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Growth faltering, previously known as failure to thrive, is a broad term describing children who do not reach their expected weight, length, or body mass index for age. Growth is assessed with standardized World Health Organization charts for children younger than two years and Centers for Disease Control and Prevention charts for children two years and older. Traditional criteria for growth faltering can be imprecise and difficult to track over time; therefore, use of anthropometric z scores are now recommended. These scores can be calculated with a single set of measurements to assess malnutrition severity. Inadequate caloric intake, the most common cause of growth faltering, is identified with a detailed feeding history and physical examination. Diagnostic testing is reserved for those who have severe malnutrition or symptoms concerning for high-risk conditions, or if initial treatment fails. In older children or those with comorbidities, it is important to screen for underlying eating disorders (e.g., avoidant/restrictive food intake disorder, anorexia nervosa, bulimia). Growth faltering can usually be managed by the primary care physician. If comorbid disease is identified, a multidisciplinary team (e.g., nutritionist, psychologist, pediatric subspecialists) may be beneficial. Failure to recognize and treat growth faltering in the first two years of life may result in decreased adult height and cognitive potential.

Failure to thrive in childhood is a state of undernutrition due to inadequate caloric intake, inadequate caloric absorption, or excessive caloric expenditure. In the United States, it is seen in 5 to 10 percent of children in primary care settings. Although failure to thrive is often defined as a weight for age that falls below the 5th percentile on multiple occasions or weight deceleration that crosses two major percentile lines on a growth chart, use of any single indicator has a low positive predictive value. Most cases of failure to thrive involve inadequate caloric intake caused by behavioral or psychosocial issues. The most important part of the outpatient evaluation is obtaining an accurate account of a child's eating habits and caloric intake. Routine laboratory testing rarely identifies a cause and is not generally recommended. Reasons to hospitalize a child for further evaluation include failure of outpatient management, suspicion of abuse or neglect, or severe psychosocial impairment of the caregiver. A multidisciplinary approach to treatment, including home nursing visits and nutritional counseling, has been shown to improve weight gain, parent-child relationships, and cognitive development. The long-term effects of failure to thrive on cognitive development and future academic performance are unclear.

Children with very low weight for age or height and those who do not maintain an appropriate growth pattern may have failure to thrive (FTT), also known as weight faltering. If confirmed by repeated valid measurements, FTT should prompt a search for causes of undernutrition, including neglect, family food insecurity, and underlying medical conditions. Inadequate caloric intake is the most common cause of FTT, but inadequate nutrient absorption or increased metabolism is also possible. Difficulty attaining or maintaining appropriate weight is the first indication of FTT, and sustained undernutrition can impede appropriate height, head circumference, and the development of cognitive skills or immune function in extreme cases. Early identification and management of the issues causing undernutrition are critical. In most cases, an appropriate growth velocity can be established with outpatient management based on proper nutrition and family support. Primary care physicians can effectively treat most children with FTT, and subspecialist consultation or hospitalization is rarely indicated.

Background Early-onset chronic diarrhoea often indicates a congenital disorder. Mutation in diacylglycerol o-acyltransferase 1 ( DGAT1 ) has recently been linked to early-onset chronic diarrhoea. To date, only a few cases of DGAT1 deficiency have been reported. Diarrhoea in those cases was severe and developed in the neonatal period or within 2 months after birth. Case presentation Here, we report a female patient with DGAT1 mutations with delayed-onset chronic diarrhoea. The patient had vomiting, hypoalbuminemia, hypertriglyceridemia, and failure to thrive at early infancy. Her intractable chronic diarrhoea occurred until she was 8 months of age. A compound heterozygous DGAT1 mutation was found in the patient, which was first found in the Chinese population. Her symptoms and nutrition status improved after nutritional therapy, including a fat restriction diet. Conclusions This case expanded our knowledge of the clinical features of patients with DGAT1 mutations. Intractable diarrhoea with delayed onset could also be a congenital disorder.

