Rate Of Catch-up Growth Research Articles

Born small for gestational age: consequences for growth.

A large number of studies have documented a strong correlation between size at birth and subsequent height, although the reported incidence of catch-up growth and consequently the impact on final height has varied with time and between countries. These variations may be real, but could also be related to a number of methodological problems. The aim of this study was to explore two important aspects related to postnatal growth after disturbed fetal growth: first, the definition of small for gestational age (SGA), including the selection of cut-off points in defining shortness; and, secondly, the importance of the general socio-economic status of the population with regard to the incidence of growth faltering in early life. Data were analysed from two longitudinal population-based studies, one from Sweden and one from Hong Kong. Of the Swedish cohort, 3.8% had a birth length below -2 SD scores; in the Hong Kong population the corresponding value was 11.9% (Swedish reference values were used in both studies). The following conclusions were made. Size at birth is important for postnatal growth, and the difference in length at birth of 9-10 cm between the two extreme birth length subgroups remains, on average, until maturity. This seems to be true for the two study populations with different degrees of socio-economic development. However, the rate of catch-up growth is highly dependent on the definition of SGA, on the rate of catch-up growth in early life and on the incidence of growth faltering between 6 and 18 months of age.

The Effects of Illness on Neonatal Metabolism and Nutritional Management

In summary, careful attention to nutrient delivery in the IUGR infant is important to prevent and treat neonatal metabolic derangements and to improve postnatal growth. Carbohydrates are the essential fuel in the first days of life, to prevent hypoglycemia. Subsequent delivery of protein and fat helps rectify reduced muscle and fat stores and promotes weight gain. Calcium supplementation to prevent further bone demineralization and iron supplementation to replete iron stores may be necessary. Of special interest is that the neurologic outcome of these infants appears linked to the rate of catch-up growth. The rate of postnatal head growth depends on many perinatal and neonatal risk factors, and is a strong predictor of early developmental outcome in low-birthweight infants. Insufficient energy delivery beyond 2 weeks postnatal age in SGA premature infants results in failure to initiate subsequent catch-up head growth, with consequently smaller head circumferences at 1-year follow-up.

Body composition of children recovering from severe protein-energy malnutrition at two rates of catch-up growth

Twenty-two children with severe protein-energy malnutrition were randomly assigned to dietary treatments that permitted either moderate (4-6 g.kg-1.d-1) rates of weight gain (MG, n = 11) or rapid (12-16 g.kg-1.d-1) rates of weight gain (RG, n = 11) to test the hypothesis that restoration of weight deficits by the RG group restores reference body composition. Final total body water was 60 +/- 4% of body weight in the MG group and 62 +/- 3% in the RG group (NS) indicating reference body composition was attained by both groups. Composition of weight gained was measured by energy and nitrogen balance from doubly labeled water and metabolic collection data. In early recovery, the percent (+/- SEM) protein, fat, and water in weight gain was 20 +/- 1%, 40 +/- 8%, and 40 +/- 10% in the MG group and 14 +/- 1%, 43 +/- 4%, and 43 +/- 12% in the RG group. In late recovery these were 13 +/- 1%, 42 +/- 7%, and 47 +/- 14% in the MG group and 12 +/- 1%, 46 +/- 4%, and 42 +/- 6% in the RG group. We conclude that the nutritional therapy used to promote rapid weight gain restores reference body composition and significantly reduces time required for catch-up growth.

Transient neonatal hypothyroidism probably related to immaturity of thyroidal iodine organification

roid hormone replacement then may cause thyrotroph regression and expose the pituitary gland and sella to CSF pressure or arachnoid pulsations, which may produce an empty sella. 13 In general, only a minority of patients with empty sella develop pituitary hormone deficiencies, 14 so additional damage to the pituitary gland must occur in some individuals. One might wonder whether slower thyroxine treatment (e.g., less than full replacement dosage) might have altered the development of an empty sella and hypopituitarism. This has been suggested by McVie, ~3 although we know of no studies to support this recommendation. Our patient was initially given a relatively 10w dose of thyroxine, 1.67 /~g/kg body weight, and subsequently required increased dosage. Evidence is accumulating that pituitary enlargement and subtle visual field defects and pituitary alterations occur more commonly with primary hypothyroidism than previously appreciated. Our case report outlines the full spectrum of these changes during childhood, when the development of hGH deficiency has more impact. The initial CT scan was obtained somewhat serendipitously; with the diagnosis of primary hypothyroidism, we would recommend CT scan of the brain only if the patient has signs of increased intracranial pressure or visual field deficits. With pituitary enlargement or mild visual field defects, we believe a conservative approach with thyroxine therapy and close observation is warranted. If the expected clinical response is not seen (in particular, failure to return to normal or catch-up growth rate), the clinician must consider the development of hypopituitarism, which may be associated with an empty sella. We thank Douglas Livermore, M.D., for referring the

Team management of failure to thrive

A multidisciplinary team approach to treatment of failure to thrive in infancy and early childhood permits the simultaneous consideration of nutritional, medical, and psychosocial risk factors associated with this complex syndrome. The registered dietitian works with the physician, nurse, and social worker to provide an integrated evaluation of nutrition history, feeding patterns, medical status, social situation, developmental level, and interactional qualities of the child with failure to thrive. Nutritional management of failure to thrive emphasizes: (a) ongoing assessment of nutritional status and rate of catch-up growth, including regular collection of anthropometric measurements; (b) provision of energy and protein in amounts sufficient to meet requirements for catch-up growth; and (c) concrete, individualized nutrition instruction. Long-term follow-up at regular intervals in coordination with other members of the failure-to-thrive team provides the opportunity to reinforce nutrition instruction and to reassess and adapt meal plans to meet the growing child's changing nutritional needs.

Abuse‐dwarfism syndrome: After rescue, statural and intellectual catchup growth correlate

In 32 cases of abuse dwarfism followed for varying periods of time, the growth rate, including catchup growth rate of intelligence and stature (height) measured as IQ and HQ, respectively, correlated (r=0.42; p<0.01). This finding lends support to the hypotheses that neurohormones (probably ACTH and MSH) and/or neurotransmitters (probably B‐endorphin) jointly govern hormonal secretion from the pituitary and growth of intelligence. In both instances growth may be arrested in response to the external, socially imposed stimuli of child abuse and neglect.