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Hamish M. Fraser and Robert W. Shaw

Abstract. Dysfunctional uterine bleeding is a disorder which presents problems for effective treatment and management. We have utilized the ability of chronic LRH agonist treatment to suppress ovarian steroid production to examine its effects on stumptailed macaques with a detailed history of excessive days of menstrual bleeding. Five monkeys were treated for 6 months with daily injections of D-Ser[But]6 LRH (1–9) nonapeptideethylamide. This was successful in suppressing ovarian steroid production in all monkeys as indicated by the maintenance of serum concentrations of oestradiol at < 100 pg/ml and progesterone at < 1 ng/ml. All monkeys menstruated for their typical time period during the first treatment cycle, but thereafter bleeding stopped in 2 monkeys and was considerably reduced in a further 2. In the remaining monkey, no significant improvement occurred. The results indicate that suppression of ovarian function in this way may have a significant role to play in the treatment of dysfunctional uterine bleeding.

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Stephen J Gallacher, Robert A Cowan, William D Fraser, Fraser C Logue, Andrew Jenkins and Iain T Boyle

Gallacher SJ, Cowan RA, Fraser WD, Logue FC, Jenkins A. Boyle IT. Acute effects of intravenous 1α-hydroxycholecalciferol on parathyroid hormone, osteocalcin and calcitriol in man. Eur J Endocrinol 1994;130:141–5. ISSN 0804–4643

The acute effects of a single intravenous injection of 2 μg of 1α-hydroxycholecalciferol (alfacalcidol) were studied for a 24-h period in six normal males (mean age 33 years), six women with primary hyperparathyroidism (mean age 72 years) and six women with established osteoporosis (mean age 63 years). In all three groups, serum calcitriol levels rose to a peak 2–3 h after administration of alfacalcidol. Basal levels were highest in the primary hyperparathyroidism group at (mean ±sem) 81±2 vs 62±12 (normal males) (p<0.05) and 56±5 pmol/l (osteoporosis) (p<0.01). Highest peak levels were found also in the primary hyperparathyroidism group at 150±15 vs 114±15 (normal males) (p<0.05) and 127 ± 1 5 pmol/l (osteoporosis) (p<0.01). The rise in calcitriol was higher in the primary hyperparathyroidism group than either the normal males or osteoporotic patients (p<0.05). No significant differences were evident in basal serum calcidiol concentrations among the three treatment groups. As might be expected, highest basal concentrations of parathyroid hormone (PTH). serum calcium and serum osteocalcin were noted in the primary hyperparathyroid group (PTH: 17.1±7.7 vs 1.9±0.5 (normal males) (p<0.01) and 2.1±0.3 pmol/l (osteoporosis) (p<0.01): calcium: 3.06±0.08 vs 2.50±0.02 (normal males) (p<0.01) and 2.43±0.02 mmol/l (osteoporosis) (p<0.01): osteocalcin: 1.10±0.08 vs 0.56±0.16 (normal males) (p<0.05) and 0.53±0.21 nmol/l (osteoporosis) (p<0.05). Following treatment with alfacalcidol, no significant change was observed in PTH, calcium or osteocalcin serum concentrations in any group. These results show that maximal conversion of alfacalcidol to calcitriol occurs within a few hours of administration of alfacalcidol in normal males and patients with primary hyperparathyroidism and osteoporosis. Whilst this may reflect differences in activity of the enzyme 2 5-hydroxylase among these groups, other explanations, such as differences in calcitriol clearance, cannot be excluded.

SJ Gallacher, University Department of Medicine, Queen Elizabeth Building, Glasgow Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK

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Christopher J. Kenyon, William B. Brown, Robert Fraser, Giancarlo Tonolo, Fiona McPherson and David L. Davies

Abstract.

Low-dose infusions of dexamethasone (2 μg/day for 2 and 4 weeks) increased systolic blood pressure and decreased body weight gain in male rats. Total body sodium, calcium and magnesium were increased by dexamethasone treatment; potassium was unaffected. These changes have been evaluated bearing in mind that glucocorticoids have profound catabolic effects. Relative to pretreatment values, dexamethasone decreased exchangeable body sodium for the first two weeks of treatment although values were not significantly different from vehicle-treated controls. Hematocrit, plasma cholesterol and transaminase activities were increased by dexamethasone; white cell numbers and plasma volumes were decreased; plasma Na+, K+ and Ca2+, red cell numbers, extracellular fluid volume, and glomerular filtration rate were not significantly affected. It is concluded that glucocorticoids cause plasma volume to contract, possibly as a result of glucocorticoid-induced natriuresis. Any effects of dexamethasone on whole-body ionic composition are obscured by simultaneous changes of intermediary metabolism.