[Child growth and malnutrition].
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Anorexia Nervosa↗
Biomedical subjects
J Pozo
Publications and source records attributed to J Pozo.
The growth hormone axis: control and effects.
Many important advances in our understanding of the growth hormone (GH) axis have occurred during the last decade. A number of neurotransmitters and neuropeptides are implicated in the control of growth hormone-releasing hormone (GHRH) and somatostatin release; however, the role of many of these, such as serotonin, gamma-aminobutyric acid and dopamine, is still a matter of discussion. As a newly isolated hypothalamic peptide with a possible role in the control of GH secretion, pituitary adenylate cyclase activating peptide has received considerable attention. Synthetic hexapeptides that stimulate GH release (GH-releasing peptides 1, 2 and 6) have been identified. Pituitary-specific transcription factors involved in the expression of the GH gene have been identified, the GHRH receptor gene has been cloned, as well as a number of somatostatin receptor genes, and advances in our understanding of the insulin-like growth factor-binding proteins, and growth hormone-binding proteins have been made.
Animals↗
Insulin-like growth factor I, insulin-like growth factor binding proteins, and growth hormone binding protein in Spanish premature and full-term newborns.
The normal values of insulin-like growth factor I (IGF-I), IGF-binding proteins 1 and 3 (IGFBP-1 and IGFBP-3), and the high-affinity growth hormone binding protein (GHBP) are not well established in large series of healthy fullterm newborns. We report the normative data for IGF-I, IGFBP-I, IGFBP-3, and GHBP in 271 normal Spanish full-term newborns, born between 37 and 42 weeks of gestation, and compare these results with the same parameters studied in 39 premature infants. Furthermore, we report the relationship between results found in the normal full-term newborns and those of 252 healthy prepubertal (Tanner stage I) Spanish children. Serum GHBP, IGF-I, and IGFBP-3 levels are very low in the premature infant and show a significant increase in full-term newborns, and continue to decline during childhood (p < 0.001; analysis of variance). A positive correlation between GHBP, IGF-I, and IGFBP-3 versus gestational age was observed. In contrast, we found a negative correlation between IGFBP-I and gestational age. There is a direct relationship between the ponderal index and IGF-I and IGFBP-3. When the group of premature newborns was divided into infants born before or after 32 weeks of gestation, we found higher levels of IGF-I and IGFBP-3 (p < 0.01 and p < 0.05, respectively, by Student's test) in the group with the higher gestational age; however, the IGFBP-I level was lower in this group (p < 0.001 by Student's t test), with no differences seen in serum GHBP concentrations. The presence of IGFBPs in the premature infant suggests that they are important modulators of IGF-I action during fetal growth and development.
Carrier Proteins↗
Growth hormone-releasing peptides: clinical and basic aspects.
Growth hormone (GH)-releasing peptides (GHRPs), a family of synthetic oligopeptides which stimulate GH release, were identified more than a decade ago. The effects of these peptides on GH release have been described in vivo and in vitro, in both animals and humans, using various doses and administration routes. It is generally accepted that GHRPs stimulate the release of GH by acting at the level of the pituitary through a receptor different to that for the endogenous GH-releasing hormone (GHRH). In addition, it has been reported that there are specific binding sites for these peptides in the hypothalamus and that systemic administration of GHRPs increases the expression of the immediate early gene c-fos in a subpopulation of hypothalamic neurons. However, the identity of these hypothalamic neurons and the mechanism of action of GHRPs at both the hypothalamic and pituitary levels remain unknown. One interesting aspect of GHRPs is that they are orally active and this phenomenon has been demonstrated in both animals and humans. Furthermore, these drugs stimulate GH secretion in humans dose-dependently with the magnitude and duration of this response being comparable to that seen with an intravenous peptide bolus. We have studied the oral activity of GHRP-2 on GH release in normal children. In addition, we have analyzed the response to GHRP-2 of obese adolescents, as well as the effects of an intravenous bolus of GHRH alone and GHRH plus GHRP-2. Orally administered GHRP-2 stimulates GH secretion in normal children and, although it seems that this drug is more potent in girls, there were no statistical differences between the groups. Characteristically, GH levels started to increase by 15 min, peaked at 60 min and returned to basal concentrations by 180 min. The effect of GHRP-2 was synergistic with GHRH 1-29 NH2. In addition, obese subjects appeared to have a greater response to this peptide than did normal controls. To study the effects of GHRPs on hypothalamic GHRH and somatostatin neurons, female dwarf rats (dw/dw) were treated continuously with GHRP-6 (1 mg/kg per 24 h) for 14 days. In situ hybridization for GHRH and SS was performed. We found that GHRP-6 stimulated GHRH mRNA levels in the posterior arcuate nucleus (ARC), with no significant effect in the anterior ARC or ventromedial hypothalamic neurons. SS mRNA levels in the posterior periventricular nucleus (PeN) were decreased after GHRP-6 treatment, while no effect was seen in the anterior PeN, ARC, or lateral paraventricular nucleus. These results suggest that GHRP-6 treatment modulates hypothalamic neurons controlling GH secretion; however, whether this effect is direct or mediated through another factor remains to be elucidated.
