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.     

Plasma homocysteine levels in hyperinsulinemic patients

In order to evaluate the clinical characteristics of metabolic syndrome, a screening procedure was performed and in a cohort of middle-aged (40-60 years) hyperinsulinaemic (fasting plasma insulin > 15 microU/ml) and/or postprandial [120 min after 75 g glucose load] insulin > 45 microU/ml) subjects (n = 91; men/women: 38/53; age mean +/- SD 47.6 +/- 4.3 years; body mass index: 34.6 +/- 4.9 kg/m2; waist-hip ratio: 0.92 +/- 0.07; actual blood pressure 146 +/- 16/87 +/- 9 mmHg; fasting insulin: 24.2 +/- 11.3 microU/ml; postprandial insulin 125.5 +/- 103.8 microU/ml; serum LDL-cholesterol: 3.73 +/- 1.09 mmol/l; HDL-cholesterol: 1.12 +/- 0.30 mmol/l; triglycerides: 2.97 +/- 2.38 mmol/l; uric acid 279 +/- 79 mumol/l) plasma fasting homocysteine, vitamin B12 and folic acid levels were simultaneously determined. The values were separately evaluated according to the stages of glucose tolerance (normal glucose tolerance [n = 47]; impaired glucose tolerance [n = 24] and diabetes mellitus [n = 20]). Laboratory normal values were determined in 47 healthy subjects (control group, age: 45.0 +/- 7.8 years, men/women: 19/28). There was no significant difference between hyperinsulinaemic and control subjects regarding plasma homocysteine (9.28 +/- 3.81 mumol/l vs. 9.63 +/- 2.70 mumol/l), folic acid (8.5 +/- 5.9 ng/ml vs. 7.5 +/- 2.1 ng/ml) and vitamin B12 levels (423 +/- 141 pg/ml vs. 356 +/- 121 pg/ml). Plasma homocysteine levels were significantly (p < 0.001) higher in hyperinsulinaemic men than women (11.34 +/- 4.72 mumol/l [n = 38] vs. 7.86 +/- 2.13 mumol/l [n = 53]). There was no significant difference between subgroups classified according to the stages of glucose tolerance in hyperinsulinaemic groups. Plasma homocysteine values exceeding the upper limit of normal range (> 12.45 mumol/l) were detected at a similar prevalence rate in control (4/47 = 8.5%) and in hyperinsulinaemic subjects (10/91 = 10.9%). A weak but statistically significant correlation was found between plasma homocysteine values and age of subjects (r = 0.222; p < 0.05) whereas a stronger correlation was documented between plasma homocysteine and serum creatinine values (r = 0.658; p < 0.001) in hyperinsulinaemic groups (n = 91). Plasma homocysteine values independently from the stages of glucose tolerance are not elevated in hyperinsulinaemic subjects. Hyperhomocysteinaemia is not a characteristic feature of hyperinsulinism suggesting that plasma homocysteine levels are of no considerable importance in the complex pathomechanism of atherosclerosis at early stages of metabolic syndrome.     

Comparison of a high-protein disease-specific enteral formula with a high-protein enteral formula in hyperglycemic critically ill patients

