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Biomedical subjects

P D Woolf

Publications and source records attributed to P D Woolf.

At least 73 records · Page 4Linked to original sources
PubMed1979

Counterregulatory hormonal responses to rapid glucose lowering in diabetic man.

To define whether rapid rate of fall in blood glucose stimulates counterregulatory hormonal responses in diabetic man, blood glucose in eight hyperglycemic diabetic subjects was rapidly lowered by intravenous insulin administration. Despite precipitous declines in blood glucose, plasma epinephrine and growth hormone remained virtually unchanged. In contrast, norepinephrine and cortisol increased significantly (P less than 0.025) in the face of hyperglycemia or euglycemia, while glucagon was suppressed (P less than 0.025). A transient modest fall in mean arterial pressure and a rise in pulse rate were noted. No correlation was observed between glucose disappearance rate or decrement in glucose concentration and the hormonal responses. After sham insulin administration, no change was observed in plasma epinephrine, norepinephrine, and cortisol levels. These findings suggest that rate of fall in blood glucose per se is not a primary signal for counterregulatory hormonal response. Cortisol but not growth hormone release during falling blood glucose in diabetic subjects can occur despite elevated blood glucose levels. The etiology of norepinephrine and cortisol change is unclear.

Adult↗
PubMed1979

Hypothalamic-hypopituitarism due to temporal arteritis.

Hypothalamic hypopituitarism developed in a 74-year-old woman who was in the active phase of temporal arteritis. Hypopituitarism was established by low basal gonadotrophin, thyroxine, and thyroid-stimulating hormone levels. The failure of growth hormone and prolactin to respond to insulin hypoglycemia and an inadequate prolactin response to the administration of chlorpromazine provided further evidence of hypopituitarism. The hypothalamic origin of the hypopituitarism was suggested by quantitatively normal prolactin and gonadotrophin responses to the administration of gonadorelin (gonadotrophin-releasing hormone) and protirelin (thyrotrophin-releasing hormones). Despite the frequency of other intracranial neurological lesions, injury to the hypothalamus and pituitary gland is rare in temporal arteritis. This apparent protection may be due to the abundant blood supply to the hypothalamic-pituitary region.

Aged↗
PubMed1979

Hypothalamic-pituitary-ovarian axis in uremic women.

Menstrual abnormalities are common with decreasing renal function and uremia. Maintenance hemodialysis therapy partially corrects some of the abnormalities. Since the pathophysiology of the menstural irregularities is unknown, the secretion of LH, FSH, estrogen, and PRL was studied under basal conditions and after provocative testing in 13 women undergoing chronic maintenance hemodialysis. Elevated LH concentrations were found in all six premenopausal (44.1 +/- 26.4 mlU/ml, normal follicular phase 4 to 30) and seven postmenopausal (246.1 +/- 171.4 mlU/ml, normal 35 to 200) women studied. FSH values were normal both in the premenopausal women (7.9 +/- 4.1 mlU/ml, normal 2 to 20) and in postmenopausal women (88.0 +/- 69.0 mlU/ml, normal 40 to 200). FSH and LH levels did not show typical ovulatory spikes in three of four women studied. Pulsatile hormonal release was absent. The pituitary response to LH-RH was adequate and prolonged, but the response to clomiphene citrate was variable. The study documents the existence of abnormalities at various levels of the hypothalamic-putuitary-ovarian axis.

Adult↗
PubMed1978

Dopamine affects basal and augmented pituitary hormone secretion.

