Biomedical subjects
Publications and source records attributed to H M Lloyd.
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.
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.
Experience of primary hyperparathyroidism (PHPT) at the Royal Brisbane Hospital was reviewed to determine the effect of multiphasic biochemical screening, introduced during 1970, on the rate of diagnosis of this disease. In the period 1959-1970, there were 28 proved cases and, in the period 1971-1974, 41 cases, an increase from 2.5 to 11.7 cases per annum. The main factor contributing to this increase was the inclusion of plasma calcium in the multiphasic screening programme, together with correction of the plasma calcium for the total protein concentration in the same blood sample.