Biomedical subjects

N Kelepouris

Publications and source records attributed to N Kelepouris.

3 recordsLinked to original sources

PubMed1995

Severe osteoporosis in men.

OBJECTIVE: To evaluate men with severe osteoporosis for pathogenetic factors and to review the reported features of primary osteoporosis in men. DESIGN: Case series and clinical review. PATIENTS: 47 men consecutively referred to a metabolic bone center because of atraumatic (or minimally traumatic) fractures (91%) or radiographic osteopenia (9%). MEASUREMENTS: Clinical assessment, radiographs, chemical analyses of serum and urine, hormone assays, skeletal densitometry, and histomorphometry of iliac crest biopsy specimens. RESULTS: 27 of the 47 men (57%) had vertebral fractures, and 16 (34%) had appendicular fractures. Causal factors identified in 30 men (64%) included glucocorticosteroid treatment (8 men); hypogonadism (7 men); excessive alcohol consumption (7 men); and anticonvulsant use, osteomalacia, severe hyperthyroidism, or bone marrow neoplasia (8 men). Seventeen men (36%) had no medical conditions or known risk factors associated with bone disease. Spinal mineral density was well below the mean value for healthy young men in 94% of the patients with primary osteoporosis tested. Examination of biopsy specimens from 13 of 17 men with primary osteoporosis showed reduced trabecular bone volumes, normal bone formation rates, and slightly increased resorption surfaces. Fasting hypercalciuria was seen in some men (41%). In the primary osteoporosis group, eight men were followed serially (range of follow-up, 6 months to 9 years) while they were receiving a nonpharmacologic regimen (diet and activity); the mean axial bone mineral density of these men increased slightly. CONCLUSIONS: A thorough evaluation for identifiable causes of severe osteoporosis in men is warranted because definable pathogenetic factors are seen in many cases. A few men with severe osteoporosis have primary or idiopathic osteoporosis. Primary osteoporosis in men is probably caused by many factors because heterogeneous clinical, laboratory, and histologic features were seen in our series and in those of others. Further studies of primary osteoporosis are needed to define the course of the disease, to identify pathogenetic mechanisms, and to develop therapeutic interventions.

Adult↗

PubMed1995

Hemifacial spasm and osteitis deformans.

PURPOSE/METHODS: A patient with osteitis deformans (Paget's disease) and hemifacial spasm underwent magnetic resonance tomographic angiography. Bone-modulating bisphosphonates and botulinum injection were administered to treat the hemifacial spasm. RESULTS/CONCLUSIONS: Computed tomography showed marked temporal bone overgrowth. Magnetic resonance tomographic angiography showed no vascular compression of the facial nerve root. The hemifacial spasm failed to resolve with intravenous pamidronate. Subsequent botulinum injection rendered the patient spasm free for 22 weeks. Further research on the use of bisphosphonates in the treatment of pagetoid hemifacial spasm is required.

Aged↗

PubMed1991

Estradiol down-regulation of the rat uterine estrogen receptor.

We have previously shown that neonatal exposure of rats to pharmacologic doses of diethylstilbestrol via daily injections resulted in a significant decrease in the estrogen-binding capacity of the uterine estrogen receptor (ER). In this study, we examined the effects of physiologic and pharmacologic doses of estradiol (E2) administered to adult ovariectomized rats via Silastic implants. Two days after implantation, uteri were removed, weighted, and homogenized, and ER levels were determined in the supernatant (hydroxylapatite assay) and low-speed pellet (nuclear exchange assay). Implants containing E2 concentrations of 0.005 or 0.05 mg/ml increased cytosolic but not total ER-binding capacity, whereas 0.5 or 5.0 mg of E2/ml implants decreased the binding capacity of cytosol ER to 40% and total ER to 50% of control values. The 0.005-mg/ml dose increased cytosol ER without increasing uterine weight; all higher doses significantly increased uterine weight. Determination of ER protein by an ER radioimmunoassay showed the same extent of reduction of ER concentration as the binding assays, demonstrating that the loss in E2 binding capacity is homologous down-regulation. The down-regulation of ER was maximal at 24 hr and was completely reversible after implant removal, although the time required to recover from down-regulation was dose dependent. Uterine weight also returned to control levels slowly after implant removal. Neither the sedimentation rate of the down-regulated ER nor the Kd of the cytosolic ER changed following long-term implantation; however, the Kd of the nuclear ER decreased significantly. This is the first demonstration of in vivo homologous down-regulation of uterine ER. ER down-regulation may play a role in several biologic processes.

Animals↗