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Biomedical subjects

R A Donald

Publications and source records attributed to R A Donald.

At least 163 records · Page 9Linked to original sources
PubMed1977

The pituitary-thyroid axis following surgery for thyrotoxicosis: thyrotrophin-releasing hormone tests in diffuse thyroid hyperplasia and toxic uninodular goitre.

The pituitary-thyroid axis was assessed 1 month after surgery by thyrotrophin releasing hormone (TRH) testing in thirty thyrotoxic patients treated by subtotal thyroidectomy and eleven patients with toxic uninodular goitre. All toxic nodule patients gave essentially normal TRH responses and have remained clinically and biochemically euthyroid at follow-up. Only seven of the thirty subtotal thyroidectomy patients had normal TRH tests when assessed 1 month post thyroidectomy -sixteen patients showed increased response, six gave flat responses, and one showed an anomalous minimal response. Follow-up TRH tests 12 months postthyroidectomy have shown a tendency for TRH responsiveness to return towards normal, but two patients with flat TRH tests have required radioiodine for relapse and four TRH hyperresponders are currently receiving thyroxine replacement therapy.

Adult↗
PubMed1977

Bromocriptine suppression of plasma growth hormone in acromegaly.

Twelve acromegalic patients were studied in one or more of three protocols to establish the response of plasma growth hormone (hGH) concentraions to (a) a single oral test dose of bromocriptine, (b) incremental dose therapy from 10 mg/day to 40 mg/day over 4 weeks, and (c) sustained therapy with 20 mg/day over a 3 month period. Ten of the patients studied had previously been treated by yttrium implantation, external pituitary irradiation or surgical hypophysectomy. A high incidence of side effects including postural hypotension, hallucinations and peripheral vasospasm was noted reducing the numbers of patients completing the three protocols. Suppression of hGH concentrations was disappointing; significant reductions in hGH concentraions occurred in five of eleven patients in response to a single test dose of bromocriptine, and in only one of seven patients treated with the drug over a sustained period. An impression of clinical improvement was gained in one patient, but there was no associated reduction in plasma hGH concentrations. It seems likely that acromegalic patients who have failed to respond to conventional treatment may be more resistant to bromocriptine therapy.

Acromegaly↗
PubMed1976

Measurement of pituitary hormones: clinical applications. 5. Prolactin.

A sensitive and specific assay for human prolactin has been developed using human prolactin and antiserum distributed by the United States National Pituitary Agency. Plasma prolactin concentrations in control subjects ranged from 0-20 ng/ml. No sex difference in prolactin concentration was observed. A brisk increase in plasma prolactin levels occurred in normal subjects during the administration of chlorpromazine and thyroid stimulating hormone releasing factor (TRH). These stimulatory tests of prolactin release should therefore be useful in the assessment of hypothalamic pituitary function. Basal plasma prolactin values were raised in most patients who were being treated with phenothiazines and were helpful diagnostically in patients with amenorrhoea, galactorrhoea, hypogonadism, cranio-pharyngioma, "non-functioning" pituitary tumours and acromegaly. In many of these disorders a significant reduction in the plasma prolactin concentration was observed following oral administration of bromocriptine. Plasma prolactin determinations should be useful in evaluating the response to medical treatment or pituitary ablation.

Acromegaly↗
PubMed1976

Studies with the autotransplanted ovine pancreas: glucagon and insulin secretion.

Basic studies on the secretion of glucagon and insulin by the ovine pancreatic autotransplant in the neck are described. Of the 17 transplants in the series none failed to secrete glucagon and only three failed to secrete insulin in detectable amounts. The longest surviving transplant actively secreted both hormones 3 years after transplantation and five other transplants were functional and the animals healthy after 16 months. Exocrine secretion disappears shortly after transplantation. Sodium butyrate and alanine each promoted the secretion of both hormones by the transplant. Glucagon failed to promote insulin secretion by the transplant, although it apparently stimulated the ovine in situ pancreas. The immediate (presumably direct) effect of insulin was to inhibit transplant glucagon secretion. Hypoglycaemia induced by peripheral insulin administration failed to stimulate glucagon secretion by the transplant, although it did promote glucagon secretion by the ovine in situ pancreas. Heparin did not markedly suppress basal transplant secretion of either glucagon or insulin. Phasic response patterns occurred with both hormones during long butyrate perfusions, although first-phase responsiveness was not a constant feature. In one trial, first-phase responses fell off with repeated short butyrate infusions. Glucagon and insulin secretory patterns in response to butyrate were remarkably alike, suggesting a common mechanism. Loss of specific functions by the ovine pancreas after transplantation is discussed.

