The metabolic response to rapid intravenous glucose injection in acute falciparum malaria

Because hypoglycaemia is common in severe malaria, intravenous glucose is often given empirically to patients on admission to hospital. To investigate the metabolic response to rapid glucose injection in acute malaria, 50 ml of 50% w/v (25 g) dextrose was given over 5 min to 10 adult patients (7 males, 3 females; mean age 30 years) with acute falciparum malaria. Five patients with severe infections were studied between doses of intravenous quinine; 5 cases were uncomplicated and previously untreated. The patients with severe malaria had lower pre-injection plasma glucose concentrations than patients with uncomplicated infections (mean +/- standard deviation, 4.2 +/- 0.9 vs 5.8 +/- 1.1 mmol/litre, 2P less than 0.015). However, peak glucose concentrations (18.6 +/- 4.8 vs 17.0 +/- 2.4 mmol/litre) and integrated responses (AUC0-245 min) were similar in the groups (2P greater than 0.1 in each case), and pre- and post-injection plasma insulin concentrations and AUC0-245 min values were also not significantly different (2P greater than 0.05 in each case). No 'rebound' hypoglycaemia was observed. The patients with severe malaria had higher peak plasma lactate concentrations than the uncomplicated patients (2.5 +/- 0.7 vs 1.5 +/- 0.9 mmol/litre, 2P less than 0.05), but the highest plasma lactate achieved and the greatest maximum post-injection rise were only 3.8 and 0.8 mmol/litre respectively. The average maximum reduction in plasma potassium after injection was 0.2 mmol/litre at 35 min. These data suggest that injections of hypertonic dextrose given empirically in conventional doses to non-acidotic patients with acute, severe malaria are not harmful, but the metabolic response in patients with an established acidosis remains unknown.     

Pharmacokinetics of quinine in young and elderly subjects.

The effect of age on the pharmacokinetics of quinine was investigated by comparing its kinetic behaviour in 12 young healthy adults and 8 healthy elderly subjects after a single 600 mg oral dose of quinine sulphate. Peak plasma quinine concentration and the time of peak concentration were similar in the young and elderly subjects. The mean oral clearance of quinine was found to be significantly decreased in the elderly (P less than 0.05, 0.062 litre/h/kg vs 0.084 litre/h/kg) as compared to the young. This was accompanied by a significant increase in the mean elimination half-life of quinine in the elderly group (18.4 +/- 5.7 [standard deviation] h vs 10.5 +/- 1.6 h, P less than 0.05). There was no significant difference in the renal clearance of quinine between the young and the elderly (P greater than 0.05). However, elderly subjects excreted 16.6 +/- 3.7% of the dose as unchanged quinine in the urine and this was significantly greater (P less than 0.005) than the amount excreted by the young (11.2 +/- 2.5%). The results of this study indicate that the elimination processes for quinine are impaired in normal elderly subjects. The clinical significance of these findings is unknown, but they indicate the need for caution in the administration of quinine to elderly patients.     

Circulating and secretory antibodies to specific food proteins in adults

Indirect enzyme-linked immunosorbent assays (ELISA) for the detection of antibodies to gliadin, beta-lactoglobulin and ovalbumin have been developed. Specific antibody immunoglobulin levels were quantified. Serum and saliva samples were collected from twenty normal subjects and measured for the presence of specific antibodies. For each subject food intake was calculated from a 7-d weighed food inventory record. The total IgG level was 14.2 +/- 4.3 mg/ml (mean +/- s.d.). Levels of beta-lactoglobulin IgG were significantly lower than ovalbumin IgG levels (130 +/- 130 micrograms/ml versus 637 +/- 703 micrograms/ml, P less than 0.01). Gliadin IgG levels were also significantly lower than ovalbumin IgG levels (262 +/- 398 micrograms/ml versus 637 +/- 703 micrograms/ml, P less than 0.05). However, no significant difference was observed between gliadin and ovalbumin IgA levels in the subjects (29 +/- 39 per cent versus 56 +/- 122 per cent). A significant correlation was observed between ovalbumin IgG levels in serum and dietary intake of egg protein (r = 0.46, P less than 0.05). No other significant correlations were observed.     

