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Biomedical subjects

R Lanes

Publications and source records attributed to R Lanes.

At least 55 records · Page 3Linked to original sources
PubMed1986

Growth hormone secretion in patients with constitutional delay of growth and pubertal development.

Growth hormone levels were measured every 30 minutes during sleep over 9 hours in 20 prepubertal patients with constitutional delay of growth and puberty (CGD) and in 10 age-matched controls, all of whom had had normal GH responses to an orally administered dose of clonidine. We found no significant difference in the mean 9-hour overnight GH concentration between groups (4.5 +/- 1.8 ng/ml (mean +/- SD) in the CGD group, 4.4 +/- 2.8 ng/ml in the control group). Total GH output (258 +/- 99 U vs 222 +/- 135 U), total number of nocturnal GH pulses (3.6 +/- 0.8 vs 3.3 +/- 1.3), mean peak GH response during nocturnal sampling (13 +/- 1.2 ng/ml vs 13.2 +/- 1.3 ng/ml), and basal somatomedin C concentrations were not different in the children with growth delay and controls. We conclude that prepubertal patients with constitutional delay of growth and puberty secrete GH normally and do not seem to have any abnormality in GH regulation.

Adolescent↗
PubMed1986

Breast feeding and insulin-dependent diabetes mellitus in children.

We have evaluated the hypothesis of a protective effect of human milk on the development of insulin dependent diabetes mellitus (IDDM). We studied the feeding histories of 95 diabetic children and compared them with controls consisting of their non-diabetic siblings and a pair matched group of nondiabetic peers of the same age, sex, geographical location, and social background. The incidence of breast feeding in diabetic children was 18%. This was similar to the control group. The duration of breast feedings was also similar among all three groups. There was no difference in the age of introduction of solid food between diabetic and nondiabetic children. Twice as many diabetic children, however, received soy containing formula in infancy as compared to control children. The mean age of onset of IDDM was not related to the type of feeding during infancy. The incidence of positive thyroid antibodies was two and one half times higher in formula-fed diabetic children than in breast-fed ones. In our studies we were unable to document any relationship between the history of breast feeding and subsequent development of IDDM in children.

Adolescent↗
PubMed1985

Low-dose oral clonidine. A simple and reliable growth hormone screening test for children.

We evaluated the efficacy and side effects of a low dose of oral clonidine hydrochloride on growth hormone release in 24 healthy short children; ten received 100 micrograms (group A) and 14 received 50 micrograms (group B). The mean +/- SD growth hormone peak at 60 minutes was 14.5 +/- 6.3 mg/mL in group A v 11.6 +/- 6.1 mg/mL in group B. Failure rate (growth hormone less than 10 mg/mL) was 10% in group A and 36% in group B. The drop in cortisol levels was similar in both groups. Blood pressure did not change significantly, and only mild somnolence was noted in all. A single dose of oral clonidine hydrochloride approximating 100 micrograms/sq m, followed by one blood sample after 60 minutes seems to be an effective and safe screening test for growth hormone deficiency in short children.

Adolescent↗
PubMed1985

Effect of asphyxia on free thyroid hormone levels in full term newborns.

Alterations in the thyroid metabolism of hypoxic, fasted, and chronically ill adults and older children have been described. We evaluated the effects of asphyxia on thyroidal indices of term newborns and compared them to those of a control population. Blood was drawn from the cord and then serially at 5 min and 3, 24, and 48 h after delivery in all patients. Seven term healthy newborns (group 1)increased their free thyroxine (FT4) concentrations significantly after delivery from a mean +/- SD baseline of 0.94 +/- 0.13 ng/dl in cord blood to a mean +/- SD peak of 2.6 +/- 0.6 ng/dl 48 h after delivery (p less than 0.001 at 3, 24, and 48 h), while their free triiodothyronine (FT3) levels increased from a mean +/- SD baseline level of 2.3 +/- 0.5 pg/ml in cord blood to a mean +/- SD peak of 3.7 baseline level of 2.3 +/- 0.5 pg/ml 48 h after delivery (p less than 0.001 at 24 and 48 h). Seven term newborns with transient low Apgar scores at birth (group 2) and seven term neonates born to mothers with toxemia or hypertension (group 3) failed to increase their FT4 and FT3 concentrations above baseline during the first 48 h of life. FT4 and FT3 values at 3, 24, and 48 h were significantly higher in the control group than in groups 2 and 3. Cord blood thyroid-stimulating hormone, FT4, and FT3 levels were not statistically different in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1985

Impaired somatomedin generation test in children with insulin-dependent diabetes mellitus.

