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Biomedical subjects

G Iñiguez

Publications and source records attributed to G Iñiguez.

13 recordsLinked to original sources
PubMed2006

Comparison of clinical, ultrasonographic, and biochemical differences at the beginning of puberty in healthy girls born either small for gestational age or appropriate for gestational age: preliminary results.

CONTEXT: There are limited and controversial data concerning puberty characteristics in girls born small for gestational age (SGA). OBJECTIVE: The objective of the study was to document clinical, ultrasonographic, and biochemical characteristics at the beginning of puberty in matched healthy girls born either SGA or appropriate for gestational age (AGA) recruited from the community. PATIENTS: Inclusion criteria were breast Tanner stage II and a body mass index between the 10th and 95th percentiles. INTERVENTIONS: Recruited subjects underwent a complete physical exam, bone age, and ultrasound measurements of the internal genitalia. Hormonal assessment included fasting early morning dehydroepiandrosterone sulfate, androstenedione, SHBG, inhibin-B, FSH, LH, estradiol (E2), 17-hydroxyprogesterone (17OH Prog), and testosterone. Thereafter, a GnRH agonist test (leuprolide 500 microg, sc) was performed with FSH and LH at time 3 and 24 h for E2, 17OH Prog, and testosterone. RESULTS: Sixty-five girls (35 AGA, 30 SGA) with a mean age of 9.9 +/- 1.03 (7.8-12.5) yr, similar bone age/chronological age (1.02 +/- 0.8 in AGA and 1 +/- 0.76 in SGA), median height of 1.35 +/- 0.06 cm, and similar waist to hip ratio were included. No differences in the presence of pubic hair, axillary hair, apocrine odor, or ultrasound measurements were found. SGA girls had increased baseline E2 as well as stimulated E2 and 17OH Prog. CONCLUSIONS: In a preliminary sample of lean, healthy girls recruited from the community born either SGA or AGA, we observed slight hormonal differences at the beginning of puberty. Longitudinal follow-up of this cohort will allow us to understand whether these differences are maintained and have a clinical impact in their pubertal development.

17-alpha-Hydroxyprogesterone↗
PubMed2006

Treatment of central precocious puberty with triptorelin 11.25 mg depot formulation.

A new triptorelin 11.25 mg long depot formulation is now available for the treatment of central precocious puberty (CPP). The aim of our study was to evaluate the efficacy of triptorelin 11.25 mg administered every 90 days to suppress gonadotropin and sex steroid secretion and pubertal signs in children with CPP during 2 years of treatment. Inclusion criteria were clinical pubertal development before the age of 8 years in girls or 9 years in boys, advanced bone age and a pubertal LH response (peak >5 mIU/ml) to GnRH. We studied 20 patients (19 girls and 1 boy), with a median age at entry into the study of 7.5 +/- 0.2 years for girls, and 9 years for the boy. The basal and GnRH-stimulated serum levels of LH and FSH decreased significantly from baseline to 3 months of therapy (p <0.0001). All patients had a GnRH-stimulated peak below 3 mIU/ml between 6 and 24 months of treatment. The pituitary-gonadal axis recovered adequately after discontinuation of therapy. These results suggest that 3-month depot triptorelin is a satisfactory alternative for the therapy of children with CPP. The longer interval between injections may increase acceptability and compliance with treatment.

Breast↗
PubMed2005

Longitudinal changes in insulin sensitivity and secretion from birth to age three years in small- and appropriate-for-gestational-age children.

AIMS/HYPOTHESIS: Insulin resistance and type 2 diabetes risk in human subjects who were small-for-gestational-age (SGA) at birth may be a consequence of rapid early postnatal weight gain. MATERIALS AND METHODS: We prospectively studied early changes in fasting insulin sensitivity and insulin secretion, assessed by a short intravenous glucose tolerance test that was conducted several times from birth to 3 years of age in 55 SGA (birthweight below fifth percentile) newborns and in 13 newborns with a birthweight appropriate for gestational age (AGA). RESULTS: Most SGA infants showed postnatal upward weight centile crossing and by 3 years were similar in size to AGA infants. SGA infants had lower pre-feed insulin levels at postnatal age 48 h than AGA infants (median 34.4 vs 59.7 pmol/l, p<0.05), but by the age of 3 years they had higher fasting insulin levels (median 38.9 vs 23.8 pmol/l, p<0.005), which were related to rate of weight gain between 0 and 3 years (r=0.47, p=0.0003). First-phase insulin secretion did not differ between SGA and AGA infants, but SGA infants had a lower glucose disposition index (beta cell compensation) (median 235 vs 501 min mmol(-1) l(-1), p=0.02), which persisted after allowing for postnatal weight gain (p=0.009). CONCLUSIONS/INTERPRETATION: SGA infants showed a marked transition from lower pre-feed insulin and increased insulin sensitivity at birth to insulin resistance over the first 3 years of life. This transition was related to rapid postnatal weight gain, which could indicate a propensity to central fat deposition. The additional observation of reduced compensatory beta cell secretion underlines the need for long-term surveillance of glucose homeostasis in all SGA subjects, whether or not they show postnatal catch-up growth.

