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Biomedical subjects

E O Reiter

Publications and source records attributed to E O Reiter.

At least 19 recordsLinked to original sources
PubMed1993

Serum bioactive luteinizing and follicle-stimulating hormone concentrations in girls increase during puberty.

FSH plays an essential role in folliculogenesis and ovarian growth. However, cross-sectional studies have not shown an increase in bioactive FSH (B-FSH) during puberty. To eliminate intersubject variability, we used a longitudinal design and tested the hypothesis that B-FSH increases during puberty. Thirty normal, healthy girls were enrolled in a longitudinal study from pubertal stages I to IV. The subjects were evaluated at 6-mo intervals; each visit consisted of pubertal staging, bone age determination by x-ray, measurements of serum immunoreactive FSH (I-FSH) and B-FSH (n = 14) or immunoreactive LH (I-LH) and bioactive LH (B-LH) (n = 18), and adrenal and ovarian steroids. All girls had clinical and hormonal characteristics of puberty. Both I-FSH and B-FSH levels were relatively elevated before puberty, whereas serum I-LH and B-LH were low. From pubertal stages I to III, there was a modest yet significant rise in serum I-FSH (p < 0.001) and serum B-FSH (p < 0.01). Serum I-LH and B-LH concentrations showed the expected increases with puberty (p < 0.001), with serum B-LH concentrations exhibiting a greater rise than I-LH (p < 0.001). Our results demonstrate that serum B-FSH and I-FSH increase during puberty. Relatively elevated B-FSH concentrations from early to midpuberty may be an important factor for ovarian growth while circulating LH and estrogen are still low. As puberty progresses, the continued and selective increase in LH induces a rise in estradiol and ultimately leads to ovulation.

Adolescent↗
PubMed1993

Serum bioactive gonadotropins during male puberty: a longitudinal study.

To evaluate the relative changes in serum bioactive (B) and immunoreactive (I) plasma gonadotropin concentrations during pubertal maturation, 28 healthy boys were enrolled at Tanner stage I and followed at 6-month intervals until achievement of Tanner stage V of pubertal maturation. At each visit, a careful interview, complete physical examination, sexual maturation staging, and bone age x-ray study were done, and a blood sample was obtained. Serum concentrations of PRL, dehydroepiandrosterone, and its sulfate, delta 4-androstenedione, estrone, estradiol, and testosterone (T) were determined by RIA. Samples from 20 boys were assayed for I-LH by RIA and for B-LH by the rat interstitial cell testosterone production assay, using 2 standards [Second International Reference Preparation-Human Menopausal Gonadotropin (2nd IRP-hMG) and LER 960]. Samples from 11 boys (3 from LH group and 8 others) were assayed for I-FSH by RIA and B-FSH by the rat Sertoli cell aromatase induction assay. The results were analyzed by regression analysis for B and I LH and FSH by Tanner stages of puberty, and by correlation of B to I LH and FSH as well as B and I LH and FSH to T. The results from both LH standards correlated well to each other (r = 0.967 and 0.882 for B- and I-LH, respectively), and the data are presented for 2nd IRP-hMG standard. In both groups of boys serum T concentrations increased progressively with pubertal development (P < 0.001). The boys bone age, testicular volume, serum T, dehydroepiandrosterone sulfate, dehydroepiandrosterone, delta 4-androstenedione, estrone concentrations correlated well with pubertal maturation, similar to previously published data and indicate that this group of boys had progressed through puberty in the expected normal manner. Mean serum I-LH concentrations increased progressively from Tanner stage I to V of puberty (P < 0.001), and serum B-LH exceeded the increase in serum I-LH levels. Mean serum I-LH concentrations were 2.0 +/- 0.1, 2.9 +/- 0.2, 4.7 +/- 0.4, 6.7 +/- 0.7, and 10.4 +/- 2.0 IU/L 2nd IRP-hMG whereas mean serum B-LH concentrations were 0.8 +/- 0.1, 2.2 +/- 0.2, 5.9 +/- 0.2, 10.3 +/- 1.2, and 22.3 +/- 3.8 IU/L 2nd IRP-hMG for Tanner stages I-V of puberty, respectively. This resulted in a progressive increase of LH B/I ratio with advancing pubertal maturation (P < 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗
PubMed1992

The influence of diabetes mellitus on cardiovascular function in children and adolescents.

