Reduction of plasma cortisol levels in childhood obesity.
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Adolescent↗
Biomedical subjects
S A Chalew
Publications and source records attributed to S A Chalew.
Does growth hormone influence the severity of phosphopenic rickets?
The severity of bone disease in phosphopenic rickets is not correlated with serum phosphate levels. In order to determine whether growth hormone (GH) secretion may influence rachitic changes, we evaluated the 24 h integrated concentration of growth hormone (IC-GH) in five children with phosphopenic rickets. Two patients with marked clinical and roentgenographic rachitic abnormalities had normal IC-GH levels. In contrast, three patients with low IC-GH levels had mild rachitic changes. We suggest that the level of spontaneous GH secretion may be one factor which influences the severity of phosphopenic rickets.
Adolescent↗
Cornstarch ingestion after oral glucose loading: effect on glucose concentrations, hormone response, and symptoms in patients with postprandial hypoglycemic syndrome.
In susceptible individuals ingestion of glucose can lead to clinical symptoms of hypoglycemia as well as a reflex rise of counterregulatory hormones. We hypothesized that cornstarch, a slowly absorbed starch, might prevent hypoglycemic-symptom episodes. Eight patients who had characteristic signs, symptoms, and reflex hormonal responses of hypoglycemia at the glucose nadir after ingesting 75 g glucose (OGTT) participated. Patients ingested 75 g glucose followed by 75 g raw cornstarch (OGTT + CS). None of the patients reported symptoms or had signs of hypoglycemia in response to OGTT + CS. The glucose nadir concentration during OGTT + CS (3.8 +/- 0.6 mmol/L) was significantly higher than during OGTT (3.2 +/- 0.6; P less than 0.03). The responses of cortisol (331 +/- 166 nmol) and epinephrine (491 +/- 589 pmol/L) at the glucose nadir during OGTT + CS were significantly lower than the responses of cortisol (524 +/- 193 nmol/L; P less than 0.003) and epinephrine 1834 +/- 1135 pmol/L (P less than 0.0005) during OGTT. A slowly absorbed starch such as cornstarch may be an effective component in dietary management of this disorder.
Administration, Oral↗
Assessment of growth hormone secretion in normal stature children using 24-hour integrated concentration of GH and pharmacological stimulation.
The integrated concentration of serum GH (IC-GH) is used for the assessment of spontaneous GH secretion. In order to use the IC-GH as a diagnostic tool a normative reference range needs to be established. We determined the IC-GH by continuous blood withdrawal in 119 children of normal height, weight and growth rate. Although the mean IC-GH increased with pubertal status, 4.4 +/- 1.2 micrograms/L at Tanner I (n = 36), 5.5 +/- 2.1 micrograms/L at Tanner II-III (n = 43), and 5.8 +/- 1.6 at Tanner IV-V (n = 40) (P less than 0.03), there was a considerable overlap of individual IC-GH levels between the pubertal groups. Gender affected the mean IC-GH level slightly, but not the range. Although the mean IC-GH of girls tended to be higher than that of boys this difference was not statistically significant. Ninety five percent of the IC-GH values were above the 3.2 micrograms/L level. The response to pharmacological stimulation (clonidine, insulin, or arginine) was also evaluated in 68 of the subjects. The peak GH response to pharmacological stimulation (micrograms/L) with clonidine 21.0 +/- 10.7 (n = 66) was significantly higher than to either arginine 13.1 +/- 6.1 (n = 23) or insulin 14.2 +/- 6.3 (n = 19) (P less than 0.01). The peak response to clonidine increased significantly with pubertal status (P less than 0.001) and there was an interactive effect of gender and pubertal stage where the GH response of prepubertal boys exceeded that of prepubertal girls but the response of pubertal girls exceeded that of pubertal boys (P less than 0.02). The peak stimulated GH levels was correlated with IC-GH in this subgroup r = 0.52, P less than 0.0001). This study provides a large normative data base for IC-GH and the GH provocative tests in normally growing children of varying pubertal status.
Adolescent↗
Hypocortisolemia in children undergoing evaluation for growth hormone deficiency.