AIMS: To determine whether a specific high-protein enteral formula with a similar caloric percentage of fat and carbohydrates achieves greater control over glycemic levels and reduces insulin requirements in hyperglycemic critically ill patients when compared to a control high-protein enteral formula. DESIGN: A prospective, randomized, controlled, single-blind trial in two University Hospital Intensive Care Units in Spain. METHODS: We enrolled 50 patients with diabetes mellitus or stress hyperglycemia with basal glycemia > or =160 mg/dl and indication for enteral nutrition > or =5 days. Patients with severe kidney failure, liver failure or obesity were excluded from the study. In the first 48 h of admission, after randomization, 26 patients received the study diet and 24 patients received the control diet. The variables were monitored for 14 days. The Harris-Benedict formula with a fixed stress factor of 1.2 was used to calculate caloric needs. Insulin was administered by continuous infusion. An intention-to-treat analysis was performed. RESULTS: On admission, there were no differences between the study and control group in plasma glucose levels (mg/dl) (190.9+/-45 vs 210.3+/-63) and capillary glucose levels (mg/dl) (226.1+/-73 vs 213.8+/-67). After the feeding trial, there were differences between the study and control group in plasma glucose levels (mg/dl) (176.8+/-44 vs 222.8+/-47, P=0.001), capillary glucose levels (mg/dl) (163.1+/-45 vs 216.4+/-56, P=0.001), insulin requirements/day (IU) 8.73 (2.3-27.5) vs 30.2 (21.5-57.1) (P=0.001), insulin/received carbohydrates (UI/g) 0.07 (0.02-0.22) vs 0.18 (0.11-0.35) (P=0.02) and insulin/received carbohydrates/kg 0.98 (0.26-3.59) vs 2.13 (1.44-4.58) (P=0.04). These differences remain in a day-to-day comparison. There were no differences in the analytical tests, or in digestive or infectious complications. Intensive Care Unit length of stay, mechanical ventilation and mortality were similar in both groups. CONCLUSIONS: Hyperglycemic critically ill patients fed with a high-protein diet with a similar caloric percentage of fat and carbohydrates show a significant reduction in plasma glucose levels, capillary glucose levels and insulin requirements in comparison to patients on a conventional high-protein diet. This better glycemic control do not modify Intensive Care Unit length of stay, infectious complications, mechanical ventilation and mortality.     

Low serum selenium and glutathione peroxidase activity in patients receiving short-term total parenteral nutrition

Selenium status was determined in 15 consecutive postoperative patients receiving short-term total parenteral nutrition (TPN) using both serum selenium concentration and glutathione peroxidase (GSH-Px) activity as an indicator of body selenium status. The serum selenium concentration was significantly (p less than 0.001) lower in TPN patients (0.52 +/- 0.16 mumol/l, mean +/- SD) than in age- and sex-matched controls (1.08 +/- 0.17 mumol/l). Serum selenium in TPN patients ranged from 0.28 to 0.79 mumol/l and was associated with the duration of TPN. The lowest selenium values was found in patients who had received TPN over 3 weeks (0.35 +/- 0.06 mumol/l) as compared to patients receiving TPN for 1-3 weeks (0.61 +/- 0.13 mumol/l; p less than 0.01). Serum GSH-Px activity in TPN patients was also low (116 +/- 21 U/l) and ranged from 75 to 159 U/l. A significant positive correlation was found between serum selenium and GSH-Px activity (r = 0.520; p less than 0.05) whereas serum selenium and GSH-Px activity did not correlate significantly with liver function tests and body mass index. This study suggests that also short-term TPN patients may be at risk of selenium deficiency.     

Liver composition and histology in growing infant miniature pigs given different total parenteral nutrition fuel mixes

Although young infants are at greater risk for total parenteral nutrition (TPN)-related liver disease than adults, previous studies on the effect of the TPN energy source on the development of hepatic steatosis have been carried out in adult rats and adult humans. We studied the effect of a glucose and a glucose/fat TPN energy regimen on hepatic chemical composition and the development of steatosis in newborn miniature pigs. Twenty miniature pigs were randomized at 10 days of age to receive a TPN regimen which utilized either glucose (group A) or glucose/fat (group B) as the non-nitrogen energy source. After 8 days, blood was drawn for insulin, glucagon, SGPT, albumin, and bilirubin determinations. Samples of liver were obtained at 9 days. Plasma insulin levels were significantly higher and glucagon levels lower in group A piglets than in those in group B. Normal values were obtained for SGPT, albumin, and bilirubin, and no differences were found between groups. Chemical analysis of the livers revealed no differences between groups in the concentrations of glycogen, fat, protein, DNA, and RNA. Group A animals had significantly higher concentrations of water than group B (group A: 0.75 +/- 0.01 liter/kg; group B: 0.74 +/- 0.01; p less than 0.03). A significant correlation was found in group B between the plasma insulin/glucagon ratio and the hepatic glycogen concentration (r = 0.73, p less than 0.05). Group A animals had fat vacuoles in centrilobular hepatocytes, in contrast with group B animals who had visible fat only in Kupffer cells.(ABSTRACT TRUNCATED AT 250 WORDS)     

