.7 +/- 11.0 micrograms/l). Serum selenium level was related to the severity of liver disease, and most reduced in subjects with decompensated alcoholic cirrhosis. Their serum selenium level (29.2 +/- 13.7 micrograms/l) was below (p less than 0.05) that obtained in alcoholics with normal liver and fatty liver respectively. Both inadequate dietary selenium intake and alcohol-induced changes in hepatic structure and function may have contributed to the decrease of serum selenium in the subjects studied.     

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.     

Selenium status in term and preterm infants during the first months of life

OBJECTIVE: We hypothesized that very low birth weight (VLBW) infants have reduced serum and red blood cell (RBC) selenium (Se) at birth, which decrease further with current nutrition and are associated with chronic lung disease and septicaemia. DESIGN: We studied Se intake, concentration in serum and RBCs and glutathione peroxidase (GSH-Px) activity in preterm and term infants from birth until 16 weeks. Data are mean+/-standard deviation (s.d.). SETTING: Seventy-two preterm infants in two groups, born in Berlin, gestational age 26+0/30+0 weeks, birth weight 845/1270 g, with low Se intake (2.2+/-0.8/2.5+/-1.2 microg/kg/day), and 55 term infants, gestational age 39+1 weeks, birth weight 3160 g, born in Venezuela (high Se intake: 29+/-8 microg/day). RESULTS: A balance study in 10 preterm infants showed that Se is well absorbed from human milk (77+/-9%). Serum concentration was higher in term (142.0+/-40.0 microg/l) than in preterm infants (17.8+/-8.1/19.9+/-2.2 microg/l) at 4/7 weeks. Serum and RBC concentration of Se declined in all infants, low values in preterm infants did not correlate with chronic lung disease and septicaemia. GSH-Px activity in RBCs remained stable until 6 weeks of age in all infants and was not correlated with Se in RBCs. CONCLUSIONS: Se concentration in serum decreases during the first weeks of life and depends on intake. GSH-Px activity is not useful as a marker for Se status in infants up to 16 weeks after birth.     

Reduced concentration of hepatic alpha-tocopherol in patients with alcoholic liver cirrhosis.

The concentration of alpha-tocopherol was measured in liver biopsy specimens obtained from 83 patients with alcoholic and non-alcoholic liver diseases. The mean hepatic vitamin E content (as alpha-tocopherol) was significantly lower in 23 patients with alcoholic cirrhosis (17.6 +/- 12.1 nmol/mg wet weight liver), compared with 12 patients with normal liver histology (39.2 +/- 29.7 nmol/mg, P less than 0.01). The mean serum concentration of alpha-tocopherol was lower in patients with alcoholic cirrhosis (13.9 +/- 7.0 mumol/l) than in individuals with alcoholic fatty liver (21.3 +/- 9.3 mumol/l, P less than 0.01) and patients with normal liver histology (23.4 +/- 11.6 mumol/l, P less than 0.01). A decreased ratio of serum alpha-tocopherol/total serum lipids was also observed in patients with alcoholic cirrhosis, compared with patients with normal liver histology (P less than 0.05). There was a significant correlation between concentrations of alpha-tocopherol in liver and serum (r = 0.43, P less than 0.001). Furthermore, serum alpha-tocopherol correlated with retinol (r = 0.53, P less than 0.001), selenium (r = 0.45, P less than 0.001), and albumin (r = 0.37, P less than 0.001) in serum. We suggest that the reduced content of hepatic alpha-tocopherol observed in some patients may play a role in ethanol-induced lipid peroxidation.     

Glucose-based versus fat-based total parenteral nutrition (TPN): effects on hepatic function in septic patients complicated with cholestatic jaundice

A prospective study of two types of total parenteral nutrition (TPN) was carried out in 34 patients suffering from sepsis and complicated liver dysfunction. Group 1 (18 patients) received non-protein energy as glucose plus fat emulsion in a caloric ratio of 19:1, while group 2 (16 patients) received the same energy intake but with a ratio of 1:1. Group 1 exhibited higher levels of bilirubin and alkaline phosphatase with values of 93.5 +/- 25.5 mumol/l and 160 +/- 30 IU/l respectively compared to Group 2, in which the corresponding values were 81.6 +/- 32.3 mumol/l and 120 +/- 10 IU/l (p < 0.05). On the other hand, group 1 had lower levels of serum albumin and serum transferrin with values 25 +/- 1.3 g/l and 40 +/- 20% of normal, compared to group 2 in whom the corresponding values were 28 +/- 8 g/l and 48 +/- 30% of normal (p < 0.05). There were no differences between the two groups, in the absolute number of T-lymphocytes and in transaminase levels. In sepsis complicated by liver dysfunction a 50:50 glucose: fat regimen caused less disturbance of liver function than one consisting almost entirely of glucose.     

