Arm span as measurement of response to growth hormone (GH) treatment in a group of children with meningomyelocele and GH deficiency.

Satin-Smith, Marta; Katz, Lorraine Levitt; Thornton, Paul; Gruccio, Denise; Moshang, Thomas

doi:10.1210/jcem.81.4.8636383

Cited by 9 publications

(6 citation statements)

References 14 publications

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“…Other factors that can affect linear growth in children with spina bifida and hydrocephalus are endocrinologic disorders such as growth hormone deficiency [Rotenstein and Breen, 1996;Satin-Smith et al, 1996;Hochhaus et al, 1999], hyperthyroidism [Hochhaus et al, 1997], and precocious puberty [Meyer and Landau, 1984;Perrone et al, 1994;Trollmann et al, 1996;Hochhaus et al, 1997].…”

Section: Obesitymentioning

confidence: 99%

Feeding and swallowing dysfunction in genetic syndromes

Cooper-Brown

Copeland

Dailey

et al. 2008

Dev Disabil Res Revs

150

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Children with genetic syndromes frequently have feeding problems and swallowing dysfunction as a result of the complex interactions between anatomical, medical, physiological, and behavioral factors. Feeding problems associated with genetic disorders may also cause feeding to be unpleasant, negative, or even painful because of choking, coughing, gagging, fatigue, or emesis, resulting in the child to stop eating and to develop behaviors that make it difficult, if not impossible, for a parent to feed their child. In addition, limited experiences with oral intake related to the medical or physical conditions, or other variables such as prematurity, often result in a failure of the child's oral motor skills to develop normally. For example, a child with Pierre Robin sequence may be unable to successfully feed orally, initially, due to micrognathia and glossoptosis. Oral-motor dysfunction may develop as a result of both anatomical problems, (e.g., cleft lip/palate), lack of experience (e.g., s/p. surgery), or oral motor abnormalities (e.g., brain malformation). Neuromotor coordination impairments such as those associated with Down syndrome (e.g., hypotonia, poor tongue control, and open mouth posture) frequently interfere with the acquisition of effective oral-motor skills and lead to feeding difficulties. Management of these phenomena is frequently possible, if an appropriate feeding plan exist that allows for three primary factors: (1) feeding program must be safe, (2) feeding program must support optimal growth, and (3) feeding program must be realistic. Researchers have demonstrated the utility of behavioral approaches in the treatment of feeding disorders, such as manipulations in the presentation of foods and drink and consequences for food refusal and acceptance (e.g., praise, extinction, contingent access to preferred foods). However, because a child's failure to eat is not frequently the result of a single cause, evaluation and treatment are typically conducted by an interdisciplinary team usually consisting of a behavioral psychologist, pediatric gastroenterologist, speech pathologist, nutrition, and sometimes other disciplines. This chapter provides an overview of some of the feeding difficulties experience by some of the more common genetic disorders including identification, interventions, and management.

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Section: Obesitymentioning

confidence: 99%

Feeding and swallowing dysfunction in genetic syndromes

Cooper-Brown

Copeland

Dailey

et al. 2008

Dev Disabil Res Revs

150

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“…In children with MMC, muscle wasting due to denervation is observed. What is more, MMC children often have impaired linear growth [14]. In these cases, Cr and precise estimation of eGFR may be impossible.…”

Section: Discussionmentioning

confidence: 99%

Are Tubular Injury Markers NGAL and KIM-1 Useful in Pediatric Neurogenic Bladder?

Bagińska

Korzeniecka‐Kozerska

2021

JCM

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The lack of early biomarkers of renal damage in children with neurogenic bladder (NB) prompts us to investigate the role of promising proteins: neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). This prospective analysis was conducted on 58 children with NB and 25 healthy children. We assessed urinary levels of NGAL and KIM-1 in both groups. Age, sex, anthropometric measurements, activity assessment, renal function, and urodynamics parameters were analyzed. The differences between the median uNGAL and uKIM-1 in the NB group compared to control were recorded. However, only uNGAL levels were statistically significantly higher. Statistically significant correlation was found between gender, recurrent urinary tract infections, bladder trabeculation, its compliance, activity assessment, and uNGAL. To conclude, elevated levels of uNGAL may be considered a biomarker of tubular injury in children with NB due to MMC in contrast to uKIM-1.

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“…A limited number of biochemical studies documented that short stature in MMC patients is not only the result of neurological lesion with impaired growth of lower limbs and trunk but also the consequence of hypothalamo-pituitary growth hormone deficiency [6, 7, 9]. Furthermore, patients are at risk of premature activation of hypothalamo-pituitary-gonadal axis resulting in central precocious puberty [5, 8].…”

Section: Discussionmentioning

confidence: 99%

“…Several former reports documented endocrine disorders in MMC patients such as obesity, short stature, premature sexual development [2, 3, 4, 5]. Central precocious puberty and growth hormone deficiency (GHD) were the most common biochemical findings [6, 7, 8, 9]indicating disturbed regulation of the hypothalamopituitary axis.…”

Section: Introductionmentioning

confidence: 99%

Spontaneous Nocturnal Leptin Secretion in Children with Myelomeningocele and Growth Hormone Deficiency

et al. 2002

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Objective: To examine the spontaneous leptin secretion in patients with myelomeningocele (MMC) and growth hormone deficiency (GHD). Methods: Serum leptin levels were studied in 10 prepubertal MMC patients with GHD (CA 6.2 ± 0.5 years), 10 patients with idiopathic GHD (IGHD; CA 7.6 ± 0.7 years) and 12 children with normal variant short stature (NVSS; CA 7.6 ± 0.5 years). Mean BMI (kg/m²) values of the groups did not differ significantly. Nocturnal leptin levels were analyzed over 10 h (blood samples every 20 min) and measured by specific radioimmunoassay. Results: Mean leptin concentrations did not correlate with BMI in MMC patients. Nocturnal leptin secretion of MMC patients was significantly different to those of children with IGHD and NVSS. Morning leptin levels did not decline as observed in both other groups. Conclusion: Since all groups were matched for BMI values, we suggest a hypothalamic dysregulation of leptin secretion in MMC patients.

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Arm span as measurement of response to growth hormone (GH) treatment in a group of children with meningomyelocele and GH deficiency.

Cited by 9 publications

References 14 publications

Feeding and swallowing dysfunction in genetic syndromes

Feeding and swallowing dysfunction in genetic syndromes

Are Tubular Injury Markers NGAL and KIM-1 Useful in Pediatric Neurogenic Bladder?

Spontaneous Nocturnal Leptin Secretion in Children with Myelomeningocele and Growth Hormone Deficiency

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