Experimental carnitine depletion in rats

We studied tissue carnitine concentrations after long-term peroral feeding with carnitine-free parenteral nutrient solutions in rats. Group I (n = 22) was fed perorally for 6 weeks with the carnitine free experimental diet. The control group (group II, n = 22) was pair-fed a standard laboratory pellet diet containing carnitine 60 nmol/g. The carnitine free experimental diet caused approximately 50% depletion of carnitine in serum, muscle, and liver while the concentrations in the pair-fed rats were normal. The free and total carnitine concentrations in serum were 25.5 +/- 7.8 and 32.9 +/- 9.3 mumol/l (group I), and 69.3 +/- 13.7 and 84.1 +/- 16.5 mumol/l (group II, p < 0.001), in muscle 2.1 +/- 0.3 and 2.3 +/- 0.4 mumol/g dry weight (group I), and 3.8 +/- 0.6 and 4.3 +/- 0.8 mumol/g dry weight (group II, p < 0.001), and in liver 0.5 +/- 0.1 and 0.6 +/- 0.1 mumol/g dry weight (group I), and 1.2 +/- 0.1 and 1.3 +/- 0.1 mumol/g dry weight (group II p < 0.001). Daily supplementation of the experimental liquid diet with I-carnitine caused normal tissue carnitine concentrations, indicating the exclusion of dietary carnitine as the cause of carnitine depletion. We conclude that in rats carnitine depletion in serum, muscle, and liver can be induced by prolonged peroral feeding with carnitine free diet.     

Stimulation of thermogenesis in men after combined glucose-long-chain triglyceride infusion

The effect of combined long-chain triglyceride infusion (Intralipid 20%) with graded doses of insulin/glucose on energy expenditure was examined in 17 healthy young male volunteers by using the euglycemic insulin clamp technique in combination with indirect calorimetry. Intralipid was infused for 90 min at a constant rate of 0.23 g/min; plasma free fatty acids increased from base-line values of 380 +/- 8 mumol/l to steady state levels of 650 +/- 12 mumol/l. After 90 min the Intralipid was continued and insulin was infused at three rates (0.5, 2, and 4 mU/kg . min) to achieve steady state hyperinsulinemic plateaus of 63 +/- 4, 167 +/- 10, and 410 +/- 15 microU/ml. Plasma glucose concentration was maintained constant at basal euglycemic levels (insulin clamp technique) by infusing glucose at 0.24, 0.48, and 0.59 g/min, respectively. Glucose storage during the insulin clamp (ie, glucose uptake minus glucose oxidation) was 0.13, 0.33, and 0.40 g/min for each group and exogenous lipid storage was 0.17, 0.18, and 0.19 g/min, respectively. The net increment in energy expenditure was 0.15, 0.24, and 0.26 kcal/min, respectively, which represents 8.5% of the energy content of the total amount of glucose and lipid stored. The experimentally determined value (approximately 9%) for the cost of storing both glucose and lipid was found to be significantly greater than predicted by stoichiometric calculations. However, the experimental value for the combined infusion was less than that observed for glucose storage alone (12%). This finding provides support for the use of combined glucose/fat infusions in parenteral nutrition as it is used more economically than when glucose is infused alone.     

On the disturbances in carbohydrate metabolism in pre-dialysis patients with chronic renal failure

