Rapid Catch-up Growth Research Articles

Catch-up Growth and Discontinuation of Fludrocortisone Treatment in Aldosterone Synthase Deficiency.

Aldosterone synthase deficiency (ASD) caused by mutations in the CYP11B2 gene is characterized by isolated mineralocorticoid deficiency. Data are scarce regarding clinical and biochemical outcomes of the disease in the follow-up. Assessment of the growth and steroid profiles of patients with ASD at the time of diagnosis and after discontinuation of treatment. Children with clinical diagnosis of ASD were included in a multicenter study. Growth and treatment characteristics were recorded. Plasma adrenal steroids were measured using liquid chromatography-mass spectrometry. Genetic diagnosis was confirmed by CYP11B2 gene sequencing and in silico analyses. Sixteen patients from 12 families were included (8 females; median age at presentation: 3.1 months, range: 0.4 to 8.1). The most common symptom was poor weight gain (56.3%). Median age of onset of fludrocortisone treatment was 3.6 months (range: 0.9 to 8.3). Catch-up growth was achieved at median 2 months (range: 0.5 to 14.5) after treatment. Fludrocortisone could be stopped in 5 patients at a median age of 6.0 years (range: 2.2 to 7.6). Plasma steroid profiles revealed reduced aldosterone synthase activity both at diagnosis and after discontinuation of treatment compared to age-matched controls. We identified 6 novel (p.Y195H, c.1200 + 1G > A, p.F130L, p.E198del, c.1122-18G > A, p.I339_E343del) and 4 previously described CYP11B2 variants. The most common variant (40%) was p.T185I. Fludrocortisone treatment is associated with a rapid catch-up growth and control of electrolyte imbalances in ASD. Decreased mineralocorticoid requirement over time can be explained by the development of physiological adaptation mechanisms rather than improved aldosterone synthase activity. As complete biochemical remission cannot be achieved, a long-term surveillance of these patients is required.

493 Using human monogenic disease to quantify the contribution of fetal insulin to birth weight

Fetal insulin affects birth weight, but the extent of this relationship has not been established in humans, nor whether it has any implications for postnatal growth. We sought to investigate this by studying birth size and postnatal growth in individuals with monogenic diseases which result in absent insulin secretion in utero. We studied birth size in individuals with a homozygous insulin gene (INS) mutation or pancreatic agenesis (n=64 for weight, n=17 for length) born after 31 weeks gestation and compared with international growth standards for gestational age and sex (SDS). Postnatal growth was studied in individuals with INS mutations. We analyzed serial measures of weight and length until the age of four years (n=10 and 9, respectively) and most recent available weight and height (n=16 and 15, respectively). In all individuals birth weight and length were low (median (IQR) SDS -3.11 (-3.53,-2.61) and -2.86 (-3.62,-1.90), respectively). Birth weight adjusted to 40 weeks gestation was 1711 g (95% CI 1601,1821 g) vs expected of 3320 g (Fig. 1), showing non-insulin-mediated growth represents 52% of normal birth weight at term. Catch-up growth was rapid with median (IQR) weight and length SDS -0.27 (-0.37,-0.17) and -0.30 (-1.33,0.002), respectively, at 12 months, and 0.02 (-0.35,0.78) and 0.00 (-0.34,0.21), respectively, at 24 months (Fig. 2). Most recent available weight and height SDS were 0.19 (-0.67,1.33) and -0.78 (-1.78,-0.19), respectively. Monogenic diseases resulting in absent fetal insulin have enabled us to answer fundamental questions about early growth in humans. Ultimately, fetal insulin accounts for half of birth weight at term and could be an important cause of fetal growth restriction that is characterised by rapid catch-up growth. Future studies investigating outcomes arising from low and high birth weight should determine differences in insulin and non-insulin-mediated fetal growth, and consider whether they might have different implications for pregnancy outcomes and long-term risk of disease.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Early life growth and associations with lung function and bronchial hyperresponsiveness at 11-years of age