The group of children who have clinical manifestations of GH deficiency may potentially contain a large number of patients with secretory defects of cortisol. We assessed physiological cortisol secretion by measuring the 24-h integrated concentration of cortisol (IC-F) in a series of 105 patients, aged 7-19 yr, undergoing endocrinological evaluation for growth impairment possibly due to GH deficiency. The reference value for IC-F, established from 30 normal stature, normal weight children (controls), aged 7-18 yr, was 157 +/- 41 nmol/L (mean +/- 1 SD). There was no effect of age, gender, or pubertal status on IC-F in controls. The IC-F of patients was 150 +/- 72 nmol/L. Twelve patients (11%) had IC-F values more than 2 SD below the mean (i.e. less than 75 nmol/L) of the controls (P less than 0.001). An IC-F below 75 nmol/L was associated with a blunted peak cortisol response to insulin-induced hypoglycemia (367 +/- 160 nmol/L compared to 464 +/- 155 nmol/L in the other patients; (P less than 0.05). None of the patients had obvious clinical symptoms of hypocortisolemia at the time of testing. In general, IC-F levels were not correlated with IC-GH. However, 10 patients who had subnormal IC-F values also had laboratory evidence of GH secretory defects; 7 had subnormal IC-GH levels but normal stimulated GH responses, and 3 had both subnormal responses to stimulation as well as subnormal IC-GH. The long term prognosis and management implications of hypocortisolemia diagnosed in this patient group require further evaluation.
Adolescent↗
Reproducibility of growth hormone testing procedures: a comparison between 24-hour integrated concentration and pharmacological stimulation.
The purpose of this study was to compare the reproducibility of two approaches to the evaluation of GH secretion: the integrated concentration of GH (IC-GH), a physiological test of GH secretion, and pharmacological stimulation tests. IC-GH was determined in 40 poorly growing children twice within 4 weeks. The first and second IC-GH were highly correlated r = 0.859, P less than 0.001. One hundred and thirteen poorly growing children underwent pharmacological GH stimulation tests twice within 6 weeks. A moderate correlation was found between the first and second pharmacological test r = 0.524, P less than 0.01. Among the three pharmacological stimuli studied, clonidine (n = 81) had the highest reproducibility followed by arginine (n = 20), and insulin (n = 12). We conclude that IC-GH is more consistently reproducible than the GH response to repeated pharmacological stimulation.
Adolescent↗
Evidence for elevated glucose threshold in patients with impaired glucose tolerance and symptoms of hypoglycemia during OGTT.
We evaluated the relationship between hypoglycemic symptoms, glucose nadir levels, and hormone changes in patients with impaired glucose tolerance (IGT) after an oral glucose tolerance test (OGTT). The peak counterregulatory hormone response was determined at the glucose nadir identified by continuous glucose monitoring. Eight patients with IGT who had symptoms and signs typical of hypoglycemia at the glucose nadir were compared with completely asymptomatic subjects (5 IGT patients and 13 patients who had normal glucose tolerance [NGT]). The mean glucose nadir of symptomatic IGT patients was 3.50 +/- 0.46 mM, which was not statistically different from the mean of asymptomatic NGT patients (4.10 +/- 0.56 mM) but was significantly lower than that for asymptomatic IGT patients (5.10 +/- 0.81 mM, P less than 0.001). Seven of 8 symptomatic IGT patients had glucose levels that never fell below the range of glucose nadirs for asymptomatic NGT patients. However, the symptomatic IGT group had significantly higher levels of growth hormone, cortisol, epinephrine, and norepinephrine than the asymptomatic groups in response to the nadir. We conclude that patients with IGT are capable of experiencing signs and symptoms of hypoglycemia at physiological glucose levels during OGTT with reflex stimulation of counterregulatory hormone release. This may indicate that symptomatic IGT patients have a higher glucose threshold for eliciting characteristic hypoglycemic symptom episodes than individuals with NGT.
Adult↗
Quantitative monitoring of brain function, vital signs, and hormonal response during acute insulin-induced hypoglycemia.