Animals↗
Decreased expression of placental growth hormone in intrauterine growth retardation.
During normal pregnancy, the levels of placental GH in the maternal circulation increase significantly until 35 wk of gestation. We have previously shown that these levels are significantly reduced in cases of intrauterine growth retardation (IUGR). To better understand the basis of this observation, we have studied the expression of placental GH in placentas from normal births (n = 6) and births with IUGR (n = 5). In situ hybridization histochemistry was used to determine the mean number of cells per area expressing this message, as well as the mean level of specific mRNA per cell. We have found that the mean mRNA signal level per cell of placental GH did not differ between normal or IUGR placentas. However, the mean number of cells/ area expressing this mRNA was significantly greater in normal placentas compared with IUGR placentas (normal 12.8 +/- 0.9 cells/unit area, IUGR 4.9 +/- 2.4 cells/unit area, analysis of variance: p < 0.004). These data suggest that the decreased levels of placental GH in the maternal circulation in IUGR are not due only to the reduced size of the placenta, but also to changes in the placental tissue which result in a reduced number of cells per area that are capable of producing this peptide.
Female↗
Insulin-like growth factor I, its binding proteins 1 and 3, and growth hormone-binding protein in children and adolescents with insulin-dependent diabetes mellitus: clinical implications.
Values of IGF-I after extraction, its binding proteins, and the high affinity GH-binding protein (BP) are not well established in pediatric patients with insulin-dependent diabetes mellitus (IDDM). We report data for IGF-I, IGFBP-1, and -3, and GHBP in 92 Spanish children with IDDM, separated according to pubertal stage: prepubertal (n = 49); pubertal onset (n = 17); mid-puberty (n = 17), and complete puberty (n = 9), as well as to metabolic control (HbA1 < 9% or > or = 9%). IGF-I levels in IDDM patients increased throughout development (p < 0.001), but were diminished at every developmental stage when compared with marched control subjects. IGF-I concentrations showed a negative correlation with the degree of metabolic control, in particular during the prepubertal stage of development. A negative correlation (r = -0.22; p < 0.005) between IGF-I concentrations and HbA1 was found. Serum IGFBP-I levels diminish during maturation in diabetic patients (p < 0.001). However, IDDM patients have significantly higher levels of IGFBP-1 than control subjects at every stage of development, and IDDM patients with inadequate metabolic control exhibit even greater differences when compared with matched control subjects. A positive correlation (r = 0.22; p < 0.005) between IGFBP-1 concentrations and HbA1 was found. IGFBP-3 serum levels were similar to those observed in normal subjects, and no correlation was observed in relation to the metabolic control. In IDDM patients, GHBP levels change significantly during maturation, as they do in normal control subjects; however, significantly lower GHBP levels were found in prepubertal and pubertal IDDM patients. GHBP levels were independent of metabolic control, although a tendency toward lower levels of GHBP was seen when HbA1 levels increased. We suggest that a partial GH resistance syndrome exists in IDDM patients, and this may be related to the metabolic control. Hence, the biochemical markers measured here may be of value in evaluating the smaller pubertal growth spurt in diabetic patients.
