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Biomedical subjects

W H Daughaday

Publications and source records attributed to W H Daughaday.

At least 127 records · Page 7Linked to original sources
PubMed1975

The Jewish Hospital of St. Louis therapeutic grand rounds no. 9. Diagnosis and therapy of acromegaly.

Acromegaly, the clinical expression of chronic hypersecretion of growth hormone, develops insidiously and is too often not recognized until the disease is advanced. However, a useful screening procedure, the measurement of serum growth hormone after an oral glucose load, is available. Though evidence suggesting that acromegaly may be a disorder of defective hypothalamic regulation of pituitary growth hormone secretion has accumulated, the pathogenesis of the diease is not sufficiently understood to permit consistently effective medical therapy. Current therapy, therefore, is directed toward destruction of growth hormone producing pituitary tissue. Patients with major suprasellar extension and chiasmal compression usually require transfrontal surgery. Patients without major suprasellar extension can be treated with external irradiation or with transsphenoidal surgery. It is our current practice to limit the former to young patients withe relatively modest elevation of the serum growth hormone concentration.

Acromegaly↗
PubMed1975

Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion.

Methysergide, a clinically-used blocker of serotonin receptors, was administered to 10 normal young men at a dose of 2 mg every 6 h for 48 h. After drug treatment, serum levels of growth hormone during sleep were 41.9% higher than placebo values (less than 0.001). In contrast, drug treatment was associated with a 36.4% decrease in stimulated growth hormone secretion during insulin tolerance testing (P less than 0.01). These opposite effects of methysergide suggest that different mechanisms are responsible for sleep-related and insulin-induced growth hormone secretion. Accordingly, data obtained with pharmacologic stimuli may lead to erroneous inferences regarding physiologic growth hormone control mechanisms. Administration of methysergide profoundly suppressed sleep-related prolactin secretion; overall nocturnal mean prolactin fell by 70.3% from 4.30+/-0.19 to 1.28+/-0.06 ng/ml (P less than 0.0001). It appears that serotonin may be significant modulating neurotransmitter for the control of growth hormone secretion, limiting sleep-related release, and enhancing insulin-induced release. It seems likely from these data that the role of serotonin in the control of prolactin secretion is relatively more important, since serotonin receptor blockade dramatically reduced sleep-related prolactin secretion.

Adult↗
PubMed1975

Steroid hormone effects on sonatomedin. I. Somatomedin action in vitro.

The effects of cortisol, estradiol, and testosterone on somatomedin action on cartilage incubated in vitro have been examined. The addition of hormones in the absence of serum had no effect on the incorporation of sulfate by cartilage from hypophysectomized rats, embryonic chicks, or normal young pigs. Normal human serum provided a source of somatomedin which stimulated the incorporation of sulfate by cartilage in a dose-response relationship; the potency of serum with and without added steroid hormone was determined after formal parallel-line analysis. Moderately supraphysiologic levels of cortisol, 17 beta-estradiol, and testosterone generally had little effect on somatomedin action in the test systems. Very high levels of serum cortisol (100-1000 mug/100 ml) inhibited somatomedin action on pig cartilage, but had little effect on rat or chick cartilage. A 20 ng/100 ml increase in serum estradiol had no effect on somatomedin action on chick cartilage, but appeared to enhance somatomedin action on pig cartilage. A 5 mug/100 ml increase in serum testosterone did not affect somatomedin action on either chick or pig cartilage. These studies suggest that the alteration of somatomedin action is not a major mechanism in the effect of steroid hormones on growth. In addition, since modest increases in serum levels of cortisol, estradiol, and testosterone had little effect on somatomedin action in our assay systems, these systems should be satisfactory for the study of hormone effects on somatomedin generation.

Animals↗
PubMed1975

Marked hyperthermia as a manifestation of hypoglycemia in long-standing diabetes mellitus.

Hyperthermia has recently been recognized as a manifestation of hypoglycemia. We describe two episodes of hypoglycemia associated with nausea, vomiting, chills, and impaired consciousness which were followed by marked hyperthermia. We suggest that the hyperthermia may result from excessive reaction to preceding hypothermia caused by the hypoglycemia. We would like to alert the clinician to the possibility of a previous, severe hypoglycemic episode in any diabetic patient with hyperthermia and coma.

Diabetes Complications↗