Recent studies have suggested a partial block in somatomedin (SM) production or growth hormone (GH) action in IDDM. Twelve well-nourished diabetic children (9 males and 3 females with a mean age of 11.2 +/- 3.3 yr), six with an HbA1c of 7.9-11.2% (group A) and six with an HbA1c of 12.5-15.6% (group B), were studied as follows: the GH response after 100 micrograms of oral clonidine and the SM generation capacity after i.m. administration of 0.2 U/kg/dose of human growth hormone (hGH) for 4 days. Group B diabetic subjects had a significantly higher mean +/- SD GH increase after clonidine than did group A patients (delta of 17.4 +/- 4.9 versus 5.7 +/- 6.0 ng/ml, P less than 0.01); the basal GH of both groups were similar (1.6 +/- 0.7 versus 2.3 +/- 1.4 ng/ml). In contrast, the SM response to hGH was significantly decreased in group B children as compared with those in group A (delta of 0.3 +/- 0.3 versus 1.2 +/- 0.4 U/ml, P less than 0.01). The basal SM levels of both groups were normal for age. GH and SM correlated with HbA1c levels (r = +0.80, P less than 0.01; r = -0.79, P less than 0.01, respectively); there was no correlation with plasma and urine glucose or serum cholesterol, cortisol, and transferrin. Our data indicate a blunted SM response to hGH in group B diabetic subjects; this defect in SM generation is apparently not present in group A subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Abnormalities of thyroid function in infants with Down syndrome.

We describe 12 of 1130 infants with Down syndrome in whom various degrees of thyroid dysfunction were detected by neonatal screening. These aberrations were confirmed subsequently in 11 patients. In eight of 11 children, persistent primary hypothyroidism, was diagnosed, whereas in the remaining three patients transient thyroid abnormalities were noted. The twelfth patient died and could not be retested. We found an incidence of persistent primary congenital hypothyroidism in infants with Down syndrome of 1:141, or about 28 times more than in the general population. The cause of thyroid aberrations in these infants remains unclear; none of the studied patients had agenesis or ectopia of the thyroid gland. On initial screening most infants with Down syndrome had only mild biochemical abnormalities, with gradual decompensation occurring thereafter. Infants with Down syndrome are therefore at high risk for congenital hypothyroidism and should have careful follow-up to prevent further deterioration of their mental development or growth.

Child, Preschool↗
PubMed1984

A clinical syndrome of mild androgen insensitivity.

We studied four patients from three kindreds who had normal male body habitus and external genitalia except for short penile length and gynecomastia. Prostate size was small in all patients and spermatogenesis was decreased markedly in one and absent in three. Testicular biopsies in two patients revealed normal histology but evidence of spermatogenic arrest at the spermatocyte stage. Circulating levels of testosterone and LH were increased and the testosterone-dihydrotestosterone ratios were normal. Plasma estradiol was elevated in three of the four patients. Serum FSH levels were significantly elevated in only one patient. The response of LH and FSH to LHRH stimulation was normal in the two patients who were tested. Despite the normal male phenotype, the laboratory studies suggested the diagnosis of androgen insensitivity. This was confirmed in two patients by finding decreased dihydrotestosterone-binding capacity in genital skin fibroblasts. Two of the patients had normal levels of androgen receptor binding, suggesting that their defect represented a mild form of androgen insensitivity with normal receptor activity. These results demonstrated that mild forms of androgen insensitivity exist in which the only obvious clinical manifestations may be the presence of reduced penile length, gynecomastia, and/or infertility. The incidence of androgen insensitivity among men with these subtle phenotypic abnormalities, including infertility, remains to be determined.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1983

Decreased secretion of cortisol and ACTH after oral clonidine administration in normal adults.

Clonidine, a selective noradrenergic receptor agonist, has been shown to affect various hormones acutely. It increases growth hormone levels in animals and in human adults and children. The effect of clonidine upon ACTH and cortisol levels is not as clear, and both stimulatory and inhibitory effects have been reported. We found a significant decrease in plasma cortisol decreased. No changes in FSH, LH, or prolactin were seen after oral clonidine. Our data are compatible with an inhibitory noradrenergic mechanism modulating ACTH and cortisol secretion in normal adults.

Adrenocorticotropic Hormone↗
PubMed1983

Calcitonin and calcium therapy in an infant with osteogenesis imperfecta congenita.

Calcitonin has been helpful in the treatment of osteogenesis imperfecta tarda inhibiting bone mineral resorption. The experience with salmon calcitonin in the early treatment of osteogenesis imperfecta congenita is very limited. Here we report an infant with this disorder treated with calcitonin from 3 to 15 months of age with clinical and radiographic improvement.

Bone Resorption↗
PubMed1983

Turner syndrome patients with a ring X chromosome.

A patient with clinical features of Turner syndrome and a 45,X karyotype in repeated blood cultures was re-evaluated when she spontaneously entered puberty. A ring X cell line was found in a small proportion of fibroblasts. A review of 35 previously published ring X cases is presented. All are mosaic, the major cell line in most cases being 45,X. There is wide variation in the frequency with which the abnormalities associated with Turner syndrome are found in these patients. All have short stature. Some are sexually developed and fertile. Cardiovascular anomalies are uncommon. This phenotypic variation may have at least two causes: the size of the deleted portion at each end of the X chromosome, and the relative frequency and distribution of 45,X and 46,X,r(X) cell lines in various body tissues.