Adolescent↗
Failure of the sliding hip screw in the treatment of femoral neck fractures: 'left-handed surgeons for left-sided hips'.
The pre-operative radiographs of 265 patients consecutively treated with sliding hip screws were reviewed. In 244 cases the fixation was for a basicervical or intertrochanteric fracture. The post-operative radiographs of these 244 patients were examined for technical failure of the device. Of the 15 failures analysed, one had occurred where insufficient sliding length had been available to the screw within the barrel, and one was due to jamming of the screw within the barrel. Of the remaining 13 fixations, 12 had occurred where the screw had been poorly positioned within the femoral head, and one device had failed for no obvious reason. Malpositioning of the failures occurred significantly more frequently on the left than on the right, in a Unit where all the surgeons were right-handed. We conclude that the majority of technical failures of the sliding hip screw occur because of poor positioning of the screw. This occurs more commonly on the left side when the surgeon is right-handed.
Bone Screws↗
Growth hormone secretion in children with normal variants of short stature.
Pulsatile growth hormone (GH) secretion plays a central role in human growth during the prepubertal period of life. In order to investigate whether or not short stature in prepubertal children with normal variants of short stature (NVSS) may be explained, at least in part, by the presence of abnormalities in the pulsatile pattern of GH secretion, we have studied the spontaneous secretion of GH/24 h in 139 prepubertal children with short stature (< or = -2 SD) and normal growth velocity (> -1 SD) and in 37 prepubertal children with normal height and growth velocity. All of the subjects included in this study exhibited a body mass index (BMI) lower than 1 SD. The patients with short stature were divided into three groups according to their bone age and the existence of familial antecedents of short stature. These groups were: (1) familial short stature without bone age retardation (FSS-1); (2) constitutional, nonfamilial short stature, with bone age retardation suggesting further delay of puberty (possible constitutional delay of growth and puberty), and (3) familial short stature with bone age retardation (FSS-2). Spontaneous GH secretion was analyzed by using a computerized mathematical algorithm of pulsatility (Cluster). In addition, in all of the patients with short stature, the GH secretory response to three different pharmacological stimuli was evaluated, including: clonidine, growth hormone-releasing hormone (GHRH) and hypoglycemia after insulin administration. The mean values of GH/24 h exhibited a wide range of distribution (1.4-7.8ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
Body Height↗
Normative data for insulin-like growth factors (IGFs), IGF-binding proteins, and growth hormone-binding protein in a healthy Spanish pediatric population: age- and sex-related changes.
The normal values of insulin-like growth factors (IGFs) after extraction, their binding proteins, and the high affinity GH-binding protein are not well established in infancy or childhood. We report the relationship between serum IGF-I, IGF-II, their binding proteins IGFBP-1 and IGFBP-3, and GH-binding protein in 600 normal Spanish children who were divided into 5 groups according to Tanner stage: I, 150 males and 102 females; II, 40 males and 42 females; III, 45 males and 45 females; IV, 42 males and 55 females; and V, 23 males and 56 females. Serum IGF-I levels increase slowly during childhood in both sexes, exhibiting a dramatic increase during puberty and a significant decline [P < 0.001, by analysis of variance (ANOVA)] during adulthood. The pubertal peak occurs approximately 2 yr earlier in girls than in boys. In contrast, serum IGF-II levels remain stable throughout childhood, showing no pubertal peak. In boys, there is a significant decline in IGF-II levels during adulthood (P < 0.001). Serum IGFBP-3 levels show a pattern similar to that of IGF-I, with a significant increase during childhood and a significant decline during adulthood (P < 0.001, ANOVA) in both males and females. In contrast, serum IGFBP-1 levels decrease dramatically during childhood in both boys and girls (P < 0.001 and P < 0.005, respectively, by ANOVA). A significant decline in serum GH-binding protein levels is observed between prepubertal and pubertal children of both sexes (P < 0.001). There is a close linear correlation between the sum of serum IGF-I plus IGF-II levels vs. serum IGFBP-3 (r = 0.724; P < 0.0001). In contrast, there is a nonlinear correlation between serum IGF-I vs. serum IGFBP-3 (concave curve) as well as between serum IGF-II and serum IGFBP-3 (convex curve). A negative correlation was found between serum IGF-I vs. IGFBP-1 (r = -0.51; P < 0.0001) as well as between the sum of serum IGF-I plus IGF-II vs. IGFBP-1 (r = -0.47; P < 0.0001), but not between serum IGF-II and IGFBP-1. These data emphasize that when these tests are performed in the clinic, their interpretation should be based upon age- and sex-specific criteria.