Failure to thrive (FTT) is an inadequate growth in young children. It can increase the risk of overweight or obesity later in life. Patients with renal tubulopathies can present FTT due to solute losses in the urine. We aimed to test our hypothesis that children with tubulopathies have an increased risk of overweight and obesity due to rebound following FTT that could complicate these conditions. We enrolled 26 patients with tubulopathies and evaluated for the first time within the first 12 months of life (mean age: 4.8 months ± 2.6 SDS). FTT was evident in 17 out of 26 patients (65.4%). The mean age at the last follow-up was 14.1 years ± 5.5 SDS. The mean age at overweight/obesity onset was 9.0 years ± 3.6 SDS. The prevalence of overweight/obesity was 73.1% (19/26). Among the patients with FTT, 15 (88.2%) developed overweight/obesity compared to 4 out of the 9 patients (44.4%) without FFT ( p  = 0.028). The presence of FTT determined an OR for obesity/overweight of 9.4 (95% CI: 1.3–67.6; p  = 0.026). FTT continued to be significantly associated with obesity/overweight also after adjustment for preterm birth and birth weight <10th percentile (OR = 23.3; 95% CI: 1.95–279.4; p  = 0.01). In conclusion, in our series, patients with tubulopathies presented an increased risk of overweight/obesity due to the FTT that can complicate these conditions.

Extrapulmonary manifestations of COVID-19 are associated with a much higher mortality rate than pulmonary manifestations. However, little is known about the pathogenesis of systemic complications of COVID-19. Here, we create a murine model of SARS-CoV-2-induced severe systemic toxicity and multiorgan involvement by expressing the human ACE2 transgene in multiple tissues via viral delivery, followed by systemic administration of SARS-CoV-2. The animals develop a profound phenotype within 7 days with severe weight loss, morbidity, and failure to thrive. We demonstrate that there is metabolic suppression of oxidative phosphorylation and the tricarboxylic acid (TCA) cycle in multiple organs with neutrophilia, lymphopenia, and splenic atrophy, mirroring human COVID-19 phenotypes. Animals had a significantly lower heart rate, and electron microscopy demonstrated myofibrillar disarray and myocardial edema, a common pathogenic cardiac phenotype in human COVID-19. We performed metabolomic profiling of peripheral blood and identified a panel of TCA cycle metabolites that served as biomarkers of depressed oxidative phosphorylation. Finally, we observed that SARS-CoV-2 induces epigenetic changes of DNA methylation, which affects expression of immune response genes and could, in part, contribute to COVID-19 pathogenesis. Our model suggests that SARS-CoV-2-induced metabolic reprogramming and epigenetic changes in internal organs could contribute to systemic toxicity and lethality in COVID-19.

ObjectiveTo characterise the association between sepsis and postnatal weight growth when accounting for the degree of growth restriction present at birth.DesignRetrospective matched cohort study using data from the Postnatal Growth and Retinopathy of Prematurity study. Participants were born with birth weights of <1500 g or gestational ages of <32 weeks between 2006 and 2011 at 29 neonatal centres in the USA and Canada. Sepsis was defined as a culture-confirmed bacterial or fungal infection of the blood or cerebrospinal fluid before 36 weeks’ postmenstrual age (PMA). Growth was assessed as the change in weight z-score between birth and 36 weeks’ PMA.ResultsOf 4785 eligible infants, 813 (17%) developed sepsis and 693 (85%) were matched 1:1 to controls. Sepsis was associated with a greater decline in weight z-score (mean difference −0.09, 95% CI −0.14 to −0.03). Postnatal weight growth failure (decline in weight z- score>1) was present in 237 (34%) infants with sepsis and 179 (26%) controls (adjusted OR 1.49, 95% CI 1.12 to 1.97). Longitudinal growth trajectories showed similar initial changes in weight z-scores between infants with and without sepsis. By 3 weeks after sepsis onset, there was a greater decline in weight z-scores relative to birth values in those with sepsis than without sepsis (delta z-score −0.89 vs −0.77; mean difference −0.12, 95% CI −0.18 to −0.05). This significant difference persisted until 36 weeks or discharge.ConclusionInfants with sepsis had similar early weight growth trajectories as infants without sepsis but developed significant deficits in weight that were not apparent until several weeks after the onset of sepsis.

SUMMARY POINTS Weight faltering is not a disease, but rather a description of a relatively common growth pattern It is most commonly caused by undernutrition relative to a child's specific energy requirements Causes tend to be multifactorial and often involve problems with diet and feeding behaviour that usually respond to simple targeted advice More rarely, weight faltering may be associated with neglect or maternal mental health problems or addiction The health visitor (public health nurse) is often best placed to assess and advise in the first instance Organic disease is rare in otherwise asymptomatic children, but it is reasonable to rule out organic disease if dietary and behavioural interventions are unsuccessful