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)     

口服亚硒酸钠和维生素E对高海拔地区心血管病患者甲状腺激素的影响

目的探讨使用亚硒酸钠和维生素E对高海拔地区心血管病患者甲状腺激素的影响.方法将心血管病患者随机分为3组A组42例患者口服亚硒酸钠,同时加服维生素E;B组28例患者口服亚硒酸钠;对照组20例,未服用亚硒酸钠及维生素E.观察对象分别于治疗前和治疗6个月后抽血检测血清硒(Se)、血浆谷胱甘肽过氧化物酶(GSH-Px)活力、丙二醛(MDA)含量及甲状腺激素(T3、T4)等指标,以观察远期疗效.结果治疗后A组和B组血清Se含量[(0.71±0.22)、(0.68±0.18)μmol/L]明显高于治疗前[(0.31±0.17)、(0.33±0.14)μmol/L],差异有显著性(P＜0.01);A组和B组血浆GSH-Px活力分别为(87.12±13.61)、(84.79±12.13)U/L,较治疗前[分别为(58.43±18.93)、(57.12±17.36)U/L]明显增加.A组和B组MDA含量[(4.86±1.18)、(4.18±1.23)nmol/ml]较治疗前[(8.66±0.96)、(8.71±0.87)nmol/ml]明显降低,差异均有显著性(P＜0.01);A组和B组患者T3和T4较对照组明显降低,趋于正常.血清Se与血浆GSH-Px呈正相关(r=0.781,P＜0.01),与MDA、T3、T4浓度呈负相关(r=-0.385;r=-0.687;r=-0.412,均P＜0.05).甲状腺激素恢复正常者A组31例(73.81%)、B组20例(71.42%);部分恢复者A组4例(9.52%)、B组2例(7.43%),其恢复率明显高于对照组,差异有显著性(P＜0.05),远期疗效较好.结论补充适量硒和维生素E可纠正高原环境下因低Se而引起的甲状腺激素代谢异常.     

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.     

Long-term parenteral nutrition in unrestrained nonhuman primates: an experimental model

A freely mobile jacket and tether system was developed for the investigation of total parenteral nutrition (TPN)-induced metabolic bone disease and complications of prolonged TPN in 12 Macaca fascicularis nonhuman primates. The animals received TPN for 49 +/- 7 d (means +/- SEM), providing 82 +/- 2 kcal.kg-1.d-1. Serum glucose increased from 3.6 +/- 0.2 mmol/L at baseline to 8.3 +/- 1.9 mmol/L (p less than 0.01) during TPN, and serum albumin decreased from 38 +/- 1 g/L at baseline to 29 +/- 1 g/L (p less than 0.001) during 2.75% amino acid TPN and 30 +/- 2 g/L (p less than 0.01) during 5% amino acid TPN infusion. No significant changes were seen in serum prealbumin, total protein, bilirubin, alanine aminotransferase, and 5'-nucleotidase during TPN infusion. Major complications included catheter sepsis, hyperglycemia, diarrhea, and premature death in six animals. Thus, metabolic complications of prolonged TPN support may be investigated in a freely mobile nonhuman primate.     

Trace element nutrition status and dietary intake of children with phenylketonuria

The trace element status (copper, iron, zinc, manganese, chromium, and selenium) of 20 dietetically treated phenylketonuric (PKU) children was assessed. Significantly higher intakes of copper (p = 0.002) and iron (p = 0.005) were noted in PKU children compared with their siblings. No significant differences were found for zinc, manganese, or chromium. Intake of selenium was significantly lower (p = 0.0001) in PKU children (8.4 +/- 3.9 micrograms/d) than in siblings (41.6 +/- 9.4 micrograms/d). Plasma and urine selenium and erythrocyte glutathione peroxidase activity (GSHpx) were significantly lower (p = 0.001) in PKU children (0.38 +/- 0.11 mumol/L, 58.0 +/- 34.5 nmol/d, and 14.2 +/- 5.5 U/g Hb, respectively) than in siblings (0.82 +/- 0.15 mumol/L, 165.2 +/- 49.4 nmol/d, and 22.7 +/- 5.2 U/g Hb, respectively). No differences were found in plasma and urine concentrations of other elements. Intake of selenium was significantly correlated with erythrocyte GSHpx (r = 0.87, p = 0.0001) and plasma selenium (r = 0.71, p = 0.0001) for the combined groups. The need and possible procedures, including dietary manipulation, for increasing selenium intake in PKU subjects are discussed.     

