Search PubMed⌕ Search

Biomedical subjects

J C Gallagher

Publications and source records attributed to J C Gallagher.

At least 19 recordsLinked to original sources
PubMed1992

Thalassemia minor: a risk factor for osteoporosis?

A case report of a 53 year old postmenopausal woman with severe osteoporosis occurring in association with beta thalassemia trait is presented. She was found to have marked axial osteopenia with lumbar spine bone mineral density that was more than three standard deviations below the mean, but had normal bone mineral density of the proximal radius. A biopsy of the iliac crest showed evidence of high turnover osteoporosis. Bone densitometry of the spine and hip in a consecutive series of eleven asymptomatic individuals with thalassemia trait also is reported. Bone mineral density was diminished in the spine (z-score = -0.78, P less than 0.03) and hip (z-score = -0.54, P = 0.05) of patients with thalassemia trait. It is postulated that thalassemia minor may be a risk factor for osteoporosis.

Adult↗
PubMed1992

Vitamin D metabolism and therapy in elderly subjects.

Serum 25-hydroxyvitamin D declines in elderly subjects. This decrease reflects, in part, a lower vitamin D intake. But changes in serum 25-hydroxyvitamin D are more marked in the northern latitudes of the world because less vitamin D synthesis occurs n the skin as a result of a reduced amount of ultraviolet light. Consequently, vitamin D deficiency leading to osteomalacia is more common in thr northern latitudes, particularly among the elderly. The Recommended Daily Allowance of 200 IU of vitamin D in the elderly may be insufficient, since higher doses of 800 IU/day have been shown to reduce the incidence of osteoporotic fractures. The use of more potent analogues of vitamin D, such as calcitriol (Rocaltrol), should be reserved only for those patients who have established vertebral osteoporosis and who generally have more pronounced malabsorption of calcium.

Aged↗
PubMed1991

Effect of progestin therapy on cortical and trabecular bone: comparison with estrogen.

PURPOSE: To determine the effect of progestin therapy on bone mineral density in postmenopausal women and to compare its effects to those of estrogen. SUBJECTS AND METHODS: A prospective, randomized clinical trial was performed in 81 postmenopausal women aged 51.7 +/- 4.4 years (mean +/- SD). They were assigned to one of four groups: Provera 20 mg, Premarin 0.6 mg, Premarin 0.3 mg plus Provera 10 mg, and a placebo. In addition, all women received calcium supplementation, if necessary, to a calcium intake of 1,000 mg/day. We used single- and dual-photon absorpiometry, metacarpal radiogrammetry, and computed axial tomography to measure bone mineral density in the total skeleton, spine, radius, and metacarpal. RESULTS: Women receiving placebo lost bone at all sites (p less than 0.01). The Provera-treated group showed no change in total body calcium, but there were decreases in radial density (p less than 0.01), metacarpal cortex (p less than 0.01), and spine density (p less than 0.01). The Premarin-treated group had an increase in spine density and total body density (p less than 0.05), but a decrease in radial density (p less than 0.05). The Premarin-plus-Provera group showed no change in spine density, total body calcium, or radial density but had a decrease in metacarpal cortex (p less than 0.01). CONCLUSIONS: Compared to placebo, Provera reduced the rate of loss in cortical areas of the skeleton, but not in the spine, which contains more trabecular bone. In contrast, Premarin reduced the rate of loss in both cortical and trabecular areas of the skeleton. The low-dose combination of Premarin plus Provera was similar in its effect on bone to that of Premarin alone, suggesting that there may be a synergistic effect of this hormone combination on bone. Serum cholesterol levels decreased with Provera, Premarin, and the combination of both, whereas levels of serum triglycerides increased with Premarin treatment, decreased with the Provera regimen, and were unchanged with the combination therapy. Provera does not adversely affect the lipid profile.

Bone Density↗
PubMed1991

The effects of estrone (Ogen) on spinal bone density of postmenopausal women.

The effects of cyclical treatment with estrone sulfate (0.3, 0.625, or 1.25 mg), plus calcium carbonate, on spinal trabecular bone density were compared with placebo in 120 postmenopausal women in this 2-year, multicenter, double-blind study. While the placebo and 0.3-mg treatment groups lost bone density (-3.6% and -5.1%), the 0.625- and 1.25-mg treatment groups experienced no significant change from baseline at 24 months (-0.8% and +0.7%). The 1.25-mg treatment group was significantly different from the placebo group at 12, 18, and 24 months. Although the 0.625-mg treatment group was significantly different from the placebo group only at 18 months, the data suggest that 0.625 and 1.25 mg of estrone sulfate had different effects than placebo and 0.3 mg of estrone sulfate and, given with supplemental calcium, are effective doses for the prevention of spinal bone loss.