Birth Weight↗
PubMed2002

Regulation of steroid synthesis and apoptosis by insulin-like growth factor I and insulin-like growth factor binding protein 3 in human corpus luteum during the midluteal phase.

The aim of the present study was to investigate the action of insulin-like growth factor I (IGF-I) and insulin-like growth factor-binding protein 3 (IGFBP-3) on steroidogenesis and apoptosis in human corpus luteum during the midluteal phase. Slices from corpora lutea were incubated for 4 h with IGF-I or IGFBP-3. Progesterone, oestradiol, androstenedione and testosterone concentrations were determined by radioimmunoassay; caspase 3 expression was assessed by immunohistochemistry; bcl-2, bax and P(450arom) expression were assessed by RT-PCR; and apoptosis was detected by in situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling. The results showed that addition of IGF-I stimulated progesterone production (150%, P < 0.01), oestradiol production (65%, P < 0.05) and bcl-2 gene expression (approximately 200%, P < 0.05), but decreased apoptosis (P < 0.05). In contrast, IGFBP-3 reduced steroid production and increased bax gene expression and the percentage of apoptotic cells (P < 0.05). Neither IGF-I nor IGFBP-3 had an effect on P(450arom) expression or on the concentrations of its substrates. However, maximum expression of caspase 3 was detected in corpus luteum during the midluteal phase. In conclusion, these results indicate that IGF-I and IGFBP-3 act as regulatory peptides of the function of the human corpus luteum during the midluteal phase. This action may be direct or mediated by steroid production or by bcl-2-bax expression.

Adult↗
PubMed2001

Effect of nitric oxide on the expression of insulin-like growth factors and the insulin-like growth factor binding proteins throughout the lifespan of the human corpus luteum.

The presence of insulin-like growth factors (IGF), IGF binding proteins (IGFBP) and IGF receptor type 1 (IGF-IR) in the human corpus luteum was investigated by examining the expression and production of related proteins throughout the lifespan of the corpus luteum and the action of nitric oxide upon their production. The expression of proteins in corpora lutea from the early, mid-and late luteal phases was assessed by immunohisto-chemistry, evaluated by a semi-quantitative analysis and the functional study was performed in corpus luteum explants incubated with nitric oxide donors. IGF-I and -II and IGFBP-1 and -3 were measured in the culture media by specific immunoassays. The results showed that IGF-I and -II, IGFBP-1 to -6 and IGF-IR were detected in the human corpus luteum throughout the luteal phase. Moreover, the expression and production of IGF-I and IGFBP-1 increased progressively from corpora lutea from the early to late luteal phases (P < 0.05), whereas the expression and production of IGFBP-2, -4 and -5 were significantly higher in corpora lutea from the mid-luteal phase (P < 0.05). No differences were observed in the expression of IGF-II, IGFBP-3 and -6 and IGF-IR throughout the lifespan of the corpus luteum. However, functional studies showed that nitric oxide donors elicited a stimulatory action on production of IGF-I in corpora lutea from the early luteal phase (80%) and on production of IGFBP-1 in corpora lutea from the late luteal phase (50%) (P < 0.05), whereas production of IGF-II and IGFBP-3 was not affected by nitric oxide. In conclusion, the components of the IGF-IGFBP system are expressed in the human corpus luteum throughout its lifespan. Nitric oxide regulates IGF-I and IGFBP-1 production, indicating that the growth factors may serve, at least in part, as mediators of the action of nitric oxide in the human corpus luteum.

Adult↗
PubMed2001

[Reference values of growth hormone binding protein (GHBP) for a normal pediatric population].

