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Biomedical subjects

C W Burke

Publications and source records attributed to C W Burke.

At least 37 records · Page 2Linked to original sources
PubMed1987

Factors in the outcome of transsphenoidal surgery for prolactinoma and non-functioning pituitary tumour, including pre-operative bromocriptine therapy.

Radical transsphenoidal surgery in 58 patients with large non-functioning pituitary tumours relieved pressure symptoms and disconnection hyperprolactinaemia without loss of pituitary function, and verified the diagnosis. Pre-operative bromocriptine did not cause any shrinkage of non-functioning tumours (n = 8), even up to 48 weeks. Thirty-two patients not given postoperative radiotherapy are being followed-up, and although two show minor CT scan evidence of tumour regrowth, for the others the delay in radiotherapy is enabling reproduction where required. In 20 patients with non-invasive macroprolactinomas radical surgery caused no loss of pituitary function but cured eight, of whom one has relapsed; none of eight invasive prolactinomas was cured by surgery. Pre-operative bromocriptine caused marked size reduction in seven of seven macroprolactinomas, but if continued beyond 6 weeks induced tumour fibrosis and uneven shrinkage which made surgery dangerous and unproductive. Selective transsphenoidal surgery relieved hyperprolactinaemia in 70% of patients with meso- (n = 15) or microprolactinoma (n = 24) usually without loss of pituitary function: the relapse rate was 1 per 88 patient years of follow-up. Invasive prolactinomas, and macroprolactinomas showing uneven shrinkage with a short (up to 4 weeks) course of bromocriptine should have radiotherapy rather than surgery, while the patients most suited to surgery are those with mesoprolactinomas, or some macroprolactinomas with compact intrasellar shrinkage after short-term bromocriptine. Microprolactinomas generally did not benefit from surgery as compared to conservative therapy. In none of the tumour groups were the surgical findings an accurate predictor of postoperative pituitary function.

Adenoma↗
PubMed1987

Cushing's syndrome in pregnancy: the timing of definitive treatment.

Cushing's syndrome in pregnancy is rare but associated with a high fetal loss rate, premature labour and excessive maternal morbidity. There has been controversy regarding the safety and efficacy of surgical treatment during pregnancy. We describe two further cases, both due to adrenal adenomas, in whom the diagnosis was made at 28 and 31 weeks gestation. Both cases suffered from severe myopathy. The first case was not treated during pregnancy and developed wound and urinary infections after caesarean section and subsequent adrenalectomy. An incisional hernia in the caesarean section scar has been repaired twice. The second had an adrenalectomy when 29 weeks pregnant with rapid resolution of the features of Cushing's syndrome, particularly the myopathy, and had an uneventful vaginal delivery. The second case, and a review of those previously described, indicates that surgical treatment during pregnancy is safe and significantly reduces fetal losses, premature labour and maternal morbidity.

Adenoma↗
PubMed1987

The human leucocyte sodium pump in adrenocortical insufficiency.

In view of the known effects of cortisol and related compounds on sodium balance, we examined leucocyte 22Na+ efflux in patients with adrenocortical insufficiency. The ouabain-sensitive 22Na+ efflux rate constant, which reflects sodium pump activity, was lowered in secondary hypoadrenalism (mean 1.95 +/- SD 0.25 vs 2.33 +/- 0.45 h-1, P less than 0.002, n = 6). Patients with hypoadrenalism also had higher intracellular sodium content (mean 34.9 +/- SD 3.5 vs 27.8 +/- 9.5 mmol/kg dry weight, P less than 0.008) and lower intracellular potassium to sodium ratios (mean 9.7 +/- SD 0.7 vs 12.9 +/- 3.6, P less than 0.001). These defects in cellular sodium balance were corrected following replacement therapy with cortisol, prednisolone or dexamethasone. In-vitro incubation of normal leucocytes with 5-20 nmol/l dexamethasone led to an increase in the Na+/K+-ATPase activity. The effect of cortisol and related compounds on the distribution of sodium between intra- and extra-cellular fluid may be mediated by their action on the sodium pump.

