Effect of an acute fast on energy compensation and feeding behaviour in lean men and women.

AIM: Humans appear to defend against energy deficit to a greater extent than energy surplus. Severe dietary energy restriction resulting in 5-30% weight loss often leads to hyperphagia and weight regain in lean subjects. However, the period of time over which fasting is often endured in Western society are far shorter, approximately 1-2 days. This study examined how a 36 h fast effected the subsequent day's energy and nutrient intake in a group of 24 healthy, lean men and women. METHOD: Subjects underwent two 2 day treatments, termed 'fast' and 'maintenance'. During the 'fast' treatment, subjects were fed a maintenance diet on the day prior to the fast (day -1) to prevent overeating. They then consumed non-energy drinks only, from 20:00 h on day -1 to 08:00 h on day 2 (ad libitum feeding day), thus fasting for 36 h. On the 'maintenance' protocol, subjects received a maintenance diet throughout day 1. Throughout day 2 they had ad libitum access to a range of familiar foods, which were the same for both treatments. Body weight, blood glucose and respiratory quotient were used as compliance checks. Hunger was monitored on day's -1, 1 and 2 for the fast treatment only. RESULTS: On day 2, average energy intake was 10.2 vs 12.2 MJ/day (s.e.d. 1.0) on the post-maintenance and post-fast periods, respectively (P=0.049). Subjects altered feeding behaviour, in response to the fast, only at breakfast time, selecting a higher-fat meal (P<0.005). Compared to day -1, motivation to eat was elevated during the fast (P<0.05). This continued until breakfast was consumed during the re-feeding period (day 2), when values then returned to baseline. CONCLUSION: These data suggest that a 36 h fast, which generated a negative energy balance of approximately 12 MJ, did not induce a powerful, unconditioned stimulus to compensate on the subsequent day.

Fecal calprotectin: validation as a noninvasive measure of bowel inflammation in childhood inflammatory bowel disease.

BACKGROUND: Calprotectin is an abundant neutrophil protein, which is extremely stable in feces. This study aimed to validate fecal calprotectin as a marker of bowel inflammation against invasive measures in children with inflammatory bowel disease (IBD), including colitis and small bowel Crohn disease. METHODS: Fecal calprotectin was measured using a simple enzyme-linked immunosorbent assay in 36 spot stool samples from 22 children before colonoscopy and from 14 children before technetium-99 (99Tc) scanning. Using standard scoring systems, the severity of inflammation was assessed macroscopically and histologically at six standard sites in those who underwent colonoscopy and also at six standard sites in those who underwent 99Tc scanning. The subscores from each site were summated to give combined severity and extent scores for macroscopic and for histologic inflammation in the group undergoing colonoscopy and total inflammation in the group undergoing 99Tc scanning. RESULTS: In the 22 children who underwent colonoscopy, median fecal calprotectin was 4.9 mg/L (0.1-272.5 mg/L) (range). Disease groups included six normal cases, nine ulcerative colitis cases, two isolated Crohn colitis cases, two indeterminate colitis cases, and three allergic colitis cases. Fecal calprotectin correlated closely with colonic macroscopic inflammation (r = 0.75, P < 0.001) and histologic inflammation (r = 0.85, P < 0.001). Of the 14 children undergoing 99Tc scanning, 10 had Crohn disease, 3 had ulcerative colitis, and 1 had allergic colitis. Median fecal calprotectin was 9.1 mg/L (0.3-141.7 mg/L), and this correlated closely with the 99Tc scanning score (r = 0.80, P = 0.001). CONCLUSION: Fecal calprotectin correlates closely with the best invasive measures of colonic and small bowel inflammation in childhood inflammatory bowel disease. As a sensitive objective measure of bowel inflammation that is risk-free and noninvasive, fecal calprotectin lends itself particularly to the monitoring of and assessment of therapeutic interventions in children with inflammatory bowel disease.

Fecal calprotectin as a measure of disease activity in childhood inflammatory bowel disease.