Vitamin E (tocopherols) in human cerebrospinal fluid

Cerebrospinal fluid (CSF) and blood were obtained at the time of myelographic examinations from 40 adult, male, human subjects with no neurologic or metabolic abnormalities. Vitamin E (tocopherols) concentrations were determined by liquid chromatography. In subjects with normal concentrations of CSF protein (n = 22), the alpha- and gamma-tocopherol concentrations were 29.2 +/- 9.5 (mean +/- SD) and 6.5 +/- 3.6 nmol/L, respectively, in CSF and 26.0 +/- 8.1 and 6.0 +/- 3.6 mumol/L, respectively, in serum. The concentrations of alpha-tocopherol in CSF correlated significantly (P less than 0.001) with both total protein and albumin concentrations, suggesting that tocopherol transport into CSF is linked with that of plasma proteins. In vitro oxidation of vitamin E in CSF by the free-radical generator 2,2'-azobis-(2-amidinopropane) hydrochloride showed a measurable induction (lag) period. This is due to the presence of other antioxidants in human CSF.     

Blood mononuclear cell magnesium in normal pregnancy and preeclampsia

Magnesium (Mg) is effective in the treatment of pregnancy-induced hypertension (PIH). In order to determine if patients with PIH are Mg deficient, we assessed mononuclear cell magnesium content (mMg) and serum Mg concentrations (sMg) in 23 normal pregnant women and in 12 women with PIH admitted in active labor. The sMg concentration in women with PIH was 1.74 +/- 0.1 mg/dl (mean +/- SD) and was not significantly different from normal pregnant women at 1.69 +/- 0.2 mg/dl. Both groups had sMg concentrations lower than in normal, non-pregnant controls (sMg = 1.96 +/- 0.1 mg/dl, p less than 0.001). The mMg content in normal pregnant women did not differ significantly from that in women with PIH (1.54 +/- 0.26 micrograms Mg/mg protein and 1.50 +/- 0.26 micrograms Mg/mg protein respectively). The normal control mean mMg was 1.36 +/- 0.17 micrograms Mg/mg protein, slightly lower than in normal pregnancy (p less than 0.005) and PIH (p less than 0.02). Mononuclear Mg content did not correlate with sMg concentration. These data suggest that PIH is not associated with an intracellular Mg deficit. Further studies utilizing other measures of intracellular Mg are indicated to assess the presence or absence of Mg deficiency in patients with both normal pregnancy and pregnancy complicated by PIH.     

Effect of dietary control and exercise training on daily food intake and serum lipids in postmyocardial infarction patients.

The effects of 12 weeks of exercise training without dietary control (n = 30) and exercise training with dietary control by dietition counseling (n = 30) and exercise training with dietary control by dietition counseling (n = 30) on serum cholesterol, serum triglycerides, and total substrate contents were studied in 60 postmyocardial infarction patients. Both groups showed reductions (P less than 0.01) in mean total daily kilocalories consumed (2867 +/- 82 versus 2088 +/- 77 and 2848 +/- 15 versus 1285 +/- 68, respectively); however, no significant change occurred in total body weight. The dietary control group consumed relatively more kilocalories as protein than the group without dietary control (285 of 1,285 versus 389 of 2,088, respectively) and less (P less than 0.05) as fat (443 of 1285 versus 804 of 2,089, respectively). Both groups had lower (P less than 0.01) mean daily dietary cholesterol after 12 weeks (811 +/- 44 versus 232 +/- 17 mg) versus (325 +/- 18 versus 309 +/- 23 mg, respectively). A reduction in serum cholesterol (P less than 0.05) was seen in the dietary control group (270 +/- 8 versus 243 +/- 7 mg/dl) but not in the group without dietary control (260 +/- 6 versus 261 +/- 7 mg/dl). The dietary control group had a lower mean triglyceride level (P less than 0.05) (229 +/- 24 versus 155 +/- 18 mg/dl)) but no differences were seen in the group without dietary control (189 +/- 15 versus 180 +/- 13 mg/dl). It is concluded that significant reductions in caloric intake and daily cholesterol compliment the effects of exercise training in postmyocardial infarction patients by increasing substrate protein:fat consumption ratio and by reducing serum cholesterol and triglycerides. These effects are not seen with exercise training alone.     

The relationship between the response of Plasmodium falciparum malaria to mefloquine in African children and its sensitivity in vitro.