We describe some of the aspects of impaired carbohydrate metabolism in predialysis uremic patients. METHODS: A total of seventy-five nondiabetic patients with chronic renal failure (CRF) were enrolled in the present study. The level of glycosylated hemoglobin was measured in 51 patients using kits from Merck and an oral glucose challenge test was performed in 20 according to a standard protocol. The levels of immunoreactive insulin and growth hormone (GH) were measured in all predialysis patients using original kits and an automatic minigamma counter (Abbott, USA). The results were compared with those from 30 healthy controls. RESULTS: In patients with first degree CRF the level of glycosylated hemoglobin was 5.9 +/- 05%. In patients with second and third degree CRF there was a trend towards higher glycosylated hemoglobin levels--6.3 +/- 0.6% (P > 0.05; u = 1.1) as compared with the controls--5.5 +/- 0.4%. The analysis of the results from the oral glucose challenge test revealed impaired glucose tolerance in 12 predialysis patients with CRF with blood glucose levels of 9.1 +/- 1.6 mmol/l at the second hour following the ingestion of glucose. Nine of those had second or third degree CRF. The baseline levels of plasma immunoreactive insulin showed a tendency towards increase in the patients with uremia as compared with the controls (7.2 +/- 1.1 IU/ml versus 6.4 +/- 0.7 IU/ml) whereas no significant difference was found at the 1st, 2nd or 3rd hour following the ingestion of glucose as compared with the healthy controls. Five of our patients had significantly elevated basal insulin levels. With regard to GH levels, we found similar baseline values in our study patients and the controls. At the 1st hour following the glucose challenge the GH values showed a tendency towards increase in the uremic patients--6.1 +/- 1.1 ng/ml. In 4 of our study patients we found significantly elevated GH levels at the 1st hour following the ingestion of glucose (6.6 +/- 0.7 ng/ml). CONCLUSIONS: 1. No significant disturbances in carbohydrate metabolism were found in patients with mild (initial) CRF. 2. In patients with moderate and advanced CRF we found changes consistent with impaired carbohydrate metabolism and a tendency towards an increase in the basal immunoreactive insulin levels. 3. Growth hormone levels showed a different pattern of change in predialysis patients and those changes cannot be explained by the changes in carbohydrate metabolism.     

Substrate fuel kinetics in enterally fed trauma patients supplemented with ornithine alpha ketoglutarate

BACKGROUND: Ornithine-alpha-ketoglutarate (OKG) is a promising anticatabolic agent and the mechanisms of its potential use in trauma patients are not clearly understood. AIM: To determine the altered whole-body protein, lipid and glucose substrate kinetics in trauma victims in the early flow-phase of injury when they were fed enterally with or without OKG. METHODS: Fourteen adult, multiple trauma patients who were highly catabolic and hypermetabolic were studied. Whole-body protein ((15)N glycine), fat (2 stage glycerol infusion) and glucose ((3H)glucose) kinetics (t/o) and plasma parameters were measured (A) within 48-60 h after injury before starting nutritional support and then (B) after 4 days of enteral feeding. Group A (n=7, control) received a defined enteral formula (Two Cal HN, 1.4 times BEE calories) and Group B (n=7, OKG) received same isonitrogenous diet replacing 2.62gN/d from the enteral diet by OKG-N (20g OKG/d). RESULTS (Mean+/-SEM): Protein turnover is significantly (P<==0.05) increased in OKG treated patients (4.68+/-0. 15 vs 3.90+/-0.23, gP/kg/day) and glycerol turnover is decreased (0. 87+/-0.16 vs 1.46+/-0.16, micro mole/kg/min). Glucose turnover is not changed. Significant (P<== 0.05) increases in circulating plasma levels of hormones (insulin, 44.2+/-8.4 vs 15.7+/-5.0 ulU/ml, growth hormone 1.68+/-0.33 vs 0.92+/-0.16, ng/ml and IGF-1, 106+/-13 vs 75+/-18, ng/ml) and free amino acids (glutamine, 383+/-20 vs 306+/-25, Proline, 203+/-18 vs 146+/-13 and ornithine, 164+/-27 vs 49+/-5 micro mole/l) are found in OKG treated patients, compared to non OKG patients. CONCLUSION: Increased hormone secretion due to OKG and the rapid interaction between the metabolites of OKG at the intermediary metabolism level may be responsible for altered substrate fuel kinetics.     

Beneficial influence of an indigenous low-iron diet on serum indicators of iron status in patients with chronic liver disease