Early manifestations of non-atherosclerotic cardiomyopathy, a recognized complication of diabetes in adults, have been suggested to contribute to depressed levels of aerobic fitness described in children and adolescents with this disease. This study measured components of aerobic fitness and cardiovascular function during maximal cycle ergometer exercise in 11 insulin-dependent diabetic boys aged 10.2-16.5 years. Mean duration of diabetes was 4.5 years. Eleven non-diabetic subjects matched for age, body size, and regular physical activity served as controls. No differences in maximal oxygen uptake or heart rate were observed between the two groups, nor were any significant differences recorded in submaximal stroke volume, cardiac output, heart rate, and pressure-rate product. This study failed to reveal any evidence of functional myocardial disease in children and young adolescents with diabetes, suggesting that manifestations of diabetic cardiomyopathy should not be expected during the pediatric years. Moreover, these findings indicating normal cardiovascular function in young diabetic subjects imply that regular levels of habitual physical activity are more likely to affect aerobic fitness in these patients rather than influences of the diabetic state itself.

Adolescent↗
PubMed1992

Serum growth hormone (GH)-binding protein/receptor: an important determinant of GH responsiveness.

Individual growth rates (or responses to GH therapy) and adult heights vary over a wide range. The reasons for this variation are poorly understood. Based on the reciprocal relationship between GH production and serum GH-binding protein/receptor (GH-BP), we hypothesized that genetic growth potential was achieved by a specific combination of GH-BP/receptor and GH production in each individual. To address the question whether GH production regulates GH-BP, or vice versa, we studied GH-deficient children, where one of the parameters, GH exposure, could be controlled through exogenous administration. Forty-three untreated prepubertal GH-deficient children were studied before and after 6 and 12 months of GH replacement therapy (0.18 mg/kg.week). Growth velocity, height, bone age, weight and their respective Z scores, serum GH-BP, and serum insulin-like growth factor I (IGF-I) were measured at each time point. The patients responded with significant increases in serum IGF-I, age-adjusted growth velocity, and height (P < 10(-6) for all). Before therapy, GH-BP correlated directly with chronologic and bone age (P < 10(-4), but not with either growth velocity or IGF-I. In contrast, GH-BP correlated strongly with the response to therapy whether assessed as the incremental change in IGF-I (P < 10(-6)) or as the increase in growth velocity (P approximately 0.003). GH treatment had no consistent effect on GH-BP/receptor levels. These findings support the concept that the GH-BP/receptor endowment is characteristic for an individual and plays a pivotal role in somatic growth. The GH-BP/receptor system and its ontogeny appears relatively independent of regulation by GH. Differences in individual GH-BP/GH receptor complement account for some of the variability in the response to GH, and GH-BP levels may serve as a predictor for the degree of response. The reciprocal relationship between GH production and GH-BP in normal subjects probably results from adjustment of GH secretion to accommodate the prevailing GH-BP/receptor environment.

Adolescent↗
PubMed1992

The role of body mass in the response to growth hormone therapy.

Obesity is associated with normal or increased growth despite diminished GH secretion compared to lean children. The mechanism by which adequate growth is maintained in the presence of low GH levels is unknown, but is possibly mediated at the GH receptor level. To probe this hypothesis, we examined the relationship between GH responsivity, body mass index (BMI) and plasma GH-binding protein (GH-BP)/receptor level in 43 GH-deficient children during treatment with a fixed dose of GH (0.18 mg/kg.week). Before treatment, BMI [expressed as standard deviation score (SDS) for age (BMI-SDS)] did not correlate with either growth velocity or serum insulin-like growth factor-I (IGF-I). In contrast, after 12 months of GH therapy BMI-SDS correlated directly with plasma IGF-I (P < 10(-5)) and growth velocity (P < 10(-3)). These findings parallel those obtained for GH-BP vs. the response to GH, suggesting that BMI and GH-BP are covariants. The interrelationships among BMI, GH-BP, and response to GH were further probed by multiple regression analysis. Partial correlation coefficients vs. response to GH were consistently stronger for GH-BP than for BMI-SDS, indicating that GH-BP is the dominant factor between these two covariants in determining responsiveness to GH. The data suggest a primary role for GH-BP/receptor levels in determining GH action, with secondary but significant effects of nutrition and degree of adiposity. The latter may be mediated through the impact of nutrition and body mass on GH-BP/receptor levels.

Body Height↗
PubMed1992

Urinary excretion of IGF-I and growth hormone in children with IDDM.