Bone Density↗
PubMed1991

Estimation of bone mineral density in children with juvenile rheumatoid arthritis.

Bone mineral content of different areas of the skeleton was measured by dual photon absorptiometry in 20 children with juvenile rheumatoid arthritis (JRA) and compared to 20 age and sex matched healthy children. Spinal density was similar in both groups in prepubertal children but decreased in the postpubertal girls with JRA. Total bone density was also decreased in the postpubertal girls. Six children with JRA had repeat scans 12 to 24 months later; in 3 children total bone mineral content increased significantly with an intensive management program. Our study suggests that bone mineral density does not show a pubertal increase in children with JRA, as it does in healthy children.

Absorptiometry, Photon↗
PubMed1990

Treatment of postmenopausal osteoporosis with high doses of synthetic calcitriol. A randomized controlled study.

OBJECTIVE: To study the efficacy of synthetic 1,25 dihydroxyvitamin D3 (calcitriol) in the treatment of osteoporosis. DESIGN: Two-year, double-blind, randomized clinical trial. SETTING: University medical center. PATIENTS: Fifty postmenopausal women with vertebral fractures recruited by referral. INTERVENTION: Calcium intake was adjusted to 25 mmol/d (1000 mg/d) at baseline. Patients were then randomized to treatment with either calcitriol or placebo. During the study, calcium intake was reduced to 15 mmol/d (600 mg/d) and the dose of calcitriol was adjusted to maintain serum calcium less than 2.74 mmol/L (less than 11.0 mg/dL) or urine calcium less than 9.96 mmol/d (less than 400 mg/d). MEASUREMENTS AND MAIN RESULTS: After 2 years, the mean dose of calcitriol in the treated group was 0.62 micrograms/d. Bone mineral density of the spine increased 1.94% with calcitriol therapy and decreased 3.92% with placebo (P = 0.001). Total body calcium increased 0.21% with calcitriol therapy and decreased 1.85% with placebo (P = 0.004). Patients receiving placebo had significant decreases in spine density (P = 0.0007) and total body calcium (P = 0.0004). There were no differences in vertebral fracture rates between the groups. Renal function studies were not statistically different between the groups after 2 years. CONCLUSION: The treatment of postmenopausal osteoporotic women with synthetic calcitriol for 2 years was associated with increases in spine density and total body calcium. No adverse effects on renal function were seen after long-term calcitriol therapy.

Aged↗
PubMed1990

Evaluation of a continuous combined low-dose regimen of estrogen-progestin for treatment of the menopausal patient.

Menopause constitutes a sizable proportion of the adult women's life, and it is reasonable to consider that most women will benefit from hormone-replacement therapy. Also, it is important to realize that cardiovascular disease is a major cause of morbidity and death in the menopausal patient. Two regimens of hormone-replacement therapy were evaluated in postmenopausal women with 0.625 mg of conjugated equine estrogen with either 2.5 or 5 mg of medroxyprogesterone acetate taken continuously for 52 weeks in 92 patients. The data demonstrated an improvement in menopausal symptoms, a beneficial effect in lipoprotein profiles, the establishment of an atrophic endometrium, and a marked decrease in vaginal bleeding after 13 weeks and a further decrease after 26 weeks. Ideally this regimen will offer better patient compliance and, if the favorable lipoprotein profiles offer protection to the cardiovascular system, the overall health of the American woman will be markedly affected.

Cholesterol↗
PubMed1990

Metabolic effects of synthetic calcitriol (Rocaltrol) in the treatment of postmenopausal osteoporosis.

The long-term safety and efficacy of synthetic 1,25-(OH)2D3 (calcitriol; Rocaltrol) in the treatment of women with type 1 osteoporosis is being assessed in a randomized trial. Patients were allocated in double-blind fashion to 1,25-(OH)2D3 or matching placebo. Initially, the calcium intake was adjusted to 1,000 mg/d. The study protocol called for increasing the dose of 1,25-(OH)2D3 until patients developed either hypercalcemia or hypercalciuria. However, in order to maintain a higher dose of calcitriol on a long-term basis, the calcium intake had to be reduced to 600 mg/d in those receiving calcitriol; if that was not successful in eliminating hypercalcemia and hypercalciuria, then the dose of 1,25-(OH)2D3 was reduced as necessary. During the hypercalcemic phase, the indices of bone resorption decreased significantly, demonstrating that calcium absorption is solely responsible for hypercalcemia. The maintenance dose was established after 8 to 10 weeks, and the 24-hour urine calcium and creatinine clearance remained constant throughout the remainder of the study period. On a calcium intake of 600 mg/d, the long-term maintenance dose of 1,25-(OH)2D3 averaged 0.675 micrograms/d. Long-term therapy on an average dose of 0.675 micrograms/d was not associated with nephrotoxicity.