The main Fe storage organ in the body is the liver. In patients with chronic liver disease, secondary Fe overload is common. Phlebotomy, often used in the West to reduce Fe overload to improve the efficacy of interferon therapy, is not socially acceptable in India. We assessed the efficacy of a low-Fe diet in reducing serum Fe levels. Nineteen patients with hepatitis B- and C-related chronic liver disease, ten with normal (< 25 mumol/l) baseline serum Fe levels (group A) and nine with high (> 25 mumol/l) serum Fe levels (group B) were included. All the subjects were advised to eat a low-Fe diet. The daily Fe intake was reduced approximately 50% by consumption of the rice-based diet. Haemoglobin, serum Fe, transferrin saturation index (TSI), ferritin and alanine transaminase (EC 2.6.1.2) levels were studied at 1 and 4 months. Dietary Fe intake and body weight were closely monitored. All patients complied with the dietary regimen and at 4 months significant (P < 0.001) reductions from baseline were seen in serum Fe (20 (SD 3) v. 12 (SD 4) mumol/l group A; 30 (SD 3) v. 19 (SD 7) mumol/l group B) and TSI (38 (SD 8) v. 23 (SD 9)% group A; 53 (SD 15) v. 34 (SD 13)%, group B) in both the groups, albeit earlier in group B subjects. Serum ferritin levels, however, reduced only in group A (112 (SD 62) v. 43 (SD 25) ng/ml, P < 0.05) and not in group B. Non-significant reductions in haemoglobin levels were seen in both groups. Alanine transaminase levels reduced significantly (P < 0.05) in both the groups (95 (SD 49) v. 44 (SD 25) IU/l, group A; 82 (SD 16) v. 51 (SD 14) IU/l group B). Thus, a low-Fe diet results in significant reductions in serum Fe and TSI levels, irrespective of baseline Fe levels. This diet should be evaluated to improve the efficacy of interferon therapy in patients with hepatitis B- and C-related chronic liver disease.     

Essential fatty acid deficiency in patients receiving simultaneous parenteral and oral nutrition

Essential fatty acid deficiency is a common finding in patients nourished parenterally with hypertonic glucose and amino acids. In this study, we measured the linoleate concentration in the livers of 3 groups of patients. All the patients had operable upper gastrointestinal tract malignancies. Group I ate the hospital's regular diet ad libitum. Group II were given total parenteral nutrition (TPN), Group III received both enteral and parenteral nutrition and obtained about 35% of their caloric intake from food. The percentage of total liver fatty acids as linoleate were group I, 15.2 +/- 1.2%, group II, 3.7 +/- 1.4%, and group III, 2.8 +/- 1.6%. Data are expressed as the mean +/- 1 SEM. The patients who received 35% of their calories by mouth as food and the patients on TPN were found to be equally depleted in linoleate.     

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.     

Effects of supplementary parenteral nutrition on thyroid hormone patterns in surgical patients with liver cirrhosis.

The relationship between nutritional intervention and circulating thyroid hormones and rapid-turnover proteins was investigated in surgical patients with liver cirrhosis. Fourteen patients with well-compensated liver cirrhosis who were subjected to operations for esophageal varices or hepatoma were divided into two groups. The oral group was offered an oral diet containing 2200 kcal/day before surgery and conventional intravenous infusions of 5% glucose after the operation (500-600 kcal/day). The supplementary parenteral nutrition (SPN) group was offered the same oral diet as the oral group, combined with intravenous 50% glucose, fat emulsion, and branched-chain enriched amino acid solution, 600-1000 kcal and 7.32 g nitrogen/day during the 10 days before surgery and 800-1800 kcal and 7.32-9.76 g nitrogen/day during the first 2 wk postoperative. Plasma triiodothyronine (T3) was higher in the SPN group (1.26 +/- 0.09 ng/ml) than in the oral group (0.91 +/- 0.08 ng/ml) (P less than 0.001), and reverse T3 (rT3) was lower in the SPN group (297 +/- 33 pg/ml) than in the oral group (351 +/- 29 pg/ml (P less than 0.01) on the day of surgery. In addition, SPN significantly attenuated the low T3 and high rT3 levels found in the oral group throughout the 2 postoperative wk. In addition, attenuation of decreases in rapid-turnover proteins was achieved in the SPN group. It is likely that the SPN contributed to the partial correction of liver dysfunction and metabolic imbalance in traumatized cirrhotic patients.     

Total parenteral nutrition in the newborn: amino acids-energy interrelationships

As part of an ongoing study on the influence of intravenous glucose and fat on nitrogen metabolism we evaluated the relationship between the source of infused energy and plasma amino acid levels. Thirty-two studies were performed in 16 appropriate-for-gestational-age newborn infants (birth weight, 2150 +/- 115 g; means +/- SEM). In a crossover design each patient received two 6-d periods of isocaloric and isonitrogenous infusions, differing only by the source of calories (high or low fat intakes). For an energy intake of 80 kcal.kg-1.d-1 (335 kJ.kg-1.d-1) there was a significant hypoaminoacidemia (2338 +/- 185 vs 2937 +/- 196 mumol/L, high fat vs low fat) under the high-glucose intake. These data suggest that above an energy intake of 60 kcal.kg-1.d-1 (251 kJ.kg-1.d-1) there is a threshold at which changes in plasma amino acid levels are triggered by variations in the source of infused energy. Careful examination of all variables, including energy sources, is essential when aminograms are compared.     

