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Biomedical subjects

S M Sprague

Publications and source records attributed to S M Sprague.

41 records · Page 3Linked to original sources

Parathyroid hormone-mediated aluminum deposition and egress in the rat.

Exogenous PTH significantly enhances tissue aluminum concentration in normal rats fed an aluminum-supplemented diet. In this study, we examined the effect of PTH withdrawal on brain and whole carcass aluminum concentrations. Four groups of rats were fed an aluminum diet while receiving injections of PTH for 5 days. On day 5, one group of rats was sacrificed, and the treatment regimen of the remaining groups altered. PTH, the aluminum diet, or PTH and the aluminum diet were withdrawn respectively for an additional 5 days. An additional group of rats was fed the aluminum diet for 10 days. PTH dramatically increased the concentration of aluminum in both brain and carcass above that found in tissues of rats given aluminum alone. Brain and whole carcass aluminum concentrations remained elevated in rats continued on PTH even in the absence of continued supplemental dietary aluminum. In contrast, following PTH withdrawal, brain and whole carcass aluminum concentrations were significantly lower and independent of dietary aluminum. Thus, PTH may be an important mediator of specific tissue aluminum burdens.

Aluminum↗

Factors affecting tissue aluminum concentration.

Elevated concentration of aluminum has been reported in serum, whole blood and tissue samples of patients with renal insufficiency. Evidence incriminating aluminum as a neurotoxin among the dialysis population is strong. The source of this aluminum has not been clearly defined, although both gastrointestinal and parenteral routes may be involved. Data from this laboratory suggest that an effect of parathyroid hormone on tissue aluminum burdens may, in part, explain why only certain patients exposed to high dialysate aluminum develop the dialysis encephalopathy syndrome and the occasional occurrence of this syndrome in the absence of dialysis or increased dialysate aluminum.

Administration, Oral↗

The pathogenesis of beta(2)-microglobulin-induced bone lesions in dialysis-related amyloidosis.

Dialysis-related amyloidosis (DRA), also referred to as beta(2)-microglobulin amyloidosis (A beta(2)M), is an important cause of morbidity in patients with chronic renal failure and in those who are on dialysis. Although DRA deposits from affected joints have been characterized as a unique amyloid fibril protein, beta(2)M, less is known about the pathologic role of beta(2)M as a mediator of bone and joint disease. Potential mechanisms for beta(2)M pathologic interaction in bone include bone growth factors, cytokines, and advanced glycation end products (AGEs). It appears that DRA is the result of a complex interaction between bone resorption and surrounding tissue destruction culminating in beta(2)M deposition and amyloid formation. More work is required to elucidate the relationship between beta(2)M accumulation and progressive tissue destruction.

Amyloidosis↗