Adrenal Insufficiency↗
PubMed1986

Non-functioning pituitary adenomas do not regress during bromocriptine therapy but possess membrane-bound dopamine receptors which bind bromocriptine.

Dopaminergic binding to membranes from 20 well-characterized non-functioning pituitary tumours was investigated using the radioligand [3H]spiperone; nine had failed to regress during pre-operative bromocriptine therapy. Five macroprolactinomas and six normal pituitaries were similarly investigated. High affinity dopaminergic binding sites were defined in all tissues studied. Mean dissociation constants were similar for the three groups (0.92, 0.55 and 0.51 nmol/l, respectively) but mean site numbers were greater in the prolactinomas (698) than in non-functioning tumours (131) or normal pituitaries (136 fmol/mg protein). In a pool of non-functioning tumour membranes ligand competition experiments confirmed that binding was dopaminergic. Stereospecificity was demonstrated using the (+) and (-)isomers of butaclamol. Bromocriptine was present in three non-functioning tumours that had been exposed to the drug within 24 h of surgery and it largely prevented [3H]spiperone binding; membrane washing restored [3H]spiperone binding to control values. We conclude that non-functioning tumours possess high affinity membrane-bound dopaminergic binding sites similar to those in normal pituitary and macroprolactinomas, but apparently fewer in number than in the latter. Though bromocriptine binds to dopamine receptors on non-functioning tumours in vivo, this does not result in tumour regression.

Adenoma↗
PubMed1986

Sensitive and specific bromocriptine radioimmunoassay with iodine label: measurement of bromocriptine in human plasma.

Plasma bromocriptine assays must have high sensitivity because plasma concentrations are low, and high specificity because bromocriptine is extensively metabolised. This paper describes the simple preparation of a radioiodine-labelled derivative of dihydroergocriptine and its use in a radioimmunoassay employing an antiserum directed against the intact bromocriptine molecule. The method could measure plasma bromocriptine at concentrations of 0.05 nmol/L, had between-assay coefficients of variation of less than 10% and was more convenient than previous assays using tritium radiolabels.

Adenoma↗
PubMed1986

Spironolactone in the treatment of idiopathic hirsutism and the polycystic ovary syndrome.

Forty-eight hirsute women were treated with spironolactone 100 mg twice daily for 3 to 12 months. Both facial and body hirsuties improved by 30-40%, and there was a threefold reduction in frequency of local treatments such as waxing or shaving. Plasma testosterone fell by 30%, though the improvement in hirsuties grading did not correlate with the fall in plasma testosterone. Six subjects discontinued treatment because of lack of effect, and 4 because of menstrual disturbance. Spironolactone was equally effective in the treatment of idiopathic hirsutism and of the polycystic ovary syndrome.

Adolescent↗
PubMed1986

Effect of bromocriptine treatment on the fibrous tissue content of prolactin-secreting and nonfunctioning macroadenomas of the pituitary gland.

We performed a quantitative study using a point-counting technique at the light microscope level of the fibrous tissue content of PRL-secreting and nonfunctioning pituitary macroadenomas from patients treated or untreated with bromocriptine (BC) before surgery. There was a significant increase in the fibrous tissue content of PRL-secreting, but not nonfunctioning, tumors after BC treatment. The extent of the increase in fibrous tissue in prolactinomas correlated with the duration of treatment with BO.

Adenoma↗
PubMed1985

Adrenocortical insufficiency.

Adrenocortical insufficiency causes difficulty in diagnosis and morbidity out of proportion to its rarity, because of the non-specific, multi-system nature of the clinical features. Most of these are due to cortisol deficiency. Prominent features are well-known ones such as weight loss and asthenia, and hypoglycaemia. Less prominent in recent accounts are those due to failure of cellular sodium export and to vasopressin excess, which are frequent and clinically significant. For this reason, the clinical features of isolated ACTH deficiency, isolated glucocorticoid deficiency and Addison's disease overlap greatly. In addition, cortisol deficiency has secondary endocrine effects, e.g. glucocorticoid-reversible hypothyroidism, hyperprolactinaemia and hypercalcaemia. Further overlap between the various steroid insufficiency syndromes occurs because of the association of various organ-specific autoimmune endocrinopathies with Addison's disease. Over 80% of Addison's disease is of the autoimmune type, though almost any systemic destructive process can cause similar steroid insufficiency. Demonstration of adrenal insufficiency requires various combinations of tetracosactrin adrenal stimulation tests, and hypoglycaemia or equivalent tests, if the cause is ACTH deficiency but the correct test can only be chosen to suit a firm clinical diagnosis. The treatment of adrenocortical insufficiency is described.

