The clinical and metabolic effects of porcine calcitonin were assessed in six patients with Paget's disease and two patients with osteoporosis under metabolic balance conditions. The administration of calcitonin for 4-17 wk resulted in an amelioration of the clinical phenomena associated with Paget's disease, including bone pain, increased skeletal vascularity, congestive heart failure, and neurologic deficits secondary to skeletal impingement. The major metabolic effects of calcitonin in Paget's disease included the induction of positive calcium balance of +50 to +240 mg/day, reduction in hyperphosphatasia and hydroxyprolinuria of 15 to 60%, and a deceleration of radiocalcium turnover by 12 to 46%. Natriuresis, phosphaturia, and reduced urinary calcium excretion were observed, whereas sustained hypocalcemia and hypophosphatemia did not occur. The administration of porcine calcitonin was not associated with adverse objective or subjective reactions, toxic effects, or allergic phenomena. There was no evidence of antibody formation or loss of therapeutic potency. Although the response of individual patients with Paget's disease varied widely, the data indicate that calcitonin, presumably through its skeletal anti-resorptive action, is able to reduce skeletal turnover and volume in Paget's disease, and thereby improve the associated clinical and metabolic abnormalities. Long term therapeutic studies in progress suggest that prolonged periods of control of the generalized condition may be feasible. In osteoporosis, neither clinical improvement nor consistent metabolic changes indicative of amelioration of the skeletal disease were observed.

Aged↗

PubMed1971

Bone collagenase in assessment of the clinical course of metabolic bone disease.

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Bone Diseases↗

PubMed1970

The cellular transport of magnesium in rat liver.

The bidirectional transport of Mg in rat liver was studied using slices labeled with (28)Mg in a closed two-compartment system under steady-state conditions. The influx (K(bs)) and efflux (K(sb)) transfer coefficients governing transport between the extracellular phase and a rapidly exchanging cell fraction were 0.074 and 0.019 per min, respectively. An increased extracellular concentration of Mg(++) caused a 30% decrease in K(bs) and a 31% increase in K(sb). A decreased extracellular Mg(++) had an opposite effect. At 0 degrees C, both transfer coefficients were reduced by 65%. Increased pH and NaCN increased transport, whereas Ca(++) reduced transport. Reduced pH, altered Na(+):K(+) ratio, Sr(++), glucose deletion, iodoacetate, ethanol, and lactate had no significant influence. Dinitrophenol reduced K(sb) but had no effect on K(bs). These data support the thesis that the intracellular concentration of Mg is in part regulated by a reciprocal change in the influx transfer coefficient and a parallel change in the efflux transfer coefficient in response to altered extracellular concentrations of Mg(++). The qualitative and quantitative similarities of Mg and Ca transport in this system suggest that Mg and Ca share a common transport mechanism which is primarily dependent upon the binding of these divalent cations to macromolecular ligands within the cell membrane or within the cell.

Animals↗

PubMed1970