Acute insulin-induced hypoglycemia provokes changes in central nervous system activity and release of counterregulatory hormones. The clinical relationship between central nervous system activity, hormone secretion, and vital signs has not to our knowledge been previously reported. We used computerized electroencephalographic (CEEG) analysis to monitor 5 nondiabetic subjects during acute insulin-induced hypoglycemia (0.75 U/kg intravenous push). Their glucose nadir was 38 +/- 6 mg/dl (mean +/- 1 SD). A three-phase pattern of change in CEEG power in response to hypoglycemia was observed: phase 1 was characterized by an increase in total CEEG power (natural log of activity = 9.1 +/- 1.3 microV2) over baseline (8.7 +/- 1.2 microV2) in the theta, delta, and beta frequency bands. This phase preceded and coincided with the glucose nadir. During phase 2, power in all frequency bands fell significantly below baseline. A nadir in CEEG power (8.0 +/- 1.6 microV2) occurred 40 to 55 minutes after insulin injection as glucose levels were rising. During phase 3 there was a return to baseline in CEEG power and frequency spectra. Heart rate increase just before phase 1; peak heart rate (91 +/- 8 beats/min) coincided with peak CEEG power and was significantly higher than basal rate (71 +/- 11, P less than 0.05). A significant increase in respiratory rate occurred during phase 1 of the CEEG and persisted through phase 2. A significant decrease in mean blood pressure (nadir = 73 +/- 6 mm Hg) below preinsulin blood pressure (81 +/- 8 mm Hg, P less than 0.05) coincided with the nadir of CEEG power in phase 2.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Tumor-induced osteomalacia and rickets.
Tumor-induced osteomalacia is a clinicopathological entity in which vitamin D-resistant osteomalacia or rickets occurs in association with a tumor. A total of 72 cases (three current, 69 from review of literature) has been reported to date. Men and women are equally affected. The majority are adults over 30 years old who exhibit progressive lower leg and back pain. Forty bone and 31 soft-tissue tumors were responsible for this syndrome; two-thirds occurred in the extremities. Chemical findings are typical: low serum phosphorus, normal serum calcium, and elevated alkaline phosphatase. Serum levels of 1,25-dihydroxyvitamin D were low or undetectable. Histologically, more than a third were classified as vascular tumors, and half of these cases were hemangiopericytomas that were distributed equally between bone and soft tissues. Other common diagnoses included nonossifying fibromas, "mesenchymal" and giant-cell tumor variants. Features common to all tumors were prominent vascularity, and giant and primitive stromal cells. Only 10 were histologically malignant. Ultrastructural studies have not shown any secretory granules suggestive of a hormone-secreting tumor. It is clear, however, that the tumor is responsible for the osteomalacia because the complete removal generally results in a dramatic reversal of all symptoms and signs.
Adolescent↗
Surgically curable hypophosphatemic rickets. Diagnosis and management.
Childhood hypophosphatemic rickets (HR) is most often caused by a defect in renal tubular resorption of filtered phosphorus. However, HR can also be caused by secretion of a phosphaturetic factor from a tumor. The presentation of patients with the different HR syndromes may be identical. Distinguishing between the HR syndromes is essential, however, because HR caused by renal defect requires life-long therapy with Vitamin D and phosphate replacement, but tumor-associated HR is cured by removal of the tumor. A case of hemangiopericytoma occurring in bone and causing HR is reported. Children with HR typically have normal levels of serum calcium and parathyroid hormone but very low levels of serum phosphorus. In a child with HR, the following features should prompt a thorough evaluation for a causative tumor: lack of other family members who have hypophosphatemia; presence of aminoaciduria, particularly glycinuria. Causative lesions are most commonly found in the bone or skin.
Child↗
Growth without growth hormone: the "invisible" GH syndrome.
Growth hormone (GH) deficiency, diagnosed by radioimmunoassay (RIA) measurements of GH in blood after provocation or in continuous 24 h samples of venous blood, is usually associated with growth failure. 4 non-obese boys have been identified who had normal linear growth despite apparent GH deficiency by standard RIA. All 4 patients had normal GH concentrations as measured with an IM-9 cell radio-receptor assay (RRA). The RRA/RIA ratio of the 4 patients significantly exceeded that of controls. Thus, these patients secrete a molecule with normal GH receptor binding and bioactivity which is "invisible" to the standard GH RIA. This variant GH is possibly expressed from the human GH-V gene or a mutant allele.