OBJECTIVE: To compare the urinary output of insulinlike growth factor I (IGF-I) and growth hormone (GH) in prepubertal and pubertal children with insulin-dependent diabetes mellitus (IDDM) versus nondiabetic subjects and to analyze the relationship between the urinary excretion of these peptides and degree of metabolic control. RESEARCH DESIGN AND METHODS: Group 1 included 30 IDDM patients who had had diabetes for 4.9 +/- 0.7 yr and had normal renal function (mean age 11.6 +/- 0.9 yr); group 2 consisted of 31 control subjects (mean age 9.2 +/- 0.6 yr). Sensitive radioimmunoassays were used to measure IGF-I and GH in urine aliquots from 12-h timed overnight collections that had been dialyzed, concentrated 50-fold, and lyophilized. RESULTS: Significantly lower IGF-I and GH outputs per kilogram body weight per 12 h were observed in IDDM subjects compared with control subjects. When data were expressed per kilogram of body weight, no difference was observed between the urinary output of IGF-I and GH between prepubertal and pubertal subjects within group 1 or group 2. The prepubertal children had significantly lower HbA1 than the pubertal population; however, no correlation was found between urinary output of IGF-I or GH and HbA1. A positive correlation was observed between urinary IGF-I and GH (r = 0.85, P less than .001). CONCLUSIONS: Patients with long-standing IDDM excrete significantly lower urinary levels of IGF-I and GH compared with normal subjects. Serial measurements of these peptides from onset of IDDM are needed to define whether the changes observed are present at diagnosis or are secondary to duration of disease.

Child↗
PubMed1991

Growth hormone therapy in hypophosphatemic rickets.

The effects of growth hormone therapy on the biochemical measures of bone metabolism were studied in 11 children aged 3.5 to 17 years who had familial hypophosphatemic rickets; five were male. Subjects were maintained on a regimen of stable doses of conventional therapy (calcitriol and phosphate). Subjects were studied at baseline receiving conventional therapy and during three sequential treatment periods: no therapy (4 weeks), growth hormone only (0.05 mg/kg per day for 4 weeks), and conventional therapy plus growth hormone (2 weeks). The nine youngest subjects were continued on a regimen of triple therapy for an additional 24 weeks. Serum phosphate averaged 0.93 +/- 0.13 mmol/L (mean +/- SD) at entry and decreased when the subjects were not receiving any therapy. During the 4 weeks of growth hormone only treatment, phosphate rose in all 11 subjects (0.70 +/- 0.08 mmol/L to 0.83 +/- 0.08 mmol/L). With triple therapy, phosphate remained higher than with no therapy. Calcitriol, osteocalcin, and parathyroid hormone increased as the subjects received growth hormone alone. Insulinlike growth factor I z scores rose significantly in response to growth hormone therapy alone. All nine subjects receiving 6 months of triple therapy increased their growth rate z scores. Exogenous growth hormone therapy may be useful in familial hypophosphatemic rickets.

Adolescent↗
PubMed1991

Pubertal growth and growth hormone secretion.

A dramatic increase in linear growth velocity, often referred to as the pubertal growth spurt, is a central feature of pubertal development. Despite the existence of numerous investigative attempts, a precise understanding of the hormonal events subserving this process has proved elusive. Nevertheless, evidence has gradually accumulated that indicates that sex steroid-induced modulation of growth hormone secretion is a central and critical feature of the pubertal growth spurt. As a result, disorders of either growth hormone or sex steroid hormone production may result in clinical growth disorders during puberty.

Body Height↗
PubMed1990

Pharmacological testing of growth hormone secretion.

The laboratory confirmation of growth hormone (GH) deficiency (GHD) has been extensively studied. Multiple stimuli induce GH release, but insulin-induced hypoglycemia usually is considered the 'gold standard'. Seventy-five to 90% of normal children have significant increments of hGH to any single test. Complete and partial syndromes of GHD have been defined, but some patients with a clinical appearance of GHD release hGH during provocative testing. Discordant results on varied tests may occur in the same child. Sequential and simultaneous tests have been attempted with diverse time patterns; testing sequence may significantly affect data interpretation. Persistent problems with GH provocative tests remain: normal data not strictly defined throughout childhood, multiple tests with discordant results, and substantial discrepancies of immunopotency estimates with different radioimmunoassays. Some children with 'normal' hGH increments during provocative tests, despite clinical GHD, may require short-term treatment with hGH to finally establish the diagnosis.

Arginine↗
PubMed1989

Increased insulin-like growth factor I binding to red blood cells of normal prepubertal children.

