Arsenic, selenium, and African trypanosomiasis.
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Brain Diseases↗
Biomedical subjects
M H Golden
Publications and source records attributed to M H Golden.
Coagulase-negative staphylococcal bacteremia in severely malnourished Jamaican children.
Immunosuppression increases the susceptibility to infection and changes the inflammatory response in children with severe protein-energy malnutrition. In this 5-year prospective study bacteremia was documented in 16% of 336 severely malnourished children, 2 to 34 months of age, who were hospitalized consecutively in the Tropical Metabolism Research Unit, Kingston, Jamaica. The 53 children had 60 episodes of nosocomial and community-acquired bacteremia with 69 blood isolates. Community-acquired bacteremia accounted for 72% (43 of 60) of bacteremic episodes. Thirty-five percent (24 of 69) of the strains were coagulase-negative staphylococci, 19% (13 of 69) were Staphylococcus aureus and 11% (8 of 69) were Streptococcus Group D. Seventeen episodes of coagulase-negative staphylococcal bacteremia were acquired in the community and 7 were nosocomial. These patients were more likely to have pneumonic consolidation than children with all other bacteremias combined (P < 0.02, Fisher's exact test). The bacteremia-related case fatality rate was 8% (5 of 60). Polymicrobial and Gram-negative septicemia were independent positive predictive factors for mortality when compared with single-agent and Gram-positive sepsis (P < 0.02). This 71% (49 of 69) prevalence of Gram-positive organisms suggests a change in the epidemiology from the predominant Gram-negative etiologies (76%) described in previous reports.
Bacteremia↗
Ultrasonographic assessment of the extent of hepatic steatosis in severe malnutrition.
Ultrasonographic, blinded assessment was made of the extent of hepatic steatosis in 55 children with severe malnutrition: undernutrition (n = 6), marasmus (n = 18), marasmickwashiorkor (n = 17), and kwashiorkor (n = 14). The children were examined on admission, in early recovery (considered as baseline), and again at discharge. Eleven healthy control children and eight of the previously malnourished children were studied as comparison groups. Both oedematous and non-oedematous malnourished children had significantly more steatosis than the comparison groups at each time. Children with oedematous malnutrition had significantly greater steatosis than non-oedematous children at admission. Half of the non-oedematous malnourished children had appreciable hepatic steatosis at both admission and at baseline. Hepatic fat was only slowly mobilised. The rate constant was 1.4 +/- 0.3%/day. One quarter of the children did not change steatosis grades during the period they were in hospital. There was no overall correlation between the extent of steatosis and liver size. Hepatic steatosis in childhood malnutrition is not confined to oedematous children: it is frequently present in marasmic and undernourished children. Its extent is not necessarily related to the degree of hepatomegaly and accumulated lipid is only slowly mobilised.
Child, Preschool↗
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.
Child, Preschool↗
The exocrine pancreas in kwashiorkor and marasmus. Light and electron microscopy.
Histological sections of pancreas and liver from 65 cases of children dying from childhood malnutrition were reviewed. The extent of pancreatic atrophy and fibrosis was compared with fatty change in the liver. Pancreatic atrophy was common, and often associated with severe fatty change in the liver, but also occurred in marasmic children with scanty liver fat. Pancreatic fibrosis, when present, was only of mild degree. Among 16 patients with marasmus, fibrosis was only seen in one pancreas. Fibrosis was recorded in 8/25 cases of kwashiorkor, and in 7/24 cases diagnosed as marasmic-kwashiorkor. Electron microscopy of the pancreas was performed in seven cases, using tissue collected at immediate autopsy. Atrophy and variable amounts of degranulation of acinar cells were seen. There was often disorganization of the endoplasmic reticulum with intracisternal sequestration. Mitochondrial swelling was consistent with terminal anoxia. Centro-acinar cells were prominent. Some acini were dilated and contained fibrillar material. These findings support the pioneer paper by Blackburn and Vinijchaikul (1969) and underline the importance of pancreatic atrophy in the pathology of protein-energy malnutrition.
Child, Preschool↗
The zinc sandwich and growth.
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Child Nutrition Disorders↗
Peroxisomes and the fatty liver of malnutrition: an hypothesis.
Peroxisomes play a role in hepatic beta-oxidation of fat, a process that results in the production of hydrogen peroxide. The fatty infiltration of the liver that occurs in severely malnourished children remains unexplained. We observed an almost total absence of peroxisomes in the hepatocytes of these children. We suggest that lack of available peroxisomes could contribute to the development of fatty liver.
Child↗
The nature of nutritional deficiency in relation to growth failure and poverty.
A new classification of essential nutrients is proposed based on whether the major response to a deficiency is either (a) specific defects which lead to loss of particular functions and characteristic clinical signs and symptoms or (b) a primary cessation of growth. Diagnosis of deficiency of the nutrients which give rise to growth failure (nitrogen, essential amino acids, potassium, sodium, phosphorus, sulphur, zinc, magnesium) is particularly difficult because of the nature of the response and the lack of a body store. The implications of the differences in the types of deficiency are explored in relation to assessment of the likelihood that widespread deficiency exists. Poverty is particularly likely to be associated with unrecognised deficiency of these "growth" nutrients because of the monotony of the diet. This will lead to slow growth. There is probably a difference in the nutrient requirements for longitudinal and ponderal growth. Of the growth nutrients sulphur is likely to be required in much higher amounts for skeletal growth than soft tissue growth.
