Experience Growth Failure Research Articles

Prolonged enteral leucine supplementation improves lean growth in neonatal pigs fed a restricted protein diet (258.6)

Many low birth weight infants experience growth failure due to feeding intolerance resulting in reduced nutrient intake. The branched‐chain amino acid, leucine, has been shown to have anabolic effects on skeletal muscle. The objective of the study was to determine if prolonged enteral leucine supplementation improves lean growth in neonatal pigs fed a restricted protein diet. Five‐day‐old pigs (N = 22; 1.9 ± 0.3 kg initial BW) were fed by gastric catheter either a control protein (CP; 22.5% protein, 0.98% leucine) or restricted protein (RP; 11.2% protein, 0.49% leucine) milk replacement diet or RP supplemented with leucine to the same level as in the CP diet (RP+L). Pigs were fed 40 ml/kg BW per meal every 4 h for 21 d. Body composition was determined by dual‐energy x‐ray absorptiometry on d 0 and 20. Feeding the CP diet resulted in greater total body weight and lean body mass after 21 d compared to RP fed pigs (P < 0.05). Mass of the longissimus dorsi muscle, heart, and kidney were also greater in the CP than RP fed pigs (P < 0.05). Body weight, lean body mass, and mass of the longissimus dorsi, heart, and kidney in pigs fed the RP+L diet were intermediate to the RP and CP fed pigs. Fat content and gain were similar for all groups. Prolonged leucine supplementation of a marginal protein diet has the potential to improve overall growth in neonatal pigs and infants with restricted protein intake through an increase in lean tissue growth.Grant Funding Source: Supported by NIH HD072891 and USDA/ARS 6250‐51000‐055

349 Effects of Postnatal Energy and Macronutrient Intakes on Growth in Extremely Preterm Infants: a Population-Based Study

BackgroundExtremely preterm infants often experience growth failure and adequate nutritional supply may be difficult to achieve. It is still debated to what extent nutrition affects growth at an early stage...

Normal Interstage Growth After the Norwood Operation Associated With Interstage Home Monitoring

After stage 1 palliation (S1P) with a Norwood operation, infants commonly experience growth failure during the initial interstage period. Growth failure during this high-risk period is associated with worse outcomes. This study evaluated the growth patterns of patients enrolled in the authors' interstage home-monitoring program (HMP), which uses a multidisciplinary team approach to nutrition management. From 2000 to 2009, 148 infants were enrolled in the HMP after S1P. Families recorded daily weights during the interstage period and alerted the interstage monitoring team about protocol violations of nutritional goals. Interstage monitoring and inpatient data from the S1P hospitalization were reviewed to identify risk factors for poor growth. Growth outcomes were compared with published norms from the Centers for Disease Control. Interstage survival for patients in the HMP was 98 % (145/148). Growth velocity during the interstage period was 26 ± 8 g/day. The weight-for-age z-scores decreased from birth to discharge after S1P (-0.4 ± 0.9 to -1.3 ± 0.9; p < 0.001) but then increased during the interstage period to the time of S2P (-0.9 ± 1; p < 0.001). The factors associated with improved growth during the interstage period included male gender, greater birth weight, full oral feeding at S1P discharge, and a later birth era. After S1P, infants enrolled in an HMP experienced normal growth velocity during the interstage period. Daily observation of oxygen saturation, weight change, and enteral intake together with implementation of a multidisciplinary feeding protocol is associated with excellent interstage growth and survival.

Early Nutrient Supply and the Preterm Infant

Early Nutrient Supply and the Preterm Infant

Specific considerations in the treatment of pediatric inflammatory bowel disease

Inflammatory bowel disease is one of the most prevalent chronic inflammatory disorders and commonly presents during childhood or adolescence. Occurring during a critical period of growth and development, pediatric Crohn’s disease and ulcerative colitis require special consideration. Children often experience growth failure, malnutrition, pubertal delay and bone demineralization. Medical treatment must be optimized to promote clinical improvement and reverse growth failure with minimal toxicity. In addition to pharmacologic and surgical interventions, nutritional therapies play a vital role in the management of pediatric inflammatory bowel disease. This review will outline the epidemiology and clinical complications that are unique to pediatric inflammatory bowel disease, current trends, and recent advances in nutritional and pharmacologic treatment, and projected future therapeutic direction.

