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Biomedical subjects

V V Weldon

Publications and source records attributed to V V Weldon.

At least 19 recordsLinked to original sources
PubMed1986

Outcome in children with normal growth following removal of a craniopharyngioma.

Ten children who had normal or excessive growth rates following surgical removal of a craniopharyngioma have been followed. Final adult heights for three were more than 2.5 standard deviations below the mean adult height for sex. Nine of the 10 children showed a deceleration in growth rate that occurred 1.5-6 years following surgery. The deceleration in linear growth did not appear to correlate with changes in weight gain, somatomedin-C, or the integrated insulin response to an oral glucose load. These results suggest that the mechanisms whereby some children with growth hormone deficiency have normal growth rates following neurosurgic procedures are complex. The authors recommend that these children have continued follow-up so that growth hormone therapy may be instituted when appropriate.

Body Height↗
PubMed1985

Hypopituitarism and septooptic "dysplasia" in first cousins.

Although familial forms of hypopituitarism are known, to our knowledge familial septooptic "dysplasia" in association with hypopituitarism has not been reported. We describe two first cousins with panhypopituitarism, one of whom had septooptic dysplasia. We discuss the possibility that septooptic dysplasia-hypopituitarism may be inherited as an autosomal dominant, or recessive, or multifactorial trait.

Adult↗
PubMed1984

Somatomedin C response to growth hormone in psychosocial growth retardation.

Three children with psychosocial growth retardation increased their serum somatomedin C levels from 0.20 +/- .02 to 0.81 +/- 0.2 U/ml in response to exogenous growth hormone. The pattern of somatomedin C response to growth hormone was no different from that seen in 11 prepubertal children with growth hormone deficiency who received growth hormone according to the same acute treatment regimen. This result suggests that the poor growth response of children with psychosocial growth retardation to exogenous growth hormone is not due to an inability to synthesize somatomedin C, and that it may represent a degree of resistance to the actions of somatomedin C.

Child↗
PubMed1982

Fetal and maternal virilization associated with pregnancy. A case report and review of the literature.

A masculinized female infant was born to a mother who had virilizing signs dating from the fourth month of pregnancy. Serum 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, and testosterone levels were all normal in the infant. Maternal testosterone level was markedly elevated one week post partum. Dexamethasone phosphate suppression was normal. Human chorionic gonadotropin stimulation five weeks post partum revealed further elevation of high baseline free and total testosterone levels. Free and total testosterone levels 30 weeks post partum were normal, and all maternal virilizing signs had regressed with the exception of her deepened voice. The child has had no progression of masculinization. The mother is believed to have had a luteoma of pregnancy.

Adult↗
PubMed1982

Growth hormone--dependent growth failure.

Growth failure may be associated with low serum somatomedin concentrations despite normal to increased concentrations of serum growth hormone. We have recognized five patients who responded to GH administration with an increase in serum Sm and an acceleration in skeletal growth, and have characterized the circulating GH in an homologous human GH radioreceptor assay employing the IM-9 lymphocyte as a source of human GH receptor. These five prepubertal children, who had a mean height 7.8 SD below the mean for age, had a mean RIA-GH of 34.2 +/- 3.5 ng/ml in response to stimulation, a basal Sm activity by hypophysectomized rat cartilage bioassay of less than 0.3 IU/ml, and a mean peak Sm of 0.9 +/- 0.1 IU/ml in response to 48 hours of GH therapy. During a one-year trial of GH therapy, four of these children significantly increased their growth velocity as compared to their growth rate before GH therapy. These children had a mean RIA-GH/RRA-GH ratio of 2.f. The fifth patient had a low RIA-GH/RRA-GH ratio and had no increase in growth rate. These studies suggest that growth in certain growth retarded children may be dependent on exogenous GH, even though they are not GH deficient by standard criteria.

Body Height↗
PubMed1982

Kinetics of the somatomedin C/insulin-like growth factor I: response to exogenous growth hormone (GH) in GH-deficient children.

The somatomedin C/insulin-like growth factor I (SMC/IGF-I) response to human GH (hGH) therapy and the t1/2 of SMC/IGF-I after the cessation of hGH were determined in 15 children with GH deficiency. After 5 injections of hGH (0.1 U/kg), there was a significant increase in total SMC/IGF-I [from 0.27 +/- 0.06 to 1.19 +/- 0.17 U/ml (mean +/- SEM)]. Both the pretreatment SMC/IGF-I and the maximal SMC/IGF-I levels attained were correlated with chronological age and bone age. Body size, as indicated by height and weight, also correlated with pretreatment and maximal SMC/IGF-I levels. For both pretreatment and maximal SMC/IGF-I levels, there was a better correlation of SMC/IGF-I levels with bone age than with chronological age. While the correlation between height and the pretreatment SMC/IGF-I level was stronger, weight was a better predicter of the maximal SMC/IGF-I level. Maximal SMC/IGF-I levels were reached 18.8 +/- 2.9 h after the last hGH injection. The t1/2 for SMC-IGF-I after the attainment of maximal levels was 20.7 +/- 2.3 h, or 39.5 +/- 3.8 h from the last injection of hGH. The t1/2 of SMC/IGF-I determined in this way was longer than previous values reported from studies in the rat. The relatively long t1/2 of SMC/IGF-I which we observed may in part explain the success of present GH treatment regimens which involve every other day injections of hGH.

Adolescent↗
PubMed1980

Topically applied testosterone and phallic growth. Its effects in male children with hypopituitarism and microphallus.