Protective effect of some tropical vegetables against CCl4-induced hepatic damage

In the present study, ethanolic extracts of some tropical vegetables were investigated for their hepatoprotective effect against CCl4-induced liver damage in rats. CCl4 at a dose of 0.5 mL/kg of body weight produced liver damage in rats as manifested by the rise in the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total protein in serum (40.60 +/- 3.50 IU/L, 80.60 +/- 5.10 IU/L, and 73.20 +/- 1.87 g/L, respectively) and in liver homogenate (1,300.00 +/- 7.38 IU/L, 1,660.00 +/- 13.69 IU/L, and 250.00 +/- 7.51 g/L, respectively) compared to the control. The extracts at doses of 250 and 500 mg/kg of body weight were administered to the CCl4-treated rats. The vegetables at a dose of 250 mg/kg of body weight produced a significant hepatoprotective effect by decreasing the serum levels of ALT, AST, and total protein to values in the range of 11.21 +/- 1.90-16.22 +/- 1.00 IU/L, 29.00 +/- 2.70-48.00 +/- 2.10 IU/L, and 62.10 +/- 2.40-70.13 +/- 2.00 g/L and at a dose of 500 mg/kg of body weight to 13.00 +/- 1.20-21.00 +/- 1.30 IU/L, 40.00 +/- 2.5-59.00 +/- 2.20 IU/L, and 68.00 +/- 2.40-72.00 +/- 2.10 g/L, respectively. Similar results were obtained for liver homogenate levels of ALT, AST, and total protein with decreasing values compared with the CCl4-treated rats: 900.00 +/- 3.05-1,020.00 +/- 4.25 IU/L, 1,150.00 +/- 5.57-1,530.00 +/- 4.99 IU/L, and 150.00 +/- 3.12-185.00 +/- 3.00 g/L and 900.00 +/- 3.05-1,030.00 +/- 8.80 IU/L, 1,400.00 +/- 6.95-1,530.00 +/- 8.50 IU/L, and 165.0 +/- 5.50-210.00 +/- 4.41 g/L, respectively, at doses of 250 and 500 mg/kg of body weight, respectively. Furthermore, the effect of the extracts on lipid peroxidation, measured as malondialdehyde (MDA), was estimated on the liver homogenate. A significant hepatoprotective effect was also noticed with a decreased value of the MDA levels: 46.00 +/- 0.08-52.00 +/- 0.06 and 47.00 +/- 0.07-60.00 +/- 0.10 nmol of thiobarbituric acid-reactive substances/g of liver protein at doses of 250 and 500 mg/kg of body weight, respectively. It could be concluded that all the evaluated vegetables exhibit good hepatoprotective activities, though to varying degrees.     

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.     

Cerebrospinal fluid angiotensin converting enzyme levels in the diagnosis of neurosarcoidosis.

Cerebrospinal fluid angiotensin converting enzyme (CSF-ACE) level was measured in two patients considered to have neurosarcoidosis, three patients with possible neurosarcoidosis and in 38 control patients suffering from prolapsed intervertebral discs. Both neurosarcoidosis patients had elevated levels (1.8 and 5.4 mumol/l/min) while the possible neurosarcoidosis patients had values similar to the control patients (mean 0.59 +/- 0.42 mumol/l/min). We suggest that CSF-ACE values may be of use in some patients as a diagnostic test for neurosarcoidosis and provide a reference range of normal controls.     