Low birthweight and being born small-for-gestational age (SGA) are linked to asthma and impaired lung function. Particularly, poor intrauterine growth followed by rapid catch-up growth during childhood may predispose for respiratory disease. Bronchial hyperresponsiveness (BHR) is an essential feature of asthma, but how foetal and early childhood growth are associated with BHR is less studied. Our hypothesis was that children born SGA or with accelerated early life growth have increased BHR and altered lung function at 11-years of age.We studied the associations between SGA and early childhood growth with lung function and BHR at 11-years of age in a subgroup of 468 children from the Norwegian Mother, Father and Child Cohort Study (MoBa), and included data from the Medical Birth Registry of Norway (MBRN).Weight at 6 months of age was positively associated with forced vital capacity (adjusted Beta: 0.121; 95% Confidence interval: 0.023, 0.219) and negatively associated with the ratio of forced expiratory flow in first second/forced vital capacity (−0.204; −0.317, −0.091) at 11-years of age. Similar patterns were found for weight at 36 months and for change in weight from birth to 6 months of age. SGA or other various variables of early childhood growth were not associated with BHR at 11-years of age.Early life growth was associated with an obstructive lung function pattern, but not with BHR in 11-year old children. Foetal growth restriction or weight gain during early childhood do not seem to be important risk factors for subsequent BHR in children.

Post-discharge growth of extremely premature infants within corrected age of 24 months

Objective: To demonstrate the post-discharge catch-up growth of extremely premature infants (EPI) within 24 months of corrected age. Methods: This study retrospectively collected the anthropomorphic measurements of 311 EPI who visited Shenzhen Maternity and Child Healthcare Hospital from August 2013 to April 2020. These infants were stratified according to gestational age at birth (GA): 23-24+6weeks, 25-26+6weeks, 27-27+6weeks; and birth weight:<750 g, 750-999 g, ≥1 000 g. The anthropomorphic measurements, including weight, length, and head circumference for age, were recorded timely from discharge to 24 months of corrected age. And the growth curve stratified by GA and birth weight were fitted in both chronological age and corrected age, which were then compared with the World Health Organization Child Growth Standards for term infant (2006 version), to investigate the catch-up growth pattern of EPI. And appropriate catch-up was defined as the measurements reached the 25th percentile of WHO growth curve. Results: In these 311 EPI, 184 were males and 127 females, with gestational age of 23-27+6 weeks and birth weight of 480-1 430 g. Regardless of the GA and birth weight, the growth curves fitted in corrected age failed to overlap with that in chronological age by 24 months of corrected age. The growth velocity of weight, length and head circumference in both corrected and chronological age were all positively correlated with GA and birth weight: the 27-27+6weeks group showed a preferable growth pattern than the 25-26+6weeks group, and the curve of the 23-24+6weeks group was most unfavorable; and the same pattern was observed between the subgroups of different birth weight. Furthermore, the GA had more significant impact on the catch-up growth pattern than birth weight did. When assessed with corrected age curve, the weight and length of both male and female EPIs achieved appropriate catch-up by 24 months, as well as the head circumference of girls; whereas, boys' head circumference reached appropriate catch-up at the corrected age of 9 months, but fell behind the 25th percentile after that. However, when assessed with chronological age curve, both boys and girls failed to achieve appropriate catch-up in weight, length and head circumference by age 24 months. And no matter in corrected or chronological age, all physical measurements of girls were lower than those of boys. Conclusions: The rapid catch-up growth of EPI happens within 6 months of corrected age. The lower the birth weight and gestational age, the lower the physical measurements at each corresponding month of age, and the longer it takes to achieve appropriate catch-up. Gestational age has a greater impact on the longitudinal catch-up growth than birth weight does. And girls generally grow slower than boys in either correct or actual age. Before 24 months of corrected age, the growth should be assessed with corrected age rather than chronological age.

Mild maternal sleep-disordered breathing during pregnancy and offspring growth and adiposity in the first 3 years of life

Sleep-disordered breathing (SDB) during pregnancy has been linked to adverse fetal outcomes. Since the intrauterine milieu plays a critical role in childhood growth, we explored the interactions between maternal SDB and offspring growth and adiposity patterns during infancy. Fifty-eight healthy women with uncomplicated pregnancies underwent an objective sleep study and laboratory evaluation during the third trimester, their offspring underwent a 3-year growth surveillance. The 14 (24.1%) women with SDB had a higher body mass index (BMI) (P = 0.003), elevated C-reactive protein levels (P = 0.003), and decreased HDL-cholesterol levels (P = 0.009) than the women without SDB. A general linear model evaluated the interactions between maternal SDB and offspring growth and adiposity measurements after controlling for gestational age and maternal and paternal BMIs. The offspring of mothers with SDB had a significantly smaller head circumference at birth (P = 0.004), with a distinctive pattern of catchup growth by the end of the first year of life (P = 0.018). Their growth pattern was distinguished by compromised birth weight-to-length, rapid catch-up growth, and an increase in both weight-to-length and triceps thickness by the age of three (P < 0.001 and P = 0.001, respectively). Our findings suggest that maternal SDB during pregnancy affects head circumference growth and adiposity acquisition from birth through infancy.