UNLABELLED: Circulating concentrations of the high affinity growth hormone binding protein (GHBP) may be a marker of GH receptor density as well as GH sensitivity. GOAL: To determine values of GHBP for a normal Chilean pediatric population. METHODS: We determined GHBP levels in 73 males and 73 females between 4 to 15.5 years and 4 to 16.8 years respectively, divided in 7 groups according to age and puberal status. RESULTS: The population was normally distributed in weight, height and body mass index (BMI). GHBP activity increased up to Tanner IV in males and Tanner III in females, and decreased slightly thereafter in Tanner V and IV respectively. There was a significant difference between GHBP levels of preschool children and those found in Tanner II to V in both sexes (p < 0.05). In addition, we found a positive correlation between GHBP vs weight, height and BMI (p < 0.001) in males and females. CONCLUSION: The availability of this methodology allows us to establish the normative value of GHBP in our population and provides useful information to interpret GH circulating levels in children with growth disorders.

Adolescent↗
PubMed2000

Nitric oxide induces apoptosis in the human corpus luteum in vitro.

The present study aimed to investigate the role of nitric oxide (NO) in regression of the human corpus luteum. We therefore examined the effect of both NO and human chorionic gonadotrophin (HCG) on luteal cell apoptosis, and Bcl-2 production. The effect of NO on oestrogen production during corpus luteum regression was also studied. Slices from corpus luteum collected throughout the luteal phase were incubated for 4 h with the nitric oxide synthase (NOS) substrate, L-arginine (L-Arg, 1 mmol/l), the NOS inhibitor N-monomethyl-L-arginine (L-NMMA) (1 mmol/l), or with HCG (10 IU/ml). Oestradiol concentrations were determined by radioimmunoassay; Bcl-2 concentrations were measured by enzyme-linked immunosorbent assay; apoptosis was detected in-situ by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling; and inducible nitric oxide synthase (iNOS) was assessed by immunohistochemistry. Consistent with our previous findings, L-Arg elicited an inhibitory action on the production of oestradiol (P< 0.05). The number of apoptotic cells increased (P<0.05) from early to late corpus luteum, as did the number of cells positive for the expression of iNOS. The percentage of apoptotic cells in mid and late luteal phase was increased by L-Arg (56% and 310% respectively; P <0.05), and decreased by L-NMMA and HCG. Although no changes were observed in Bcl-2 concentration during the corpus luteum life span, L-Arg inhibited, and HCG augmented, Bcl-2 production (P<0.05) from mid and late corpus luteum cells in vitro. In summary, these results suggest that the opposite actions of L-Arg and HCG on human corpus luteum viability may, in part, be mediated by changes in the level of the anti-apoptotic activities caused by oestradiol and Bcl-2 protein.

Adult↗
PubMed1998

Effects of eight months treatment with graded doses of a growth hormone (GH)-releasing peptide in GH-deficient children.

Stimulation of pituitary GH secretion with administered GHRH can be effective therapy for those GH deficient (GHD) patients whose disorder results from insufficient endogenous GHRH secretion. We have previously shown that most such patients also respond acutely to the GH-releasing peptides (GHRP's), which have a different mechanism of action from GHRH, with release of GH. In this study we tested whether the GH response to a newer GHRP, GHRP-2, would be sustained over time. Six prepubertal children with GHD and growth failure received stepwise increasing s.c. doses of GHRP-2, at 0.3, 1.0, and 3.0 micrograms/kg/day, in successive 2-month treatment periods, with monitoring of overnight 12 h episodic GH secretion and toxicity measures at the end of each period. During a fourth 2-month period, they received 3 micrograms/kg GHRP-2 together with 3 micrograms/kg s.c. GHRH. Serum levels of IGF-I and IGFBP-3 were also measured, and stadiometer height measurements were recorded. GHRP-2 administration produced a dosewise increase in overnight GH secretion. GH profiles showed that the effect of GHRP-2 injections was relatively brief, with little effect upon GH secretion later in the night. Serum levels of IGF-I and of IGFBP-3 did not increase. Growth velocity was higher during GHRP-2 treatment than during pretreatment and post-treatment evaluations. There were no side effects or toxicities observed. Thus GHRP-2 is well tolerated and is able to stimulate GH secretion. Formulations or routes of administration that allow for a longer duration of action will likely be needed to use GHRP-2 in therapy.

Adolescent↗
PubMed1995

The effects of beta 1-adrenergic blockade on the growth response to growth hormone (GH)-releasing hormone therapy in GH-deficient children.

