Osteoporosis in Primary Biliary Cirrhosis: Effects of 25-Hydroxyvitamin D3 Treatment
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Osteomalacia
Osteopenia
Iliac crest
Primary Biliary Cirrhosis
Bone disease
The bone histology in patients with chronic renal failure and aluminum-related bone disease does not always show the excess accumulation of unmineralized osteoid (matrix) characteristic of osteomalacia. Frequently, bone aluminum accumulation is associated with normal or reduced amounts of unmineralized osteoid and low bone formation and is referred to as aplastic bone disease. In this study, we compared static and dynamic bone histomorphometric parameters and plasma PTH and aluminum levels in 12 patients with osteomalacia and 18 patients with aplastic bone disease who had been receiving dialysis for the same duration to determine if the difference in osteoid accumulation in these 2 lesions might be explained by differences in aluminum accumulation or PTH levels. The stainable bone surface aluminum level was significantly higher in the patients with osteomalacia compared to that in the group with aplastic bone [61 ± 5% (±sem) vs. 43 ± 4%; P < 0.02]. The rates of bone apposition and bone formation were lower in the group with osteomalacia (P < 0.01). Plasma amino-terminal PTH was not significantly different in the 2 groups. The increment in plasma aluminum levels after a single infusion of deferoxamine was higher in the osteomalacic group than in the aplastic group, suggesting that the patients with osteomalacia accumulated more total body chelatable aluminum than did those with aplastic bone disease during a comparable length of time on dialysis. We conclude that the excess unmineralized osteoid in aluminum-related osteomalacia results from the high rate of total body aluminum accumulation, which directly causes uncoupling of matrix mineralization and matrix production, independent of PTH levels. Patients with aplastic bone disease who have accumulated lesser amounts of total body aluminum fail to develop excess unmineralized osteoid because production and mineralization of matrix are more closely coupled than in the osteoma-lacic lesion, despite a decline in osteoblast numbers.
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Osteopenia is a condition of reduced bone mineral content including osteoporosis, characterised by a reduced bone mass but normal mineral composition of bone tissue, and osteomalacia, characterised by unchanged bone mass but a deficient level of calcification of the protein matrix. Both conditions possess multifactorial etiopathogeneses and may affect the skeleton as a generalised or local manner, thus creating syndromes of circumscribed osteomalacia (osteomalacia of the patella, of the jaw). In some cases of local osteopenia, genetic, ethnic, dietary (inadequate intake of calcium, vitamin D), behavioural (abuse of smoking, coffee or alcohol), mechanical (reduced muscular exercise) and jatrogenic factors can play an important pathogenetic role. The definition of the exact nature of osteopenia (osteoporosis or osteomalacia), now possible using instrumental and laboratory tests, and the identification of the pathogenetic factors involved enable a correct therapy to be commenced.
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Osteomalacia
Osteoid
Bone disease
Primary Biliary Cirrhosis
Chronic liver disease
Metabolic bone disease
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Hyperphosphatemia leads to the development of osteitis fibrosa in patients with chronic renal failure. In contrast, crippling osteomalacia may appear in uremic patients who are hypophosphatemic or aluminum intoxicated or who undergo total or subtotal parathyroidectomy. Thus, strict phosphorus control by use of aluminum-containing gels may ameliorate renal osteitis fibrosa, but may potentiate the development of osteomalacia. To evaluate this possibility, we compared the bone histologies of 10 chronic renal hemodialysis patients who consistently maintained predialysis phosphorus levels between 4–5 mg/dl (Strict-P) to those of 46 randomly selected dialysis patients (Random-P). We found that the Strict-P group had lower circulating immunoreactive PTH (P <0.02) and alkaline phosphatase (P < 0.05) levels and, as expected, less evidence of hyperparathyroid bone disease. On the other hand, the Strict-P patients had osteomalacia, as evidenced by moderate osteoid accumulation and reduced capacity of bone to assume a fluorescent tetracycline label. Furthermore, all Strict-P patients had histological evidence of bone aluminum accumulation. We conclude that maintenance of normal serum P levels with aluminum-containing gels in hemodialysis patients prevents severe hyperparathyroid bone disease. Such treatment, however, is also attended by a moderate degree of aluminum-associated osteomalacia.
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Osteopenia
Osteomalacia
Bone disease
Bone remodeling
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Osteomalacia
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Osteodystrophy
Liver disease
Chronic liver disease
Metabolic bone disease
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ABSTRACT: In a 71-year-old woman with severe anticonvulsant osteomalacia and Paget's disease, vitamin D (50,000 units orally twice/week and 400 units orally daily) produced dramatic subjective improvement. Bone biopsies showed a striking increase in areas of mineralized bone after treatment, although the pagetoid appearance of bone trabeculae remained unchanged. The patient's blood and urinary calcium levels were low initially, and did not increase significantly after vitamin D administration. When Paget's disease is associated with anticonvulsant osteomalacia, moderately high doses of vitamin D may safely reverse the course of the osteomalacia and induce remineralization of the skeleton.
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Primary Biliary Cirrhosis
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