Serum zinc, retinol and retinol-binding protein levels in cirrhotics with hypogonadism

Levels of serum zinc, retinol and retinol-binding protein (RBP) were measured in 16 male hypogonadal cirrhotics and compared with 13 male cirrhotic patients without evidence of hypogonadism. Their ages ranged from 20 years to 76 years with a mean of 40.06 +/- 15.6 years (+/- s.e.m.) while non-hypogonadal patients had an age range of 30-55 years with a mean of 41.23 +/- 7.2 years. Mean testicular volume for hypogonadal patients was 6.69 +/- 3.5 cm3 (+/- s.e.m.) while for non-hypogonadal ones it was 12.15 +/- 6.0 cm3. Mean serum zinc level in hypogonadal patients was 4.43 +/- 0.05 mumol/l which was significantly lower than for those without hypogonadism (6.8 +/- 0.09 mumol/l). Similarly serum retinol was lower in hypogonadal patients (0.40 +/- 0.07 mumol/l) than in patients without hypogonadism (0.53 +/- 0.12), although this difference was not statistically significant. RBP was also lower in the hypogonadal patients (0.79 +/- 0.49 mumol/l) than in those without (1.36 +/- 0.74 mumol/l, P less than 0.05). It is concluded that hypogonadal cirrhotics have lower levels of serum zinc and RBP than those without hypogonadism. These deficiencies may contribute to the genesis of hypogonadism in cirrhosis of the liver and supplementation of zinc alone or with vitamin A early in the disease may retard the development of this feature of the disease.     

Critically-ill patients receiving total parenteral nutrition show altered amikacin pharmacokinetics

The purpose of this clinical study was to characterise the kinetic behavior of amikacin in the parenterally-fed critically-ill adult patient. 22 critically-ill adult patients treated with amikacin (15.5 +/- 7.9 mg/kg/day) for severe gram-negative infections were enrolled into a non-randomised control trial. Malnourished patients were administered total parenteral nutrition (TPN, n = 11), while well-nourished patients received fluid therapy (FT, n = 11). Amikacin pharmacokinetic parameters were estimated by non-linear regression analysis, assuming a one-compartment model and central first-order elimination. Patients receiving TPN showed an expanded amikacin distribution volume (0.403 +/- 0.0961/kg vs. FT 0.298 +/- 0.083 l/kg, p < 0.05), and a tendency towards increased total body clearance (0.089 +/- 0.029 l/kg/h vs. FT 0.069 +/- 0.0201/kg/h, p = 0.09). TPN produced lower peak concentrations (19.3 +/- 3.1 mcg/ml vs. 23.1 +/- 3.5 mcg/ml, p < 0.05), but had no significant influence on trough concentrations (p = 0.56). Patients on TPN also showed increased body temperature (p < 0.05) and fluid intake (p < 0.05), and decreased hematocrit (p < 0.05). Stress, malnutrition, parenteral nutrition itself, fluid and osmotic overload, and fever often occur concurrently in parenterally-fed patients and appear to produce lower amikacin serum levels. Consequently, critically-ill patients receiving TPN need higher amikacin doses and individualised treatment by monitoring serum concentrations, to ensure optimal therapeutic response.     

Serum levels of coenzyme Q10 and lipids in patients during total parenteral nutrition

Serum levels of coenzyme Q10 (CoQ10) as well as lipids were determined in patients during total parenteral nutrition (TPN). The mean CoQ10 levels (M +/- SD) were 0.77 +/- 0.30 microgram/ml for 108 normal subjects and 0.59 +/- 0.35 microgram/ml for 95 patients before TPN. The mean CoQ10 level of the patients decreased significantly to 0.35 +/- 0.23 microgram/ml one week after the start of TPN, and then remained almost unchanged during TPN for up to 6 weeks. When the patients receiving TPN (TPN patients) were grouped according to their clinical diagnoses, the mean CoQ10 level of patients with cancer was significantly lower than that of the other patients without cancer in 4 week therapy, but there was no difference in the levels between the patients with and without diseases of the gastrointestinal tract. Serum levels of total cholesterol (T-Chol) and esterified cholesterol in TPN patients also declined below their respective normal ranges, but not to the same extent in comparison to CoQ10. The levels of triglycerides (TG), phospholipids (PL), non-esterified fatty acids, low density lipoproteins, very low density lipoproteins, chylomicrons, and cholesterol in the high density lipoprotein fraction in serum of TPN patients were within their normal ranges. The levels of CoQ10 in TPN patients were correlative to those of T-Chol, TG, and PL, and decreased rapidly prior to the latter levels.     