Adverse effects of prenatal mercury exposure on neurodevelopment during the first 3 years of life modified by early growth velocity and prenatal maternal folate level

Background and aimsPrevious studies have suggested that mercury exposure and folate levels during pregnancy may influence early childhood neurodevelopment. Rapid catch-up growth in children is associated with an increased risk of pathological nervous system development. We evaluated whether the association between prenatal folate and mercury-related neuropsychological dysfunction was modified by growth velocity during childhood. MethodsThe Mothers and Children's Environmental Health (MOCEH) birth cohort study began in 2006 and by 2010, 1751 women had been enrolled before the second trimester of their pregnancy along with their partners. Participants visited the research center at birth and 6, 12, 24, and 36 months. We measured mercury levels in maternal and cord blood and folate in maternal serum. Questionnaires to evaluate the environment and health of their child were administered and anthropometric factors including body weight and height were measured. Certified investigators used the Bayley test to measure neurobehavioral outcomes. We calculated postnatal growth change as the change in infant weight for-age z-score between birth and 3 years. Multiple linear regression and mixed models were used to examine the association between mercury exposure and children's neurodevelopment as well as the modifying effects of folate and growth velocity. ResultsA total of 30.6% of children experienced rapid growth during the first 3 years of life. Median values of mercury in the low folate group were significantly higher in rapid growers (3.41 μg/L in maternal blood and 5.63 μg/L in cord blood) than in average/slow growers (3.05 μg/L in maternal blood and 5.19 μg/L in cord blood). Rapid growers were also significantly associated with decreased psychomotor development scores during the first 3 years of life and with having mothers who had low prenatal folate levels, even after adjusting for potential confounders. ConclusionPrenatal mercury exposure adversely affects infant neurodevelopment and is associated with rapid growth during the first 3 years of life. This effect was limited to children whose mothers had low prenatal folate levels, suggesting a protective effect of folate against developmental neurotoxicity due to mercury exposure and rapid catch-up growth.

Prenatal exposure to ambient air multi-pollutants significantly impairs intrauterine fetal development trajectory.

Impaired in utero fetal growth trajectory may have long term health consequences of the newborns and increase risk of adulthood metabolic diseases. Prenatal exposure to air pollution has been linked to fetal development restriction; however, the impact of exposure to ambient air pollutants on the entire course of intrauterine fetal development has not been comprehensively investigated. During 2015-2018, two cohorts of mother-infant dyads (N=678 and 227) were recruited in Shanghai China, from which three categories of data were systematically collected: (1) daily exposure to six air pollutants during pregnancy, (2) fetal biometry in the 2nd (gestational week 24, [GW24]) and 3rd trimester (GW36), and (3) neonatal outcomes at birth. We investigated the impact of prenatal exposure to air pollutant mixture on the trajectory of fetal development during the course of gestation, adjusting for a broad set of potential confounds. Prenatal exposure to PM2.5, PM10, SO2 and O3 significantly reduced fetal biometry at GW24, where SO2 had the most potent effect. For every 10 μg/m3 increment increase of daily SO2 exposure during the 1st trimester shortened femur length by 2.20mm (p=6.7E-21) translating to 5.3% reduction from the average of the study cohort. Prenatal air pollution exposure also decreased fetal biometry at GW36 with attenuated effect size. Comparing to the lowest exposed quartile, fetus in the highest exposed quartile had 6.3% (p=3.5E-5) and 2.1% (p=2.4E-3) lower estimated intrauterine weight in GW24 and GW36, respectively; however, no difference in birth weight was observed, indicating a rapid catch-up growth in the 3rd trimester. To our knowledge, for the first time, we demonstrated the impact of prenatal exposure to ambient air pollutants on the course of intrauterine fetal development. The altered growth trajectory and rapid catch-up growth in associated with high prenatal exposure may lead to long-term predisposition for adulthood metabolic disorders.

