Slow turnover of manganese in active rheumatoid arthritis accelerated by prednisone.

Total body and area counts of intravenously injected (54)Mn 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 (54)Mn 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 tracemetal deficiency and called for an alternative explanation of these findings.