Animals↗
PubMed1976

A comparison of the effect of levodopa and somatostatin on the plasma levels of growth hormone, insulin, glucagon and prolactin in acromegaly.

The acute suppressive effects of L-dopa and somatostatin (growth hormone release inhibiting hormone) on the elevated plasma GH concentrations of seven patients with acromegaly were compared. In addition the effects of the two agents on fasting concentrations of plasma glucose, insulin, glucagon and prolactin were studied. In six of the seven patients hourly samples for GH assay were taken from 08.00 to 20.00 hours on a control day. Synthetic cyclic somatostatin (100 mug) was infused intravenously in an albumin/saline solution over 75 min with a Harvard constant infusion pump. Levodopa 500 mg was given orally. Somatostatin infusion produced a reduction in plasma GH concentrations in six of seven patients (mean reduction 55%). L-Dopa produced a reduction in plasma GH concentrations in the same six patients (mean reduction 52%). The minimum GH concentrations achieved in the two tests were comparable and did not differ significantly from the minimum GH concentrations recorded during the 12 h control study. Mean plasma insulin and glucagon concentrations were also significantly reduced during the somatostatin infusion (P less than 0-025; P less than 0-05 respectively). Plasma glucose concentrations did not change. L-Dopa did not alter mean plasma glucose, insulin or glucagon values. Somatostatin did not alter prolactin values but L-Dopa suppressed basal values to less than 2 ng/ml in five patients. This study shows that the plasma GH change after the administration of L-dopa and somatostatin in acromegaly is comparable and confirms the pancreatic effects of somatostatin.

Acromegaly↗
PubMed1976

Lithium associated thyroid disease--a report of 14 cases of hypothyroidism and 4 cases of thyrotoxicosis.

Thyroid function was assessed in 80 patients receiving long-term lithium therapy. Three of the 80 patients were biochemically hypothyroid and a further patient was receiving thyroxine for lithium associated hypothyroidism. A further eight patients had elevated TSH levels and eight patients had subnormal serum triiodothyronine levels. After a 24 month follow up period seven of the 80 patients have developed clinical hypothyroidism. One patient had elevated thyroid parameters and clinical features of mild hyperthyroidism. Additional clinical and laboratory data are included from seven patients with lithium associated hypothyroidism and three patients with lithium associated thyrotoxicosis who were not included in the survey population.

Adolescent↗
PubMed1976

The effect of cyproterone acetate on the plasma gonadotrophin response to gonadotrophin releasing hormone.

Cyporterone acetate (100-150 mg daily) was administered to 8 male patients with excessive libido. Within 3 months a significant fall (P less than 0.02) in plasma testosterone was demonstrated. The plasma luteinising hormone (LH) and follicle stimulatin hormone (FSH) responses to gonadotrophin releasing hormone (LH/FSH-RH) were also significantly impaired (P less than 0.05). A direct correlation between the resting plasma testosterone level and the LH response to LH/FSH-RH was demonstrated (r = 0.743). It is concluded that the fall inplasma testosterone levels in patients receiving cyproterone acetate may be attributed to suppression of LH release, rather than an antiandrogen effect on the testis or hypothalamus.

Adult↗
PubMed1976

Aldosterone and renin-angiotensin responses to stimuli in patients with treated congestive heart failure.

Aldosterone responses to physiologic doses of known regulatory factors have been studied in 8 patients with treated congestive heart failure under standard conditions of electrolyte balance and controlled body posture. The response of plasma aldosterone, plasma renin activity (PRA), and in some instances angiotension II, to the brief (120 minute) intravenous administration of ACTH (1.25 mug beta1-24 ACTH in 60 minute and 5 mug in 60 minutes), angiotensin II (30 mug) and potassium (30 mEq.), and to 2 hours in the upright posture, was measured. The plasma aldosterone increase was greatest in response to ACTH (mean increment 20.8 ng. per 100 ml.) followed by that with upright posture (mean rise 17.1 ng. per 100 ml.), potassium (mean 6.7 ng. per 100 ml.) and angiotensin II (5.8 ng. per 100 ml.). PRA rose vigorously following 2 hours of upright posture and fell with angiotensin II infusion, but showed no definite change in response to potassium or ACTH. A diurnal pattern of PRA, angiotensin II, and plasma aldosterone on control days was observed in these patients, with higher prenoon levels falling to a nadir at midnight. The electrolyte and hormone response to administered aldosterone (75 mug over 2 hours) was also studied in the same patients. During aldosterone infusions, plasma aldosterone increased (increment range 36 to 110 ng. per 100 ml.), urine sodium excretion decreased, but no significant change in urine potassium excretion or in PRA was observed. It is concluded that small fluctuations in ACTH secretion, as well as change in body posture, produce marked effects on plasma aldosterone in patients with controlled congestive heart failure. Aldosterone responses to ACTH in these patients is similar to that observed in normal subjects.