Young children are growing at a time when circulating levels of IGF-I measured by RIA are generally less than or equal to values in nongrowing adults. 125I-Thr59-IGF-I binding to receptors on conveniently available red blood cells was studied in 33 normal adults (nine males, 24 females) and 13 normal prepubertal children aged 3-10 y (10 boys, three girls; all Tanner stage 1). Red blood cell specific binding of 125I-Thr59-IGF-I was determined by displacement of labeled Thr59-IGF-I by unlabeled Thr59-IGF-I or insulin in a dose-dependent manner. Mean (+/- SEM) 125I-Thr59-IGF-I specific binding was significantly higher (p = 0.01) in prepubertal children than in adults (13.9 +/- 0.7% versus 11.6 +/- 0.5%/3 x 10(9) cells/mL). Specific binding did not differ between adult males and females. There was no significant correlation between specific binding and reticulocyte count. Scatchard analysis demonstrated a linear plot. Increased binding to red blood cells in the prepubertal children appeared to be due to an increase in receptor affinity (Ka = 4.97 +/- 0.42 x 10(8) M-1 versus 3.70 +/- 0.41 x 10(8) M-1; children versus adults; p = 0.03). Mean receptor concentrations were not different in children and adults (64.4 +/- 8.5 versus 58.0 +/- 5.6 binding sites/cell). There was a significant positive correlation between 125I-Thr59-IGF-I specific binding and affinity (p = 0.007, r = 0.39). We speculate that the greater specific binding of labeled Thr59-IGF-I to red blood cells in prepubertal children may provide a mechanism for enhanced cellular responsiveness to relatively low levels of circulating IGF-I.

Adult↗
PubMed1989

Absence of nonclassical congenital adrenal hyperplasia in patients with precocious adrenarche.

We studied 31 patients (28 girls and 3 boys), ranging in age from 3.2-7.9 yr, with precocious adrenarche defined by the presence of early sexual hair development, no signs of virilization, and bone age within +3 SD of the mean for chronological age. To determine if this symptom complex stemmed from any form of nonclassical (late-onset) congenital adrenal hyperplasia, an ACTH stimulation test was performed on each patient using a standard 0.25-mg dose of Cortrosyn, given as an iv bolus. Twelve pubertal children (7 girls and 5 boys) and 18 prepubertal children (11 girls and 7 boys) served as normal controls. Baseline and stimulated 17-hydroxypregnenolone (17-OHPreg), 17-hydroxyprogesterone, (17-OHP), 11-deoxycortisol, dehydroepiandrosterone, androstenedione, testosterone, and cortisol levels were measured. Using published nomogram standards for serum 17-OHP response to ACTH, no child with precocious adrenarche was diagnosed as having nonclassical 21-hydroxylase deficiency. Eight girls, however, had a stimulated 17-OHP value that exceeded the mean response for pubertal and prepubertal controls by more than +2 SD [range, 295-670 ng/dL (8.94-20.3 nmol/L)]. Stimulated 11-deoxycortisol values [less than 400 ng/dL (11.6 nmol/L)] ruled out any cases of nonclassical 11 beta-hydroxylase deficiency. No patient had nonclassical 3 beta-hydroxysteroid dehydrogenase deficiency, as defined by both the stimulated 17-OHPreg and the 17-OHPreg/17-OHP ratio to be more than +2 SD above the mean for pubertal children [1354 ng/dL (41.0 nmol/L) and 10.4, respectively]. In conclusion, we could not provide any biochemical evidence for nonclassical congenital adrenal hyperplasia in a large group of children with precocious adrenarche.

17-alpha-Hydroxypregnenolone↗
PubMed1988

Diagnostic value of the growth hormone-releasing factor stimulation test.

Growth hormone (GH) responses to growth hormone-releasing factor (GRF) were evaluated in 55 children with growth failure. The study groups consisted of group 1, severe GH deficiency; group 2, partial GH deficiency; group 3, patients with prior cranial radiation for nonpituitary brain tumors; and group 4, children with idiopathic growth failure. Children in group 1 were unresponsive to GRF (mean GH peak +/- SEM, 1.6 +/- 0.5 ng/ml). Higher GH responses to GRF were observed in both groups 2 (17.2 +/- 4.1 ng/ml) and 3 (10.4 +/- 2.8 ng/ml). The highest GH responses to GRF were observed in group 4 (35.9 +/- 4.3 ng/ml). ANOVA revealed a significant difference between groups (F = 12.9; df = 3; p less than 0.01), and further analysis by the Scheffe and Student-Newman-Keuls tests revealed that group 4 was significantly higher than groups 1, 2, or 3 (p less than 0.05). These data suggest that GRF unresponsiveness is a reliable predictor of severe GH deficiency. In patients with partial GH deficiency or idiopathic growth failure, the GRF gives semiquantitative information about somatotrope responsivity to exogenous stimulation.

Adolescent↗
PubMed1988

Variable estimates of serum growth hormone concentrations by different radioassay systems.