Long-Term Metabolic Consequences of Intrauterine Growth Restriction

To summarize recent findings on the associations of intrauterine growth restriction (IUGR) and long-term metabolic consequences such as obesity, type 2 diabetes (T2D), and cardiovascular diseases and the underlying mechanisms. Recent evidence suggests that metabolic diseases such as obesity, T2D, hypertension, and coronary artery disease are related to developmental programming in fetal period and early childhood. Rapid postnatal catch-up growth is also an important factor that contributes to the development of these long-term metabolic complications. The underlying mechanisms include oxidative stress, changes in hormonal milieu, vascular endothelial dysfunction, epigenetic regulation, and the potential alteration of microbiome. Fetal and early life environment is an important determinant of long-term cardiometabolic risks. Children with IUGR need close follow-up for early detection of these complications.

Impact of catch-up growth on bone age development in preterm infants from a cohort study

Objective To evaluate the catch-up growth features of preterm infants and to explore the influence of catch-up growth on bone age development. Methods The two-way cohort study was conducted.The preterm infants who visited the Child Health Department of Wuhan Children′s Hospital from January 1st to December 31th in 2015 were selected as the exposed group and the full term infants with age, gender and ethnicity matched with the exposed group ones were selected according to the ratio of 1∶1 for the non-exposed group who visited the same hospital at the same time non.Information of those childeren as the birth history, past birth and development history were collected in both groups were followed up till 3 years old and photographed on the left wrist X-ray film for bone age evaluation at 3 years old. Results At the time of enrollment, 392 subjects were selected in the exposed group and non-exposed group and 239 infants in the exposed group and 247 infants in non-exposed group were followed up till 3 years.During the follow-up period, there was a conspicuous catch-up growth trend of body length and weight in the exposed group, and weight Z score was the lowest at 2 months old, but the overall level of body length and weight were still lower than the non-exposed group.The start of catching up growth in body weight took precedence over the length, which was reflected in the time when the weight caught up to Z=-2 and Z=-1 as 3.78 months old and 16.18 months old, whereas the time of length catching up to Z=-2 and Z=-1 was 7.24 months old and 22.21 months old.The length catch-up growth was slower during the period of 5-10 months old and 12-21 months old.The age of bone age assessment in the 2 groups was between 2.80 and 3.20 years old(mean 3.03 years old). The bone age of boys in the exposed group was higher than that of the non-exposed ones[(3.13±0.61) years old vs.(2.75±0.51) years old], and there was statistical significance (t=-5.52, P 0.05). Body length Z-score at the age of 1 month, 2 months, 4 months, 5 months, 6 months, 12 months and weight Z-score at 2 months, 3 months, 4 months were the facilitating factors for skeletal development, whereas body length Z-score at 15 months, 18 months, 36 months and weight Z-score at 15 months were obstacles. Conclusions Premature infant have a catch-up trend before 3 years old.In order to delay the skeletal development, it is necessary to avoid rapid catch-up growth of weight and length in premature infants before 1 year old. Key words: Preterm infants; Catch-up growth; Bone age development; Cohort study

Tracking of Serum DHEAS Concentrations from Age 1 to 6 Years: A Prospective Cohort Study

ContextAdrenarche is a gradual process, but its programming is unknown.ObjectiveThe objective of this article is to examine the trajectory of dehydroepiandrosterone sulfate (DHEAS) from age 1 to 6 years and the associations of early growth with DHEAS concentration by age 6 years.Design and participantsLongitudinal data from a population sample of 78 children (43 girls) with serum samples for DHEAS and insulin-like growth factor 1 (IGF-1) measurements available at ages 1 and 6 years.Main outcome measureSerum DHEAS concentration at age 6 years.ResultsDHEAS concentration at age 1 year correlated with DHEAS concentration at age 6 years (r = 0.594, P < .001). DHEAS levels at age 6 years increased with tertiles of DHEAS at age 1 year (medians (µg/dL); 4.2, 14.4, 22.6; P < .001) and with those of greater increase in length by age 1 year (6.0, 11.7, 16.4; P = .047), and decreased with tertiles of birth length (17.7, 13.3, 7.1; P = .042). In a regression model including birth size, biochemical covariates at age 1 year, and growth measures by age 6 years, higher DHEAS concentration at age 1 year was an independent determinant of falling into the highest DHEAS tertile at age 6 years.ConclusionsHigher serum DHEAS concentrations already at age 1 year are associated with those at age 6 years. Also, shorter birth length and rapid catch-up growth in length by age 1 year are associated with higher DHEAS concentrations at age 6 years. These results corroborate the early origin of adrenarche and strongly suggest that part of adrenarchal programming already takes place by the end of infancy.