The clinical efficacy of two doses of mefloquine (15 and 25 mg/kg body weight) was evaluated in 85 children suffering from acute symptomatic falciparum malaria. The cure rate on day 28 was 100% in both groups. There was no significant difference (P > 0.05) in the mean parasite and fever clearance times in both groups (48.5 +/- 14.6 and 32.0 +/- 12.7 h respectively for the 25 mg/kg group and 49.0 +/- 15.1 and 30.0 +/- 13.3 h respectively for the 15 mg/kg group). There was also no significant difference (P > 0.05) in these values between children with hyperparasitaemia (53.6 +/- 11.1 and 36.0 +/- 17.0 h respectively) and those without hyperparasitaemia (49.1 +/- 13.6 and 31.8 +/- 14.6 h respectively). Recurrence of parasitaemia was observed after day 30 in 2 patients in the 15 mg/kg group and in 1 patient in the 25 mg/kg group. In vitro, 3 of 21 isolates showed reduced susceptibility to mefloquine, with minimum inhibitory concentrations (MIC) > 67 nM/litre. The MIC and 50%, 90% and 99% inhibitory concentrations were 200.8, 6.27, 31.7 and 119.6 nM/litre respectively. Four of 22 isolates were resistant to chloroquine (MIC > 108 nM/litre). Isolates that showed low sensitivity to mefloquine in vitro were sensitive to chloroquine in vitro, and the 4 that were resistant to chloroquine were sensitive to mefloquine. Irrespective of MIC and dose of mefloquine, parasitaemia cleared in all subjects in 96 h or less.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ascorbate deficiency impairs the muscarinic-cholinergic and ss-adrenergic receptor signaling systems in the guinea pig submandibular salivary gland

Ascorbic acid is preferentially concentrated in the hypothalamus, pituitary and adrenal glands. Its level in the acini of salivary glands is relatively high. We therefore hypothesized that ascorbate may have a role in salivary gland function. Ascorbate-deficient guinea pigs had lower stimulated whole salivary flow rates than well-fed, age-matched controls (P: < 0.005). Total salivary protein concentration was also markedly (P: < 0.005) reduced in the deficient guinea pigs. SDS-PAGE and densitometric quantification of protein bands confirmed significant reduction in specific salivary proteins (e.g., amylase, proline-rich proteins) in the saliva samples of malnourished guinea pigs. Some protein bands not seen in control saliva were detected in the saliva of malnourished guinea pigs. Ascorbate deficiency also produced a significant (P: < 0.005) reduction in the ss-adrenergic receptor density (subtype 1; 95 +/- 19 fmol/mg protein compared with 179 +/- 27 fmol/mg protein for the controls). No significant difference was observed between the two groups with respect to the ss-adrenergic receptor subtype 2. Additionally, ascorbate-deficient guinea pigs had significantly lower muscarinic-cholinergic receptor densities (50 +/- 5 vs. 74 +/- 8 fmol/mg protein for controls). Our data support the conclusion that diminished membrane receptors might impair the capacity of the transmembrane signaling system, resulting in salivary gland hypofunction in ascorbate-deficient guinea pigs. Without implying extrapolation of our findings in experimental animals to humans, it is perhaps relevant that many conditions often associated with salivary gland hypofunction in humans (e.g., smoking or drug ingestion) deplete cellular ascorbate.     

Combination of quinine, quinidine and cinchonine for the treatment of acute falciparum malaria: correlation with the susceptibility of Plasmodium falciparum to the cinchona alkaloids in vitro

Thirteen patients with acute symptomatic uncomplicated falciparum malaria were enrolled in an open, randomized, phase 2, dose-finding clinical trial of a fixed dosage combination of quinine, quinidine and cinchonine (LA40221, Sanofi Recherche, France), which contained equal parts of the 3 alkaloids and was administered orally every 8 h in doses of 400 mg (7 patients) or 500 mg (6 patients) for 7 d. There was prompt clearance of parasitaemia and fever in all patients. The mean clearance times (+/- standard deviation) of parasitaemia, fever and other symptoms were 29 +/- 11.0 h, 10.7 +/- 4.1 h and 14.9 +/- 9.7 h respectively for the 400 mg dose group, and 35 +/- 20.0 h, 16 +/- 7.0 h and 17.6 +/- 8.7 h respectively for the 500 mg dose group. There was no recrudescence of parasitaemia during the 28 d observation period. Minor gastrointestinal side effects occurred in 2 patients, but there was no major side effect. Haematological, biochemical and other measurements were not adversely altered by treatment. QTc prolongation occurred in 3 patients--2 from the 400 mg and 1 from the 500 mg dose group. Testing in vitro against Plasmodium falciparum isolates from 47 patients (including the 13 patients enrolled in the trial) of the combination and its individual components suggested that the relative potencies in vitro, in decreasing order, were quinidine, LA40221, cinchonine and quinine. The minimum inhibitory concentrations were 0.32, 0.64, 0.64 and 1.28 mumol/litre of blood-medium mixture respectively, and the 50% inhibitory concentrations were 0.083, 0.11, 0.12 and 0.22 mumol/litre of blood-medium mixture. The respective 99% inhibitory concentrations were 0.27, 0.45, 0.50 and 1.20 mumol/litre of blood-medium mixture.     

