Bone-density measurement.
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Biomedical subjects
Publications and source records attributed to D W Purdie.
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Forty-five healthy postmenopausal women participated in a study designed to examine the effects on bone and mineral metabolism of SHD 386L, a new hormone replacement therapy (HRT) regime. This oral preparation delivers 2 mg estradiol valerate daily and 75 micrograms of levonorgestrel from days 17-28 inclusive of a 28-day cycle. The study was double-blind, randomized and placebo controlled. Patients who received SHD 386L exhibited significant falls in plasma calcium, ionised calcium, phosphate and total alkaline phosphatase. No alteration, however, was observed in plasma osteocalcin. No significant changes in mineral metabolism were observed in a parallel group receiving levonorgestrel alone. The results indicate that SHD 386L is likely to be protective to the skeleton through inhibition of bone resorption and that such actions are attributable to the estrogen component. The preparation was well tolerated, compliance was satisfactory and serious adverse affects were not seen. The above biochemical evidence for skeletal protection will require to be supplemented by prospective biophysical evidence of the effect of SHD 386L on bone mineral density.
OBJECTIVE: To determine if women who suffer from early pregnancy loss are at increased risk of osteoporosis later in life. DESIGN: Part of a community screening project for bone mineral density (BMD). SUBJECTS: 392 women aged 50-54 who had had from 0 to 6 miscarriages out of 0 to 8 term pregnancies. TECHNIQUE: BMD measured using dual energy X-ray absorptiometry at both the lumbar spine and the proximal femur. RESULTS: The mean BMD in nulligravid women was not significantly different from those whose only pregnancies ended in early loss. There was no significant correlation between the BMD at either the lumbar spine or the proximal femur and the number of miscarriages (r = 0.03 and 0.01, respectively). The BMD of the lumbar spine and femoral neck were not affected by parity (P = 0.08 and P = 0.87, respectively). CONCLUSION: The risk of osteoporosis was not influenced by parity or the number of previous miscarriages.
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A radioimmunoassay based on an antiserum to human parathyroid hormone-related protein PTHrP(1-16) was used with PTHrP(1-34) standard to measure the concentration of immunoreactive PTHrP in extracts of fetal parathyroid glands from lambs and calves and also placental membranes obtained from several species, including man. Dilution curves from these sources were parallel to those obtained for PTHrP(1-34) standard. It was demonstrated that this parallelism was not the result of tracer damage caused by enzymic activity in the tissue extracts. Extracts of human placental membranes were subjected to high-pressure liquid chromatography with a linear acetonitrile gradient. Co-elution of cytochemical biological activity with 125I-labelled PTHrP(1-34) was noted. These results provide further evidence for both the fetal parathyroid glands and the placenta containing material resembling PTHrP which may be responsible for sustaining the activity of the placental calcium pump which maintains the fetus hypercalcaemic relative to its mother.
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The clinical manifestations of severe pre-eclampsia are normally separated from those of mild pre-eclampsia and normal pregnancy on arbitrary grounds. A clinical index, based on the increase in diastolic blood-pressure and the presence of proteinuria, was developed to reflect the spectrum of disease from mild to severe pre-eclampsia. This was related to a coagulation index based on the platelet-count, plasma-factor-VIII, and serum-fibrinolytic-degradation-products. The two indices were shown to be strongly correlated. All cases of perinatal death associated with pre-eclampsia had coagulation indices in the most severely abnormal range. These results suggest that intravascular coagulation is a highly characteristic feature of pre-eclampsia and that the coagulation index may be of value in monitoring the progress of the disease.
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Osteoporosis is a prevalent disease without a curative treatment. Agents that will prevent fracture are known and bone mineral density can now be measured. Thus there is a prima-facie case for screening, which should be explored.