1,720,998 research outputs found
Analysis of growth hormone receptor gene expression in tall and short stature children
No full textBACKGROUND:
The majority of children who present for evaluation of tall stature fall under the diagnosis of constitutional tall stature (CTS).
METHODS:
To investigate mechanisms of tall stature, we evaluated serum IGF-I values and the expression of the GHR gene in the peripheral blood cells of 46 subjects with normal height, 38 with tall stature and 30 healthy children with short stature.
RESULTS:
Our results showed significantly lower IGF-I levels in children with short stature (-0.57±0.18 SDS) compared to control children (0.056±0.19 SDS; p<0.0001) and to subjects with tall stature (0.594±0.17; p=0.00067). Furthermore, we found significantly higher GHR gene expression levels in tall children (321.84±90.04 agGHR/5×105agGAPDH) compared with other groups of subjects (short children: 30.13±7.5 agGHR/5×105agGAPDH, p<0.0001; controls: 86.81ag±19.5 GHR/5×105agGAPDH, p=0.035). The GHR gene expression level in short children was significantly lower compared with control subjects (p=0.0068).
CONCLUSIONS:
Significantly higher GHR gene expression levels in tall subjects suggests a sensitization of the GHR-IGF system leading to overgrowth in CTS
The effect of two different GH dosages on final height and bone geometry
No full textBackground: Growth hormone (GH) has a strong positive influence on bone, stimulating both bone elongation and increase in size. The aim of the study was to compare the effect of two different GH dosages on final height and bone geometry in two groups of GH-deficient children. Methods: We evaluated 121 children (86 m, 35f). Group 1 (77 patients) treated with GH at a mean dose of 0.16 mg/kg/week and group 2 (44 patients) at 0.3 mg/kg/week. Bone geometry was evaluated at final height from a digitalized X-ray of the left hand considering the following parameters: metacarpal index (MI), cross-sectional area (CSA), cortical area (CA) and medullary area (MA). Results: At baseline, group 2 was shorter than group 1 (-1.54 vs -1.01 SDS; p < 0.005), while at final height there was no difference. Height gain was significantly greater in group 2 than in group 1 (1.62 vs 1.13 SDS; p < 0.001). Bone geometry: MI was significantly greater in group 2 (0.62 vs 0.55; p < 0.001) as well as CA (46.87 vs 42.69 cm2; p < 0.005), while MA was significantly lower in group 2 (8.48 vs 11.65 cm2; p < 0.002). Conclusion: Higher GH doses elicit a significantly greater statural gain and a greater bone cortical area
Growth hormone bioactivity, insulin-like growth factors (IGFs), and IGF binding proteins in obese children.
No full textThe influence of growth hormone treatment on glucose homeostasis in growthhormone-deficient children: A six-year follow-up study
No full textBackground: Growth hormone (GH) influences glucose homeostasis by negatively affecting insulin sensitivity, leading to a compensatory increase in insulin secretion. It has recently been reported, in animals and humans, that GH might also stimulate insulin secretion by directly affecting the growth and function of pancreatic Î2-cells. The aim of this work was to longitudinally study the insulin sensitivity (HOMA-S), insulin secretion [insulinogenic index (IGI)] and capacity of Î2-cells to adapt to changes in insulin sensitivity [oral disposition index (ODI)] in GH-deficient (GHD) children under GH treatment. Methods: We studied 99 GHD (62 male, 37 female; age 8.9 ± 3.5 years) children for a median period of 6 years (range 1.5-16.2). Every year, our patients underwent an oral glucose tolerance test, which was used to calculate the HOMA-S, IGI and ODI. Results: Although HOMA-S remained unchanged, an increase in IGI and ODI was observed, becoming significant after 6 years of treatment (1.25 ± 1.28 vs. 2.35 ± 2.38, p < 0.05 and 0.57 ± 0.68 vs. 1.50 ± 1.92, p < 0.01, respectively). Conclusion: Our results suggest a positive influence of GH treatment on the Î2-cell secretory capacity in children with GH deficiency
Growth hormone bioactivity and levels of growth hormone, growth hormone-binding protein, insulin-like growth factor I, and insulin-like growth factor-binding proteins in premature and full-term newborn during the first month of life.
No full textAltered thyroid function and structure in overweight and obese children and adolescents: reversal after weight loss
No full textObesity is associated with hypothyroidism and goiter
The level of bioavailable growth hormone (GH) after the first GH injection predicts the first year's growth response in GH-deficient children.
No full textCurrent clinical management of constitutional delay of growth and puberty
Full text linkAbstract Background: Constitutional delay of growth and puberty (CDGP) is classifed as the most frequent cause of delayed puberty (DP). Finding out the etiology of DP during frst evaluation may be a challenge. In details, pediatricians often cannot diferentiate CDGP from permanent hypogonadotropic hypogonadism (PHH), with defnitive diagnosis of PHH awaiting lack of puberty by age 18 yr. Neverthless, the ability in providing a precise and tempestive diagnosis has important clinical consequences. Main text: A growth failure in adolescents with CDGP may occur until the onset of puberty; after that the growth rate increases with rapidity. Bone age is typically delayed. CDGP is generally a diagnosis of exclusion. Nevertheless, other causes of DP must be evaluated. A family history including timing of puberty in the mother and in the father as well as physical examination may givee information on the cause of DP. Patients with transient delay in hypothalamicpituitary-gonadal axis maturation due to associated conditions, such as celiac disease, infammatory bowel diseases, kidney insufciency and anorexia nervosa, may experience a functional hypogonadotropic hypogonadism. PHH revealing testosterone or estradiol low serum values and reduced FSH and LH levels may be connected to abnormalities in the central nervous system. So, magnetic resonance imaging is required in order to exclude either morphological alterations or neoplasia. If the adolescent with CDGP meets psychological difculties, treatment is recommended. Conclusion: Even if CDGP is considered a variant of normal growth rather than a disease, short stature and retarded sexual development may led to psychological problems, sometimes associated to a poor academic performance. A prompt and precise diagnosis has an important clinical outcome. Aim of this mini-review is throwing light on management of patients with CDGP, emphasizing the adolescent diagnosis and trying to answer all questions from paediatricians
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