Deficiency Diseases↗
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.
Capillaries↗
Effacement of glomerular foot processes in kwashiorkor.
In a study of the pathogenesis of the oedema of kwashiorkor the ultrastructure of the kidneys from 6 children was examined shortly after they died from oedematous malnutrition. There was a generalised effacement of the glomerular epithelial cells onto the basement membrane. The filtration slits that remained were narrowed. The picture was similar to that seen in minimal-change nephrotic syndrome--but none of the children had albuminuria. The degree of effacement was statistically related to treatment with gentamicin. The findings suggest that there is a defect in the anionic charge of the glomerular basement membrane in oedematous malnutrition, that the membrane charge is more easily neutralised by cations such as gentamicin, and that, because proteinuria is not a feature of oedematous malnutrition, the proteinuria in other conditions associated with glomerular epithelial cell effacement (eg, minimal-change nephrotic syndrome) is due to something more complex than simple loss of charge.
Basement Membrane↗
The effect of DPT inoculation on the hormonal control of glucose homeostasis in children recovered from malnutrition.
The effect of a controlled stress (DPT inoculation) on the hormonal control of glucose homeostasis was investigated in children nutritionally rehabilitated from severe malnutrition. The age range of the 15 children studied was 6-26 months. Plasma insulin (INS), growth hormone (GH) and interleukin-1 (IL-1) were measured by radioimmunoassay; plasma glucose (GLU) by a glucose oxidase method; and red cell insulin binding (%SB) was determined, using A-14 monoiodinated insulin. Measurements were made on two occasions: (T-0) at 10 a.m., 12 hr before DPT inoculation, and (T-36) 36 hr. after inoculation. On both occasions, 4 hr post-prandial blood samples were used, and the mean body temperature (T) on the day of the test was determined. Red cell insulin binding (%SB) was significantly higher at T-36 than at T-0 (16.8 +/- 1.7 vs 12.1 +/- 1.2 (14), p = 0.005). (Results were expressed as mean +/- SEM, numbers of paired observations in parentheses). The higher %SB after DPT was accompanied by an increase in the number of receptor sites (S) (29.05 +/- 6.5 vs 15.6 +/- 2.5 (14), p = 0.025). However, insulin receptor affinity (K x 10(9) M-1) was decreased (0.7 +/- 0.1 vs 1.5 +/- 0.3 (14), p = 0.008). There were no significant differences in the plasma levels of insulin, glucose and interleukin-1, but plasma growth hormone (microU/ml) was increased after DPT, (18.0 +/- 3.0 vs. 11.5 +/- 1.2 (13), p = 0.04). Body temperature (degree C) was also significantly increased after DPT, (99.6 +/- 0.4 vs. 98.3 +/- 0.2 (14), p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Glucose↗
Changes in red cell insulin receptors during recovery from severe malnutrition.
Red cell insulin binding was studied in 13 Jamaican children (age range 4-24 months), while malnourished (MAL), during early recovery (GI), late recovery (GII), and after anthropometric recovery (REC). The rate of weight gain (RW), the energy intake (EN), and the protein intake (PR) were monitored at each phase of the study. Four-hour fasting blood samples were used, and the insulin binding characteristics were investigated in the physiological range of insulin concentrations (16.7-1670 pM). Analyses of variance were used to examine differences in the variables measured at the four phases. Red cell-specific insulin binding (SB) was lower in MAL than in GI (P less than 0.001) and in (GII) (P = 0.026). SB in REC and MAL were not significantly different. Insulin receptor affinity (K) was also lower in MAL than in GI (P less than 0.001). GII (P = 0.001), and REC (P = 0.012). The insulin receptor number (S) appeared to be high in malnutrition and to decrease as recovery progressed; however the decrease was not significant. Children with fever demonstrated high insulin binding. Plasma insulin (IN) rose during recovery, and was significantly higher in GII than in MAL (P = 0.01). There was no difference in plasma glucose (G) at any phase of the study. The interrelationships among the variables measured were investigated longitudinally using multiple regression analyses, SB was positively associated with S (P = 0.032), EN (P = 0.029), and PR (P = 0.0076). S was negatively associated with K (P less than 0.001). The associations of S and K with PR were positive and approached significance (P = 0.09 and P = 0.07 respectively). RW was positively associated with PR (P less than 0.001), and with EN (P = 0.001). There were no significant relationships between G and any of the other variables longitudinally. However, correlations of the variables within phases demonstrated that in MAL, G was negatively associated with SB (P less than 0.05) and with K (P less than 0.05); but in REC, G was positively associated with SB (P less than 0.05). These results demonstrated that in severe malnutrition, the red cell insulin receptor affinity was low. During catch-up growth when protein and energy intakes were increased, both insulin receptor affinity and specific insulin binding were also increased. The negative relationship between insulin binding and plasma glucose during malnutrition may be related to carbohydrate intolerance.