Adolescent↗
[The growth hormone axis in malnutrition].
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Animals↗
[Methodologic aspects of the determination of growth hormone in urine].
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Growth Hormone↗
[Neuroregulation and the growth hormone].
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Amino Acid Sequence↗
[Therapeutic implications of growth hormone in infancy and childhood].
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Body Height↗
Subcellular structure of prenatal human ovary: mitochondrial distribution during meiotic prophase.
The dynamics of mitochondrial population during the first meiotic prophase in the fetal human ovary was studied in sequential stages of development, from week 13 to week 23 of intrauterine life; the study was performed by means of electron microscopy. Two mitochondrial translocations were observed: first, from a random cytoplasmic distribution during leptotene, the mitochondria translocate toward a perinuclear location during zygotene. Second, from this perinuclear position they migrate toward a pole of the cell where they contribute during diplotene to form the Balbiani's vitelline body. Coincident with these mitochondrial redistributions, changes in mitochondrial cristae morphology were observed. From a tubular profile during early leptotene, they turn parallel with a more electron dense matrix during zygotene and pachytene, and finally arciform in diplotene. Since meiosis is a process that probably requires high levels of energy, these dynamic changes in mitochondrial population and the close association between mitochondria and nuclear membrane may be related with energy producing reaction that may be necessary for insuring the completion of the first meiotic prophase.
Cell Cycle↗
[Recurrent infection of the urinary tract in girls].
A group of 18 girls, studied in a period between 1979 and 1985 with recurrent urinary tract infections (RUTI), with at least three culture documented episodes of bacteriuria in the previous year and without radiologic evidence of urinary tract abnormality is described. Incidence was 6.1% amount a selected group of 295 girls with urinary tract infection. The period of follow-up was between 2 and 6 years (X 3.33). Symptomatology was light. No predominance of urinary symptoms were found. E. coli was the most frequent germ isolated. The number of recurrences/year/girl were significantly lower with prophylactic treatment and with years of evolution. Renal damage was not found. Vesicoureteral reflux appeared in two girls only. They had a benign course and a good prognosis. Reduction of aggressive investigation in this group of patients is proposed.
Child↗
[Moschowitz's thrombocytopenic thrombotic purpura].
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Adrenal Cortex Hormones↗
Molecular diagnosis and endocrine evaluation of a patient with a homozygous 7.0 kb deletion of the growth hormone (GH) gene cluster: response to biosynthetic GH therapy.
A significant proportion of cases of GH deficiency (5-30%) may be due to genetic causes. At least four Mendelian types of isolated GH deficiency (IGHD) have been delineated based on the mode of inheritance and the degree of GH deficiency, with IGHD type IA being the most severe. A 2 year-old girl, the second child of consanguineous parents, with short stature was diagnosed with IGHD type IA. The analysis of the genomic DNA of this patient, performed by polymerase chain reaction (PCR) amplification of the flanking regions of the GH-1 gene, showed a homozygous deletion of 7.0 kb of sequence including the GH-1 gene. She was treated with biosynthetic GH resulting in long-lasting catch-up growth during at least three years, despite a clinically irrelevant appearance of low binding capacity GH antibodies. Growth hormone-binding protein (GHBP) levels were normal at the time of diagnosis. In addition, GHBP plasma levels did not show any significant change during the three years of therapy with GH. Diagnosis of carrier status in family relatives was done by genotyping GH gene alleles by PCR amplification from blood spots on filter paper.
Antibodies↗