Why and How Imprinted Genes Drive Fetal Programming.

Imprinted genes mediate fetal and childhood growth and development, and early growth patterns drive fetal programming effects. However, predictions and evidence from the kinship theory of imprinting have yet to be directly integrated with data on fetal programming and risks of metabolic disease. I first define paternal-gene and maternal-gene optima with regard to early human growth and development. Next, I review salient evidence with regard to imprinted gene effects on birth weight, body composition, trajectories of feeding and growth, and timing of developmental stages, to evaluate why and how imprinted gene expression influences risks of metabolic disease in later life. I find that metabolic disease risks derive primarily from maternal gene biases that lead to reduced placental efficacy, low birth weight, low relative muscle mass, high relative white fat, increased abdominal adiposity, reduced pancreatic β-cell mass that promotes insulin resistance, reduced appetite and infant sucking efficacy, catch-up fat deposition from family foods after weaning, and early puberty. Paternal gene biases, by contrast, may contribute to metabolic disease via lower rates of brown fat thermiogenesis, and through favoring more rapid postnatal catch-up growth after intrauterine growth restriction from environmental causes. These disease risks can be alleviated through dietary and pharmacological alterations that selectively target imprinted gene expression and relevant metabolic pathways. The kinship theory of imprinting, and mother-offspring conflict more generally, provide a clear predictive framework for guiding future research on fetal programming and metabolic disease.

The Crafts–Harley view of German industrialization: an independent estimate of the income side of net national product, 1851–1913

AbstractNovel information on land rent is used to estimate the income side of German net national product (NNP) in 1851–1913 without recourse to output side aggregates. The new series shows higher values during the initial part of the period of observation, which narrows the wedge that opens up between existing estimates of NNP before the 1880s. The results support a modified Crafts–Harley view of the first phase of German industrialization: despite rapid catch-up growth of industrial leading sectors from the 1840s to the 1870s, the pace of aggregate growth accelerated only gradually. The initially small size of the modern sector and the simultaneity of the first phase of industrialization and the first wave of globalization account for this paradox. The labor share remained largely constant; the decline of the land share in NNP was compensated by a rise of the capital share.

Postnatal growth in children born small for gestational age with and without smoking mother.

Maternal smoking impairs fetal growth; however, if postnatal growth differs between children born small for gestational age (SGA) with smoking and non-smoking mother is unknown. Cohort-study of term born children born appropriate for gestational age with non-smoking mother (AGA-NS, n = 30,561), SGA (birthweight <10th percentile) with smoking mother (SGA-S, n = 171) or SGA with non-smoking mother (SGA-NS, n = 1761). Means of height and weight measurements, collected at birth, 1.5, 3, 4, and 5 years, were compared using a generalized linear mixed effect model. Relative risks of short stature (<10th percentile) were expressed as adjusted risk ratios (aRR). At birth, children born SGA-S were shorter than SGA-NS, but they did not differ in weight. At 1.5 years, SGA-S had reached the same height as SGA-NS. At 5 years, SGA-S were 1.1 cm taller and 1.2 kg heavier than SGA-NS. Compared with AGA-NS, SGA-S did not have increased risk of short stature at 1.5 or 5 years, while SGA-NS had increased risk of short stature at both ages; aRRs 3.0 (95% CI 2.6;3.4) and 2.3 (95% CI 2.0;2.7), respectively. Children born SGA-S have a more rapid catch-up growth than SGA-NS. This may have consequences for metabolic and cardiovascular health in children with smoking mothers.

Risk of metabolic consequences of rapid weight gain and catch-up growth in the first two years of life: a systematic review protocol.

The specific review question to be addressed in this review is: what is the risk of metabolic outcomes for individuals who experience rapid weight gain or catch-up growth during the first two years of life?

Reduced body weight at weaning followed by increased post-weaning growth rate interacts with part-per-trillion fetal serum concentrations of bisphenol A (BPA) to impair glucose tolerance in male mice.

