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Biomedical subjects

R M Blizzard

Publications and source records attributed to R M Blizzard.

At least 109 records · Page 6Linked to original sources
PubMed1972

Serum follicular-stimulating hormone and luteinizing hormone as measured by radioimmunoassay correlated with sexual development in hypopituitary subjects.

Serum follicular-stimulating hormone (FSH) and luteinizing hormone (LH) as determined by radioimmunoassay, were correlated with sexual development in 29 patients with hypopituitarism (ages 14.2-29.9 yr).16 of 25 idiopathic hypopituitary patients (20 males and 5 females) exhibited some degree of sexual development. Stage III of sexual development or beyond was achieved by 12 of the 16. Of 13 patients with growth hormone (GH), adrenocortical-stimulating hormone (ACTH), and thyroid-stimulating hormone (TSH) deficiency, 8 did not develop beyond stage I. In contrast, five of six patients with GH deficiency without ACTH or TSH deficiency developed to stage III of sexual development or beyond. The mean (+/-sd) serum LH concentration while in stage I (4.3 +/-0.9 mIU/ml) of eight patients (seven males and one female) who developed beyond stage I was significantly (P < 0.005) greater than the mean serum LH concentration (2.3 +/-0.9 mIU/ml) in nine patients (seven males and two females) who had not developed beyond stage I. Mean serum FSH concentrations were not different. Three of four males with organic hypopituitarism did not develop beyond stage I of sexual development. Serum FSH and LH concentrations in the idiopathic and organic hypopituitary patients were more compatible with stage of sexual development than with age. A serum LH concentration below the range of normal for stage I of sexual development in a prepubertal patient suggests that the patient will remain sexually infantile as an adult.

Adolescent↗
PubMed1972

Serum thyrotropin responses to synthetic thyrotropin-releasing hormone in normal children and hypopituitary patients. A new test to distinguish primary releasing hormone deficiency from primary pituitary hormone deficiency.

Synthetic thyrotropin-releasing hormone (TRH) was administered intravenously in a dose of 7 mug/kg to 20 normal children ages 4-13 yr. Serum thyroid-stimulating hormone (TSH) was measured by radioimmunoassay and rose from a mean value of 1.7 muU/ml (range = < 1.25-7.2) to a mean peak value of 21.5 muU/ml (5.2-33.2) at 15 or 30 min after administration.13 patients with idiopathic hypopituitarism and apparent normal thyroid function, ages 3-19 yr, responded to TRH in a manner very similar to the control subjects: TSH rose from a mean value of 1.8 muU/ml (range < 1.25-4.3) to a mean peak value of 18.5 muU/ml (range = 9.5-45.0) which occurred between 15 and 60 min after TRH.13 idiopathic hypopituitary patients with documented thyroid deficiency were tested after thyroid therapy had been discontinued for a minimum of 10 days. The serum TSH values in 10 of 13 patients rose from a mean base line level of 2.2 muU/ml (< 1.25-5.3) to a peak mean value of 32.5 muU/ml (9.6-61.3) between 30 and 120 min after TRH. In three patients, however, little or no TSH response was detected, even when serum thyroxine levels were extremely low. Similar to the latter group, three of five patients with hypopituitarism secondary to craniopharyngiomas had undetectable or barely measurable TSH levels before and after TRH. Two of these five patients had significant responses which were compatible with hypopituitarism resulting from damage to the hypothalamus or hypothalamic vessels instead of the pituitary. Side effects were experienced in 41 of 54 patients (76%). The effects were limited to a mild nausea-like sensation in 63% of the patients and occurred within the first 5 min after receiving TRH. No evidence of serious toxicity or long-term side effects was noted. The TRH test is a safe, effective way to measure TSH reserve in children. The positive response in 10 of 13 patients with secondary hypothyroidism supports data previously accumulated that most patients with idiopathic hypopituitarism have an abnormality of their hypothalamic-releasing hormone function, whereas the remaining minority probably have primary pituitary disease.

Adolescent↗
PubMed1972

Human prolactin and thyrotropin concentrations in the serums of normal and hypopituitary children before and after the administration of synthetic thyrotropin-releasing hormone.