Adrenocorticotropic Hormone↗
PubMed1975

Isochromosome for the short arm of X: a human mosaic 45,x/46,XXpi.

An 18 year female patient with short stature, amenorrhoea and poorly developed secondary sexual characteristics, has subnormal oestrogen excretion and increased levels of plasma gonadotrophin. Laparoscopy revealed streak ovaries. A reduced number of buccal mucosal cells showed positive sex chromatin. Chromosome studies of blood lymphocytes indicated mosaicism: the major cell line was characterized by an isochromosome for the X short arm, 46,XXpi; the minor cell line had a single X chromosome, 45,X.

Adolescent↗
PubMed1975

Regression of acromegaly following pituitary apoplexy.

A case of acromegaly complicated by pituitary apoplexy is described. The pituitary apoplexy occurred while the patient was under investigation in a metabolic ward permitting full assessment of pituitary function both before and immediately after the event. This demonstrated a remarkably selective reduction in the plasma growth hormone concentration with preservation of other pituitary function excluding mild diabetes insipidus. The plasma growth hormone fell from values greater than 120 ng/ml to less than 4 ng/ml. The brisk inappropriate release of growth hormone observed on stimulation with thyrotrophic hormone releasing hormone, associated with a severe headache and the onset of pituitary apoplexy two days later raised the possibility of provocative tests of pituitary function precipitating pituitary apoplexy.

Acromegaly↗
PubMed1975

Abnormal pancreatic alpha-cell function in first-degree relatives of known diabetics.

A standard intravenous glucose tolerance test utilizing a 25g glucose load was administered to 15 first-degree relatives of known diabetics and 19 normal control subjects with no known diabetic relatives. Despite normal glucose tolerance, 5 of the first-degree relatives had a significantly lower release of first-phase insulin (p 0.05). In contrast to 8 normal subjects and the remaining 10 first-degree relatives the secretion of glucagon by the 5 first degree relatives with abnormally low insulin release was not suppressed by induced hyperglycaemia. These findings provide evidence of abnormal alpha-cell function in a very early stage of genetic diabetes.

Adult↗
PubMed1975

The plasma cortisol and corticotropin response to hypoglycemia following adrenal steroid and ACTH administration.

The plasma cortisol response to hypoglycemia is widely used as a test of hypothalamic-pituitary-adrenal function. It was the aim of this study to determine whether this test gives a reliable indication of pituitary corticotropin (ACTH) release in patients recovering from adrenocortical suppression due to corticosteroid or ACTH therapy. The 16 patients who were studied (6 on more than one occasion) had received in excess of 5 mg predinisone or equivalent daily for over 12 months. The insulin tolerance tests were carried out 18 h after stopping steroid therapy. The tests were then repeated three to four days after adrenal function had been restored (as indicated by urinary oxogenic steroid excretion of greater than 35 mg/24 h) by zinc tetracosactrin administration. The ACTH response to hypoglycemia was significantly impaired in the steroid-treated group. However with the exception of one patient who had persistently elevated resting ACTH levels there was a significant correlation (P less than 0.01) between the maximum increments in plasma cortisol and ACTH during hypoglycemia. No significant difference in sensitivity to endogenous ACTH could be demonstrated between the steroid-treated group and 12 normal control subjects. Following ACTH administration the plasma ACTH and growth hormone responses to hypoglycemia were significantly reduced, but the response in plasma cortisol was not significantly affected. It is concluded that the plasma cortisol response to hypoglycemia gives a useful indication of ACTH release in steroid-treated patients provided that they have not recently received exogenous ACTH.

Adolescent↗
PubMed1975

Plasma aldosterone response to low dose ACTH stimulation.

The brief (60-min) infusion of a small amount (1.25 mug) of ACTH into 7 normal subjects on an unrestricted sodium intake resulted in a vigorous plasma aldosterone response in each case. This finding suggests that physiologic fluctuations in ACTH may significantly alter aldosterone secretion in normal man.

Adrenocorticotropic Hormone↗