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Biomedical subjects

H A Morris

Publications and source records attributed to H A Morris.

At least 91 records · Page 5Linked to original sources
PubMed1991

Evidence for a renal calcium leak in postmenopausal women.

We have measured calcium, albumin, globulin, bicarbonate, and anion gap in the plasma; and calcium, sodium, and creatinine in the urine, in 115 premenopausal and 140 postmenopausal normal women after an overnight fast, and calculated the calcium fractions in the plasma and the calcium/and sodium/creatinine ratios in the urine. The total ultrafiltrable calcium was significantly higher in the postmenopausal group, mainly due to their higher complexed calcium fraction, due in turn to their higher bicarbonate and anion gap concentrations. Urinary calcium was also significantly higher in the postmenopausal group even after correcting for sodium. After matching for total calcium and each of the calcium fractions in turn, the urinary calcium remained significantly higher in the post- than in the premenopausal sets even after correction for sodium. The implication is that the rise in urinary calcium at the menopause is due to reduced tubular reabsorption of calcium rather than to an increase in filtered load. We suggest that estrogens promote tubular reabsorption of calcium and that the rise in bone resorption at the menopause could be accounted for, at least in part, by the effect of estrogen deficiency on the kidney.

Acid-Base Equilibrium↗
PubMed1991

Effects of three different calcium preparations on urinary calcium and hydroxyproline excretion in postmenopausal osteoporotic women.

Some authors have claimed that 'solubilized' calcium preparations are better absorbed than calcium carbonate, while others have reported that all forms are equally well absorbed. We measured radiocalcium absorption in 35 postmenopausal osteoporotic women and then gave them on three successive evenings, in random order, three different proprietary calcium preparations (Sandocal containing 1 g of effervescent calcium, Calsup containing 1 g of calcium as the carbonate, and Caltrate containing 1.2 g of calcium as the carbonate). The daily urinary calcium excretion rose significantly and similarly on all three supplements and was greater in the high calcium absorbers than the low calcium absorbers. The fasting urinary hydroxyproline excretion was significantly decreased the morning after administration of each preparation, and one-way analysis of variance showed no significant difference between the days of administration or the type of supplement. The decrease was greater for high absorbers than for low absorbers on all three supplements but the differences did not reach statistical significance. By 36 hours after the last calcium supplement the urinary hydroxyproline had returned to baseline. The response of hydroxyproline excretion (and by implication bone resorption) appears to be rapid in onset and short lived. Strict compliance is therefore important in patients on calcium therapy.

Absorption↗
PubMed1991

Effect of salt restriction on urine hydroxyproline excretion in postmenopausal women.

Fasting calcium and hydroxyproline excretion are related to fasting sodium excretion in postmenopausal women. We postulate that calcium excretion is sodium dependent and that hydroxyproline excretion is calcium dependent. Therefore, we sought to lower urinary hydroxyproline, which is a marker of bone resorption, by lowering urinary sodium. Fasting urine samples were obtained from 59 postmenopausal women before and after 2 to 7 days of dietary salt restriction. The urinary sodium-to-creatinine ratio fell from 16 to 7; calcium to creatinine, 0.30 to 0.26; and hydroxyproline to creatinine, 18.2 to 16.8. In the 28 subjects with starting sodium-to-creatinine ratios greater than 15, the hydroxyproline-to-creatinine ratio fell from 19.6 to 16.3. Salt restriction may be one way of reducing bone resorption in postmenopausal women, particularly in those whose sodium intake is high.

Aged↗
PubMed1990

Progressive cancellous bone loss in rats after adrenalectomy and oophorectomy.

Female Sprague-Dawley rats (n = 72), 6 months old, underwent either sham operation, oophorectomy, adrenalectomy, or combined oophorectomy and adrenalectomy (O&A). They were all maintained on normal saline ad libitum and 20 g/day 1.1% calcium chow. Nine weeks after operation, the trabecular bone volume of the distal femoral shaft was significantly lower (P less than 0.001) in the adrenalectomized (11.1%), oophorectomized (7.0%), and O&A (8.3%) animals than in sham-operated animals (19.8%). Eighteen weeks after operation, the trabecular bone volume in O&A animals had fallen to a mean of 3.8% (sham 17.0%), and the length of the femur had increased to 38.8 mm after O&A (sham 36.8 mm, P less than 0.01). O&A animals treated with 0.35 mg/kg/week nandrolone decanoate from 9 weeks postoperatively onward, had twice the femoral trabecular bone volume of untreated animals at 18 weeks (P less than 0.05). By contrast, no significant differences were found in vertebral body trabecular bone between any groups, including groups receiving treatment with androgens. We have found that, by 9 weeks after operation, adrenalectomy alone causes significant loss of metaphyseal trabecular bone, similar to the progressive loss seen after oophorectomy.