Differential effects of retinoids and chronic ethanol consumption on membranes in rats

Liver plasma membranes (LPM) were prepared from vitamin A-deficient and -sufficient rats as well as from animals treated with retinoic acid, with or without ethanol. Although the fluorescence polarization value of LPM prepared from retinoic acid-fed animals was significantly lower than that of controls (0.201 +/- 0.008 vs. 0.254 +/- 0.005, P less than 0.001), no effect was seen with a vitamin A-deficient diet (0.259 +/- 0.005). No change in the fluorescence polarization was observed in erythrocyte ghost membranes with either vitamin A deficiency or chronic ethanol consumption. The sialic acid concentration of the membranes was significantly higher in LPM and erythrocyte ghosts obtained from vitamin A-deficient animals (37.6 +/- 1.1 vs. 29.6 +/- 0.7 nmol/mg protein for LPM, P less than 0.01, and 77.7 +/- 0.6 vs. 62.0 +/- 1.7 for erythrocyte ghosts, P less than 0.001); the LPM of retinoic acid-treated animals had the lowest values (26.9 +/- 1.6 nmol/mg protein). This sialic acid concentration of LPM was positively correlated with the fluorescence polarization (r = 0.775, P less than 0.001). Chronic ethanol feeding resulted in lower hepatic and LPM vitamin A and greater LPM fluidity with higher cholesterol esters in all diet groups (P less than 0.001). Because increased sialic acid concentration has been incriminated in the pathogenesis of tumor development, it may provide a mechanism whereby lowered hepatic vitamin A promotes carcinogenesis and retinoic acid feeding opposes this process.     

急性1，2-二氯乙烷中毒脑脊液常规指标的动态监测

  目的  探讨脑脊液（cerebral spinal fluid,CSF）常规检查在急性1,2-二氯乙烷（1,2-DCE）中毒诊治中的价值。
  方法  68例急性1,2-DCE中毒患者入院后行CSF压力、常规及生化检查,并在病程中动态监测及分析CSF各项指标的变化。
  结果  急性1,2-DCE中毒患者入院时CSF外观无色透明、细胞数均正常;CSF压力增高阳性率为47.1%（32/68）,其中脑水肿组为66.7%,无脑水肿组无增高;脑水肿组CSF压力均值高于无脑水肿组（P < 0.01）;蛋白质浓度正常或轻微升高占16.2%,无脑水肿组总蛋白与白蛋白浓度高于脑水肿组（P < 0.05）;葡萄糖和氯化物大致正常;重度中毒组CSF压力均值显著高于轻度中毒组（P < 0.05）;急性1,2-DCE中毒患者入院后CSF压力持续升高,于病程（脱离接触）31~60 d最高,治疗后期患者CSF压力恢复缓慢,CSF压力的回落滞后于高颅压的临床表现及CT、MR等影像学改变。
  结论  动态监测CSF压力及各项常规指标对急性1,2-DCE中毒的临床诊治具有重大价值。
     

Development of a dietary model for the study of mild zinc deficiency in humans and evaluation of some biochemical and functional indices of zinc status

After a 1-wk baseline period, a dietary regimen was developed to induce mild zinc deficiency in 15 males (aged 25.3 +/- 3.3 y, mean +/- SD). The regimen consisted of 1 wk on a liquid diet containing 0.6 mg Zn/d and molar ratios of phytate to zinc (phy:Zn) and of phytate X calcium to zinc [(phy X Ca): Zn] of 209 and 4116, respectively, followed by 6 wk on a diet based on soy protein and egg albumin containing 4 mg Zn/d and with phy:Zn and (Ca X phy):Zn of 70 and 2000, respectively. Subjects were then repleted with 30 mg Zn/d for 2 wk. Fasting blood and urine samples were taken weekly. Changes were observed in mean plasma (mumol/L) and urinary zinc (mumol/d): baseline 97.0 +/- 10.9 and 8.0 +/- 2.7, depletion 80.1 +/- 13.4 and 4.3 +/- 2.3, and repletion 100.8 +/- 13.6 and 8.2 +/- 3.1, respectively (P less than 0.05); taste acuity (0.05 less than P less than 0.10); and cellular immune responses (P less than 0.05). Activities of plasma angiotensin-1-converting enzyme and acidic alpha-D-mannosidase were unchanged. Mild zinc deficiency was induced by the dietary regimen.     