Growth Failure in Early Life: An Important Manifestation of Turner Syndrome

The goals of this study were to test the hypothesis that girls with Turner syndrome (TS) experience growth failure early in life and to establish model-based normative growth charts for 0- to 8-year-old American girls with TS. Full-term girls with TS who had 5 or more measurements of height obtained during their first 10 years of life prior to initiation of growth hormone, estrogen and/or androgen therapy were eligible for this study. A nonlinear mixed-effects model comprising the first two components of the infancy-childhood-puberty (ICP) model of growth was fitted to the longitudinal height measurements and compared with those of healthy American girls. Height measurements (n = 1,146) from 112 girls with TS (45,X: 57.1%; 45,X/46,XX: 12.5%; 46,X, iso(X): 4.5%, and other: 25.9%) were analyzed. Mean height SDS fell from –0.68 at birth to –1.60 at 1 year, –1.80 at 2 years and –1.95 at 3 years. When compared to controls (676 girls, 4,537 measurements), girls with TS grew more slowly due to three principal factors: a slow growth rate of the infancy component, a slow growth rate at the onset of the childhood component, and delayed onset of the childhood component. Traditional concepts of growth failure in TS should be revised. Physicians should consider the diagnosis of TS in any girl with unexplained failure to thrive or short stature, even in the first 3 years of life.

TNF-alpha downregulates murine hepatic growth hormone receptor expression by inhibiting Sp1 and Sp3 binding.

Children with chronic inflammatory diseases experience growth failure and wasting. This may be due to growth hormone resistance caused by cytokine-induced suppression of growth hormone receptor (GHR) gene expression. However, the factors governing inflammatory regulation of GHR are not known. We have reported that Sp1 and Sp3 regulate hepatic GHR expression. We hypothesized that TNF-alpha suppresses GHR expression by inhibiting Sp1/Sp3 transactivators. LPS administration significantly reduced murine hepatic GHR expression, as well as Sp1 and Sp3 binding to GHR promoter cis elements. TNF-alpha was integral to this response, as LPS did not affect hepatic Sp1/Sp3 binding or GHR expression in TNF receptor 1-deficient mice. TNF-alpha treatment of BNL CL.2 mouse liver cells reduced Sp1 and Sp3 binding to a GHR promoter cis element and downregulated activity of a GHR promoter-driven luciferase reporter. Combined mutations within adjacent Sp elements eliminated GHR promoter suppression by TNF-alpha without affecting overall nuclear levels of Sp1 or Sp3 proteins. These studies demonstrate that murine GHR transcription is downregulated by LPS, primarily via TNF-alpha-dependent signaling. Evidence suggests that inhibition of Sp transactivator binding is involved. Further investigation of these mechanisms may identify novel strategies for preventing inflammatory suppression of growth.

MEASURES OF ENERGY INTAKE AND EXPENDITURE BY DOUBLY LABELLED WATER IN INFANTS RECOVERING FROM BRONCHOPULMONARY DYSPLASIA UP TO 3 MO CORRECTED AGE.▴ 1815

Premature infants (PI) with bronchopulmonary dysplasia (BPD) commonly experience growth failure beyond early infancy. Elevated basal energy expenditure (EE) combined with inadequate energy intake (EI) may be responsible. Objective: To describe patterns of energy intake and expenditure during recovery from BPD. Methods and Subjects: A longitudinal descriptive trial in which BPD infants (n=38, birth weight=867± 194 g, gestational age=26 ± 1.4 wk) were fed a standard premature formula (810 kcal/L) prior to 36.5 ± 1.6 wk post-mentural age(PMA), and then were fed an energy enriched formula (900 kcal/L) until 3 mo corrected age (CA). Measurement of EE by oral dosing of doubly labelled water(0.3 g/kg 18O and 0.1 g/kg deuterium with urine analysis by mass spectrometry at 1 and 7 days) was done at 34.5 ± 1.3 wk PMA(in-hospital), at 1 (0.75 ± 0.4) and 3 (3.3 ± 0.4) mo CA at home. Energy intake at home was determined by weighed intake.Results: The Table shows EE as a% of EI(EE/EI) and total EE of BPD infants compared to reference infants (REF): 34.5 wk-healthy PI (Jensen et al, 1992); 1 and 3 mo-infants born at term (Davies et al, 1990). EI at 34.5 wk, 1 and 3 mo (119±8, 118±20 and 114±24 kcal/kg/d, respectively) met or exceeded recommended EI for infants. Although EE of BPD infants was more variable than term REF infants, they appeared to have greater basal EE, depleting the proportion of energy available for storage. Weight gain patterns supported this trend, since no catch-up growth was observed from 1 to 3 mo CA. Conclusions: Prolonged excessive EE during recovery from BPD reflects the need for aggressive nutritional therapy beyond the neonatal period, and possibly beyond 3 mo CA. (Funded by MOH and Wyeth-Ayerst, USA)

Mother-to-child transmission of human immunodeficiency virus type 1: report from the Nairobi Study.

Mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1) is a significant problem in countries with endemic HIV-1 infection. Between 1986 and 1991, 365 children of HIV-1-infected mothers and 363 control children were studied in Kenya. The overall risk of transmission from mother to child, determined by serologic evidence of infection by age > or = 12 months and excess mortality in the HIV-1-exposed group, was 42.8% (range, 27.6%-62.2%). Marriage was the only maternal characteristic associated with transmission (odds ratio, 2.2; 95% confidence interval, 1.2-4.2; P < .05). Children who experienced growth failure were more likely to be infected. In 44% of children ultimately infected, the pattern of antibody response implied intrapartum or postnatal exposure to HIV-1. Of potential postnatal exposures examined, duration of breast-feeding beyond age 15 months and the mother being married were independently associated with increased risk of infection and seroconversion of children. The percentage of HIV infection attributable to breast-feeding > or = 15 months was 32%. The frequency of mother-to-child transmission of HIV-1 was high; a substantial proportion of infection occurred postnatally, possibly through breast-feeding.

Essential fatty acid deficiency associated with the use of a medium-chain-triglyceride infant formula in pediatric hepatobiliary disease

Serum phospholipid fatty acid patterns were determined by gas chromatography in four infants with hepatobiliary disease receiving a formula with a high content of medium-chain-triglyceride (MCT) oil. All four infants demonstrated signs of essential fatty acid deficiency, characterized by decreased arachidonic acid and increased palmitoleic and oleic acids. All had substantial concentrations of the pathologic triene 5,8,11-eicosatrienoic acid. Three of four had decreased linoleic acid concentrations and abnormal ratios of triene to tetraene (5,8,11-eicosatrienoic acid: arachidonic acid), greater than 0.38. One patient may have experienced growth failure due to abnormal essential fatty acid status. Infants with the potential for fat malabsorption should only receive MCT-oil feedings with well above the generally recommended requirements for linoleic acid (3% of total caloric intake).

The Nutritional Consequences of Gastrointestinal Disease in Adolescence

The growth spurt of adolescence, during which body weight nearly doubles and height increases by 16%, demands an increased delivery of nutrients by the gastrointestinal tract. Chronic disorders of digestion and absorption at this age, therefore have a potentially profound effect upon growth, skeletal maturation and sexual development. Moreover, the emotional climate of adolescence, which requires affiliation with peer groups, and a distancing from authority figures such as doctors and parents, is often associated with a deterioration in drug and dietary compliance and with erratic clinic attendance. Nutritional problems in adolescent patients with Crohn's disease, cystic fibrosis and coeliac disease are the most common. About one third of adolescents with Crohn's disease experience growth failure and delayed sexual development, probably as a consequence of long-term undernutrition. There is a strong argument for the care of these patients being in the hands of paediatric gastroenterologists. Enteral nutrition, often administered overnight, is successful in inducing catch-up growth, and reducing steroid dosage, although resection of diseased gut is often followed by good growth, and surgery should not be overlooked. Cystic fibrosis in adolescence is commonly complicated by protein-energy malnutrition. Pathogenesis includes anorexia, maldigestion and an increase in resting energy expenditure. Malnutrition has been treated by a number of enteral regimens. In general, there is no place for repeated, short-term interventions of less than 6 months. Long-term studies have all shown good nutritional repletion and growth, but results with respect to improved respiratory function are conflicting. More prospective control trials are needed before the precise indications for enteral nutrition in cystic fibrosis can be accurately defined. Once started it is difficult to stop, although preoperative treatment of patients awaiting heart-lung transplantation seems entirely appropriate. The major problem in the management of coeliac disease in adolescence is dietary compliance. Even those patients who claim to have good dietary compliance often have jejunal biopsy evidence of gluten ingestion and tend to be underweight. This is particularly worrying, as after 5 years adherence to a gluten free diet, the increased risk of gastrointestinal malignancy appears to return to normal.