The other end of the growth spectrum, tall stature, may be perceived a sign of “healthy growth,” undermining a discussion about possible pathologic processes. Management can be facilitated by the publications of the Pediatric Endocrine Society, which detail the guidelines for initiation of growth hormone therapy ( 15). Excess of glucocorticoids suppresses IGF-1 proliferative signal ( 10) and proinflammatory cytokines induce chondrocyte apoptosis and suppress skeletal growth ( 11).įor abnormally short stature (with or without poor weight gain), many publications aimed at guiding practitioners are available to assist in a rapid diagnosis. Estrogen, when secreted in high dose in puberty, promotes growth plate closure by depletion of proliferation and promoting hypertrophic chondrocytes' death ( 9). Both hypertrophy and proliferation are stimulated by the growth hormone (GH)–insulin-like growth factor 1 (IGF-1) pathway ( 8). Chondrocyte hypertrophy is stimulated by thyroid hormones via the Wingless-int 4 (Wnt 4) β-catenin pathway it is inhibited by the IHH–PTHrP pathway. Proliferation of chondrocytes in the growth plate is upregulated by Indian hedgehog (IHH), which stimulates PTH-related protein (PTHrP), and specific bone morphogenic protein (BMP) and is repressed by the fibroblast growth factor (FGF)-FGFR3 receptor pathway (overactivation of FGFR3 results in achondroplasia). The differentiation process is regulated both by paracrinic and endocrinic hormonal axes. Proliferating chondrocytes secrete extracellular matrix (ECM) components to support the bone structure, while hypertrophic chondrocytes apoptose and promote osteoblast influx responsible for bone mineralization. Skeletal growth occurs in the epiphyseal plate of long bones owning to the unique differentiation state of chondrocytes ( 6, 7): resting chondrocytes differentiate into proliferating chondrocytes, which in turn differentiate further into hypertrophic chondrocytes. This accounts for only 12–14% variability in final height, compared with a 56–66% variability in final weight. The final height, which is the result of a complex interplay among transcription factors, hormones, and a large variety of target cells that lasts for about 18 years, eventually falls within a 19–24 cm (7.5–9.4 inches) range for the vast majority of the population. This accounts for a final height of 153–174 cm (60–68.5 inches) for girls and 165–189 cm (65–74 inches) for boys falling between then 5th and 95th centiles, according to the CDC standardized growth charts ( 5). At puberty, linear growth velocity peaks at 6–10 and 5–11 cm/year for girls and boys, respectively ( 4).
Postnatally, linear growth velocity declines to 15–17 cm/year in the first 2 years of life, which further decreases until puberty to about 5 cm/year. Following conception, the fetus follows a rapid growth phase around 13–16 weeks of gestation which gradually slows down until birth ( 3).
#Overgrowth mods not showing up serial
Nowadays, growth is routinely followed prenatally with serial ultrasonography (defined as changes between consecutive measurements of biparietal diameter, abdominal circumference, and femur length). As early as the 18th century, the importance of growth charts was recognized, and its role as a diagnostic tool is now widely appreciated ( 2). Healthy growth can be defined as a progression of changes in height, weight, and head circumference and is predicted to follow standardized growth curves, reflecting the overall health and nutritional status of an individual ( 1).
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