Glucocorticoids cause growth retardation in children. We have studied the effect of these hormones on serum somatomedin (Sm) levels in seven children with nephrosis. Intravenous administration of methylprednisolone sodium succinate, 2.2 mg/kg, causes a rapid fall in serum Sm activity. The activity remains suppressed during continuous therapy, but returns toward normal when medication is omitted during the course of alternate-day therapy. We conclude that one reason for growth retardation secondary to continuous glucocorticoid therapy is suppression of Sm generation. A direct effect of these hormones on the cartilage cell or induction of an Sm inhibitor cannot be excluded by the reported experiments.

An effect of two glucocorticosteroids on the transport of the essential trace element, manganese, is described. Mice receiving high doses of prednisolone or cortisol accumulated more radiomanganese in their carcasses and retained less in their livers than did untreated controls. In some respects this effect was similar to that seen when manganese salts were administered as significant metabolic loads. It was brought on regardless of whether the injected isotope was in the divalent ionic form or in the plasma-bound form. Treatment with mineralocorticosteroids alone did not affect manganese metabolism as tested here. Furthermore, Zn65 did not respond to the glucocorticoid effects exhibited by Mn54.

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Total body and area counts of intravenously injected 54Mn were measured periodically in 29 in-patients. A heterogeneous group of 19 control patients showed fair reproducibility in the immediate distribution, and considerable individual variance in the subsequent loss of the isotope. Eight studies of the effects of feeding excesses of manganous sulfate to five patients showed acceleration of the rate of loss of the radioisotope from the whole body and the liver. These findings seem compatible with the presence of control mechanisms in man, operating to vary the metal's excretion, while tending to preserve constancy of its concentration in tissues.Slow turnover rates of the metal were demonstrated in seven out of eight patients with active rheumatoid arthritis, in one with hydralazine disease, but not in one arthritic undergoing an impressive, spontaneous remission. Statistically significant differences were encountered in the measurements of 54Mn turnover of the total body, the thyroid, and the liver.Administration of prednisone induced clinical improvement and significant acceleration of these turnovers. Slow turnovers are characteristic of nutritional manganese deficiency. Therefore, serum and blood manganese determinations were performed by neutron activation analysis on 14 control patients, and on six patients with active rheumatoid arthritis. A statistically significant elevation of the red cell manganese concentration was encountered in patients with rheumatoid arthritis. This argued against the presence of classical trace-