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Biomedical subjects

E A Schriock

Publications and source records attributed to E A Schriock.

11 recordsLinked to original sources
PubMed1995

Octreotide enhances positive calcium balance in Duchenne muscular dystrophy.

Although receptors for somatostatin are found in bone cells, the effect of somatostatin analogs on calcium metabolism is unknown. The authors studied, in a metabolic ward, the effect of octreotide (a long-acting somatostatin analog) and a placebo in two 6-day calcium balance periods in 8 children with Duchenne muscular dystrophy. As expected, octreotide (2 micrograms/kg, subcutaneously, every 8 hours) reduced serum growth hormone and somatomedin (IGF-1) to levels found in growth hormone deficiency. Octreotide enhanced calcium retention by 30% (96 mg daily [P < 0.04]) in 7 boys for whom complete data (diet, urine, and fecal calcium) were available. In 6 children with urinary calcium excretion (Uca) greater than 50 mg daily, octreotide markedly lowered Uca, from 114 +/- 23 mg daily to 61 +/- 9 mg daily (P < 0.03). Calcium retention occurred in patients with or without initial hypercalciuria, but the higher the basal Uca, the greater was the inhibition by octreotide (r = 0.79; P < 0.03). Inactive, nonambulatory patients had a more pronounced response of Uca to octreotide (P < 0.02). Octreotide caused a mild, nonsignificant reduction in fecal calcium, with no major changes in serum calcium, phosphorus, parathyroid hormone, urinary excretion of sodium and potassium, or in creatinine clearance. Based on the current observations and the presence of receptors for somatostatin in bone cells, this hormone may have, at least on a short-term basis, an anabolic effect on calcium, perhaps favoring its deposition in bone.

Adolescent↗
PubMed1992

A method of predicting adult height and obesity in long-term survivors of childhood acute lymphoblastic leukemia.

PURPOSE: Short stature and obesity have been reported among long-term survivors of childhood acute lymphocytic leukemia (ALL). We examined factors that contribute to these adverse sequelae. PATIENTS AND METHODS: Serial height and weight measurements were analyzed for 91 long-term survivors who were treated for ALL between 1967 and 1975 at a single institution. These patients were all younger than 12 years at diagnosis, were in continuous complete remission, had reached final height, and had height and weight measurements within 1 year of age 18 years. They had received craniospinal (n = 33) or cranial irradiation (n = 58) to total doses of 24 Gy as CNS prophylaxis. Standard deviation scores (SDS) were used to reflect the deviation of height and weight measurements from population means, and the body mass index (BMI; weight divided by height squared) was used in assessing obesity at age 18 years. RESULTS: Short stature (less than fifth percentile) was seen in 41 patients (45%), and obesity (BMI greater than or equal to 24 kg/m2) in 35 (38%). Regression formulae were developed that explain 65% and 62% of the variability in patient height and BMI, respectively. CONCLUSIONS: Risk factors were identified for abnormally short stature, which was defined to be a decrease of 1.5 SDS in height from diagnosis to age 18 years. These factors include younger age and above-average height for age at diagnosis (height SDS greater than 0), craniospinal irradiation, and greater decrease in height SDS during antileukemic therapy. Risk factors for obesity at age 18 years include weight SDS greater than 0 and greater than height SDS at 1 year after the end of chemotherapy.

Adolescent↗
PubMed1991

Abnormal growth patterns and adult short stature in 115 long-term survivors of childhood leukemia.

Significant growth retardation was found in 115 survivors of childhood acute lymphoblastic leukemia (ALL) who had completed their growth. These children were diagnosed before 12 years of age and treated on four protocols in a single institution; all received either cranial (n = 78) or craniospinal (n = 37) prophylactic irradiation. Patients' heights at diagnosis were within expected ranges, but final heights were greater than or equal to 1 SD below population means in 74% of cases and greater than or equal to 2 SD in 37%. Effects on growth were more pronounced for children who had received craniospinal irradiation, but decrements were also significant in the cranial irradiation group, with adult heights greater than or equal to 2 SD below population norms in 32%. Growth retardation was significantly greater (P less than .0001) in children who had earlier disease onset. Growth deceleration occurred not only during chemotherapy but during a later period that followed an interval of improved growth in many cases. Thus, late decrements in growth may be missed in studies that do not follow patients until they have attained final heights. These findings indicate that abnormally short stature among survivors of ALL merits further clinical and research attention.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Recent advances in the management of sexual precocity in girls.