Although the role of the neurotransmitter, dopamine (DA), in the regulation of PRL has been well documented, controversy exists regarding its participation in the regulation of the other pituitary hormones. Consequently, we infused DA into six healthy male subjects (ages 19-32) and studied its effects on both basal pituitary hormone levels and augmented hormonal release induced by insulin hypoglycemia (ITT), TRH, and gonadotropin-releasing hormone (GnRH). DA alone produced a modest though significant increase in GH concentration from 2.2 +/- 0.5 to 11.9 +/- 3.7 ng/ml (P less than 0.05) by 60 min, but the peak incremental GH response to ITT was significantly inhibited by DA (43.5 +/- 5.0 vs. 16.3 +/- 3.3 ng/ml; P less than 0.01). PRL concentrations fell during the DA infusion (20.4 +/- 3.0 to 10.6 +/- 1.5 ng/ml; P less than 0.02) at 235 min, and the PRL responses to both ITT and TRH were completely abolished. Although the basal LH and FSH concentrations were unaffected by DA, the incremental LH response to GnRH was inhibited (45.5 +/- 10.6 to 24.4 +/- 5.4 mIU/ml; P less than 0.05), while the FSH response was unchanged. DA significantly reduced the basal TSH concentration from 3.9 +/- 0.2 to 2.5 +/- 0.2 micro U/ml (P less than 0.01) at 230 min and blunted the peak incremental TSH response to TRH (6.0 +/- 1.5 vs. 2.9 +/- 0.9 microU/ml; P less than 0.01). DA had no effect on basal cortisol levels, the cortisol response to ITT, basal plasma glucose, or the degree of hypoglycemia after ITT. Our data provide new evidence that DA has an inhibitory as well as a stimulatory role in the regulation of GH secretion in normal humans. It inhibits centrally as well as peripherally mediated PRL secretion and blunts the LH response to GnRH. In addition, DA lowers both basal and TRH-mediated TSH release, confirming the reports of other investigators.

Adult↗
PubMed1978

Primary empty sella syndrome with panhypopituitarism, diabetes insipidus, and visual field defects.

A 58 year old woman with a history of hypothyroidism was evaluated for marked visual impairment and found to have the primary empty sella syndrome with multiple endocrine abnormalities. Visual field determination revealed preservation of vision only in the left inferior quadrants bilaterally. Failure of growth hormone (hGH), cortisol and prolactin to respond to insulin induced hypoglycaemia (0.1 U/kg), of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to respond to gonadotrophin releasing hormone (GnRH, 100 microgram) and of thyrotrophin (TSH) and prolactin to increase after thyrotrophin releasing hormone (TRH, 500 microgram), confirmed the diagnosis of panhypopituitarism. Following water deprivation with a 9% loss in body weight, her urine osmolality remained at 204 mOsm./kg H2O), indicating that she had posterior pituitary deficiency as well. During surgical exploration, which was performed in an effort to improve her markedly impaired vision, a compromised vascular supply to the left optic nerve and chronic arachnoiditis was demonstrated. This case represents one extreme of functional impairment in a syndrome which is generally considered benign and which rarely requires therapeutic intervention. Our patient is compared to 29 reported cases of the primary empty sella syndrome with visual field defects. The operative findings in eight of these cases are reviewed. The need for a multidisciplinary approach and close follow-up of patients with an empty sella and functional deficits is emphasized. Surgical intervention including lysis of adhesions and chiasmapexy has been effective in selected cases in reversing or stabilizing visual field abnormalities.

Adolescent↗
PubMed1977

Hypothyroidism and amenorrhea due to hypothalamic insufficiency. A study in four young women.

Four women, aged 17 to 23, were evaluated for secondary amenorrhea of 12 to 36 months' duration. All were considered to have hypothalamic hypothyroidism on the basis of low thyroxine (T4) concentrations, inappropriately low thyrotropin (TSH) levels, with a normal TSH response to thyrotropin-releasing hormone (TRH, 500 microgram intravenously) in three, and absence of a pituitary lesion. Nevertheless, menses did not resume after adequate replacement with thyroid hormone. Investigation of the pituitary-gonadal axis revealed a normal increase in both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) following the intravenous administration of gonadotropin-releasing hormone (GnRH). Three subjects received clomiphene citrate, 100 mg/day for five days, but a normal menstrual cycle was not induced. It is concluded that the amenorrhea was not due to thyroid hormone deficiency but, like the hypothyroidism, to a hypothalamic abnormality involving secretion of the appropriate releasing hormone.

Adolescent↗
PubMed1977

Germinal cell aplasia: response of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone to LH/FSH-releasing hormone with histopathologic correlation.

