The immune response of children with chronic lymphocytic thyroiditis to a viral challenge.
Explore the source record for details and available documents.
Adenoviridae↗
Biomedical subjects
A W Root
Publications and source records attributed to A W Root.
Plasma glucose and insulin levels in monkeys anticipating feeding.
To see whether plasma glucose or insulin changed in anticipation of feeding, we provided seven rhesus monkeys with four-hour access to food every other day. Blood was sampled before and during a 30-minute signal which ended with food availability and before and during a 30-minute signal which was not closely and reliably linked with food availability. Plasma insulin showed no evidence of conditioning. Plasma glucose was higher during the signal than prior to the signal in both experiments. This probably reflects the arousing nature of the signal rather than appetitive-associated learning. However, the differences, while statistically significant, were probably biologically trivial because they fall within the normal fluctuations of meal-fed monkeys. Under the conditions of this experiments, it appears that conditional changes in glucose and insulin do not reliably occur in monkeys anticipating access to food.
Animals↗
Facilitation of the growth promoting effect of growth hormone (GH) by an antibody to methionyl-GH.
Despite the development of antibodies to methionyl growth hormone in a child with hypopituitarism, the patient grew at a rapid rate on low doses of somatotropin. Serum immunoglobulins from this patient stimulated the growth of Nb2 lymphoma cells in vitro in samples obtained within 48 hours after the last dose of growth hormone, while samples obtained several weeks after an injection of methionyl growth hormone did not. Immunoglobulins from normal subjects or from hyposomatotropic patients being treated with methionyl growth hormone who had not developed antibodies did not stimulate Nb2 lymphoma cell growth. We suggest that the antibodies to methionyl growth hormone in this child served as a reservoir for exogenous growth hormone or facilitated the interaction of growth hormone with the prolactin receptor on the Nb2 lymphoma cell.
Antibodies↗
Hetero- and isosexual pseudoprecocity associated with testicular sex-cord tumors in an 8 year-old male.
Enlargement of the right breast, axillary hair, and acceleration of linear growth rate were first noted at 8 years of age in an otherwise healthy male with no known exposure to exogenous hormones. At 9.5 years of age the right subareolar mass was excised; histologic examination revealed fibrous breast tissue. Subsequently pubic hair appeared. At 10.7 years of age, the patient complained of right inguinal pain after a minor injury. Examination revealed a tall (height age 12.7 years), mature, muscular boy with enlarged (R: 5 x 3 x 2 cm; L: 3 x 2 x 3 cm) firm, irregular testes, Tanner stage II pubic hair, and modest axillary hair. No perioral pigmentation was present. Testicular ultrasonography revealed multilobular echogenic foci with calcifications. Bone age was 13 years, the LH and FSH secretory responses to GnRH were minimal (LH: < 0.038-->0.28 mIU/ml; FSH: < 0.063-->0.11 mIU/ml), and basal serum testosterone (< 10 ng/dl) and estradiol (< 10 pg/ml) values were undetectable. Following administration of human chorionic gonadotropin (hCG), the serum testosterone concentration increased to 275 ng/dl, while estradiol remained unmeasurable. Spermatic vein concentrations of testosterone were undetectable in the basal state and increased after hCG administration. After bilateral orchiectomy, pathologic examination revealed multifocal tumors composed of brightly eosinophilic, large polygonal cells arranged in nests, cords, and clusters within dense connective tissue or mucinous stroma with lamellar calcifications of varying sizes. These pathologic findings were compatible with a large cell calcifying Sertoli cell (sex-cord)tumor of the testes. Testosterone, estradiol, immunoreactive and bioactive aromatase activity were not detectable in the tumor. Thus, both heterosexual (gynecomastia) and isosexual (increased musculature, pubic and axillary hair) precocious puberty may occur in boys with testicular sex-cord tumors.
Child↗
Evaluation of the clinical utility of the ultrasensitive immunofluometric assay for growth hormone (GH) and of the cortisol secretory pattern in prediction of the linear growth response to treatment with GH.