Addison Disease↗
PubMed1983

Thyroxine, 3,5,3' -triiodothyronine and 3,3', 5' -triiodothyronine in human amniotic fluid: relationships between concentrations and turnover.

We have made estimates of the possible contributions of various routes of entry and disposal to the turnover of thyroxine (T4), 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (reverse T3, rT3) in human amniotic fluid (AF). Our calculations suggest that, in normal pregnancy, AF T4 and T3 are derived mainly from the maternal circulation, and that their concentrations depend very largely on binding-protein concentrations. The majority of AF rT3 is unlikely to enter the amniotic sac directly from the maternal circulation, or from the fetal circulation by passive diffusion or fetal urinary excretion; however, our calculations are consistent with the hypothesis it is derived largely from inner-ring deiodination of T4 in the fetal membranes. We propose that the molar ratio of one AF iodothyronine to another may yield more information about fetal thyroid status than the total concentration of any single iodothyronine.

Amniotic Fluid↗
PubMed1983

Conversion of thyroxine to 3,3',5'-triiodothyronine in the guinea pig placenta: in vivo studies.

Studies of placental inner-ring deiodination of T4 were carried out in pregnant guinea pigs, by in situ placental perfusion. When [131I]T4 and [125I]rT3 were administered to the mother, the ratio of fetal side to maternal side [131I]rT3 was more than 10 times greater than the corresponding ratio for [125I]rT3. When radiolabeled T4 was supplied to the fetal side of the placenta in perfusion fluid, and the perfusate recycled through the placental circuit, there was a progressive increase in labeled rT3 concentration in the perfusate. These results indicate that the guinea pig placenta actively deiodinates both maternal and fetal T4 in the inner ring in vivo. We found evidence of very little outer ring deiodination of either T4 or rT3. The quantitative contribution of placental deiodination of maternal T4 to circulating rT3 in the fetus appears to be small; however, placental deiodination of fetal T4 (about 0.5 nmol/kg fetal BW X day) could contribute significantly to fetal rT3 levels. Our observations are consistent with the hypothesis that placental inner-ring deiodination of T4 plays a part in the regulation of fetal iodothyronine metabolism.

Animals↗
PubMed1982

Radioimmunoassay of thyroxine and 3,3',5'-triiodothyronine (reverse T3) in human amniotic fluid.

Measurement of amniotic fluid iodothyronine concentrations may enable antenatal detection of fetal thyroid abnormalities; however, the delineation of normal ranges is complicated by methodological problems associated with strong and highly variable protein-binding, and specificity of antisera. Improved radioimmunoassays of thyroxine (T4) and 3,3',5-triiodothyronine (reverse T3, rT3) have been developed to overcome these problems. In normal pregnancy, mean rT3 concentrations at less than 17 weeks, 17-22 weeks and 35-42 weeks gestation were 3.6 nmol/l (n = 21), 6.1 nmol/1 (n = 14) and 0.66 nmol/1 (n = 39) respectively; corresponding mean T4 concentrations were 2.4 nmol/1, 6.5 nmol/1 and 3.6 nmol/1. rT3 concentrations showed a strong positive correlation with T4 concentration in each age range; however, the molar ratio of rT3:T4 decreased progressively with gestational age, from 1.69 at less than 17 weeks to 0.19 at 35-42 weeks. In both mid- and late gestation, rT3 and T4 concentrations were strongly correlated with total amniotic fluid protein concentrations.

Amniotic Fluid↗
PubMed1982

Gynaecomastia.

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Adolescent↗