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Biomedical subjects

R T Kirkland

Publications and source records attributed to R T Kirkland.

At least 19 recordsLinked to original sources
PubMed1989

Growth hormone testing in short children and their response to growth hormone therapy.

Because current concepts of growth hormone (GH) testing and GH treatment have become controversial, we investigated the GH secretory patterns in children with normal and short stature. Twenty-four-hour serum GH levels were evaluated in three groups of children. Group 1 was composed of children with normal height (mean height = 0.02 SD, n = 33); group 2 was composed of short children (less than 5th percentile, n = 63) with normal results on provocative GH testing; and group 3 was composed of short children (less than 5th percentile, n = 7) with subnormal results on provocative GH testing. Mean +/- SD (range) GH levels during 24-hour studies of GH secretion were 1.6 +/- 1.1 (0.5 to 5.6), 1.8 +/- 1.2 (0.6 to 6.3), and 0.9 +/- 0.4 (0.5 to 1.7) ng/ml in groups 1, 2, and 3, respectively. No statistical difference existed in mean GH levels between groups 1 and 2 or between groups 1 and 3. The mean GH concentration from 24-hour studies in group 2 children did not correlate with chronologic age, height standard deviation, growth rates, or insulin-like growth factor 1 levels. The linear growth rate of 26 of 28 children in group 2 who received GH therapy for 6 months improved by 2 cm/yr or more; the mean +/- SD growth rate was 4.0 +/- 1.3 and 8.8 +/- 2.0 cm/yr during control and treatment periods, respectively, for these 28 children. Mean GH levels from testing did not predict response to GH during 6 months of therapy. Children with slower growth rates responded better to GH therapy (p less than 0.05). We conclude that (1) in 24-hour studies, GH levels in normal children overlapped with those of short children, including those with classic GH deficiency, (2) in 24-hour studies, GH levels did not predict responses of linear growth to short-term GH treatment, nor did they correlate with children's heights or growth velocities, and (3) the majority of short children in group 2 treated with GH for 6 months had an increase in linear growth velocity, the mean +/- SD change being 4.8 +/- 2.0 cm/yr.

Child↗
PubMed1986

Comparison of adrenal cortical tumors in children and adults.

Morphologic features (abnormal mitoses, necrosis, vascular and capsular invasion, broad fibrous bands, cellular pleomorphism, size) previously suggested to be predictors of malignant behavior in adrenal cortical tumors were assessed individually in 23 (17 benign, 6 malignant) pediatric and 42 (29 benign, 13 malignant) adult tumors. Of these features, size was the only predictor of malignancy in pediatric tumors. All pediatric tumors weighing more than 500 g were malignant and all but one weighing less than 500 g were benign. The remaining features were present in both benign and malignant pediatric tumors, and pediatric benign tumors were significantly more likely to have mitoses (P less than 0.01), necrosis (P less than 0.001), broad fibrous bands (P less than 0.005), and moderate to severe pleomorphism (P less than 0.01) than were adult benign tumors. The authors conclude that pediatric tumors are more likely to be benign than previously thought, and that size is the only morphologic predictor of their biologic behavior.

Adenoma↗
PubMed1986

Central diabetes insipidus. 22 years' experience.

The etiology of diabetes insipidus (DI) was determined in 73 children evaluated from 1962 through 1983. Intracranial tumors produced DI in 34 children, but 27 of these 34 children developed DI only after excision of the tumor. Diabetes insipidus occurred in ten children with intracranial birth defects, eight with severe central nervous system infections, and six with histiocytosis. Six had other causes. No etiology was detected in nine. Division of the cases into two time periods (1962 through 1972 and 1973 through 1983) revealed a decrease in the frequency of idiopathic DI (26.7% to 8.6%), an increase in the frequency of intracranial birth defects (0% to 17.3%), and an increase in the frequency of severe central nervous system infections (0% to 13.8%). Significant changes in therapy for DI have occurred during these 22 years. Use of desmopressin acetate has facilitated treatment of this complex management problem.

Brain Neoplasms↗
PubMed1979

Growth increments with low dose intermittent growth hormone and fluoxymesterone in first year of therapy in hypopituitarism.

The availability of a commercial preparation of human growth hormone (hGH) prompted a study in children with hypopituitarism to determine the efficacy of a lower dose of hGH. Thirteen children, ages 4 years 3 months to 13 years 7 months, were given hGH concomitant with fluoxymesterone in an intermittent regimen. The hGH was given intramuscularly, 1 IU daily for 12 to 36 days in each course. There were four courses per year. The fluoxymesterone was given orally, 1 to 2 mg. The total amount of hGH administered was between 48 and 112 IU per year, as compared with the regimen of 312 IU per year, 2 units three times a week. The growth velocity in all 13 children improved, and the mean growth velocity was 6.4 cm +/- 1.13 SD. The mean bone age increment was 0.57 years +/- 0.14 SEM in one chronological year of therapy. The low dose regimen permits a significant reduction in cost of hGH without causing undue advance in bone age.