Sexual precocity has important psychosocial implications for the prematurely developing child, as well as being associated in some cases with significant pathology. Conscientious evaluation and initiation of effective therapy can have a significant impact on improving long-term outcome. The differentiation between complete sexual precocity with activation of the hypothalamic-pituitary axis and incomplete sexual precocity without activation of the central reproductive system is of paramount importance. In incomplete sexual precocity, the sex steroids are of exogenous, adrenal, or gonadal origin. Premature adrenarche presents with the early development of pubic hair only and must be distinguished from adrenal hyperplasia or an androgen-secreting neoplasm, which may be associated with accelerated growth, advanced bone age, and virilization. When incomplete sexual precocity involves the ovary, ovarian tumors must be considered. Other causes of incomplete sexual precocity include hypothyroidism and gonadotropin-independent precocity such as McCune-Albright syndrome. Complete sexual precocity or precocious puberty of central origin is diagnosed in girls by gonadotropin-releasing hormone challenge yielding a stimulated luteinizing hormone peak greater than 15 IU/L. Radiologic evaluation of the central axis is necessary. Treatment of precocious puberty relies on the use of potent agonists of gonadotropin-releasing hormone that reversibly suppress the prematurely activated pituitary. Depot preparations are efficacious. Early initiation and careful monitoring of treatment can reduce physical signs of development, improve the likelihood for normal adult height, and postpone normal pubertal progression to a more appropriate age.

Child↗
PubMed1990

Persistent müllerian duct syndrome.

Persistent müllerian syndrome is rare. A case of phenotypically normal male with persistent müllerian structures that consisted of a bicornuate uterus, fallopian tubes, and upper third of the vagina is reported. These unusual structures were found in association with bilateral cryptorchidism and a right inguinal hernia, and were diagnosed while repairing the hernia in the neonatal period. The uterus and fallopian tubes were removed via laparotomy when the child was eighteen months old; at the same time a bilateral orchiopexy was performed. To avoid damage to the vas deferens, which lay in closely to the müllerian structures and could not be separated from the vaginal wall, a small segment of the upper third of the vagina was retained. The testicles, although normal on pathologic examination, have shown poor response to hormonal stimulation with human chorionic gonadotropin. Long-term follow-up for these patients is necessary because they have an increased risk of testicular tumors developing.

Cryptorchidism↗
PubMed1987

Evaluation of hypothalamic dysfunction in growth hormone (GH)-deficient patients using single versus multiple doses of GH-releasing hormone (GHRH-44) and evidence for diurnal variation in somatotroph responsiveness to GHRH in GH-deficient patients.

To examine the efficacy of multiple doses of GHRH-44 to enhance GH secretion and to determine the number of GHRH-44 doses required to exclude hypothalamic dysfunction, 12 doses of GHRH-44 were administered iv every 2 h to 4 GH-deficient patients beginning in the morning (group A) and to 4 GH-deficient patients beginning in the evening (group B). Five additional GH-deficient patients (group C) were given 4-18 GHRH-44 doses. The first and last doses were 5 micrograms/kg; all others were 1 microgram/kg. Higher GH responses were attained by 9 of the 13 patients after multiple GHRH-44 doses than after the initial GHRH-44 dose. After the first GHRH-44 dose, the peak plasma GH concentrations were less than 7 micrograms/L in 9 patients; 4 of 9 achieved GH concentrations above 7 micrograms/L after 5-7 GHRH-44 doses; 2 had measurable levels below 7 micrograms/L. GH concentrations remained undetectable in 3 older patients in group C. In the patients who had detectable GH levels after GHRH-44 treatment, serum somatomedin-C concentrations increased from 0.67 +/- 0.14 (+/- SEM) to 0.79 +/- 0.14 U/mL after 6 GHRH-44 doses (P less than 0.01; n = 10) then to 1.00 +/- 0.14 (+/- SEM) U/mL after an additional 4-6 GHRH-44 doses (P less than 0.05; n = 9). After 6 GHRH-44 doses in groups A and B, the integrated GH concentrations between 2000 and 0800 h were greater than the integrated GH concentrations between 0800 and 2000 h (P less than 0.02). These findings indicate that a hypothalamic defect cannot be excluded on the basis of an impaired response to a single dose of GHRH-44, that the number of GHRH doses required to stimulate GH release in GH-deficient patients is variable, and that in addition to the possibility of genetically determined GHRH insensitivity some non-responding patients have developed severe acquired resistance to GHRH. Evidence for diurnal variation in the responsiveness of somatotropes to GHRH-44 in GH-deficient patients was also found.

Adolescent↗
PubMed1985

Effect of growth hormone-releasing factor on growth hormone release in children with radiation-induced growth hormone deficiency.

Five male children who received cranial irradiation for extrahypothalamic intracranial neoplasms or leukemia and subsequently developed severe growth hormone (GH) deficiency were challenged with synthetic growth hormone-releasing factor (GRF-44), in an attempt to distinguish hypothalamic from pituitary dysfunction as a cause of their GH deficiency, and to assess the readily releasable GH reserve in the pituitary. In response to a pulse of GRF-44 (5 micrograms/kg intravenously), mean peak GH levels rose to values higher than those evoked by the pharmacologic agents L-dopa or arginine (6.4 +/- 1.3 ng/mL v 1.5 +/- 0.4 ng/mL, P less than .05). The peak GH value occurred at a mean of 26.0 minutes after administration of GRF-44. These responses were similar to those obtained in children with severe GH deficiency due to other etiologies (peak GH 6.3 +/- 1.7 ng/mL, mean 28.0 minutes). In addition, there was a trend toward an inverse relationship between peak GH response to GRF-44 and the postirradiation interval. Prolactin and somatomedin-C levels did not change significantly after the administration of a single dose of GRF-44. The results of this study support the hypothesis that cranial irradiation in children can lead to hypothalamic GRF deficiency secondary to radiation injury of hypothalamic GRF-secreting neurons. This study also lends support to the potential therapeutic usefulness of GRF-44 or an analog for GH deficiency secondary to cranial irradiation.