Acromegaly↗
The effect of testosterone therapy on spontaneous growth hormone secretion in boys with constitutional delay.
Testosterone treatment is known to improve growth hormone (GH) secretion in boys with constitutional delay (CD). To determine whether spontaneous GH secretion is normal after treatment, we assessed GH secretion before and after a four- to five-month course of testosterone enanthate in eight adolescents with CD. Before testosterone therapy, the mean (+/- 1 SD) 24-hour integrated concentration of GH (IC-GH) by constant blood withdrawal technique was 1.7 +/- 1.0 micrograms/L (normal range for age, 3.2 to 11.5 micrograms/L), and the IC-testosterone was 1.8 +/- 2.7 nmol/L. Two patients restudied during treatment had normal IC-GH values. After testosterone treatment, the mean IC-GH of the entire group was 3.3 +/- 2.6 micrograms/L, and the IC-testosterone was 6.5 +/- 5.3 nmol/L. Five of eight patients had IC-GH values that were again subnormal. A subnormal IC-GH associated with CD may persist after testosterone therapy is discontinued. Deficiency of spontaneous GH secretion may contribute to short stature and slower growth rates in this patient group. Whether GH therapy in these patients would have a beneficial effect on final height is unknown.
Child↗
Therapy in short children with subnormal integrated concentrations of growth hormone.
We evaluated the effect of growth hormone (GH) therapy on the posttreatment growth of 11 poorly growing children who had normal GH response to provocative stimuli but subnormal integrated concentrations of GH. Patients received 0.1 U/kg of GH three times per week. Their mean (+/- SD) growth rate increased from 3.3 +/- 1.0 cm/y before treatment to 6.5 +/- 1.4 cm/y after eight months of treatment. The growth rates of five patients declined to below 4.5 cm/y four months after treatment. Three of these patients resumed GH therapy and again responded with increased growth velocity (8.0 +/- 1.2 cm/y). After therapy, the growth rate of five remaining patients continued to be greater than 4.5 cm/y (6.8 +/- 1.4 cm/y). Two of these patients had entered puberty and their posttreatment growth rate might have been due to a pubertal growth spurt. The three prepubertal patients in this group had a gradual decline in growth velocity to 3.8 +/- 1.0 cm/y by the end of 12 posttreatment months. We conclude that maintenance of normal growth in patients with this pattern of GH deficiency is dependent on GH replacement therapy.
Adolescent↗
Ectopic calcitonin in adrenocortical carcinoma: a new tumor marker.
Ectopic calcitonin has never before been described in association with pediatric malignancy. This is the first report of ectopic calcitonin in a child with adrenocortical carcinoma. It may prove to be a useful tumor marker in this, as well as other childhood malignancies.
Adrenal Cortex Neoplasms↗
Linogliride fumarate, representing a new class of oral hypoglycemic agent for diabetes.
This study presents the first multiday therapy trial of linogliride fumarate, a representative of a new class of oral hypoglycemic agents. Linogliride demonstrated a significant hypoglycemic activity in 26 patients with non-insulin-dependent diabetes mellitus receiving 1 week of therapy. In a dose range of 150 to 400 mg b.i.d., fasting glucose levels fell from 237 +/- 52 mg to 199 +/- 59 mg by day 7 (P less than 0.01). Eight-hour glucose AUCs fell from 2121 +/- 617 mg/dl/8 hr baseline to 1781 +/- 631 mg/dl/8 hr on day 7 of treatment (P less than 0.01). This was associated with a significant increase in insulin AUC from 380 +/- 327 to 610 +/- 417 on day 7 (P less than 0.01). Thus its initial action appears to be by an insulin secretagogue mechanism. No patient had any major adverse effect. This initial study indicates that linogliride fumarate is an effective hypoglycemic agent that significantly lowers fasting and postprandial glucose levels with short-term use. Linogliride fumarate represents a new group of hypoglycemic agents that may be shown to have therapeutic utility.
Administration, Oral↗
Red blood cell Na+,K+-ATPase in men with newly diagnosed or previously treated essential hypertension.
