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  • 1990-1994  (2)
  • Dementia  (1)
  • Hyperparathyroidism  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Calcium carbonate ; Phosphate ; Chronic renal failure ; Aluminium ; Hyperparathyroidism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Calcium carbonate has been successfully used as a phosphate binder in patients with chronic renal failure; however, a high frequency of hypercalcaemia has been reported. To study the effects of calcium carbonate preparations with different dissolution characteristics on the incidence of this side effect, we conducted a double-blind, crossover trial in 21 patients undergoing chronic haemodialysis. Aluminium hydroxide therapy was replaced with calcium carbonate. The subjects then randomly received either an enteric-coated or a gastric-coated preparation. Calcium carbonate (3.1–3.6 g/d) controlled serum phosphate concentrations as effectively as aluminium hydroxide (2.9 g/d). Concurrently, there was a significant rise in mean serum calcium and a fall in serum concentrations of both parathyroid hormone and osteocalcin, the latter suggesting a decrease in bone turnover. Overall, hypercalcaemic episodes developed in 9 patients (43%) and occurred at a considerable frequency (33 episodes per 100 patient-months) during treatment with the gastric-coated formulation. Following conversion to enteric-coated calcium carbonate (3.6 g/d) patients had fewer occurrences of hypercalcaemia (12 episodes per 100 patient-months,P〈0.05) and, as compared to the gastric-coated preparation, increases in serum calcium 〉3.00 mmol/l were not observed at all. Hyperaluminaemia was regressive during therapy with calcium carbonate, but addition of small doses of aluminium hydroxide caused a large rise in serum aluminium concentrations after infusion of desferrioxamine, indicating an enhanced rate of absorption or aberrant compartmentalization of aluminium. We conclude that calcium carbonate can control hyperphosphataemia in dialysis patients. However, undesirable hypercalcaemic episodes may occur, the frequency and severity of which can be lowered by the use of an enteric-coated preparation. Concomitant use of aluminium hydroxide and calcium carbonate should be restricted to patients in whom the degree of aluminium accumulation is monitored by serial desferrioxamine tests.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Thromboangiitis obliterans ; Dementia ; Cortical synaptophysin expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The generalized form of von Winiwarter-Buerger's disease (WBD) occasionally involves the brain. However, pure cerebral forms of the disease were also described by Spatz and Lindenberg (“Spatz-Lindenberg's disease”, SLD). Both, the type I, which involves the large basal arteries, and the type II, which results in a sickle-shaped granular atrophy of the cerebral cortex, are often accompanied by (“vascular”) dementia, which Lindenberg and Spatz mainly attributed to the bilateral involvement of the second frontal gyrus by granular atrophy. Recently, synaptic deprivation of the cortical gray matter has been shown to occur in the dementia of Alzheimer type (DAT) and other neurodegenerative disorders. In DAT, the synaptic loss highly correlated with the degree of the mental impairment. We wanted to examine whether similar changes also occurred in dementia of vascular origin, for which SLD, although infrequent, is a typical example. In fact, we found that in three cases of typical SLD type II the synaptophysin immunoreactivity of the cortical neuropil in areas without overt infarcts or scar formation was as much reduced as in Alzheimer's disease. Although it must be taken into account that in the present cases the synapse loss might, at least in part, be due to secondary (Wallerian) degeneration as a result of the neuronal loss in the “watershed” regions of the arterial blood supply, it cannot be excluded that a decline of cortical synaptic contacts in areas without necroses or scars may occur as a primary event, contributing to the pathogenesis of the dementia. Final conclusions can only be expected from investigations into further cases of cerebro-vascular disorders with and without dementia.
    Type of Medium: Electronic Resource
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