Adolescent↗
PubMed1978

Familial hypopituitarism with large sella turcica.

We studied endocrine function in three siblings with short stature and enlargement of the sella turcica. Sellar volumes were 5.9, 3.7 and 4.0 standard deviations above age-specific means. Computed tomography or pneumoencephalography showed full sellae without suprasellar extension. Basal thyrotropin levels were low despite hypothyroidism and increments were less than 3 micromicron per milliliter after thyrotropin-releasing hormone injection. Stimulated growth hormone levels were less than 5 ng per milliliter, declining to less than 2 ng per milliliter after thyroxine treatment. Both thyroxine and growth hormone treatments were required for rapid growth. Impaired thyrotropin responses to thyrotropin-releasing hormone distinguish these patients from most cases of idiopathic or familial deficiency of thyrotropin and growth hormone. Persistent deficiency of growth hormone during thyroxine treatment indicates that the defects is not limited to thyrotropin structure or release. The findings are compatible with either familial neoplasia of the anterior pituitary or a regulatory defect promoting anterior pituitary-cell hyperplasia and inhibiting thyrotropin and growth hormone release.

Adolescent↗
PubMed1977

Bilateral testicular tumors in congenital adrenal hyperplasia.

A 22-year-old male with bilateral testicular tumors and the 21-hydroxylase variety of congenital adrenal hyperplasia (CAH) was studied. Preoperatively, on his usual glucocorticoid regimen, his urinary pregnanetriol excretion was increased (8.0-23.5 mg/day), serum LH and FSH were normal to increased (14.3-28.7 mIU/ml and 13.2-19.5 mIU/ml, respectively) and testosterone (T) was normal to decreased (176-600 ng/dl). At surgery, testicular vein concentrations of 17-alpha-hydroxyprogesterone (17-OHP) and adnrostenedione (delta) were increased (30.1 mug/dl and 38.3 mug/dl respectively) while T was decreased (1,503 ng/dl); a positive peripheral vein--testicular vein gradient was not seen for these steroids. Following injection of 10 U of crystalline ACTH into the testicular artery; testicular vein concentrations of 17-OHP, delta and T increased to 729 mug/dl, 2,390 mug/dl and 9,660 ng/dl respectively. Microscopic examination of the testes revealed multinodular tumors composed of polygonal or rounded eosinophilic cells, arranged in cords, nests and clusters. The tumors extended from the hilus and compressed the adjacent testicular tissue. Electron microscopic examination of the tumors showed features, common to steroid-secreting tissues, with abundant smooth endoplasmic reticulum in close proximity to mitochondria which was moderate in number. The adjacent testicular tissue was composed of immature tubules with normally developed Leydig cells in the interstitial tissues. From these data and a survey of previous works, it was postulated that these tumors were dependent upon ACTH for growth and steroid secretion. In view of the high serum LH concentration seen in association with incomplete suppression of adrenal steroid secretion in this study and the association of evidence of gonadotropin secretion with testicular tumors in other CAH patients, LH may also have contributed to the growth of these tumors.

17-Ketosteroids↗
PubMed1977

Male pseudohermaphroditism with partial androgen insensitivity.

Androgen insensitivity was demonstrated in two male siblings with partial masculinization of the external genitalia. They had a previously undescribed defect characterized postpubertally by high plasma testosterone and luteinizing hormone concentrations with low serum follicle-stimulating hormone levels. Studies in skin fibroblasts showed normal androgen receptor affinity and capacity for 5alpha-dihydrotestosterone (DHT), normal nuclear retention of the receptor-DHT complex, and normal conversion of testosterone to DHT.

Adult↗
PubMed1976

Gonadotropin responses to luteinizing releasing factor in boys treated with cyclophosphamide for nephrotic syndrome.

Cyclophosphamide therapy of the nephrotic syndrome has been associated with oligo- and azoospermia and with abnormalities of testicular histology in adults and pubertal boys. In 15 prepubertal boys, no abnormalities of basal serum levels of LH, FSH, or T were found when they were studied 8 months to 7 years after cyclophosphamide therapy. Five boys were pubertal during therapy were found to have elevated mean basal values of gonadotropins with normal testosterone levels and elevated LH responses to LRF; the FSH responses to LRF were elevated in four patients. One of four boys who were prepubertal during therapy but pubertal at the time of testing had an elevated basal LH and LH response to LRF. Three boys who were prepubertal at the times of therapy and testing had normal LH responses to LRF. The LRF test may provide a means of identifying the patient who has sustained testicular injury and who may require testicular biopsy.

Adolescent↗