Child↗
PubMed1983

Sibship with 17-ketosteroid reductase (17-KSR) deficiency and hypothyroidism. Lack of linkage of histocompatibility leucocyte antigen and 17-KSR loci.

A family with nine children, three with male pseudohermaphroditism due to testicular deficiency of 17-ketosteroid reductase activity (17-KSR) and four with congenital hypothyroidism is presented. The three subjects with 17-KSR deficiency were raised as females until puberty, at which time they assumed a male gender role. Only one developed gynecomastia. Laparotomy on one of the three patients revealed normal epididymi and vas deferens with absence of Mullerian structures. Testicular biopsy in all three showed Leydig cell hyperplasia, hyalinization of the tubular basement membrane, normal Sertoli cells and maturational arrest at the spermatogonial stage. The endocrine profile in peripheral blood revealed markedly increased plasma androstenedione concentrations but normal testosterone, dihydrotestosterone, progesterone, 17-hydroxyprogesterone, and dehydroepiandrosterone. The levels of estradiol and estrone and of LH and FSH were elevated. Genital skin fibroblasts from the three patients exhibited normal dihydrotestosterone-binding activity and 5 alpha-reductase activity. Congenital hypothyroidism affected one of the three siblings with male pseudohermaphroditism. All four hypothyroid patients had thyroid enlargement and significant titers of circulating antithyroglobulin but not antithyroid microsomal antibodies. Neither the locus for the 17-KSR enzyme nor that for congenital hypothyroidism were linked to the histocompatibility leucocyte antigen complex in this sibship. Transmission of the trait for both congenital hypothyroidism and 17-KSR deficiency appeared to be autosomal recessive.

17-Hydroxysteroid Dehydrogenases↗
PubMed1982

Oral clonidine-an effective growth hormone-releasing agent in prepubertal subjects.

The effects of clonidine, metoclopramide, and insulin on growth hormone, cortisol, and glucose concentrations in the blood of 17 healthy prepubertal short children (Group A) and five prepubertal growth hormone-deficient children (Group B) were evaluated. The peak serum growth hormone values after insulin and clonidine were significantly higher than after metoclopramide administration. Growth hormone values did not rise above baseline values in Group B patients with any of these three stimuli. Plasma cortisol concentrations did not change with metoclopramide but increased significantly with insulin and decreased significantly after clonidine; no changes in glucose values were noted with either clonidine or metoclopramide. Clonidine appears to be a reliable, sensitive, and safe out-patient stimulation test of growth hormone reserve in prepubertal children, whereas metoclopramide seems not to be a suitable growth hormone-releasing agent in this age group.

Administration, Oral↗
PubMed1982

Adrenal cortical carcinoma in a 4-year-old child: temporal changes in steroid secretion.

A case is reported of a 4-year-old female with an adrenal cortical carcinoma that developed at the site of a previously removed adrenal gland. Initially, the tumor was only virilizing, but with time, it also became the source of a large secretion of glucocorticoids and, to a lesser degree, mineralocorticoids. It is one of the largest and most functional tumors described in a child.

Adrenal Cortex Neoplasms↗
PubMed1980

Are constitutional delay of growth and familial short stature different conditions?

Children between 2 and 4 standard deviations below the mean height for age with no specific cause to account for their short stature are usually considered to represent either constitutional delay of growth (CDG) or familial short stature (FSS). This study was undertaken to determine whether 167 patients who were referred to our clinic for short stature could be divided into two distinct populations that fit the criteria of CDG and FSS. When the patients were artificially divided into 2 subgroups based on skeletal age greater or less than 2 standard deviations below the mean, no significant difference in growth rates or midparental heights could be found between them. Height ages were significantly more delayed in the group with greater skeletal age delay. Midparental height of our total population of short children was less than the mean midparental height of normal American children. It was concluded that our patients did not distribute into these two clear-cut entities. Whether they represented one continuum or two largely overlapping populations could not be decided on the basis of our data.

Age Determination by Skeleton↗
PubMed1980

Glucocorticoid and partial mineralocorticoid deficiency associated with achalasia.

A number of patients with ACTH unresponsiveness resulting in glucocorticoid deficiency with normal mineralocorticoid activity have been described. This could be due to an inherited defect within the adrenal gland causing primary unresponsiveness to ACTH or to an inherited progressive degenerative process. The association of achalasia, lack of lacrimation, and glucocorticoid deficiency in two pairs of siblings with normal mineralocorticoid activity has been recently reported. Our case describes an 8.8-yr-old female with glucocorticoid insufficiency, partial mineralocorticoid deficiency, achalasia, and evidence of decreased lacrimation. Sodium depletion produced hyponatremia, and she was unable to increase her plasma aldosterone levels sufficiently, although PRA was markedly elevated. Our case may be part of a progressive degenerative process, possibly affecting both the autonomic nerve structures and the adrenal gland, leading not only to glucocorticoid deficiency but also to abnormal mineralocorticoid secretion.

17-Hydroxycorticosteroids↗