BACKGROUND: Calprotectin is an abundant neutrophil protein that is extremely stable in feces. The aim of this study was to assess the effectiveness of fecal calprotectin as a noninvasive measure of disease activity in childhood inflammatory bowel disease (IBD) by comparison to a modified Lloyd-Still and Green score and laboratory inflammatory indices. METHODS: Spot fecal samples from 37 children with IBD and 31 control children were sent by ordinary mail to the laboratory. Fecal calprotectin concentration was measured by an in-house enzyme linked immunosorbent assay (ELISA). A modified Lloyd-Still & Green score (mLSS) was calculated for each child with IBD within 10 days of obtaining the fecal sample. RESULTS: Compared with control values (median, range) (2.1, 0.5-6.3 mg/L), fecal calprotectin was increased in 16 children with ulcerative colitis, (11.5, 0.6-272.5 mg/L, P < 0.001) and in 21 children with Crohn disease, (14.0, 0.7-59.7 mg/L, P < 0.001). Twelve "moderately affected" children (mLSS of 35-65) had higher fecal calprotectin concentrations (22.2, 2.7-141.7 mg/L) than 25 "mildly affected" children (mLSS > 65), (10.3, 0.6-272.5 mg/L, P = 0.002). For the total IBD group, fecal calprotectin concentration correlated negatively with the mLSS (r = -0.61, P < 0.001). It also correlated negatively with serum albumin concentration (r = -0.49, P = 0.002) and positively with erythrocyte sedimentation rate (r = 0.40, P = 0.01). CONCLUSIONS: Fecal calprotectin seems to reflect bowel inflammation in children with IBD. As a simple, safe, noninvasive test, it has the potential to reduce the number of invasive investigations performed in these children.

Malnutrition: trials and triumphs.

Severe malnutrition is uncommon but often fatal, particularly in very young infants or when oedema is present. Another major contributor to mortality is undiagnosed infection. Three pilot studies have recently been performed in severely malnourished patients in therapeutic feeding centres in sub-Saharan Africa. In each, a practical management problem was addressed and a potential solution tested. Three conclusions were reached: young breastfeeding infants were best managed using a supplemented suckling technique; routine antibiotics from admission reduced mortality; and in adults with oedematous malnutrition, therapeutic diets with a lower-than-usual protein:energy ratio were effective in reducing mortality and permitting catch-up weight gain.

Dietary fiber in weaning cereals: a study of the effect on stool characteristics and absorption of energy, nitrogen, and minerals in healthy infants.

We evaluated the effect of increased dietary fiber (DF) content in weaning cereals based on wheat/soy (8.0 and 1.8% DF) and wheat/milk (5.3 and 2.0% DF) in healthy, formula-fed infants 7-17 weeks old. The study had a cross-over design, each infant acting as his or her own control. Stool characteristics and anthropometry were monitored over 4-week periods in groups of 34 (wheat/soy) and 23 (wheat/milk) infants. Absorption of zinc (Zn) and calcium (Ca) was studied by measuring the fecal excretion of stable isotopes during 72 h (70Zn and 42Ca) in a subgroup of the infants consuming wheat/soy cereals. Iron (Fe) bioavailability was evaluated by analysis of the incorporation of 58Fe into erythrocytes 14 days after administration. Fractional absorption (X +/- SD: 8.0 versus 1.8% DF) was 45.3 +/- 27.5 versus 41.2 +/- 19.4% of 70Zn and 63.4 +/- 15.8 versus 64.4 +/- 10.6% of 42Ca. Bioavailability of 58Fe varied between 1.0% and 5.4% (8.0% DF) and from <0.9% to 9.1% (1.8% DF). No significant difference in energy (95.3 +/- 2.0% versus 95.7 +/- 1.2%) or nitrogen (92.6 +/- 2.3% versus 93.0 +/- 1.6%) apparent absorption from the total diet was found during consumption of cereal with 8.0 and 1.8% DF. The intake of cereal decreased with higher DF content in the wheat/soy product: 34 +/- 23 g/d (8.0% DF) versus 42 +/- 23 g/d (1.8% DF), p < 0.01. While consuming the 8.0% DF product, 11 infants were reported to have "gritty stools"; no other differences were observed between different groups in stool characteristics or anthropometry. These results demonstrate no negative effect on the absorption of energy and nutrients with higher dietary fiber intake in primarily formula-fed infants. The impact of increased dietary fiber levels remains unknown in less well-nourished infants.

Calprotectin as a marker of inflammation in cystic fibrosis.

Calprotectin is an abundant neutrophil cytosolic protein released during neutrophil activation or death. The use of plasma calprotectin concentration as a marker of pulmonary inflammation was tested in 31 children with cystic fibrosis, none of whom was acutely unwell or pyrexic. Twenty three were receiving antibiotics, 21 had positive sputum cultures, but none of the traditional tests clearly diagnosed ongoing infection. Plasma calprotectin was significantly higher in the cystic fibrosis group than in matched controls. Sixteen children with cystic fibrosis had values above the control range (320-1570 micrograms/l). Their chest radiograph Northern score, an index of accumulated pulmonary involvement, and their plasma copper, an index of acute phase response, both correlated with plasma calprotectin. Plasma gamma-glutamyltransferase also correlated weakly with plasma calprotectin: thus, hepatic pathology may be a confounding variable. However, the data still suggested that plasma calprotectin is a better index of inflammation than the traditional indices in general use.