Synthetic thyrotropin-releasing hormone (TRH) was administered to normal children and hypopituitary patients in a dose of 7 mug/kg i.v. over 30-60 sec. Serum thyrotropin (TSH) and prolactin (HPr) concentrations were measured by radioimmunoassay before and at 15-min intervals for 2 hr after TRH. In 20 normal children HPr rose from a mean baseline value of 7.0+/-1.2 (SEM) ng/ml to a mean peak value of 39.5+/-5 ng/ml. In 11 patients with growth hormone (GH) deficiency without TSH deficiency. HPr values rose from a mean baseline of 3.6+/-0.8 ng/ml to a mean peak value of 13.9+/-2.8, a significantly less peak response as compared with normal children (P < 0.005). The TSH responses to TRH, however, were statistically indistinguishable from those of normal children. In 10 patients with GH and TSH deficiency both the mean baseline HPr levels (25.0+/-5 ng/ml) and the mean peak HPr levels after TRH (68.5+/-10 ng/ml) were significantly higher (P < 0.005 and < 0.025) than those of normal children. Similar comparisons were also true for the peak TSH responses (P < 0.05). Two panhypopituitary patients released no TSH and only small amounts of HPr after TRH. After thyroid replacement therapy in eight of the patients with GH and TSH deficiency, the mean HPr baseline levels (7.6+/-1.0 ng/ml) and peak levels (23.3+/-4.6 ng/ml) after the same dose of TRH were significantly less than their pretreatment levels (P < 0.001 and < 0.01) and were within the range for normal children. Synthetic TRH stimulates the simultaneous release of TSH and HPr in normal children and most hypopituitary patients. When the concentrations of thyroxine (T4) and triiodothyronine (T3) are low, the levels of HPr before and after TRH are elevated. After thyroid replacement therapy, HPr levels decrease to normal. T4 and/or T3 may condition the production or effects of prolactin-inhibiting factor (PIF) activity. The TSH and HPr responses after TRH in hypopituitary patients will determine whether the primary defect resides in the pituitary or hypothalamus, but cannot delineate the hypothalamic defect as a deficiency of hypothalamic hormone production or neurohumoral transmission.

Adolescent↗
PubMed1972

Growth hormone: metabolic clearance rates, integrated concentrations, and production rates in normal adults and the effect of prednisone.

A constant withdrawal pump was used to determine the integrated concentration of growth hormone (ICGH) which was used in conjunction with the metabolic clearance rate (MCR) of growth hormone (GH) to calculate the GH production rates (GHPR) in normal adults, acromegalics, and normal controls receiving prednisone. The mean ICGH for 22 premenopausal females on no medication was 3.0+/-1.6 ng/ml (sd) which is significantly lower (P < 0.005) than the mean of 6.6+/-2.9 for 10 women receiving oral contraceptives and significantly higher than the means of 1.5+/-0.75 for 5 postmenopausal females (P < 0.05) and 1.8+/-1.0 for 16 adult males (P < 0.01) which are comparable. The mean GHPR's in mg/24 hr per m(2) for the four groups are: normal females = 0.52+/-0.24 (sd), females receiving contraceptive pills = 1.65+/-0.58 (P < 0.005), postmenopausal females = 0.26+/-0.12 (P < 0.025), and adult males 0.35+/-0.23 (P < 0.025).Three untreated acromegalic patients had ICGH's of 59, 82, and 93 ng/ml and GHPR's ranging from 14.5 to 17.9 mg/24 hr. Prednisone in a dose of 20 mg t.i.d. for 8 days significantly decreased both the ICGH and GHPR. Alternate day prednisone (60 mg in a single q.o.d. dose) resulted in less consistent inhibition of GH release which may play a role in the more normal growth seen in children receiving q.o.d. prednisone.

Acromegaly↗
PubMed1971

Sexual development, normal and abnormal.

An understanding of normal sexual development is essential to understanding abnormal sexual development. Normal differentiation of the bipotential external genitalia, reproductive ducts, and gonads are dependent upon the presence or absence of androgens from any source, the presence or absence of mullerian inhibiting factor from the fetal testes, and the number and type of sex chromosomes present respectively. Abnormal differentiation results from an imbalance of one or more of these factors or peripheral resistance to these factors.

Adrenal Hyperplasia, Congenital↗