Adolescent↗
PubMed1984

Diabetes mellitus and its effects on menarche.

In a combined mail and medical record survey of 121 non-diabetic and 90 diabetic girls greater than or equal to 9 years of age, the mean age of menarche in the control non-diabetic population was 13.0 +/- 1.2 years and 13.4 +/- 1.2 years in the diabetics. The diabetic group was divided into those whose onset was before or after age 11 years (DM less than 11, DM greater than or equal to 11). The DM greater than or equal to 11 group had a mean menarchal age of 14.0 +/- 1.2 years and the DM less than 11 group, 13.1 +/- 1.2 (p less than 0.005). The DM greater than or equal to 11 group also differed significantly from the control group. The difference between the two groups suggests that the onset of diabetes near the onset of puberty may have a more disruptive effect on hypothalamic-pituitary-gonadal axis maturation that does the prepubertal onset of diabetes.

Adolescent↗
PubMed1984

Effect of growth hormone (GH)-releasing hormone (GRH) on plasma GH in relation to magnitude and duration of GH deficiency in 26 children and adults with isolated GH deficiency or multiple pituitary hormone deficiencies: evidence for hypothalamic GRH deficiency.

Synthetic, amidated, 44 amino acid GH-releasing hormone ( GRH -44) was administered iv at a dose of 5 micrograms/kg to 20 patients with severe GH deficiency (GHD), 6 children and adolescents with partial GHD, and 6 non-GH deficient ( NGHD ) children and adolescents. The 17 patients with severe GHD that responded to GRH -44 had lower peak concentrations of plasma GH than the NGHD individuals (5.0 +/- 1.2 (SEM) vs. 27.2 +/- 3.5 ng/ml; P less than 0.0001). The children and adolescents with severe GHD tended to have higher peak GH responses to GRH -44 than the GHD adults (6.9 +/- 1.7 vs. 2.4 +/- 0.3 ng/ml) although the difference was not significant. The peak GH concentration was attained earlier in the GHD children and adolescents than in the GHD adults (28 +/- 4.7 vs. 69.3 +/- 13 min, P less than 0.004). There was a negative correlation between chronological age and peak plasma GH response to GRH in the children and adolescents with severe GHD (r = -0.758, P less than 0.02). Children and adolescents with partial GHD had a higher mean peak concentration of plasma GH (13. 1 +/- 1.8 ng/ml) than the children, adolescents, and adults with severe GHD (P less than 0.04), but one lower than the NGHD children and adolescents (P less than 0.05). In both severe and partial GHD the GH response to GRH was greater than that elicited by standard pharmacological tests. Serum somatomedin-C did not increase after a single pulse of GRH -44 in the 12 GHD patients studied. PRL increased minimally 30 min after 5 micrograms/kg iv GRH -44 in patients with multiple hypothalamic-pituitary hormone deficiencies but not in patients with isolated GHD or in NGHD individuals. The GH responses to GRH suggest that the majority of patients with isolated GHD as well as those with multiple hypothalamic-pituitary hormone deficiencies have deficiency of hypothalamic GRH . Lack of a GH response to a single pulse of GRH does not exclude GRH deficiency as priming of the somatotrope with multiple pulses of GRH may be necessary to rule out a hypothalamic defect in the nonresponders. The results of this study support the potential usefulness of GRH or its analogs in the diagnosis and treatment of selected patients with disorders of GH secretion.

Adolescent↗
PubMed1983

Synthetic human pancreas growth hormone-releasing factor (hpGRF1-44-NH2) stimulates growth hormone secretion in normal men.

A synthetic replicate of human pancreas growth hormone-releasing factor, hpGRF1-44-NH2, (hpGRF44), a 44-amino acid amidated peptide, was administered to seven normal men. In addition to placebo, 4 subjects received 3 doses of hpGRF44 (0.5 microgram/kg, 5 micrograms/kg, 10 micrograms/kg), while one subject received 2 doses (5 micrograms/kg, 10 micrograms/kg) and 2 subjects received one dose (0.5 microgram/kg or 5 micrograms/kg), each as a rapid intravenous injection. A significant increase in circulating growth hormone (GH) was observed at each dose (0.5 microgram/kg, p = 0.05; 5 micrograms/kg, p less than 0.005; 10 micrograms/kg, p = 0.01) when compared to placebo, with equivalent maximal responses. At all doses studied a rise in plasma GH occurred within 5 min, with a peak response in most patients at 30-45 min. There were no associated changes in any of the other anterior pituitary hormones or insulin. Other than transient flushing and minimal changes in vital signs, no side effects were noted. The results of these studies support the potential usefulness of hpGRF44 for the assessment of GH secretion and reserve, and of this peptide or an analog as a therapeutic agent to stimulate GH release.

Adult↗