There is evidence from longitudinal studies that being light at birth and weaning is associated with subsequent rapid weight gain in infants. This is referred to as “centile crossing”, which can lead to increased risk of lifetime obesity, glucose dysregulation and type 2 diabetes. Here, pregnant CD-1 mice were hemi-ovariectomized so that the entire litter was contained in one uterine horn to increase variability in fetal growth rate. Pregnant females were implanted on gestation day (GD) 9 with a Silastic capsule containing 6, 60 or 600 μg bisphenol A (BPA). On GD 18 the mean fetal serum unconjugated BPA concentrations were 17, 177 and 1858 pg/ml, respectively. Capsules were not removed, to avoid maternal stress, and were predicted to release BPA for at least 3 weeks. Body weight at weaning was strongly negatively correlated with post-weaning weight gain in both control and BPA-treated male mice, consistent with human data; female offspring were excluded, avoiding complications associated with postpubertal estrogens. Within each treatment group, male offspring were sorted into tertiles based on relative weight gain during the two weeks after weaning, designated as having Rapid (R), Medium (M) or Slow (S) growth rate. BPA exposure was associated with altered growth rate between weaning and postnatal week 12 (young adulthood), when a low-dose (20 mg/kg, i.p.) glucose tolerance test (GTT) was performed. We found altered glucose regulation in response to all doses of BPA. However, glucose tolerance was only significantly impaired (blood glucose levels were elevated) compared to controls in males in the rapid post-weaning growth group exposed perinatally to BPA. We conclude that male mice that are light at weaning, but then experience rapid catch-up growth immediately after weaning, represent a sensitive sub-population that is vulnerable to the metabolic disrupting effects of very low pg/ml fetal serum concentrations of BPA.

Insights into infancy weight gain patterns for term small-for-gestational-age babies

BackgroundToo fast or slow weight gain in infancy is bad for health in later life. In this study, we aim to investigate the optimal weight gain pattern during the first 2 y of life for term small-for-gestational-age (SGA) infants.MethodWe employed data from a longitudinal, community-based cohort study on the growth and development of SGAs collected between 2004 and 2010 in Shanghai, China.Latent class growth analysis (LCGA) was applied to identify weight gain patterns among 3004 SGAs. BMI curves for each latent class from 1 mo to 5 y were produced through mixed-effects regression analysis. Multivariable regression was performed to examine the association between various classes and adverse outcomes (overweight/obesity/ malnutrition) during 2–5 y.ResultFive weight gain patterns aged 0–2 y of 3004 term SGAs were identified and labeled as follows--class 1: excessively rapid catch-up growth (10.7%); class 2: rapid catch-up growth (19.7%); class 3: appropriate catch-up growth (55.7%); class 4: slow catch-up growth (10.2%); class 5: almost no catch-up growth (3.7%). A decreasing age at adiposity rebound (AR) and an increasing BMI value were observed from class 5 to 1. Class 1 and 2 showed an early appearance of AR (< 4 y). SGAs in class 1 and 2 had a higher BMI in 2–5 y of life. After adjustment for potential confounding variables, class 1 and 2 were found to have an increased risk of being overweight/ obese. At the same time, we found the risk of malnutrition was especially prominent among SGAs in classes 4 and 5.ConclusionOur results suggest that for term SGA infants, catch-up growth that crossing two centile levels, that is, from < 10th to the interval between 25th and 50th (ΔWAZ> 1.28) in the first several months, along with on track growth and maintenance at a median level by age 2 may be the optimal catch-up growth trajectory, minimizing risk of childhood adverse health outcomes.

Reevaluation of Protein Intake for Preterm Infants.

Growth failure caused by undernutrition is considered one of the major causes for psychomotor delay in extremely preterm infants, and the concept for "aggressive nutritional approach" is widely accepted worldwide. Based on this, postnatal early catch-up growth due to sufficient supply of nutrients including sufficient amounts of amino acids is believed to be essential for a better outcome; however, there is no definitive evidence of aggressive nutrition on better outcomes in mortality, growth, and neurodevelopment. On the contrary, epidemiological evidence suggests that low birth weight and a rapid catch-up growth after birth are major risk factors for insulin resistance and diabetes in later life; higher protein intake during postnatal period relates to higher cardiovascular risk in later life. Considering these, optimal nutrition, especially protein administration, should be reevaluated. In this review, current opinions on the nutrition for the preterm infants are surveyed. In addition, I propose a new concept for optimized protein amount for the preterm infants based on the difference of amino acid metabolism between fetuses and preterm infants.