Many different assays are being used to measure serum GH concentrations in children with disorders of growth. We assessed four readily available methods to determine the comparability of the immunopotency estimates: standard double antibody RIA with pituitary standards from the National Hormone and Pituitary Program (assay 1) and from a commercial source (assay 2), a double antibody RIA with serum standards (assay 4), and a commercial immunoradiometric assay (assay 3). There was a high degree of relative correlation between assays (r = 0.95-0.98), but absolute potency estimates differed. Assays 1 and 2 were almost identical. Assay 3 yielded serum GH levels about 65% those of assay 1 or 2 and 80% those of assay 4. Assay 4 gave intermediate values between the low readings in assay 3 and higher values in assay 1 and 2. We conclude that substantial variation occurs in potency estimates in different GH assays. Such differences can affect the interpretation of many GH provocative and sampling studies.

Child↗
PubMed1987

Neuroendocrine control processes. Pubertal onset and progression.

This discussion has outlined current concepts in neuroendocrinologic control of pubertal onset and progression. Central nervous system regulation of the arcuate nucleus (ventromedial hypothalamus) pulse generator that subsequently controls pituitary gonadotropin synthesis and secretion has been highlighted. Significant investigative issues that deserve assessment in the next several years include the following: 1. Systematic neuropharmacologic, electrophysiologic, and anatomic assessment of the hypothalamic arcuate nucleus. These assessments would include the use of recombinant DNA technology to probe cellular regulation of GnRH production. 2. Physiologically oriented examination of hypothalamic GnRH synthesis and secretion, along with function in the remaining reproductive endocrine system, during situations of nutritional impairment and excessive energy utilization and psychologic stress. 3. Further assessment of the neurophysiologic inhibition of GnRH production during childhood and the late prepubertal reactivation of the arcuate nucleus pulse generator. Roles of opioids, dopamine, other neurotransmitters, and metabolic signals remain to be clarified. 4. Exploration of regulators of hypothalamic, pituitary, and gonadal function when pulsatile GnRH administration has replaced the usual hypothalamic mechanisms. Pituitary-gonadal interactions may be independently assessed. 5. Assessment of pubertal growth, endocrine function, and neuropharmacologic control mechanisms in circumstances of chemical removal of pituitary gonadotrope function by GnRH agonists or antagonists. 6. Concordance and discordance of potency estimates of gonadotropins made by bioassay and immunoassay. The biologic basis for qualitative changes in bioassayable levels of LH and FSH, often related to carbohydrate content of the glycoprotein, may help to explain changes of gonadal function during the pubertal process. The potential for significant molecular heterogeneity of the gonadotropins is recognized and suggests substantial posttranslational changes of LH and FSH. 7. A cogent delineation of the hormonal, nutritional, and energy regulators of the pubertal growth spurt, though not discussed in this manuscript, remains to be accomplished. The relationship between pituitary gonadotropins and growth hormone, sex steroids, and the various peptide growth factors, especially the relationship between the growth factors and intragonadal steroidogenesis and germ-cell production, remain to be resolved. The importance of local production and action of peptide-growth factors in diverse tissues, skeletal and other, is being increasingly recognized.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1987

Pulsatile release of bioactive luteinizing hormone in prepubertal girls: discordance with immunoreactive luteinizing hormone pulses.

An assessment of pulsatile secretion of luteinizing hormone (LH), measured by both immunoassay (I-LH) and rat interstitial cell testosterone production bioassay (B-LH), as well as of follicle-stimulating hormone and glycoprotein hormone alpha-subunit was carried out in seven normal prepubertal and six normal premenarcheal pubertal girls. Samples were obtained at 20-min intervals for a 6-h period. The hormone secretion profiles were analyzed by several computerized methods yielding pulse frequency and amplitude, interpulse basal levels, and percentage increments, with bio/immuno ratios calculated for peak and basal concentrations. In these prepubertal girls, mean B-LH levels were 12% of I-LH, with B/I ratio of 0.13; 30% of samples were below assay sensitivity (0.10 mIU/ml) for B-LH, but all I-LH (1.25 mIU/ml) were detectable. In the pubertal group, B-LH levels were 30% of I-LH, with mean B/I ratio of 0.24 and undetectable B-LH in 29% of samples. Pulsatile secretion in prepubertal girls was found in five of seven (1/150 min) for B-LH and six of seven (1/212 min) for I-LH; only two of six pubertal girls had detectable pulses. Discordance of B- and I-LH pulses were frequent, with 56% of B-LH pulses lacking an I-LH pulse and 47% of I-LH pulses not having a B-LH pulse. These data demonstrate that both B- and I-LH are secreted episodically in prepubertal girls; I-LH-like material is present in higher concentrations than B-LH in these girls; and substantial discordance of B- and I-LH pulses exist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