Topical application of 5% testosterone cream for 21 days resulted in enlargement of the penis to normal size for age in five boys with normal XY karyotype who had microphallus and hypopituitarism. In four patients, testosterone cream was applied locally to the penis and in one to an area of skin in the right axilla. Serum testosterone values rose from infantile levels before the start of therapy to normal adult male levels on the last day of treatment. All patients were receiving human growth hormone at the time of therapy with testosterone. No additional acceleration of linear growth and no advance in osseous maturation occurred during or after treatment. Application of testosterone locally for this brief period is a safe, effective, and simple means of stimulating phallic growth. Our findings suggest that topical testosterone causes penile growth predominantly through its systemic action.

Administration, Topical↗
PubMed1978

Growth failure with normal serum RIA-GH and low somatomedin activity: somatomedin restoration and growth acceleration after exogenous GH.

Two three-year-old boys with dwarfism (height ages 1-4/2 and 1-11/12 years) and delayed bone ages (1-4/12 and 1-9/12 years) had normal growth hormone (GH) responses after stimulation and low levels of somatomedin. Unlike patients with Laron syndrome, the two patients generated normal levels of somatomedin after administration of exogenous hGH. Treatment with hGH (2 IU every other day) brought about a significant increase in the growth rate of both patients. The growth rate of the first patient increased from 2 cm/year before treatment to 12 cm/year on therapy. The growth rate of the second patient was 4.5 cm/year before treatment, and 8.3 cm/year while on treatment. The two cases represent a new syndrome of dwarfism which may be caused by secretion of a biologically inactive but immunoreactive GH.

Child, Preschool↗
PubMed1977

Decreased cortical thickness & osteopenia in children with diabetes mellitus.

A recent study using the photon absorption technique has revealed a high frequency of significant bone loss in diabetic adults regardless of age or duration of diabetes. In this study 107 diabetic children age 4-18 were studied using cortical bone thickness and skeletal maturation as indicators of bone development. Overall, 25% of all diabetic children had cortical thickness values below the five percent limit for normal children. This was more common in boys than girls and was unrelated to duration of diabetes. A modest increase in delayed skeletal maturation did not account for the cortical thinning and osteopenia observed. The cause of the osteopenia of diabetic children remains an enigma.

Adolescent↗
PubMed1976

The role of growth hormone and cortisone on glucose and gluconeogenic substrate regulation in fasted hypopituitary children.

Panhypopituitarism may be associated with spontaneous hypoglycemia and marked insulin sensitivity. Five children with both growth hormone (GH) and adrenocorticotrophin (ACTH) insufficiency were studied in three periods: a) on no therapy; b) during cortisone acetate; and c) during GH and cortisone acetate replacement. With total caloric restriction prior to therapy, all patients became hypoglycemic (109 +/- 18 leads to 37 +/- 3.5 mg/dl, mean +/- SEM) and ketonemic (beta-hydroxybutyrate 0.10 +/- 0.02 leads to 3.04 +/- 0.63 mM and acetoacetate 0.05 +/- .01 leads to 0.80 +/- 0.15 mM) within 30 hours. Glutamine and alanine concentrations fell with fasting (511 +/- 13 leads to 293 +/- 26 muM and 394 +/- 58 leads to 137 +/- 12 muM, respectively) but to levels lower than in normal children. However, only alanine was significantly lower (P less than 0.05). With cortisone plus GH therapy, fasting glycemia was improved (73 +/- 6 mg/dl) at 30 hours fasting and was associated with increased alanine and glutamine concentrations (206 +/- 28 muM and 448 +/- 40 muM, respectively) and less ketonemia (beta-hydroxybutyrate 1.13 +/- 0.39 mM). Cortisone therapy alone resulted in intermediate improvement of these values. Only combined therapy resulted in increased lactate and pyruvate concentrations, which fell to normal with fasting. Fasting urinary ammonia excretion was unchanged whereas urea nitrogen excretion decreased significantly with therapy. The responses to alanine infusions following each study period in one patient were normal. The glycemic response to iv glucose was similar during each study period; however, post-prandial and glucose-stimulated insulin responses were increased with cortisone and cortisone plus GH therapy. We suggest that the hypoglycemia observed in hypopituitary patients is a substrate-mediated phenomenon, and that cortisone and growth hormone replacement therapy improve fasting glucose homeostasis, increase circulating alanine and glutamine concentrations, and decrease hepatic gluconeogenesis. These effects may be mediated through an increase in fat catabolism.

Adolescent↗
PubMed1976

Cerebral edema complicating therapy for diabetic ketoacidosis.

Four cases of cerebral edema associated with therapy for diabetic ketoacidosis are reported. One patient had an inappropriate ADH-like syndrome at the time of onset of clinical symptoms of cerebral edema; he survived. The remaining patients had hyponatremia at or near the time of onset of clinical symptoms of cerebral edema, and they subsequently died. The literature is reviewed and some aspects of therapy, which might be casually related to cerebral edema observed in association with therapy of diabetic ketoacidosis, are discussed.

Blood↗
PubMed1975

Pseudohermaphroditis, with testes and a 46, XX karyotype.

A 14 4/12-year-old white girl, evaluated for progressive virilization and clitormegaly, was found to have the unusual combination of a 46, XX karyotype, well-developed Mullerian structures, and dysgenetic testes with Leydig cell hyperplasia. Although there have been previous case reports of 46, XX males, in all of these patients development of the Mullerian ducts had been suppressed. When contemporary classifications of human disorders of sexual differentation were reviewed, no report of a similar patient was found. We speculate that the genotype and phenotype in our patient correspond to the genetic intersexuality of the hornless goat, thereby raising the possibility that the human autosome may play a role in the control of sexual development.

Adolescent↗