Coeliac disease in infants: antibodies to deamidated gliadin peptide come first!

BackgroundThe onset of coeliac disease (CD) in the first year of life is uncommon and the diagnosis can be challenging due to the suboptimal sensitivity of tissue transglutaminase antibodies (tTG) at this age and the many other possible causes of malabsorption in infants. Antibodies to deamidated gliadin peptides (anti-DGPs), especially IgG, may appear earlier than IgA anti-tTG in very young children with CD.Case presentationWe report here on an 8-month-old child who was evaluated for failure to thrive, constipation and developmental delay. The symptoms started following gluten introduction in the diet. Laboratory tests showed high fecal elastase concentration, normal serum IgA levels with positive IgG and IgA anti-DGPs, whereas anti-tTG were not detected. The duodenal biopsy revealed a complete villous atrophy (Marsh-Oberhuber 3C). The culture of biopsy fragments in the presence of gliadin peptides did not stimulate the production of IgA anti-endomysial antibodies. Genetic testing proved the child was positive for HLA-DQ2 (DQA1*05; DQB1*02) and HLA-DQ8 (DQA1*03, DQB1*0302). Having initiated the gluten-free diet, the symptoms disappeared and the infant experienced rapid catch-up growth with normalization of psychomotor development.ConclusionsThis case report highlights the utility of anti-DGPs for screening infants with suspected CD. The pattern with positivity for IgG and IgA anti-DGPs only is rare in IgA-competent children with biopsy-proven CD. It could be explained in infancy as immaturity of the adaptive immune system.

Preterm Birth and its Impact on Renal Health

Preterm birth occurs in approximately 10% of all births worldwide. Preterm infants have reduced nephron numbers at birth in proportion to gestational age, and are at increased risk of neonatal acute kidney injury as well as higher blood pressure, proteinuria, and chronic kidney disease later in life. Rapid catch-up growth in preterm infants, especially if resulting in obesity, is a risk factor for end-stage kidney disease among children with proteinuric renal disease. Preterm birth, however, is a risk factor not only for the infant because mothers who deliver preterm have an increased risk of having subsequent preterm deliveries as well as hypertension, cardiovascular disease, and renal disease later in life. Preterm birth in a female infant is also a risk factor for her future risk of having a preterm delivery, gestational hypertension, and gestational diabetes, which in turn may impact the development of fetal kidneys and the offspring's risk of hypertension and renal disease. This intergenerational programming cycle, therefore, perpetuates the risks and consequences of prematurity. Interruption of this cycle may be possible through optimization of maternal nutrition and health as well as careful antenatal care, which may in turn reduce the global burden of hypertension and renal disease in subsequent generations.

Critical questions on nutrition of preterm infants

Infants born preterm represent a nutritional emergency that must be addressed immediately in order to avoid/limit the development of nutritional deficits that lead to postnatal growth retardation. When taking care of preterm infants from a nutritional point of view, it must be taken into consideration that promotion of growth is achieved by the accomplishment of their high nutritional needs, that become even more demanding with the occurrence of comorbidities. Identification of the factors that determine and/or affect nutrient requirements is therefore mandatory. A full understanding of the most appropriate biological setting that should be used for establishing preterm infants nutritional requirements is desirable. A deeper knowledge with regard to these points would allow for the provision of appropriate amount of specific essential nutrients, avoiding the under- or overexposure to certain nutrients, and for the individualization of nutritional care of preterm infants.The avoidance of early malnutrition is of major importance since adequate postnatal growth has been associated with improvement of later neurodevelopment outcome. Limitation of extrauterine growth restriction prevents the need for rapid catch-up growth after discharge which, in turns, has been linked to later adverse metabolic consequences. Increasing evidence has indicated that postnatal growth retardation is accompanied by a fat-free mass deficit, probably related to immature metabolic mechanisms, delayed amino acid administration and protein intakes lower than recommendations. The potential long-lasting effects of these body composition modifications on future health, both in terms of neurodevelopment outcome and metabolic risk, are still under investigation.