Normal and Aberrant Growth in Children

Cooke, David W.; DiVall, Sara A.; Radovick, Sally

doi:10.1016/b978-0-323-29738-7.00024-1

Cited by 19 publications

(13 citation statements)

References 1,209 publications

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“…The rationale for using this limit is that 5 ng/ml at 2 SD for GH values on provocative testing of normally growing children and identifies children who will have the highest first-year growth response to GH treatment. [ 24 ] Being a clinical hospital-based study, Berksonian bias is introduced, and thus this data is not reflective of the general population. A skewed sex ratio may be a result of referral bias.…”

Section: Discussionmentioning

confidence: 99%

Clinical and biochemical phenotype of Indian children with different types of idiopathic growth hormone deficiency and their association with pituitary height on MRI

Sharma

Mathur

Purwar

et al. 2021

Indian J Endocr Metab

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Background and Objectives: Differentiation of growth hormone deficiency (GHD) into various types has been made based on peak stimulated growth hormone levels and other hormone axis involvement. The data regarding how this classification is associated with variation in clinical and biochemical phenotype and how these findings associate with pituitary morphology remains sparse, especially in the Indian population. Therefore, we aimed to ascertain the differences in the pattern of auxological, clinical features including pituitary hypoplasia, and endocrinological profile among patients with severe GHD, partial GHD, and MPHD in the Indian population and to evaluate the association of pituitary height with various clinical and hormonal parameters. Materials and Methods: We conducted a cross-sectional study in 100 patients with idiopathic GHD. Patients were grouped into severe GHD, partial GHD, and MPHD to observe the differences in clinical, biochemical, and MRI findings. The pituitary height findings were correlated clinical and biochemical presentation. Results: MPHD subjects had a significantly higher frequency of breech delivery, neonatal jaundice, neonatal hypoglycemia, and micropenis. A significant difference was observed in the chronological age, bone age retardation (CA-BA), height SDS, weight SDS, peak GH response, IGF-1, IGF-1 SDS, and prevalence of pituitary hypoplasia, pituitary height, and pituitary height SDS among these three groups. In the composite population of GHD, pituitary height SDS was correlated with peak GH, basal IGF-I SDS, and body height SDS. Conclusion: The clinical and biochemical phenotype differs significantly among the various types of GHD. Pituitary height correlates with these findings and is helpful in further assessment of these patients.

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Section: Discussionmentioning

confidence: 99%

Clinical and biochemical phenotype of Indian children with different types of idiopathic growth hormone deficiency and their association with pituitary height on MRI

Sharma

Mathur

Purwar

et al. 2021

Indian J Endocr Metab

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“…A host of medical conditions are often seen in individuals with NS, though the complete clinical presentation and severity of the associated medical conditions vary from individual to individual. Common medical concomitants of the syndrome include congenital heart defects, blood disorders, delayed puberty, ophthalmological issues, and hearing loss (Allanson, 2010;Cooke et al, 2016;Madan-Khetarpal & Arnold, 2018;Romano et al, 2010). Congenital heart defects, such as pulmonary valve stenosis or hypertrophic cardiomyopathy, are common among those with NS, occurring in up to 50% to 90% of individuals (Allanson, 2010;Allanson & Roberts, 2016).…”

Section: Impact On the Student And Outcomes Medicalmentioning

confidence: 99%

Noonan syndrome.

Margiano,

McWilliams,

deLeyer-Tiarks

et al. 2023

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“…However, such an assumption is inaccurate because it does not fully explicate the great clinical variability in the growth pattern among individuals with TS. Thus, other factors, such as abnormalities in the GH-IGF-I axis, loss of quantitative trait loci in Xp22.3, estrogen deficiency, and general chromosomal imbalance, might be involved in TS-associated short stature [ 66 ].…”

Section: Clinical Consequences Of Reduced Cell Proliferation Of 45x C...mentioning

confidence: 99%

The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome

Álvarez-Nava

Soto-Quintana

2022

JDB

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Turner syndrome (TS) is a chromosomal disorder that is caused by a missing or structurally abnormal second sex chromosome. Subjects with TS are at an increased risk of developing intrauterine growth retardation, low birth weight, short stature, congenital heart diseases, infertility, obesity, dyslipidemia, hypertension, insulin resistance, type 2 diabetes mellitus, metabolic syndrome, and cardiovascular diseases (stroke and myocardial infarction). The underlying pathogenetic mechanism of TS is unknown. The assumption that X chromosome-linked gene haploinsufficiency is associated with the TS phenotype is questioned since such genes have not been identified. Thus, other pathogenic mechanisms have been suggested to explain this phenotype. Morphogenesis encompasses a series of events that includes cell division, the production of migratory precursors and their progeny, differentiation, programmed cell death, and integration into organs and systems. The precise control of the growth and differentiation of cells is essential for normal development. The cell cycle frequency and the number of proliferating cells are essential in cell growth. 45,X cells have a failure to proliferate at a normal rate, leading to a decreased cell number in a given tissue during organogenesis. A convergence of data indicates an association between a prolonged cell cycle and the phenotypical features in Turner syndrome. This review aims to examine old and new findings concerning the relationship between a prolonged cell cycle and TS phenotype. These studies reveal a diversity of phenotypic features in TS that could be explained by reduced cell proliferation. The implications of this hypothesis for our understanding of the TS phenotype and its pathogenesis are discussed. It is not surprising that 45,X monosomy leads to cellular growth pathway dysregulation with profound deleterious effects on both embryonic and later stages of development. The prolonged cell cycle could represent the beginning of the pathogenesis of TS, leading to a series of phenotypic consequences in embryonic/fetal, neonatal, pediatric, adolescence, and adulthood life.

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Normal and Aberrant Growth in Children

Cited by 19 publications

References 1,209 publications

Clinical and biochemical phenotype of Indian children with different types of idiopathic growth hormone deficiency and their association with pituitary height on MRI

Clinical and biochemical phenotype of Indian children with different types of idiopathic growth hormone deficiency and their association with pituitary height on MRI

Noonan syndrome.

The Hypothesis of the Prolonged Cell Cycle in Turner Syndrome

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