Alterations of cellular function of Na+,K+-adenosine triphosphatase (ATPase; Na+-K+ pump) have been implicated in the pathophysiology of essential hypertension. Therefore, this aspect of red blood cell (RBC) Na metabolism was studied in black men with newly diagnosed, untreated essential hypertension (NEH) and a normotensive control group. RBC Na content, Na+-K+ pump number (ouabain binding sites), and pump activity were measured. No statistically significant differences were found between the two groups for any of these three parameters. However, a group of previously treated essential hypertensive subjects (PEH) who had been withdrawn from therapy in the preceding 6 weeks were also studied. This group differed significantly from the NEH subjects in regard to all RBC Na+-K+ pump parameters. Their RBC Na content (10.27 +/- 3.23 vs 7.77 +/- 2.52 mmol Na/LRBC; p = 0.006) was higher, and their Na+-K+ pump activity (166 +/- 50 vs 221 +/- 87 nmol inorganic phosphate/mg membrane protein/hr; p = 0.03) and Na+-K+ pump number (213 +/- 40 vs 284 +/- 85 binding sites/RBC; p = 0.001) were lower compared with those in NEH subjects. Although the PEH subjects were older and somewhat less hypertensive than their NEH counterparts, these factors were not found to influence the Na+-K+ pump parameters. These results indicate that chronic diuretic therapy of patients with essential hypertension is associated with a reduced number of RBC Na+-K+ pumps. Since RBCs are not considered target cells for diuretics, the effects of these drugs on RBC electrolyte metabolism may occur at the time of erythropoiesis by the production of RBCs with fewer Na+-K+ pumps.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Comparison of assays for growth hormone using monoclonal or polyclonal antibodies for diagnosis of growth disorders.
Current diagnostic standards for growth hormone deficiency were derived from measurement of growth hormone using polyclonal antibody assays. Recently, however, immunoassays using monoclonal antibodies to growth hormone have been commercially introduced. This study compares growth hormone levels obtained with two new monoclonal assays with levels obtained with a standard polyclonal assay. In 20 patients, the polyclonal assay (National Pituitary Agency) measured a mean growth hormone concentration of 14.0 +/- 10 (SD) ng/dl compared with monoclonal assay 1 (Hybritech) measurement of 10.4 +/- 7.2 ng/dl (P less than 0.01) and monoclonal 2 (Wellcome Co.) measurement of 18.9 +/- 9.8 ng/dl (P less than 0.01). The Hybritech monoclonal assay measured lower growth hormone levels than the polyclonal assay in all 20 patients. The Wellcome assay measured higher growth hormone levels than the polyclonal assay in 17 of 20 patients. There is not complete agreement between polyclonal and monoclonal antibody growth hormone assays in their measurement of plasma growth hormone levels. Clinicians using the new monoclonal antibody growth hormone assays will need to carefully develop separate diagnostic criteria for growth hormone deficiency that takes into account the disparity between the polyclonal assays that were used in the development of the current diagnostic standards and the new monoclonal antibody assays.
Adolescent↗
Diagnosis of reactive hypoglycemia: pitfalls in the use of the oral glucose tolerance test.
The signs and symptoms of reactive hypoglycemia mimic the manifestations of other clinical disorders. The oral glucose tolerance test (OGTT) is a widely accepted diagnostic procedure to evaluate patients suspected of having reactive hypoglycemia. The reproducibility of the OGTT has not been previously assessed in a large group of patients. We evaluated the consistency of glucose nadirs at 50 mg/dl and below during two consecutive OGTTs for diagnostic screening of 59 patients with postprandial symptoms of hypoglycemia. The mean nadirs of the consecutive OGTTs were 56 +/- 12 mg and 57 +/- 13 mg, both significantly below the mean nadir of asymptomatic subjects (P less than .001). The nadir of the first OGTT was at or below 50 mg/dl in a subgroup of 20 patients ("hypoglycemic"). On the repeat OGTT, 13 previously "hypoglycemic" patients had nadirs over 50 mg/dl on the second OGTT. Nine of the 39 remaining patients had nadirs below or equal to 50 mg/dl during their second OGTT. Thus, 37% of all patients had a change in diagnostic classification in the second OGTT based on the glucose nadir level. We conclude that the glucose nadir during OGTT is an inconsistent and unreliable screening criterion for evaluating patients with recurrent postprandial hypoglycemic symptoms in clinical practice.
Adult↗