Calprotectin is raised in endogenous posterior uveitis.

Calprotectin, the L1 leucocyte protein, is found in large quantities in the cytosol of granulocytes and monocytes. Plasma calprotectin levels are increased in infections, malignant tumours, vascular insults and various other pathogenic conditions. The authors have investigated plasma calprotectin and ANCA levels in 27 patients with endogenous posterior uveitis (EPU) and six healthy volunteers. Compared to the control values, the mean levels of plasma calprotectin were raised in patients with active uveitis (p<0.005 (ANOVA)). Raised serum ANCA titres, which are also associated with neutrophil activation, were also detected in some patients with EPU but the level of ANCA did not correlate with that of calprotectin. The authors suggest that measurement of plasma calprotectin may be a sensitive indicator of disease activity in patients with endogenous posterior uveitis.

Calprotectin-mediated zinc chelation as a biostatic mechanism in host defence.

The S-100 Ca2+ binding protein, calprotectin, isolated from neutrophil lysates, has been reported to exhibit zinc reversible biostatic activity in vitro. We verified these findings with C. albicans and investigated whether the growth inhibition resulted from zinc deprivation due to chelation by calprotectin. Calprotectin concentrations of 250 micrograms/ml significantly inhibited the growth of C. albicans. This was reversed by supplementing culture medium with 10 microM ZnSO4. Incubation of calprotectin in culture medium for 24 h prior to inoculation significantly reduced the minimum inhibitory concentration. When this latter medium was ultrafiltered to remove the calprotectin and then inoculated with C. albicans, significant growth inhibition was still present: again it was reversed by zinc. These findings implicate zinc chelation as a novel, potentially important host defence function of an abundant neutrophil protein.

Effect of zinc on lean tissue synthesis during recovery from malnutrition.

During recovery from severe wasting, malnourished children gain weight at greatly accelerated rates. To determine if additional zinc added to their basal therapeutic diets increased the retention of lean tissue and stimulated protein metabolism, we studied three groups of children taking either the basal diet alone or the basal diet supplemented with either 76 mumol (5 mg) or 153 mumol (10 mg) Zn/kg diet. The zinc-supplemented children gained similar weight and consumed the same amount of diet as the unsupplemented children. Zinc supplementation resulted in a greater net absorption of nitrogen and a higher rate of protein turnover, as estimated from urinary ammonia 15N enrichment after oral [15N]glycine. We conclude that additional zinc affected the composition of newly synthesized tissue and intermediary nitrogen metabolism.

Root canal filling materials for primary teeth: a review of the literature.

In summary, there is no known ideal root canal filling material for primary teeth. The closest to the ideal appears to be a calcium hydroxide-iodoform mixture. More histopathologic studies as well as long-term clinical studies are needed on this material.

Electron microscopy of herpes simplex hepatitis with hepatocyte pulmonary embolization in kwashiorkor.

We report a case of herpes simplex hepatitis in a child with edematous malnutrition. Electron microscopy showed virus in parenchymal cells, with pulmonary embolization of necrotic, infected hepatic cell fragments. Systemic dissemination of herpes simplex may be related both to the profound immunoincompetence associated with kwashiorkor and to a reduction in the circulating and fixed polyanions that normally inhibit viral attachment to cells.

Effect of zinc supplementation on the dietary intake, rate of weight gain, and energy cost of tissue deposition in children recovering from severe malnutrition.

Children recovering from severe malnutrition on a milk based diet have low plasma zinc concentrations: children recovering on a soya based diet have much lower plasma zinc concentrations, lower rates of weight gain, and higher energy costs of tissue deposition. However, they do not demonstrate the clinical features of anorexia, diarrhea, and skin lesions usually associated with zinc deficiency. We therefore supplemented 16 children with zinc acetate on the basis that a therapeutic response to zinc constitutes the best evidence of a preexisting zinc deficiency. Fourteen of the 16 children had an immediate and definite increase in their rate of weight gain with zinc supplementation. This was associated with a decrease in the energy cost of tissue deposition, regrowth of the thymus, and activation of the sodium pump. We conclude that the children were indeed zinc deficient. We suggest that the anorexia of zinc deficiency is related to an inability to metabolize nitrogen in the zinc deficient state, and that our children did not show an appetitive response because of the relatively low protein content of the diets we used. Based on the premise that the abnormalities seen in our children may have been secondary to mild zinc deficiency, we suggest that limitation of lean tissue synthesis, with resultant obesity, and a propensity to infection are the major features of a mild zinc deficiency. Children undergoing a period of "catch up" weight gain or growth should have supplemental zinc, particularly if they have had diarrhea or if the use of a soya based formula is contemplated.