Pathogenesis of cancrum oris (noma): confounding interactions of malnutrition with infection.
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This study showed that impoverished Nigerian children at risk for cancrum oris (noma) had significantly reduced plasma concentrations of zinc (< 10.8 micromol/L), retinol (< 1.05 micromol/L), ascorbate (< 11 micromol/L), and the essential amino acids, with prominently increased plasma and saliva levels of free cortisol, compared with their healthy counterparts. The nutrient deficiencies, in concert with previously reported widespread viral infections (measles, herpesviruses) in the children, would impair oral mucosal immunity. We postulate, subject to additional studies, that evolution of the oral mucosal ulcers including acute necrotizing gingivitis to noma is triggered by a consortium of microorganisms of which Fusobacterium necrophorum is a key component. Fusobacterium necrophorum elaborates several dermonecrotic toxic metabolites and is acquired by the impoverished children via fecal contamination resulting from shared residential facilities with animals and very poor environmental sanitation. (+info)
Growth hormone promotes somatic and skeletal muscle growth recovery in rats following chronic protein-energy malnutrition.
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The efficacy of recombinant human growth hormone (GH) and/or a diet enriched in protein and energy to improve growth recovery following prolonged malnutrition was examined in male rats food-restricted from birth until 120 d of age. At d 121, restricted rats were randomly assigned to recovery groups receiving either a control or enriched diet with or without daily subcutaneous injections of GH. Rats were killed after 16 or 47 d of recovery. At d 16, GH treatment stimulated liver, heart, plantaris, soleus, carcass and body weight gain and inhibited fat gain when compared to recovery controls. Rats receiving GH also exhibited the highest serum insulin-like growth factor-I (IGF-I) concentrations and total muscle protein. At d 47, GH effects on body and muscle recovery were minimal, and differences among recovery groups in serum IGF-I concentration and total muscle protein were no longer present. Consumption of an enriched diet increased fat pad and liver mass, but did not promote muscle recovery. There were no differences among treatment groups in skeletal muscle IGF-I mRNA levels at d 16 or 47. In summary, GH had positive effects on somatic and skeletal muscle growth early in the recovery process, possibly via endocrine IGF-I-stimulated protein accretion. In contrast, the enriched diet promoted fat deposition with no impact on skeletal muscle growth recovery. (+info)
Dietary protein, growth and urea kinetics in severely malnourished children and during recovery.
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The case mortality for severe malnutrition in childhood remains high, but established best approaches to treatment are not used in practice. The energy and protein content of the diet at different stages of treatment appears important, but remains controversial. The effect on growth, urea kinetics and the urinary excretion of 5-L-oxoproline was compared between a standard infant formula (HP group) provided in different quantities at each stage of treatment and a recommended dietary regimen, which differentiates the requirements of protein and energy during the acute phase of resuscitation (maintenance intake of energy and protein, relatively low protein to energy ratio, LP group) from those during the restoration of a weight deficit (energy and nutrient dense). The energy required to maintain weight was less in the HP than the LP group, but the HP group was not able to achieve as high an energy intake during repletion of wasting because of the high volume which would have had to be consumed. Compared to the LP group, in the HP group during catch-up growth there was significantly greater deposition of lean tissue and higher rates of urea production, hydrolysis and salvage of urea-nitrogen. These, together with higher rates of 5-L-oxoprolinuria, suggest a greater constraint of the formation of adequate amounts of nonessential amino acids, especially glycine, in the face of enhanced demands. Although more effective rehabilitation might be achieved using a standard formula, there is the need to determine the extent to which it might impose metabolic stress compared with the modified formulation. (+info)
Strong association between malnutrition, inflammation, and atherosclerosis in chronic renal failure.
