Biomedical subjects
Publications and source records attributed to H M Lloyd.
Nuclear diameter was measured and mean nuclear diameter calculated in 18 parathyroid carcinomas. In 11 of the 18 tumours mean nuclear diameter was above the range previously reported for 55 parathyroid chief cell adenomas and provides a useful discriminant in histological diagnosis.
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EDTA (calcium disodium edetate) lead mobilization and x-ray fluorescence (XRF) finger bone lead tests were done in 42 patients with chronic renal failure and without persisting lead intoxication. Nineteen of 23 patients with gout and 8 of 19 without gout had positive EDTA lead mobilization tests. Those patients with gout excreted significantly more excess lead chelate than those without gout. In the gout group 17 patients denied any childhood or industrial exposure to lead. They had a greater number of positive tests and excreted significantly more excess lead chelate than 14 patients with neither gout nor lead exposure. These results confirm that gout in the presence of chronic renal failure is a useful marker of chronic lead poisoning. Of 27 patients with positive lead mobilization tests, only 13 had elevated XRF finger bone lead concentrations (sensitivity 48%). Three of 15 patients with negative lead mobilization tests had elevated XRF finger bone lead concentrations (specificity 80%). Although the XRF finger bone lead test is a convenient noninvasive addition to the diagnostic evaluation of patients with chronic renal failure and gout, its application is limited due to the lack of sensitivity of the method.
Nuclear diameter, DNA synthesis, and mitotic index in the pituitary cells of male rats and serum prolactin were measured after a period of 8 days of treatment with a dopamine agonist and an antagonist given with and without estrogen. In the absence of estrogen, the dopamine agonist, bromocriptine, diminished the mean nuclear diameter of the pituitary cells and lowered pituitary DNA synthesis, and the dopamine-blocking agent haloperidol had no effect. Estrogen increased the mean nuclear diameter, pituitary mitotic index, and DNA synthesis. Bromocriptine prevented the estrogen-induced increase in mean nuclear diameter and pituitary DNA synthesis and mitotic index were lowered. Haloperidol augmented the estrogen-induced increase in mean nuclear diameter, pituitary DNA synthesis, and mitotic index. Positive correlations were obtained between mean nuclear diameter and DNA synthesis and serum prolactin. It was concluded that nuclear diameter was influenced by both DNA synthesis and secretory activity in pituitary cells.
Pituitary DNA synthesis and serum and pituitary concentrations of prolactin were measured in male rats given the dopamine antagonist haloperidol or pimozide, and the dopamine agonist bromocriptine. Increased DNA synthesis was observed 25h after a single injection of haloperidol and on each day of the 5-day period of pimozide administration. Haloperidol and pimozide increased serum prolactin levels. Pituitary prolactin concentrations fell 12h after haloperidol, recovering b6 24h, and 24 and 48h after pimozide, recovering by 72 h. Bromocriptine lowered pituitary DNA synthesis and serum prolactin levels and induced a transient rise in pituitary prolactin concentrations. The results indicate that dopamine agonists and antagonists modulate DNA synthesis in the pituitary gland of the rat.
DNA synthesis was measured in vitro by incorporation of [3H]thymidine into DNA in 42 parathyroid chief cell adenomas immediately after surgical removal. The results ranged from 18 to 185 DPM/microgram DNA and showed a positive correlation with pre-operative values for serum immunoreactive parathyroid hormone (r = + 0.47; P < 0.001) and plasma calcium (r = + 0.35; P < 0.05). There was no correlation between DNA synthesis and tumour weight or mean diameter of tumour cell nuclei. The results suggest that DNA synthesis and cell division in parathyroid adenomas are determined in part by the secretory activity of the tumour. DNA synthesis measured on one occasion is not necessarily an overall index of tumour growth.
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A 68-year-old white male patient suffering from Paget's disease of bone developed a sarcoma in the sacroiliac region during treatment with calcitonin. There was no evidence of its presence before treatment. Progression of the sarcoma did not appear to be influenced by calcitonin therapy.
Described here is a young woman with intermittent Cushing's disease associated with psychotic disturbance. On five occasions, over a period of four years, she became severely depressed and had acne, amenorrhea, hirsuties and moon facies. On each of the first four occasions the symptoms lasted from two to three months and disappeared spontaneously. Biochemical investigations, including plasma ACTH estimations during the last two episodes, indicated that the adrenocortical overactivity was pituitary-dependent. During the fifth relapse the patient experienced a very severe, depressive psychosis, necessitating bilateral adrenalectomy, which resulted in complete remission.