Study of the origin of hyperglycemia in acute myocardial infarct]

In order to clarify the origin of hyperglycaemia, blood glucose, glycated haemoglobin (GHb) and protein-corrected serum fructosamine (SFA) values were simultaneously determined at admission of 65 patients with acute myocardial infarction while oral glucose tolerance test was performed later at discharge. In 29 patients no alterations in carbohydrate metabolism were found (blood glucose: 5.2 +/- 0.1 mmol/l, GHb: 4.4 +/- 0.1%, SFA: 2.20 +/- 0.08 mmol/l) while in 9 patients diabetes was already recorded in the medical history (blood glucose: 11.5 +/- 1.1 mmol/l, GHb: 7.9 +/- 0.9%, SFA: 3.36 +/- 0.31 mmol/l, p < 0.001). Undiagnosed diabetes was documented in 8 patients (blood glucose: 11.8 +/- 1.3 mmol/l, GHb: 7.3 +/- 0.6%, SFA: 3.51 +/- 0.24 mmol/l) while stress-hyperglycaemia was found in 19 patients (blood glucose: 8.4 +/- 0.3 mmol/l, GHb: 4.5 +/- 0.1%, SFA: 2.55 +/- 0.17 mmol/l). Undiagnosed diabetes could be recorded in one seventh while stress-hyperglycaemia could be found in one third of non-diabetic patients with acute myocardial infarction. Due to overlapping values SFA is not suitable to distinguish between stress-hyperglycaemia and undiagnosed diabetes in patients with acute myocardial infarction.     

Nitrite plasma levels in chronic lung disease patients

BACKGROUND: The authors carried out a study in a group of lung disease patients, about the behaviour of the plasmatic levels of nitrites (stable, specific and irreversible end-products of nitric oxide). METHODS: The series consisted of 13 male patients (mean age 65 +/- 7 years) with chronic obstructive pulmonary disease with type 1 respiratory failure; 33 male subjects (mean age 58 +/- 5 years) without internistic disease were considered as controls. For each subject the determination of nitrite plasma levels by the Gutman and Hollywood method based on the Griess colorimetric reaction was performed. RESULTS: The mean value of the plasmatic nitrites was significantly reduced (p < 0.05) as compared to the controls (11 +/- 0.48 mumol/l vs 21 +/- 0.92 mumol/l). CONCLUSIONS: The authors hypothesized that in chronic lung disease patients there would be a condition of initial pulmonary hypertension; in this condition long-term endothelium-dependent nitric oxide production, aimed at the vasodilating effects with secondary excessive exhaled amount of NO, might cause a reduction in nitrite plasma levels. These levels may represent an early marker of pulmonary hypertension and suggest interesting therapeutic treatments through inhalation of exogenous NO.     

Effect of food restriction on tissue carnitine concentration in rats

The effect of feeding different amounts of a standard laboratory pellet diet on tissue carnitine concentration was studied in four groups of rats. Group I was fed ad libitum, whereas food intake was restricted to 25, 20, and 15g protein/kg body weight/day in group II, III, and IV, respectively. The intake of food, protein, energy and carnitine was constant and adjusted to actual body weight in groups 2-4. Six weeks food restriction had no effect on muscle carnitine. Restricted diet caused lowered concentrations of carnitine in serum (group I, fed ad libitum, total 95.0 +/- 13.8, free 80.2 +/- 2.7; group II total 78.4 +/- 8.4, free 56.9 +/- 4.7; group III total 81.7 +/- 8.8, free 66.0 +/- 8.8; and group IV total 73.8 +/- 8.7, free 59.5 +/- 7.6 mumol/l) and urinary carnitine excretion (group I, total 7.1 +/- 3.3, free 6.3 +/- 3.1; group II, total 2.5 +/- 0.7, free 2.2 +/- 0.7; group III, total 1.9 +/- 0.8, free 1.6 +/- 0.8; and group IV, total 1.3 +/- 0.4 free 1.1 +/- 0.3 mumol/day). In contrast, the liver carnitine tended to increase when dietary intake was reduced (group I total 1.1 +/- 0.1, free 1.0 +/- 0.1; group II total 1.5 +/- 0.2, free 1.4 +/- 0.2; group III total 1.3 +/- 0.1, free 1.1 +/- 0.1; and group IV total 1.5 +/- 0.2, free 1.4 +/- 0.2 mumol/g dry wt). The highest liver carnitine concentrations were observed during the lowest dietary intake when also the serum and urine carnitine were lowest. We conclude that the amount of food intake has a direct impact on carnitine concentrations in the liver, serum, and urine while muscle carnitine concentration remains relatively stable despite wide variations in food intake.