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BACKGROUND: Atherosclerotic cardiovascular disease and malnutrition are widely recognized as leading causes of the increased morbidity and mortality observed in uremic patients. C-reactive protein (CRP), an acute-phase protein, is a predictor of cardiovascular mortality in nonrenal patient populations. In chronic renal failure (CRF), the prevalence of an acute-phase response has been associated with an increased mortality. METHODS: One hundred and nine predialysis patients (age 52 +/- 1 years) with terminal CRF (glomerular filtration rate 7 +/- 1 ml/min) were studied. By using noninvasive B-mode ultrasonography, the cross-sectional carotid intima-media area was calculated, and the presence or absence of carotid plaques was determined. Nutritional status was assessed by subjective global assessment (SGA), dual-energy x-ray absorptiometry (DXA), serum albumin, serum creatinine, serum urea, and 24-hour urine urea excretion. The presence of an inflammatory reaction was assessed by CRP, fibrinogen (N = 46), and tumor necrosis factor-alpha (TNF-alpha; N = 87). Lipid parameters, including Lp(a) and apo(a)-isoforms, as well as markers of oxidative stress (autoantibodies against oxidized low-density lipoprotein and vitamin E), were also determined. RESULTS: Compared with healthy controls, CRF patients had an increased mean carotid intima-media area (18.3 +/- 0.6 vs. 13.2 +/- 0.7 mm2, P < 0.0001) and a higher prevalence of carotid plaques (72 vs. 32%, P = 0.001). The prevalence of malnutrition (SGA 2 to 4) was 44%, and 32% of all patients had an acute-phase response (CRP > or = 10 mg/liter). Malnourished patients had higher CRP levels (23 +/- 3 vs. 13 +/- 2 mg/liter, P < 0.01), elevated calculated intima-media area (20.2 +/- 0.8 vs. 16.9 +/- 0.7 mm2, P < 0.01) and a higher prevalence of carotid plaques (90 vs. 60%, P < 0.0001) compared with well-nourished patients. During stepwise multivariate analysis adjusting for age and gender, vitamin E (P < 0.05) and CRP (P < 0.05) remained associated with an increased intima-media area. The presence of carotid plaques was significantly associated with age (P < 0.001), log oxidized low-density lipoprotein (oxLDL; P < 0.01), and small apo(a) isoform size (P < 0.05) in a multivariate logistic regression model. CONCLUSION: These results indicate that the rapidly developing atherosclerosis in advanced CRF appears to be caused by a synergism of different mechanisms, such as malnutrition, inflammation, oxidative stress, and genetic components. Apart from classic risk factors, low vitamin E levels and elevated CRP levels are associated with an increased intima-media area, whereas small molecular weight apo(a) isoforms and increased levels of oxLDL are associated with the presence of carotid plaques. (+info)
Association of morbidity with markers of nutrition and inflammation in chronic hemodialysis patients: a prospective study.
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BACKGROUND: Numerous studies suggest a strong association between nutrition and clinical outcome in chronic hemodialysis (CHD) patients. Nevertheless, the pathophysiological link between malnutrition and morbidity remains to be clarified. In addition, recent evidence suggests that nutritional indices may reflect an inflammatory response, as well as protein-calorie malnutrition. In this study, we prospectively assessed the relative importance of markers of nutritional status and inflammatory response as determinants of hospitalization in CHD patients. METHODS: The study consisted of serial measurements of concentrations of serum albumin, creatinine, transferrin, prealbumin, C-reactive protein (CRP), and reactance values by bio-electrical impedance analysis (BIA) as an indirect measure of lean body mass every 3 months over a period of 15 months in 73 CHD patients. Outcome was determined by hospitalizations over the subsequent three months following each collection of data. RESULTS: Patients who required hospitalization in the three months following each of the measurement sets had significantly different values for all parameters than patients who were not hospitalized. Thus, serum albumin (3.93 +/- 0.39 vs. 3.74 +/- 0.39 g/dl), serum creatinine (11.0 +/- 3.7 vs. 9.1 +/- 3.5 mg/dl), serum transferrin (181 +/- 35 vs. 170 +/- 34 mg/dl), serum prealbumin (33.6 +/- 9.2 vs. 30.0 +/- 10.1 mg/dl), and reactance (50.4 +/- 15.6 vs. 43.0 +/- 13.0 ohms) were higher for patients not hospitalized, whereas CRP (0.78 +/- 0.89 vs. 2.25 +/- 2.72 mg/dl) was lower in patients who were not hospitalized. All differences were statistically significant (P < 0.05 for all parameters). When multivariate analysis was performed, serum CRP and reactance values were the only statistically significant predictors of hospitalization (P < 0.05 for both). When a serum CRP concentration of 0.12 mg/dl was considered as a reference range (relative risk 1.0), the relative risk for hospitalization was 7% higher (relative risk = 1.07) for a CRP concentration of 0.92 mg/dl and was 30% (relative risk = 1.30) higher for a CRP concentration of 3.4 mg/dl. When a reactance value of 70 ohms was considered as a reference range with a relative risk of 1.0, the relative risk of hospitalization increased to 1.09 for a reactance value of 43 ohms and further increased to 1.14 for a reactance value of 31 ohms. CONCLUSIONS: The results of this study strongly indicate that both nutritional status and inflammatory response are independent predictors of hospitalization in CHD patients. CRP and reactance values by BIA are reliable indicators of hospitalization. Visceral proteins such as serum albumin, prealbumin, and transferrin are influenced by inflammation when predicting hospitalization. When short-term clinical outcomes such as hospitalizations are considered, markers of both inflammation and nutrition should be evaluated. (+info)
T cells with a quiescent phenotype (CD45RA+) are overabundant in the blood and involuted lymphoid tissues in wasting protein and energy deficiencies.