Five male patients with infertility due to biopsy-proven germinal cell aplasia were given a 100-microng bolus of luteinizing hormone (LH)/follicle-stimulating hormone (FSH)-releasing hormone (LRH), and the resultant LH, FSH, and testosterone responses were correlated with their histologic patterns on testicular biopsy. The basal and stimulated FSH values were elevated in four of five patients. Basal LH values were elevated in three patients, while two clearly had exaggerated LH and testosterone responses to LRH. Although there was little correlation between various parameters, elevated basal LH values were associated with Leydig cell hyperplasia. Higher basal FSH levels were present when fibrosis and complete aplasia of germinal elements were found in the same biopsy specimen, and the magnitude of the FSH response to LRH correlated positively with the basal concentration. The findings of elevated basal LH values, an exaggerated LH response to LRH, lack of testosterone response, and Leydig cell hyperplasia indicate a definite disturbance of the LH-testosterone axis in many patients with germinal cell aplasia. Therefore, the regulation of secretion of both gonadotropins appears to be abnormal in this disorder.

Adult↗
PubMed1977

Effects of CNS dopamine augmentation on stimulated prolactin secretion.

The site, hypothalamic and/or pituitary, for dopaminergic inhibition of prolactin (PRL) secretion is unknown. Consequently, the effect of central dopamine (DA) augmentation on stimulated PRL release was determined in 5 healthy men. Regular insulin (o.1 U/kg i.v.), a potent central stimulus for PRL secretion, and TRH, a direct hypophyseal stimulus, were given alone or one hour after the third and fourth doses, respectively, of L-dopa plus the peripheral decarboxylase inhibitor, carbidopa (Sinemet 20/200 or 25/250 every 6 hours). PRL increased from 26.6 +/- 5.8 to 48.8 +/- 5.2 ng/ml (p less than 0.01) 40 minutes after insulin administration. In contrast, during Sinemet therapy the hypoglycemia-mediated PRL release did not occur, and the PRL levels were significantly lower than after insulin alone from 40 through 180 minutes. Following TRH, neither the maximal PRL rise (69.3 +/- 3.2, TRH alone vs 48.7 +/- 19.8 ng/ml, TRH + Sinemet) nor the maximal increment (37.5 +/- 5.5 vs 29.9 +/- 20.3 ng/ml) was significantly affected by Sinemet. It is concluded that central DA augmentation abolishes central but not peripherally mediated PRL release.

Adult↗
PubMed1976

Thyrotoxicosis with painless thyroiditis.

Four women and one man with painless subacute thyroiditis presented with hypermetabolic signs and symptoms. Thyroxine (T4) and triiodothyronine (T3) resin uptakes (T3R) were increased but the 24 hour radioactive iodine (RAI) uptakes were less than 1 per cent. Surreptitious use of thyroid hormone was excluded. The thyroid was enlarged in one patient and nontender in all. Exophthalmos was absent. The protein-bound iodine level was 1.1 to 9.5 mug/dl greater than the T4 level. The sedimentation rate was normal or minimally increased, and antithyroglobulin and antimicrosomal antibodies were undetectable. In one hospitalized patient 84 per cent of the administered dose of 131I was recovered in the urine within 48 hours (normal 64 per cent) excluding extrathyroidal uptake. In all subjects the T4 and T3R levels fell to normal or slightly below normal within one to four months. An increase in the 2 and 24 hour RAI uptake to minimally increased or high normal values and return of the T4 and T3R levels to normal occurred in four of five patients within six months. In one of these, the administration of thyroid-stimulating hormone (TSH) resulted in an appropriate increase in 24 hour RAI uptake from 14.9 to 37.1 per cent. One woman remained clinically hypothyroid for six months with a low T4 concentration (3.2 mug/dl), an elevated TSH level (48 muU/ml) and evidence of a persistent organification defect -- two hour RAI uptake decreasing from 33 to 23 per cent after the administration of perchlorate and the 24 hour RAI uptake increasing from 32 to 76 per cent following the administration of TSH. At 21 months after the initial onset of her illness, she is euthyroid but increased RAI uptake persists. The clinical course in four of the five patients is similar to that in an additional eight patients treated during the same time period who presented with typical subacute thyroiditis. Thus, these patients have a form of painless subacute thyroiditis which presents as thyrotoxicosis but is differentiated from it by a low RAI uptake and in whom recovery of thyroidal iodine trapping is the first indicator of recovery. The hyperthyroidism is self-limiting and should be treated conservatively.

Adult↗