[Glioblastoma manifested by algodystrophy of the hip].
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Biomedical subjects
Publications and source records attributed to L Moulinier.
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OBJECTIVE: The links between osteoporosis and arteriosclerosis have been established by numerous epidemiological studies. Could arteriosclerosis induce bone mineral loss via ischemia or other pathological process? We carried out a comparative study of bone mineral density in both legs of patients with unilateral arterial disease of the lower limbs. METHODS: We studied 25 patients, 22 men and 3 women, whose mean age was 62.3 years (range 35-88 years). These patients had unilateral lower limb arterial disease of at least 3 months duration with a systolic index at least 50% lower on the affected than on the healthy side. Bone mineral content (BMC) and bone mineral densities (BMD) of the femoral neck, femur, tibia, foot and ankle of the affected and the unaffected legs were measured by dual x-ray absorptiometry (Lunar DPXL) and the results compared. RESULTS: Bone mineral density was significantly lower in the femur (-3.7%, p = 0.04), the foot and the ankle (-3%, p = 0.05) of the affected leg. There was a non-significant decrease in BMD of the whole femoral neck (-1.2%) and the trochanter (-4.4%, p = 0.08) on the affected side. Tibial bone mineral density was identical in both legs. Bone mineral content was lower on the affected side (-5.3%, p = 0.05) whereas fat mass and muscle mass were the same in both legs. CONCLUSION: The ischemia resulting from arterial disease of the lower limbs appears to have a direct deleterious effect on bone mineralization.
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Two recent reports of phosphate diabetes in pagetic patients prompted us to evaluate urinary phosphate and its variations under pamidronate therapy in Paget's disease of bone. We also investigated whether Paget's disease is associated with phosphate diabetes. Urinary phosphate excretion was determined in 75 pagetic patients with a mean age of 72 years. None of the patients had received treatment during the six months preceding the evaluation. The 30 patients with clinical, laboratory test, and/or roentgenographic evidence of active Paget's disease were given intravenous pamidronate in a dosage of 60 or 120 mg. The control group was composed of thirty-seven age- and sex-matched subjects selected among patients admitted for degenerative bone or joint diseases. Phosphate and calcium levels were determined in blood and urine on two consecutive days in both cases and controls. The same assays were repeated six months after pamidronate therapy in the 30 patients with active Paget's disease. Phosphate diabetes was defined as a phosphate clearance above 20 ml/mn, a rate for tubular reabsorption of phosphate above 80%, and a ratio of the maximal rate for tubular reabsorption of phosphorus over the glomerular filtration rate (TmP04/GFR) below 0.80 mmol/l. As compared with controls, untreated cases had a nonsignificant increase in phosphate clearance (16.78 +/- 10.40 ml/mn versus 14.81 +/- 7.20 ml/mn), a significant decrease in tubular reabsorption of phosphate (83.41 +/- 5.57% versus 86.70 +/- 5.30%; p < 0.05), and a nonsignificant decrease in the TmP04/GFR ratio (0.93 +/- 0.14 mmol/l versus 0.98 +/- 0.15 mmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)