Adrenal Glands↗
PubMed1990

Malabsorption of calcium in corticosteroid-induced osteoporosis.

We have examined the relation between radiocalcium absorption and serum 1,25-dihydroxyvitamin D [1,25(OH)2D3] levels in a set of 60 postmenopausal women on corticosteroid therapy (29 with and 31 without vertebral compression fractures) and compared these results with those from 31 normal postmenopausal women age-matched with the "normal" corticosteroid-treated women. Radiocalcium absorption was a function of serum 1,25(OH)2D3 in both corticosteroid-treated groups and in the set as a whole, but the impaired calcium absorption in the corticosteroid-treated patients with osteoporosis was not accounted for by their slightly reduced serum 1,25(OH)2D3 levels. This apparent resistance to the intestinal action of 1,25(OH)2D3 was quantified by a Z score which expresses, in standard deviation units, the difference between the measured calcium absorption and that predicted from the 1,25(OH)2D3 level. The Z score was significantly reduced in the osteoporotic group. Vertebral mineral density (VMD) was measured by quantitative computed tomography in 43 of the corticosteroid-treated cases and in all the normal postmenopausal women; analysis by VMD yielded similar conclusions.

Adrenal Cortex Hormones↗
PubMed1990

Calcium and calcitriol therapy in osteoporotic postmenopausal women with impaired calcium absorption.

The effects of oral calcitriol (0.25 and 0.50 micrograms/d), together with calcium (1 g/d), on calcium absorption and bone resorption were measured in postmenopausal osteoporotic women with calcium malabsorption. Radiocalcium absorption was significantly improved and urinary hydroxyproline/creatinine excretion significantly reduced on both doses, but the higher dose caused an unacceptable incidence of hypercalcemia. In 49 patients treated for an average of 15 months with the lower dose, there was a nonsignificant gain in forearm bone mass of 0.4 +/- 0.3 mg/cm/mo (approximately 1/2% per annum) compared with a significant decrease in 17 untreated patients of 3.8 +/- 1.3 mg/cm/mo (approximately 5% per annum).

Absorption↗
PubMed1990

Relationship between plasma calcium fractions, other bone-related variables, and serum follicle-stimulating hormone levels in premenopausal, perimenopausal, and postmenopausal women.

The study comprises 186 untreated normal premenopausal, perimenopausal, and postmenopausal women in whom we measured serum follicle-stimulating hormone and a number of bone-related plasma and urinary variables. The calcium fractions in the plasma were calculated from the total calcium, albumin, globulin, anion gap, and bicarbonate concentrations. With a level of follicle-stimulating hormone within the reference range (up to 20 U/L) to define the premenopausal state, we confirmed previously reported menopausal rises in plasma calcium, phosphate, alkaline phosphatase, and bicarbonate, and in urinary calcium and hydroxyproline. However, inspection of the data, and t testing at different follicle-stimulating hormone criteria showed that these changes in bone-related variables did not generally occur until the level of follicle-stimulating hormone exceeded approximately 50 U/L. The plasma alkaline phosphatase level rose earlier than the other variables and was significantly elevated in subjects with follicle-stimulating hormone values above 30 U/L. The rise in plasma calcium was mainly a result of a rise in the ultrafiltrable fraction, which in turn was accounted for by rises in the ionized and complexed fractions, of which the complexed fraction was the most significant and proportionately the largest. The rise in the complexed fraction was accounted for by the increase in plasma bicarbonate.

Adult↗
PubMed1990

The reproducibility of bone-related biochemical variables in post-menopausal women.

Seventeen measured and derived bone-related biochemical variables were determined in 60 postmenopausal women on two occasions from 1 to 35 months apart. The coefficients of determination (r2) between the first and second observations were highly significant in respect of all measured and calculated variables except for anion gap, calculated complexed calcium, fasting urinary sodium:creatinine ratio and urinary phosphate:creatinine ratio. The variables with coefficients of determination which ranked highest include plasma alkaline phosphatase, albumin, globulins, calculated ionized calcium and fasting urinary corrected calcium:creatinine and hydroxyproline: creatinine ratios. They also showed marked individuality suggesting that changes within the conventional population based reference range possibly indicate significant physiological changes in metabolism. The critical difference for two results to be significantly different (P less than 0.05) was calculated from the total variation for each variable. We conclude that most of the measured and derived bone-related biochemical variables in fasting plasma and urine samples are sufficiently reproducible in postmenopausal women to be clinically and physiologically meaningful but that urinary sodium and phosphate are inconstant and probably dependent on the previous day's dietary intake.