Acute suppression of SRIH secretion with a beta-adrenergic antagonist can increase the GH response to GHRH. To determine whether chronic beta-blockade could enhance the growth-promoting effects of GHRH therapy, we conducted a double blind, placebo-controlled, randomized, cross-over trial of coadministration of the selective beta 1-antagonist atenolol together with GHRH in 11 GH-deficient children. In randomly chosen order, each patient received two 12-month treatment periods with a single daily injection of GHRH (20 micrograms/kg, sc, at bedtime), plus daily oral administration of either atenolol (1 mg/kg) or placebo. The growth velocity increased, rising from a mean +/- SD of 2.6 +/- 0.4 cm/yr before treatment to 5.4 +/- 1.0 cm/yr during the first year of treatment with GHRH plus placebo and to 6.8 +/- 1.2 cm/yr during the first year of treatment with GHRH plus atenolol. The mean growth velocity during treatment with GHRH plus atenolol was significantly greater than that observed during GHRH plus placebo (P < 0.05). After cross-over, however, during the second year of therapy, we did not observe any significant differences in growth velocity between the two groups (4.2 +/- 1.4 vs. 3.9 +/- 0.8 cm/yr during treatment with GHRH plus placebo and GHRH plus atenolol, respectively). The mean 24-h serum GH levels were 1.4 +/- 0.9 micrograms/L during the baseline period, 1.3 +/- 0.2 and 2.0 +/- 1.4 micrograms/L during the first year of GHRH plus placebo and GHRH plus atenolol, respectively (P = NS), and 2.7 +/- 1.4 and 1.4 +/- 0.4 micrograms/L during the second year of GHRH plus placebo and GHRH plus atenolol, respectively (P < 0.05). This is the first demonstration that alteration of neurotransmitter action can enhance the therapeutic response to a hypothalamic releasing factor.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1993

Chromatographic, immunochemical and electrophoretic studies of human uterotrophic placental factor (hUTPF).

The human uterotrophic placental factor (hUTPF) is a protein obtained from human term placentae and acts on uterine growth, mammary gland, and blastocyst development and implantation. In the present work, we further define some molecular characteristics of hUTPF using chromatographic, electrophoretic and immunochemical methods. It is concluded that in human term placenta a high molecular weight hUTPF is present, bound to albumin and immunoglobulins, which could represent a storage or transport form of this factor. hUTPF presents several molecular forms, one of them of 270 kDa and others of approximately 90 kDa and 27 kDa.

Animals↗
PubMedDate not supplied

GH-IGF axis during catch up growth in small for gestational age (SGA) infants.

The hormonal profile in 47 small for gestational age (SGA) term newborns during their first year of life was studied. The newborns had a mean birth weight of 2290 +/- 230 g and a length of 45.5 +/- 2.0 cm, and they were followed up every month. Serum IGF-I, IGF-II, and urinary growth hormone (u-GH) concentrations were measured at 3 days of age and every 3 months during one year. Serum IGFBP-3 levels were measured at 3 and 6 months of age. Catch up growth (CUG) was defined as an increase in length z score greater than 1 SD between birth and 6 months of age. According to this definition, 27 infants (57.4%) experienced CUG. We compared the hormonal profile of the infants who demonstrated evidence of CUG [CUG(+)] with those who did not [CUG(-)]. Serum IGF-II levels were significantly higher in CUG(+) infants compared to CUG(-) infants at 3 months of age. We did not find any differences in serum IGF-I, IGFBP-3 and urinary GH between CUG(+) and CUG(-) infants at any time during the study.

Birth Weight↗
PubMedDate not supplied

[Goiter and chronic lymphocytic thyroiditis].

Sixty patients with goiter, aged 3 to 16 years, 58 girls, were studied for evidence of chronic lymphocytic thyroiditis (CLT). Thirty eight patients, 63%, presented two or more diagnostic elements of TLC, according to Fisher's criteria, with a high frequency of thyroid function involvement (47.4% had hypothyroidism and 18.4% had hyperthyroidism). The rest of the patients with diffuse goiter (37%) did not meet Fisher's criteria, they were mostly euthyroid (95%) and they were designated "non thyroiditis goiter". All patients with probable CLT had positive antimicrosomal antibodies at relatively high titer (greater than 1 x 600 in 71% of the cases) and 32% of them had both antimicrosomal and antithyroglobulin antibodies. In the "non thyroiditis goiter" group we found 28% of children with positive antimicrosomal antibodies at low titers (1 x 100 and 1 x 400, respectively). In a control group of 28 children of similar ages, without endocrine diseases neither familiar history of thyroid diseases only 3 (11%) cases showed positive antimicrosomal antibodies, always at low serum titers.

Adolescent↗