Preventing bone disease requires diligent management in patients with renal failure.
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Biomedical subjects
Publications and source records attributed to F O Kolb.
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We studied 34 patients with primary hyperparathyroidism in order to assess their bone mineral status, to determine its relationship to biochemical parameters (serum calcium and parathyroid hormone) and surgical status, and to determine the relationship between peripheral cortical bone and spinal trabecular bone in this disease. These patients were studied with radiogrammetry of the metacarpals, Norland-Cameron photon absorptiometry of the radius, quantitative computed tomography (QCT) of the spine, industrial radiography of the hands, and conventional radiography of the thoracolumbar spine. We also calculated a spinal fracture index from thoracolumbar spine films. We found that the appendicular measurements correlated well together, but less well with spinal QCT. The spinal fracture index correlated best with QCT (r = -0.55), although significant dispersion was noted. We found that, in general, these hyperparathyroid patients had statistically significant decrements in bone mineral content in both the appendicular and the axial portions of the skeleton. However, the decrement in the appendicular skeleton did not correlate well with that in the axial skeleton. Therefore we conclude that it is necessary to measure both peripheral and central bone mineral content in order to reliably assess the skeletal demineralizing effects of primary hyperparathyroidism in an individual patient.
Vertebral trabecular mineral content and peripheral cortical bone mineral were measured in 94 female and 44 male osteoporotic patients and compared to vertebral mineral values obtained for 323 control subjects in a cross-sectional study. The rate of change of spinal trabecular mineral with age (measured by quantitative computed tomography) in control females averaged 1.2% per year from age 20 to 80, with an accelerated loss demonstrated at the menopause. Trabecular bone mass in male controls declined an average 0.72% per year. Female osteoporotics had a mean decrement of 48 mg cm-3 (39%) compared to age-matched controls, whereas males were decreased 66 mg cm-3 (50%). Radial cortical bone was correlated with spinal mineral in osteoporotics for both males (r = 0.48) and females (r = 0.62). Vertebral compression fractures or wedging was generally absent in patients with vertebral mineral values above 110 mg cm-3, whereas almost all patients with values below 65 mg cm-3 had fractures. Quantitative computed tomography for measurement of vertebral trabecular bone mineral density is useful for defining those patients in whom the risk of vertebral fracture is increased.
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The results presented in this article indicate that quantitative computed tomography provides a reliable means of evaluating and monitoring the many forms of osteoporosis and its various treatments. The greatest advantages of spinal QCT for noninvasive bone mineral measurement are its high precision, the high sensitivity of the vertebral spongiosa measurement site, and the potential for widespread application.
Advances in the radiologic sciences have permitted the development of numerous noninvasive techniques for measuring the mineral content of bone, with varying degrees of precision, accuracy, and sensitivity. The techniques of standard radiography, radiogrammetry, photodensitometry, Compton scattering, neutron activation analysis, single and dual photon absorptiometry, and quantitative computed tomography (QCT) are described and reviewed in depth. Results from previous cross-sectional and longitudinal QCT investigations are given. They then describe a current investigation in which they studied 269 subjects, including 173 normal women, 34 patients with hyperparathyroidism, 24 patients with steroid-induced osteoporosis, and 38 men with idiopathic osteoporosis. Spinal quantitative computed tomography, radiogrammetry, and single photon absorptiometry were performed, and a spinal fracture index was calculated on all patients. The authors found a disproportionate loss of spinal trabecular mineral compared to appendicular mineral in the men with idiopathic osteoporosis and the patients with steroid-induced osteoporosis. They observed roughly equivalent mineral loss in both the appendicular and axial regions in the hyperparathyroid patients. The appendicular cortical measurements correlated moderately well with each other but less well with spinal trabecular QCT. The spinal fracture index correlated well with QCT and less well with the appendicular measurements. Knowledge of appendicular cortical mineral status is important in its own right but is not a valid predictor of axial trabecular mineral status, which may be disproportionately decreased in certain diseases. Quantitative CT provides a reliable means of assessing the latter region of the skeleton, correlates well with the spinal fracture index (a semiquantitative measurement of end-organ failure), and offers the clinician a sensitive means of following the effects of therapy.
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Pseudohypoparathyroidism (pseudo HPT) is the prototype of a group of diseases with end organ unresponsiveness to parathyroid hormone (PTH). Patients with the classic form of this disease have both renal and osseous resistance to PTH. We describe a rare variant of pseudo HPT with classic renal unresponsiveness to PTH but normal skeletal responsiveness to this hormone. The latter patients develop metabolic bone disease in response to depressed calcium and elevated PTH levels. Skeletal abnormalities are histologically and radiologically indistinguishable from renal osteodystrophy and these patients frequently present in childhood with symptoms relating to slipped capital femoral epiphyses. The latter radiologic findings, in the face of normal renal function or the classic somatic features of the syndrome, are highly suggestive of pseudo HPT with normal skeletal responsiveness to PTH.
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Although the exact cause of renal stones is largely unknown, a greater knowledge of metabolic and other factors contributing to stone formation is the basis of current treatment. A practical program of medical management that is designed to prevent recurrent surgical procedures and the loss of renal function is outlined.
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