Aged↗
PubMed1990

The relative contributions of age and years since menopause to postmenopausal bone loss.

We have estimated the relative contributions of age and menopause to forearm mineral density in 485 normal postmenopausal women up to age 75 yr. In 87 pairs matched for years since menopause, in which 1 member was below 61 yr and the other was 61 yr or older, the mean bone density was significantly lower in the older than in the younger subjects despite their identical years since menopause (P less than 0.001). Further analysis suggested a model for bone loss after the menopause which comprises a menopausal component of exponential type and an age-related component which is linear and starts in the mid-50s. According to this model, a 70-yr-old woman has lost 11% of her bone due to menopause and 18% as a function of age. Thereafter, the age-related function is dominant. Early menopause is associated with a self-limiting loss of bone which does not progress further until aging exerts its effect. The main conclusion is that the significance of early menopause as a risk factor for osteoporosis has been overstated.

Age Factors↗
PubMed1989

The calcium deficiency model for osteoporosis.

Calcium deficiency causes osteoporosis in experimental animals because the skeleton is sacrificed for the preservation of the plasma (ionic) calcium and to meet obligatory calcium losses in the feces and urine. (Vitamin D deficiency, on the other hand, causes rickets and osteomalacia largely because of the loss of the calcemic action of vitamin D, which leads to hypocalcemia, secondary hyperparathyroidism, and hypophosphatemia.) The concept that human osteoporosis, particularly in postmenopausal women, results from negative calcium balance represents a working hypothesis that fits many, but not all of the available data. In normal women, the crucial event is a rise in obligatory urinary calcium loss, which may result from an increase in the complexed fraction of the plasma calcium, due in turn to an increase in plasma bicarbonate. Prospective trials with calcium supplements have, however, yielded conflicting results. In osteoporotic women, a further increase in urinary calcium combined with calcium malabsorption produces a further increase in bone resorption, but some impairment of bone formation due to declining androgens may constitute an additional risk factor with advancing age. The suppressibility of urinary hydroxyproline by calcium supplementation in those patients who can absorb calcium, and by calcitriol in those who cannot, supports the calcium deficiency model, but more trials are needed to establish its validity.

Aged↗
PubMed1989

Effects of nandrolone decanoate and antiresorptive therapy on vertebral density in osteoporotic postmenopausal women.

Conventional antiresorptive therapy for osteoporosis can delay bone loss, but secondary inhibition of bone formation appears to prevent an increase in bone density. Recently, anabolic steroid therapy has been shown to increase total body calcium and forearm density in osteoporotic patients, perhaps by causing an increase in bone formation. It is not known if these agents affect vertebral density. We have measured vertebral mineral density in 71 postmenopausal osteoporotic women before and after treatment with either the anabolic steroid nandrolone decanoate or antiresorptive therapy. After a mean treatment period of 14 months, there was a mean increase of 20% in vertebral mineral density in the former group, and no significant change in the latter group. The difference in the time-weighted mean rates of change between the two groups was significant. The results suggest that nandrolone decanoate therapy increases bone formation.

Aged↗
PubMed1988

Calcium and osteoporosis.

The loss of bone which starts at the menopause is self-limiting (exponential) and possibly mainly trabecular. It merges into an age-related linear loss of bone which is probably mainly cortical. The menopause is associated with a rise in obligatory urinary calcium loss resulting from an increase in the filtered load of calcium which may be due to the complexed fraction. The dependence of the urinary hydroxyproline on the urinary calcium and sodium suggests that the bone resorption is a response to calcium losses rather than a primary event. In osteoporotic women, there is a further increase in filtered load of calcium and obligatory calcium loss, frequently coupled with malabsorption of calcium. Urinary hydroxyproline can be suppressed by calcium administration in those with normal absorption and by calcitriol in those with calcium malabsorption. It is known that calcium deficiency causes osteoporosis in experimental animals, but there is controversy about the role of calcium deficiency in the pathogenesis of human osteoporosis. Calcium supplementation inhibits cortical bone loss in postmenopausal women but there is some doubt as to whether it can inhibit trabecular bone loss in women close to the menopause. This may be partly a matter of dose, formulation and time of administration.

Bone Resorption↗