Depressed immune response to tetanus in children with vitamin A deficiency.

A randomized, double-masked, placebo-controlled clinical trial was conducted with 236 preschool children, age 3-6 y, in Indonesia to assess immune status in mild vitamin A deficiency. The immune response to tetanus immunization was used as a measure of immune competence. Clinically normal children (n = 118) and children with mild xerophthalmia (n = 118) were randomly assigned to receive oral vitamin A (60,000 micrograms retinol equivalent) or placebo treatment for a total of four study groups. Two weeks after treatment, children were immunized with diphtheria-pertussis-tetanus vaccine. The immunoglobulin G (IgG) responses to tetanus at baseline and 3 wk following immunization were measured by ELISA. After adjusting for previous tetanus immunization, clinically normal and xerophthalmic children receiving vitamin A had a significantly greater IgG response to tetanus than clinically normal and xerophthalmic children receiving placebo (P less than 0.05). These results suggest that children with mild vitamin A deficiency have a relative immune depression compared with children who have been supplemented to normal vitamin A levels.     

Cardiovascular events in the course of tetanus: a prospective study on 30 cases in the infectious diseases clinic, in the Fann teaching hospital, Dakar

OBJECTIVES: This prospective study had for aim to determine the frequency and characteristics of cardiovascular events in the course of tetanus. PATIENTS AND METHODS: From September to December 2002, we studied all patients over 4 years of age presenting with tetanus without any documented underlying disease. RESULTS: Thirty cases were included (mean age 36+/-20 years; sex-ratio 2.3). Seventy-three per cent had a mild-gravity tetanus (stage II of Mollaret) upon admission. One hundred and seventeen ECG were recorded and 93.3% of the patients had more than one abnormality: arrhythmia (24 cases), prolonged QT interval (23 cases), ventricular hypertrophia (17 cases), and atrial hypertrophia (4 cases) especially left (3 cases), failure of AV conduction (3 cases), ST segment depression (3 cases), left and right axis deviation (3 cases), baseline undulation (3 cases) and repolarization disturbances (1 case). All patients had a normal Doppler echocardiographic examination. The mean hospitalization stay was 11.6+/-1.4 days and complications were noted in 60%; sinus tachycardia in apyrexia (5 cases), instable BP (5 cases), excessive sweatiness in apyrexia (1 case), and access of bradycardia with sudden cardiac arrest (2 cases). 8 patients died (26.7%). Six patients with cardiac autonomic dysfunction died, the case fatality rate being statistically higher in this group (P=0.007). A prolonged QT interval, sinus tachycardia and left ventricular hypertrophia were statistically more frequent at the acute phase of the illness. CONCLUSION: The case fatality rate of tetanus is still high, due among others to autonomic dysfunctions.     

Collagenase inhibition in the healing colon

A randomized controlled trial was performed to assess the effect of intravenous aprotinin (Trasylol) on the healing of experimental colonic anastomoses in the rabbit following a standard left colonic resection anastomosis. Assessment of tensile strength was by means of both bursting pressure and breaking strength. Those animals subjected to bursting pressure assessment received intravenous aprotinin 80 000 KIU (kallikrein inhibitory units) at the time of anaesthesia, and postoperatively 160 000 KIU per day given in divided doses for three days. Control animals received saline placebo. A further group of animals received a lower loading and maintenance aprotinin dose (40 000 KIU and 60 000 KIU per day respectively) with control animals receiving saline. Breaking strength was employed as the means of assessment. The mean bursting pressures were 47.7 +/- 2.9 mmHg and 37.5 +/- 3.4 mmHg for aprotinin and controls respectively (P less than 0.05). The mean difference in collagen content of the anastomosis compared to the resected specimen was +1.25 +/- 0.50 microgram/mg and -1.02 +/- 0.47 microgram/mg for aprotinin and placebo groups (P less than 0.005). The mean breaking strength in the aprotinin group was 169.6 +/- 74.5 g and 110.0 +/- 65.9 g for the saline group (P less than 0.02). The mean difference in collagen content of the anastomosis compared to the resected specimen was +0.95 +/- 0.69 microgram/mg and -1.5 +/- 0.78 microgram/mg for the aprotinin and saline groups respectively (P less than 0.05). The significant elevation of both bursting pressure and breaking strength assessments, with a significant improvement in the collagen content of the anastomoses, may be the result of collagenase inhibition following the use of intravenous aprotinin in the experimental model.     

