Robin A. Henderson

Effect of Enteral Tube Feeding on Growth of Children with Symptomatic Human Immunodeficiency Virus Infection

Summary Malnutrition and growth failure are frequent clinical consequences of human immunodeficiency virus (HIV) infection in children. Tube feeding is a means by which to increase the enteral intake of nutrients. We examined the effect of tube feeding in 18 children, median age 6 months (range, 3–159). Tube feedings were initiated due to growth failure in all, which was also associated with dysfunctional swallowing or aspiration in seven children and gastroesophageal reflux in two. Tube feedings were infused via nasogastric tube (n = 4) or gastrostomy tube (n = 14) and were continued for a median of 8.5 months (range, 2–24). Stoma complications developed in three children with gastrostomy tubes; these were the only tube-related side effect. Tube feedings were discontinued due to noncompliance (n = 3), gastrostomy leakage (n = 2), intolerance (n = 2), and death (n = 3). Anthropometric changes were evaluated comparing mean standard deviation scores (Z) before and after tube feeding. Tube feeding resulted in significantly increased weight for age (Z, −2.13 + 0.7 vs. −1.46 + 1.4; p = 0.04), weight for height (Z, −1.07 + 1.0 vs. −0.13 + 1.0; p = 0.004), and arm fat area (Z, −1.75 + 1.3 vs. −0.62 + 1.2; p = 0.01). However, tube feeding did not result in significant changes in height for age (Z, −1.93 + 0.8 vs. −1.74 + 1.6) or arm muscle area (Z, −1.24 + 0.9 vs. −0.57 + 1.2). Tube feedings effectively increased the weight of HIV-infected children in this study, but they were not sufficient to correct linear growth deficits.

Serum and Plasma Markers of Nutritional Status in Children Infected with the Human Immunodeficiency Virus

OBJECTIVE To determine whether reduced serum or plasma protein and micronutrient levels are common in children infected with the human immunodeficiency virus (HIV) and whether these levels are different in children with growth retardation compared to those with normal growth. SUBJECTS Children were separated into three groups: (a) HIV-infected with growth retardation (HIV + Gr); (b) HIV-infected with normal growth (HIV+); (c) HIV-uninfected with normal growth (HIV-). All children were afebrile and free of acute infection at the time of study. During a 24-hour stay in the Pediatric Clinical Research Unit, blood was drawn for analysis of total protein, albumin, zinc, selenium, and vitamin A levels; growth measurements were obtained; and dietary intake was assessed by 24-hour weighed food intake and 24-hour dietary recall. STATISTICAL ANALYSIS Mean differences between groups were assessed by analysis of variance, and differences in the frequency of nutrient deficiency were determined by chi 2 analysis. RESULTS Thirty-eight children between 2 and 11 years of age were studied: 10 HIV + Gr, 18 HIV+, and 10 HIV-. No statistically significantly differences were noted in mean levels of albumin, prealbumin, zinc, and selenium. Mean serum level of vitamin A was significantly higher in the HIV + Gr group than in the other two groups. There were no significant differences between groups in the frequency of deficiency for any nutrient studied. Mean energy and nutrient intake was similar among groups. APPLICATIONS/CONCLUSIONS Abnormal serum or plasma protein or micronutrient levels were uncommon in this cohort of HIV-infected children, even in children with growth retardation. Routine monitoring of the level of proteins and micronutrients studied is unnecessary in the absence of specific clinical indicators of deficiency.

Maternal vitamin A deficiency and child growth failure during human immunodeficiency virus infection.

Although vitamin A is thought to influence growth, the relationship between maternal vitamin A deficiency during pregnancy and child growth is unknown. A longitudinal cohort study of 467 HIV-infected women and their children was conducted in Blantyre, Malawi. The childrens weight and height were measured every 3 months until they were 24 months old. Maternal vitamin A deficiency was independently related to both linear and ponderal growth after adjustment for effects of body mass index, child gender, and child HIV status. By 12 months of age, infants born to mothers who were vitamin A-deficient during pregnancy weighed approximately 8% less (p < 0.001) and were approximately 2% shorter (p < 0.001) than infants born to mothers who were not deficient. This study suggests children born to HIV-infected women who are vitamin A-deficient during pregnancy are more likely to have growth failure.

Resting energy expenditure and body composition in children with HIV infection

The purpose of this study was to determine whether alterations in body composition, resting energy expenditure (REE), and dietary energy intake are associated with growth retardation in HIV-positive children. Body composition (deuterium oxide dilution, skinfold measurements), REE (indirect calorimetry), and energy intake (24-hour weighed food intake) were evaluated in three groups: HIV-positive with growth retardation (HIV+Gr), HIV-positive with normal growth (HIV+); and HIV-uninfected with normal growth (HIV-). Children were between 2 and 11 years of age, afebrile, and free from acute infection. Forty-two children (13 HIV+Gr, 19 HIV+, 10 HIV-) were studied. Lean body mass was significantly reduced in HIV+Gr compared with HIV- (p < .05), and fat mass was significantly reduced in HIV+Gr and HIV+ compared with HIV- (p < .05). The percentages of lean and fat mass were not significantly different between groups, suggesting that differences in lean and fat mass were proportional to differences in body size. Consistent with reduced lean body mass, mean REE was significantly lower in HIV+Gr compared with HIV- (p < .05). Differences in mean REE/kg of body weight or lean body mass between groups were not statistically significant. A significant negative correlation was found between REE (kcal/kg/day) and weight-for-age (p = .04), and a trend with height-for-age Z-score (p = .07). Mean energy intake was not significantly different between groups. This study suggests that lean and fat mass are proportionately reduced in HIV-positive children with growth retardation. Further studies are necessary to delineate the relationship between energy balance and growth in children with HIV infection.

Whole body protein turnover in children with human immunodeficiency virus (HIV) infection

The purpose of this study was to determine the rate of whole body protein turnover (WBPT) in human immunodeficiency virus (HIV)-infected children, and to determine the relationship between WBPT and growth. The rate of WBPT was calculated from the cumulative excretion of labeled urinary ammonia after a single intravenous dose of 15N-glycine in three groups of children: 1) HIV+ with growth retardation (HIV+ Gr); 2) HIV+ with normal growth (HIV+); and 3) HIV-uninfected with normal growth (HIV-). Twenty-six children between 2 and 11 y of age were studied (10 HIV+ Gr, 12 HIV+, 4 HIV-). All children were afebrile and free of acute infection during the study. Rates of WBPT (mean +/- SD) for the study groups were: HIV+ Gr, 12.2 +/- 4.8; HIV+, 10.7 +/- 5.1; and HIV-, 8.6 +/- 2.1 g.protein.kg-1.d-1 (NS, P > 0.05). Although not statistically significant, mean WBPT was 42% greater in HIV+ Gr, and 24% greater in HIV+ compared to HIV-. Statistically significant correlations were found between WBPT and Z scores for height (r = -0.39, P = 0.05) and weight-for-age (r = -0.51, P = 0.01) and dietary intake of protein (r = 0.39, P = 0.05), and between protein balance (synthesis-catabolism) and intakes of energy (r = 0.47, P = 0.02) and protein (r = 0.40, P = 0.04). There was no statistically significant correlation between WBPT and resting energy expenditure (r = 0.27, P = 0.19), or CD4 cell number (r = 0.05, P = 0.82). These data suggest an association between increased rates of protein turnover and low weight and height-for-age Z scores, and that it may be possible to achieve positive protein balance given an adequate intake of nutrients.