OBJECTIVES: To evaluate the utility of an ultrasensitive IFMA for human 22 kDa GH in assessment of GH secretion and prediction of the linear growth response to exogenous GH. METHODS: Utilizing Delfia reagents supplied by Wallac-OY, an ultrasensitive IFMA for GH was established. Serum GH concentrations from 15 children/adolescents undergoing 24 hour GH secretory profiles with sampling at 20 minute intervals were analyzed by both IFMA and RIA. Cortisol values were also measured. Twelve children were later treated with GH. The 24 hour GH and cortisol secretory profiles were analyzed by the Cluster program and the relationships of these profiles to the linear growth response to exogenous GH determined. RESULTS: The sensitivity of the IFMA for GH relative to a zero standard was 0.005 ng/ml; intra-assay coefficients of variation ranged from 12% at a GH concentration of 0.005 ng/ml to 4% at 0.038 ng/ml; interassay coefficients of variation ranged from 34% at a GH concentration of 0.005 ng/ml to 10.5% at 2.7 ng/ml and to 2.7% at 12.7 ng/ml. Above assay sensitivity, there was good correlation between GH concentrations determined by IFMA and those by IRMA and RIA (r = 0.998 and 0.992 respectively). The number of GH secretory peaks identified by IFMA was significantly greater than that detected by RIA (10.6 +/- 3.2 [SD] vs 6.7 +/- 3.3/24 hours, p = 0.0001 by paired t-test). There were few significant relationships between any parameter of GH secretion measured by RIA or IFMA (peak GH pulse amplitude, percent increase in amplitude, area under the peak, interpeak interval) and the pretreatment growth rate, the growth velocity while receiving GH therapy, or the increment in growth rate during administration of GH. The number of GH secretory peaks determined by RIA correlated weakly with the pretreatment growth rate. There was no meaningful relationship between the serum concentrations of cortisol and GH-IFMA. Peak GH concentrations and nadir cortisol values were exactly coincident in 15.7% (25/159); 42.8% of nadir cortisol values coincided with or were within +/- 20 minutes of peak GH values (68/159). However, there was no relationship between the number of cortisol secretory peaks, the pooled 24 hour and nocturnal concentrations of cortisol and the pretreatment growth velocity, the growth rate or increment in growth velocity during administration of GH. CONCLUSIONS: Despite the increased sensitivity of the IFMA and its ability to detect pulsatile GH secretion heretofore unidentified, data from this GH assay were not useful in predicting first year growth rate during administration of GH. The secretory pattern of cortisol was not helpful in predicting the growth response to GH.
Adolescent↗
Watery diarrhea, hypokalemia, achlorhydria syndrome in an infant: effect of the long-acting somatostatin analogue SMS 201-995 on the disease and linear growth.
An 8-week-old infant presented with vomiting and failure to thrive due to small bowel obstruction caused by a diffusely enlarged pancreas. Surgical bypass of the obstruction was followed by secretory diarrhea, hypokalemia, and dehydration. Plasma vasoactive intestinal peptide (VIP) (823pg/ml), pancreatic polypeptide (4,500 pg/ml), and neurotensin (680 pg/ml) concentrations were markedly elevated. No neoplastic process was identified. Therapy with the long-acting somatostatin analogue SMS 201-995 was followed by decline in VIP concentrations (900 to 200-300 pg/ml), decrease in stool frequency, and normalization of serum electrolytes. During 12 months of somatostatin analogue therapy, length and weight progressed along the 3rd percentile on the Tanner growth chart.
Achlorhydria↗
Hypophosphatasia: a case report.
Explore the source record for details and available documents.
Bone Diseases↗
Neurotransmitter control of growth hormone secretion in children after cranial radiation therapy.
Cranial radiation for childhood cancer can cause growth hormone deficiency (GHD), usually due to hypothalamic rather than pituitary dysfunction. To investigate whether this hypothalamic dysfunction is secondary to altered neurotransmitter input from other brain centers, we used neurotransmitter-excitatory substances to study the GH secretory response in 17 children who had received 12 to 60 Grey (Gy) to the cranium and 40 short children with normal endocrine function. As expected, the irradiated children had decreased mean GH secretion in response to insulin-induced hypoglycemia and arginine infusion, and decreased mean 24 hour GH concentrations, compared to the control group. In contrast, the two groups had similar GH secretory responses to GHRH stimulation and somatostatin suppression. Assessment of neurotransmitter pathways in the irradiated children revealed significantly lower mean peak GH concentrations in response to 5 of the 6 substances tested compared to control children: alpha-adrenergic stimulation (clonidine), beta-adrenergic blockade (propranolol), cholinergic stimulation, dopaminergic stimulation (L-dopa), and GABA-ergic stimulation (valproic acid). Results of serotonergic stimulation (L-tryptophan) were not statistically significant. Eleven patients who had abnormal GH secretion underwent 4 or more tests with neurotransmitter-stimulatory agents; 3 patients had peak GH concentrations of < 2.5 micrograms/l to all tests, whereas 4 patients had a peak GH concentration of > or = 7 micrograms/l to one or more tests but < 5 micrograms/l to one or more other tests. These observations suggest that radiation damage may sometimes spare growth hormone-releasing hormone (GHRH) and somatostatin secretion while affecting neurotransmitter pathways. We postulate that the hierarchy of sensitivity to radiation damage may be hypothalamic and extra-hypothalamic neurotransmitters > hypothalamic GHRH and/or somatostatin secretion > pituitary GH secretion.
Adolescent↗