The pituitary-thyroid axis in severe falciparum malaria: evidence for depressed thyrotroph and thyroid gland function

Abnormal thyroid function is strongly associated with mortality in severe non-thyroidal illness. We have assessed the pituitary-thyroid axis serially in 18 Thai adults with severe falciparum malaria and in 18 matched controls. The admission total serum thyroxine (T4) concentrations of the patients (median [range]: 64 nmol/litre [less than 30-91]) were significantly lower than those of controls (81 nmol/litre [61-133]; 2P less than 0.01), and remained depressed until after fever and parasite clearance. Two patients who died in hospital had admission serum T4 concentrations less than 35 nmol/litre. The admission basal serum thyrotropin (TSH) levels of the patients (0.9 mU/litre [less than 0.2-3.1]) were similar to those of controls (1.3 mU/litre [less than 0.2-3.7], 2P greater than 0.1) and remained normal throughout fever and parasitaemia. Thirty-minute TSH increments during a thyrotropin-releasing hormone test on admission were reduced in 13 patients with severe malaria (4.1 mU/litre [0.7-8.1]) relative to those in convalescence (7.1 mU/litre [1.7-14.4], n = 10, 2P less than 0.01) and controls (5.6 mU/litre [3.3-12.9], n = 9, 2P less than 0.05). These findings suggest that thyrotroph and thyroid gland function are depressed during acute, severe malaria. As these changes may be an adaptation to accelerated catabolism, the role of thyroid replacement in such patients is uncertain.     

Influence of dietary protein on glomerular filtration and urinary albumin excretion in insulin-dependent diabetes.

We investigated the effects of dietary constituents on glomerular filtration (GFR) and albumin excretion rates (AERs) in a cross-sectional study in 39 young subjects with insulin-dependent diabetes. Dietary protein intake correlated significantly in patients with GFRs less than 150 mL/min per 1.73 m2 (r = 0.53, n = 23, P = 0.009), but not with AER. GFR also correlated with mean blood glucose at a concentration less than 12.0 mmol/L (r = 0.61, P = 0.0035). Protein and fat intakes were similar in patients with and without microalbuminuria (AER greater than 20 mg/L) but long-term glycemic control was worse in the former [HbA1 12.4 +/- 2.9% (mean +/- SD) and 10.6 +/- 2.1%, respectively, P = 0.043]. In seven patients, short-term reduction of dietary protein from 2.0 to 1.0 to 0.5 g.kg-1.d-1 produced a progressive fall in GFR by 11.6 +/- 6.0 and 9.6 +/- 5.9 mL/min, respectively (P less than 0.05), but did not consistently affect AER. We conclude that both dietary protein and glycemic control influence GFR but neither alone appears to explain glomerular hyperfiltration. Microalbuminuria was associated with poor glycemic control but not with dietary fat or protein consumption.     

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.     

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.     

alpha 2-Macroglobulin in vitamin A-deficient children.

Serum samples were obtained from 43 children 14 years old or younger in Malaysia and Guatemala. The levels of the serum glycoprotein alpha 2-macroglobulin (alpha 2-M) were assayed by two methods: the trypsin-binding assay of Ganrot (Clin. Chim. Acta 14:493, 1960) and a radial immunodiffusion assay against alpha 2-M antiserum. The two methods gave the same results. When serum alpha 2-M levels were plotted against serum vitamin A concentrations, they were significantly correlated (r = 0.505, P less than 0.001); children with serum vitamin A levels greater than 40 micrograms/100 ml had alpha 2-M levels of 3.71 +/- 0.79 mg/ml (mean +/- SD, n = 13), while those with level less than 40 micrograms/100 ml had alpha 2-M levels of 2.78 +/- 0.51 mg/ml (n = 30); the difference was significant (P less than 0.001). Normal, apparently healthy children had alpha 2-M levels of 3.90 +/- 0.39 mg/ml. Most of the children sampled suffered from a variety of infections; of these, measles appeared to counteract the effect of vitamin A deficiency by elevating alpha 2-M levels. Vitamin A-deficient children with measles had alpha 2-M levels not significantly lower than those of normal children. The difference between deficient and normal values of alpha 2-M was still significant (P less than 0.05) when expressed per milligram of serum protein, showing that the effect was not caused by lowered serum protein concentrations associated with protein-calorie malnutrition, from which most of the deficiency children suffered.