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The objective of this investigation was to determine the influence of distinct forms of acute weight loss on the expression of the quiescence marker, CD45RA, by T cells in several lymphoid compartments including the blood. Male and female weanling mice, CBA/J and C57BL/6J strains, were allocated to the following groups: ad libitum intake of a complete purified diet; restricted intake of the complete diet; and ad libitum intake of an isocaloric low-protein diet. The restricted intake protocol produced weight loss through energy deficiency (marasmic-type malnutrition), whereas the low-protein diet caused wasting through inadequate protein nitrogen and induced a condition mimicking incipient kwashiorkor. In one experiment, weanling mice of both strains were maintained for 14 days according to each of these dietary protocols and, in a supplementary study, C57BL/6J weanlings consumed either the complete diet or the low-protein diet ad libitum for 21 days. Zero-time control groups (19-days old and 23-days old in C57BL/6J and CBA/J strains, respectively) were included in the first experiment to control for ontogeny-related change. Expression of CD45RA was assessed by two-colour flow cytometry in CD4+ and CD8+ T cells from the spleen, mesenteric lymph nodes and blood. Within 14 days, energy-restricted mice exhibited a high percentage of CD4+ T cells expressing CD45RA in all three lymphoid compartments in both mouse strains (an average of 50% CD45RA+ versus 9% in well-nourished controls), and a similar outcome was apparent in the CD8+ subset (93% CD45RA+ versus 63%). Mice fed the low-protein diet required up to 21 days to exhibit the same imbalance within the CD4+ T-cell subset (33% CD45RA+ versus 4% in well-nourished controls). A shift toward a quiescent phenotype occurs throughout the peripheral T-cell system in acute wasting disease. Consequently, the quiescence-activation phenotype of blood T cells reflects the same index in secondary lymphoid organs in such pathologies. Naive-type quiescence among T cells is implicated as a component of depressed adaptive immunocompetence in the advanced stages of diverse forms of acute weight loss. (+info)
Dietary phospholipids rich in long-chain polyunsaturated fatty acids improve the repair of small intestine in previously malnourished piglets.
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Malnourished piglets were studied to establish how a diet containing long-chain polyunsaturated fatty acids (LC-PUFA) of the (n-6) and (n-3) series, esterified in the form of phospholipids, affects intestinal recovery after severe malnutrition. Piglets (7-d-old) were randomly assigned to two groups. One group was fed a piglet milk formula and the other was malnourished by protein-energy restriction for 30 d. Healthy and malnourished piglets were then divided into two subgroups fed for 10 d either an adapted milk formula (C and M) or the same diet supplemented with LC-PUFA phospholipids (C-P and M-P). The M-P group had greater protein, DNA, cholesterol and phospholipid levels and a lower triglyceride level in the jejunal segment than did the M group. The fatty acid composition of the jejunal mucosa and microsomes of the M-P piglets did not differ from that of healthy piglets (C). However, in jejunal mucosa, microsomes and phospholipids from malnourished piglets that did not receive LC-PUFA (group M) had significantly lower percentages of (n-6) LC-PUFA than those in healthy piglets (C). The (n-3) LC-PUFA percentages of jejunal mucosa were also lower in the M group than in the C group. The small intestine of piglets fed the LC-PUFA-supplemented formula recovered more completely from histologic lesions and biochemical alterations caused by the malnutrition process than the small intestine of piglets fed the control formula without LC-PUFA. (+info)
A minimally invasive tracer protocol is effective for assessing the response of leucine kinetics and oxidation to vaccination in chronically energy-deficient adult males and children.
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In disadvantaged populations, recurrent infections lead to a loss of body nitrogen and worsen nutritional status. The resulting malnutrition, in its turn, produces a greater susceptibility to infection. This study aimed to examine the ability of a new minimally invasive tracer protocol to measure leucine oxidation, and then to use it to quantify the effect of vaccination on leucine kinetics and oxidation. Undernourished men (n = 5; body mass index 16.3 +/- 0.9 kg/m(2)) and children (n = 9; age 4.1 +/- 0.6 y; weight-for-age Z-score -2.3 +/- 0.7) underwent metabolic studies 6 d before and 1 d after vaccination with diphtheria, pertussis and tetanus (DPT). The tracer protocol was performed in the fed state and involved two 3-h sequential periods of frequent (20 min) oral doses of NaH(13)CO(3) or [1-(13)C] leucine. Frequent breath samples and urine collections were made. Blood samples were obtained from the men and used for the determination of the isotopic enrichment of alpha-ketoisocaproic acid. The prevaccination oxidation of leucine (percentage of dose +/- SD) was 18.1 +/- 2.3 (men) and 16.7 +/- 3.8 (children). One day after vaccination, these values had risen to 19. 9 +/- 1.9 (P < 0.05) in the men and to 19.5 +/- 4.6 (P < 0.01) in the children. In the adults, vaccination was associated with a rise in whole-body protein breakdown [mg protein/(kg.h)] from 200 +/- 40 to 240 +/- 10 (P < 0.05). A minor simulated infection increases leucine catabolism in undernourished humans and this new, minimally invasive protocol is sufficiently sensitive to measure these changes. (+info)