Aged↗
PubMed1990

Action of 1,25-dihydroxyvitamin D3 on calcium balance and bone turnover and its effect on vertebral fracture rate.

In postmenopausal osteoporotics, malabsorption of calcium is associated with reduced levels of serum 1,25-dihydroxyvitamin D. Metabolic studies have shown that calcium absorption can be normalized and calcium balance improved after administration of oral doses of synthetic 1,25-dihydroxyvitamin D3 (Rocaltrol) 0.25 micrograms twice daily. Further studies performed at two centers compared the effect of Rocaltrol 0.25 micrograms twice daily versus placebo on vertebral fracture rates in osteoporotics. A significant reduction in vertebral fracture rates was seen at the end of 1 year. Those patients who continued on Rocaltrol for a second and third year showed a progressive decrease in vertebral fractures. Rocaltrol, administered at a dose of 0.25 micrograms twice daily, seldom causes hypercalcuria or hypercalcemia in osteoporotic patients on a typical calcium intake of 700 to 800 mg/d. Careful measurements of renal function over a period of 3 years in patients treated with Rocaltrol, 0.25 micrograms twice daily, showed no deterioration in renal function. These data suggest that 1,25-dihydroxyvitamin D3 is a useful therapy in the management of patients with postmenopausal osteoporosis, particularly those who have malabsorption of calcium. We found that it improves calcium balance, reduces the vertebral fracture rate, and is safe to use provided that the dietary calcium is monitored and does not exceed 800 mg/d.

Aged↗
PubMed1990

The pathogenesis of osteoporosis.

Changes in the calciotropic hormones with age contribute significantly to the pathogenesis of osteoporosis. In both postmenopausal (Type I) and senile osteoporosis (Type II) it is common to find reduced levels of serum 1,25-dihydroxyvitamin D and malabsorption of calcium. In Type I patients a reduced level of serum parathyroid hormone causes a real decrease in serum 1,25-dihydroxyvitamin D production and malabsorption of calcium, whereas in Type II patients the decline in 1 alpha-hydroxylase activity in the kidney causes a decline in serum 1,25-dihydroxyvitamin D which leads to malabsorption of calcium and secondary hyperparathyroidism. In the final analysis both pathways lead to bone loss. In some Type II patients there may be a decline also in the function or number of the vitamin D-binding receptors in the gut. Treatment of patients with vitamin D analogues, however, normalizes calcium absorption and improves calcium balance. The improvement in calcium balance reduces bone resorption and prevents further bone loss; in addition recent studies have shown that therapy with vitamin D analogues leads to a reduction in fracture incidence.

Absorption↗
PubMed1990

A comparison of iliac bone histomorphometric data in post-menopausal osteoporotic and normal subjects.

Transilial bone biopsies following in vivo fluorochrome labeling were obtained from 90 women with postmenopausal osteoporosis and 34 healthy post-menopausal women. Standard histomorphometric data were collected from undecalcified sections. The distribution of values for both structural and remodelling indices was the same for each group. Bone volume was 35% lower (P less than 0.001), wall thickness was 12% lower (P less than 0.001), and trabecular thickness was 11% lower (P less than 0.02) in osteoporotics. Trabecular separation was 34% greater (P less than 0.001) and trabecular number was 36% lower (P less than 0.001) in osteoporotics. Biopsy core width was 11% less (P less than 0.02) and cortical width was 35-50% less (P less than 0.001) in osteoporotics. Static indices of remodelling, mineralizing surfaces, and mineral apposition rate were similar in the two groups. The absolute values for bone histomorphometric variables for both groups are similar to most published data. Osteoporotics had poorer bone structure, marked by decreased trabecular connectivity and thin cortices. There were no major differences in dynamic indices of remodelling. Since the histomorphometric data were distributed the same in both groups, special subsets of osteoporotic subjects not in the normal population did not exist.

Aged↗
PubMed1990

Lipid changes after hormone replacement therapy for menopause.

Three regimens of hormone replacement therapy were administered to 62 postmenopausal women for a period of 12 weeks and evaluated for their effect on blood lipids. Each group was given a continuous dose of 0.625 mg of conjugated estrogens combined with either a continuous dose of 2.5 mg of medroxyprogesterone acetate or 5.0 mg of medroxyprogesterone acetate, or a cyclic dose of 5.0 mg of medroxyprogesterone acetate on days 17-28 of the cycle. After treatment there was a significant decrease in the total cholesterol (P less than .0007) and low density lipoprotein cholesterol (P less than .0001) together with a significant increase in high density lipoprotein cholesterol (P less than .0029). There was no significant difference in the response of the blood lipids to the three hormone groups. Therefore, preference would depend on the combination that caused the least bleeding or amenorrhea.