Nutritional state after colon interposition for benign oesophageal disease

The nutritional state of 32 patients after (mean 66 months) colon interposition due to benign oesophageal disease was examined. Forty-four per cent of the patients had depleted iron stores (low serum ferritin concentration). Serum iron and blood haemoglobin concentrations were lower (P less than 0.001) in those with low than in those with normal serum ferritin concentration (115 +/- 12 g/l and 15 +/- 5 mumol/l vs 135 +/- 12 g/l and 23 +/- 9 mumol/l). Most very low blood haemoglobin concentrations (less than 110 g/l) were found in patients with depleted iron stores. Eighteen patients had serum albumin concentrations slightly below (35-39 g/l) the normal range, and two other patients had values less than 35 g/l. The patients had less dietary iron (13 +/- 6 mg/d) than age- and sex-matched controls (19 +/- 7 mg/d), but the intake of patients with depleted iron stores (12 +/- 5 mg/d) was similar to that of patients with normal iron stores (14 +/- 6 mg/d). Symptoms and/or the replacement of colon graft anti- or isoperistaltically did not have any significant association with the nutritional status, only slightly reduced blood haemoglobin and serum albumin concentration were found among the symptomatic patients and the patients with an antiperistaltic graft. Iron therapy and protein supplements, eg, from milk, egg, soy and meat, are recommended as the dietary treatment. To improve the nutritional status a short intra-abdominal colon graft loop anastomosed to the proximal stomach instead of long loop with an antral anastomosis of the present patients is suggested.     

Selenium supplementation in low-birthweight premature infants: relationship to trace metals and antioxidant enzymes

We attempted to study the effect of selenium supplementation upon trace metal metabolism in low-birthweight infants less than 1000 g birthweight. Serum levels of the trace metals copper, zinc, and selenium; and white blood cell glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were measured in conjunction with the trace metals when parenteral nutrition (TPN) was begun (sample A), at the initiation of enteral nutrition (sample B), and when TPN was discontinued (sample C). Two randomly selected groups of infants were evaluated: group S received selenium supplementation (1.34 micrograms/kg per d) in their parenteral nutrition solutions; group C was a control which did not receive selenium supplementation. Selenium levels declined to equally low levels in both groups by sample C, but were significantly higher in group S at sample B. GSH-Px activities demonstrated a significant increase at sample B in group S and then tended to decrease. In group C, GSH-Px tended to increase, then decreased significantly by sample C. Both groups received 20 micrograms/kg per d of copper in TPN, however, serum copper declined significantly at sample B in group S whereas there were no significant changes in group C. There were no significant changes in zinc and SOD levels. There were no significant differences between groups in clinical characteristics or outcome. This study suggests that a dose of supplemental selenium of 1.34 micrograms/kg per d in TPN is inadequate for low-birthweight premature infants. Selenium supplementation may also affect copper metabolism.     

Utilizing selenious acid to reverse selenium deficiency in total parenteral nutrition patients

The ability of selenious acid to reverse selenium deficiency in eight adult home TPN patients was assessed. Initially, deficiency was documented by comparing both plasma selenium levels in patients (means = 0.035 micrograms/g) to those of 10 controls (means = 0.117 micrograms/g) (p less than 0.001) and by comparing erythrocyte glutathione peroxidase (GSHPx) activity, as mumol NADPH oxidized/g Hb/min, in patients (means = 8.93) to controls (means = 31.76) (p less than 0.002). Subsequently, patients added 100 micrograms/day of selenious acid to their total parenteral nutrition solutions. Postsupplementation selenium status demonstrated a mean plasma level of 0.101 micrograms/g and a mean erythrocyte GSHPx activity of 17.56. Statistically, patients' plasma selenium levels were significantly different (p less than 0.001) when compared to pretreatment levels. Additionally, there was no significant difference between the restored levels and the levels of the controls. Postsupplementation erythrocyte GSHPx activity (means = 17.56) was not significantly different from the initial patient values, although activity did double. Additionally, there existed a significant difference between the postsupplementation enzyme activity and the controls (p less than 0.03). We conclude that selenious acid is able to normalize deficient plasma levels but not deficient erythrocyte GSHPx activity.