Nuclear diameter was measured in 55 parathyroid chief-cell adenomas to determine its value in histological diagnosis and to assess its relationship to other features of primary hyperparathyroidism. Mean nuclear diameter for the whole group of adenomas was significantly greater than that for the accompanying normal glands. Mean nuclear diameter in individual adenomas was significantly greater than that in the accompanying normal gland in 27 out of 34 cases. Nuclear diameter was correlated with tumour weight and with plasma calcium but was not correlated with duration of history. It was significantly greater in the group of patients with overt bone disease than in those with kidney stones and in those with neither kidney stones nor overt bone disease. Assessment of nuclear diameter is of value in histological diagnosis of parathyroid adenoma. The rate of growth of the adenoma may be a factor determining nuclear diameter.
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Haloperidol, bromocriptine and diethylstilboestrol dipropionate were given in various régimes to male rats to determine their effects on pituitary DNA synthesis, prolactin secretion and growth hormone secretion. Haloperidol increased serum prolactin but did not stimulate pituitary DNA synthesis or reduce pituitary prolactin concentrations. Haloperidol potentiated the effects of oestrogen on serum prolactin and on pituitary DNA synthesis; pituitary prolactin concentrations were greatly reduced, and growth hormone secretion was slightly inhibited. The inhibitory effects of bromocriptine in oestrogen-stimulated rats were demonstrated by smaller pituitary weights and decreased DNA synthesis; serum prolactin levels were lowered and pituitary prolactin concentrations were increased. Haloperidol, given to rats treated with oestrogen and bromocriptine, reversed the inhibitory effects of bromocriptine on DNA synthesis and serum prolactin; pituitary prolactin concentrations fell to well below normal. The results suggest that the haloperidol potentiation of oestrogen-induced pituitary DNA synthesis may depend upon stimulation of prolactin secretion together with reduction of intracellular prolactin levels.
The times of onset of oestrogen-induced prolactin secretion and DNA synthesis were studied in the pituitary gland of the male rat. At intervals from 3 to 96 h after injection of 10 mg diethylstilboestrol dipropionate, serum and pituitary prolactin concentrations were measured by radioimmunoassay and pituitary DNA synthesis by incorporation of [3H]-thymidine in vitro. Serum prolactin was raised significantly from 6 h onwards and DNA synthesis was increased from 30 h onwards. Pituitary prolactin concentration began to increase at 30 h. Significant correlations were obtained between serum prolactin and DNA synthesis from 24 to 72 h but not during the period of prolactin secretion from 6 to 24 h.
A case of Sipple's syndrome is reported, in which the full phenotype was expressed. The patient had the typical marfanoid habitus, with thickened lips and alae nasi, neuromas on lips and tongue, medullary carcinoma of the thyroid gland, phaeochromocytomas, and medullated corneal nerve fibres. The plasma calcitonin level was initially elevated, rose on calcium infusion before thyroidectomy, and was undetectably after thyroidectomy. The urinary catecholamine excretion was elevated. The plasma parathyroid hormone, adrenocorticotrophin and growth hormone levels and the serum calcium level were normal.
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Urinary adenosine -3' ,5' - cyclic monophosphate was measured in 14 patients with hypercalcaemia not caused by primary hyperparathyroidism. Increased levels were found in patients with malignant disease without bone metastases and believed to be examples of paraendocrine syndrome. Decreased levels were found in patients with metastatic carcinoma involving bone, and in patients with multiple myeloma, lymphoma and immobilisation after fracture. Results obtained during treatment for hypercalaemia are described in three patients. In two hypercalcaemic patients (one with hyperthyroidism and one with breast cancer with bone metastases) normal levels were found. This measurement is a useful substitute for assay of serum parathyroid hormone and is of value in the diagnosis of hypercalcaemia, in monitoring effects of treatment and in revealing underlying mechanisms.
Urinary adenosine 3' 5' - cyclic monophosphate (cyclic AMP) was assessed by a competitive protein binding method in 19 patients with primary hyperparathyroidism (PHPT) and in 15 control subjects. The mean value of 6.6 +/- S.E. 0-64 muM per 24 hours for the patients with PHPT was higher (P less than 0-001) than the mean control value of 3-2 +/- 0-24 muM per 24 hours. In all hypercalcaemic patients without renal insufficiency, urinary cyclic AMP excretion was more than 4 muM per 24 hours and decreased in the 15 patients investigated after parathyroidectomy. In a normocalcaemic hyperparathyroid patient and in three hyperparathyroid patients with renal insufficiency, urinary cyclic AMP was less than 4 muM per 24 hours.