Analysis of Variance↗
Growth suppression in the Trichuris dysentery syndrome.
The Trichuris Dysentery Syndrome (Ramsey, 1962) is an insidious, chronic condition which has clinical features similar to Crohn's ileocolitis and ulcerative colitis, diseases similarly associated with growth retardation. The attained heights and weights of 19 children at the time of diagnosis of intens, -2.4 Standard Deviation (Z) scores from the Tanner-Whitehouse median with weight, adjusted for height-age, -1.3 Z. We present data on the growth velocities of 11 of the children in the half-year following worm expulsion by mebendazole. These children returned to their home environments without food supplementation or close follow-up, but showed an average height velocity of +5.5 Z and weight velocity (for height-age) of +2.4 Z. Of 8 children with unequivocal height spurts only 3 had any weight spurt. We suggest that the pattern of catch-up growth points to the existence of some specific link between allergy or inflammation in the lower intestinal tract and suppression of linear growth, rather than to stunting due to general deprivation and undernutrition.
Animals↗
Plant protein rehabilitation diets and iron supplementation of the protein-energy malnourished child.
Thirty-eight children admitted to the paediatric ward of Obafemi Awolowo University Teaching Hospital, Ile-Ife, were treated using a local therapeutic regimen for protein-energy malnutrition (PEM). Serum transferrin concentration was measured at weekly intervals to determine the response to and nutritional adequacy of the dietary component of this therapeutic regimen. At discharge, weight for height measurements in the children showed a significant (P less than 0.001) increase in growth although the expected weight for height was not attained. Serum transferrin concentration rose significantly from a mean basal level of 132.1 +/- 17.2 mg/dl to 222.0 +/- 24.6 mg/dl at the end of the first week of hospitalization and at discharge was 403.2 +/- 27.8 mg/dl. Although not statistically significant, mortality was highest amongst children for whom iron supplementation started early on admission. Earlier studies on the aetiology and treatment of anaemia in PEM have argued in favour of routine treatment with iron to prevent the development of anaemia during the recovery phase, but data from this study suggest that iron therapy should not be instituted during the first week of treatment.
Anemia, Hypochromic↗
Febrile response in malnutrition.
The febrile response to a standard dose of triple (DPT) vaccine was assessed in sixteen malnourished children before and after recovery. The increase in temperature was significantly lower in the malnourished children (p less than 0.005).
Body Temperature↗
Clustering of Ascaris lumbricoides and Trichuris trichiura infections within households.
A survey of 428 households in a shanty town in Coatzacoalcos, Mexico, revealed high prevalences of Ascaris lumbricoides and Trichuris trichiura. The data were analysed separately for A. lumbricoides and T. trichiura in order to investigate the spatial distribution of heavy infections through the town. Within each age class, those individuals with egg counts in the upper 20% of the range for that age were classified as "heavily infected". When the data were stratified by household size, it was found that the distribution of "heavily-infected" individuals was not random in the community. "Heavily-infected" individuals were found together in households; fewer household units had a single heavily-infected individual than would be expected by chance. Such a pattern could result either from genetic similarities among family members influencing their ability to mount an effective immunological response to infection, or focal transmission in the vicinity of the home, or both. This result may have important implications for the development of community control programmes.
Adolescent↗
Quantitative assessment of geophagous behaviour as a potential source of exposure to geohelminth infection.
The most common form of pica, geophagy, has direct adverse nutritional effects and also exposes children to soil-borne infection. Existing methods for assessing geophagy are either inappropriate for field use (radiology) or unreliable (reporting). A new method is described, based on the measurement of soil-derived silica in stools. More than 90% of silica is excreted within one gut transit period of ingestion. The amount excreted is proportional to the amount ingested. Faecal levels of dietary silica (less than 2% dry wt stool) can be distinguished from levels due to geophagy (up to 25% dry wt stool). Studies in 2 children's homes in Jamaica showed that 33% and 66% of children were geophagous, ingesting up to 10 g soil day-1. The geophagy of less than 20% of the children accounted for greater than 60% of the total soil ingested. This overdispersion of exposure to soil-borne infection may contribute to the observed aggregation of geohelminth infection.
Child↗
In vivo metabolism of nitrogen precursors for urea synthesis in the postprandial rat.
(1) Adult postprandial rats were given a continuous, intravenous infusion of 15N-labelled glutamate, alanine, ammonium chloride and glutamine amide for 6 h. The enrichment in the free hepatic pool was measured for ammonia, glutamine amide, urea, aspartate, glutamate and alanine. (2) Glutamine and glutamate supplied significantly more nitrogen to urea than ammonium chloride or alanine. (3) Glutamate was not a significant source of hepatic ammonia, hence in this situation it is not necessary to impute a major role to glutamate dehydrogenase in hepatic ammoniagenesis for urea synthesis. (4) Glutamine and ammonia, mostly of intestinal origin in the postprandial state, were major precursors of hepatic ammonia. (5) The nitrogen of glutamate and alanine moved to urea primarily through aspartic acid.
Alanine↗