Alanine Transaminase↗
PubMed1990

Effect of estrone sulfate on postmenopausal bone loss.

Estrogen replacement therapy confers many beneficial effects to postmenopausal women, such as slowing the rate of bone loss and decreasing the risk of coronary artery disease. This multicenter, placebo-controlled study evaluated the lowest effective daily dose of estrone sulfate (0.3, 0.625, or 1.25 mg) combined with 1000 mg elemental calcium supplementation for preventing bone loss in the immediate supplementation for preventing bone loss in the immediate postmenopausal period. Spinal bone mineral density was measured using quantitative computed tomography. Compared with baseline, bone mineral density increased significantly (P less than .05) after 12 months of 0.625 mg daily (+ 1.9%) or 1.25 mg daily (+ 2.5%). The difference between the 0.625-mg and 1.25-mg doses was not statistically significant. Estrone sulfate administration (0.625 and 1.25 mg) produced significant changes in various lipid measurements at both the 6- and 12-month observation points. The prevalence rates for adverse events were comparable among the estrone sulfate groups and the placebo group. Estrone sulfate 0.625 mg daily, combined with 1000 mg elemental calcium supplementation, was the minimum effective dosage to prevent loss of spinal bone mineral density in postmenopausal women over a 12-month period.

Bone Density↗
PubMed1989

Increased incidence of hip fracture in osteoporotic women treated with sodium fluoride.

There has been controversy as to whether fluoride therapy increases the risk of fracture in the appendicular skeleton. In the present study we compared the incidence of hip fracture in four groups of osteoporotic women: 22 treated with placebo, 17 with fluoride and calcium, 18 treated with fluoride and calcitriol, and 21 with calcitriol alone. Four hip fractures occurred in 3 patients on fluoride and calcitriol, and two hip fractures occurred in 2 patients on fluoride and calcium. No hip fractures occurred in patients receiving either calcitriol alone or placebo. The difference in fracture rates for fluoride versus nonfluoride treatment is significant (p = 0.006). Moreover, the six hip fractures occurring in patients receiving fluoride during 72.3 patient years of treatment is 10 times higher than would be expected in normal women of the same age. The probability of observing six fractures in 2 years is extremely small (0.0003). In four of the hip fracture cases, the history suggested a spontaneous fracture. These findings suggest that fluoride treatment can increase the risk of hip fracture in osteoporotic women.

Aged↗
PubMed1989

The effect of age and menopause on bone mineral density of the proximal femur.

Although the menopause has been associated with increased bone loss at several skeletal sites, it has not previously been noted in the hip, yet estrogen therapy has been reported to reduce the incidence of hip fractures. We investigated the effect of age and menopause on bone loss in the proximal femur by measuring bone mineral density (BMD) of the femoral neck, Ward's triangle, and trochanter by dual-photon absorptiometry in 263 normal women aged 20-84. Multiple regression analyses revealed a significant decrease in BMD of the femoral neck and Ward's triangle with age in both pre- and postmenopausal women (p less than 0.001). In the trochanter the decrease with age was significant only in postmenopausal women (p less than 0.001). Further analysis revealed that BMD decreased faster at all sites in the early postmenopausal years. During the first 6 years postmenopause, the decrease in BMD of the femoral neck and trochanter was 3-10 times higher than the change in the decade prior to menopause. About 20% of the lifetime femoral neck loss and 30% of the trochanteric loss occurred in the early postmenopausal period. It is concluded that both age and menopause are major determinants of BMD in the proximal femur. These findings could explain why estrogen therapy has been reported to prevent hip fracture. The rapid early postmenopausal loss in BMD of the proximal femur demonstrates the importance of starting estrogen replacement therapy immediately after menopause for maximum effect.

Adult↗
PubMed1989

Change in vertebral shape in spinal osteoporosis.

The change in vertebral shape with increasing severity of spinal osteoporosis was studied in 139 women with atraumatic spinal fractures. The anterior height was below the normal range in 570 vertebrae, and the posterior height was below normal in 157 vertebrae. All values below the normal range were defined as fractures. Ninety-eight percent of posterior fractures were associated with anterior fractures. The fractures involved both the anterior and posterior vertebral borders in 58/356 (17%) of the fractured vertebrae in patients with 6 or less fractures, compared with 93/217 (45%) of the fractured vertebrae in patients with 7 or more fractures. The distribution of anterior fractures was biphasic with peak frequencies at T7-T8 and T11-T12. Posterior fractures had a more lumbar distribution, perhaps resulting from higher compressive forces on the posterior vertebral border of the lordotic lumbar spine than on the kyphotic thoracic spine. The mean anterior and posterior height of nonfractured vertebrae in osteoporotics was not significantly different from normal, suggesting that osteoporotics do not have smaller vertebrae than normal subjects.

Aged↗