The effect of
corticosteroids and cytotoxic chemotherapeutic agents on the excretion of
Bence Jones protein was determined for periods of 1 - 62 mo in 29 patients with
multiple myeloma and Bence Jones
proteinuria. The amount of
protein present in 24-h urine specimens collected before treatment and at frequent intervals during monthly treatment cycles was determined. Striking variations occurred in the amount of
Bence Jones protein excretion; these changes were especially evident when 75 mg of
prednisone were given daily for 7 days as part of a monthly chemotherapeutic regimen. Within the 7-day period seven patients showed essentially no decrease (<25%), whereas 13 and 9 patients had a moderate decrease (25-75%) or a marked decrease (>75%), respectively, in Bence Jones
proteinuria as compared to pre-treatment values. The decrease in excretion of
Bence Jones protein during this period was attributed mainly to
corticosteroid therapy because of the transient nature of the response in most patients and the lack of such response in three patients when the
hormone was omitted. Biosynthetic studies were performed to determine in vitro the effect of
corticosteroids on
Bence Jones protein synthesis. Plasma cells obtained from the bone marrow of 13 patients were incubated in a growth medium containing (14)C-labeled
lysine and
isoleucine and
prednisone in concentrations up to 240 mug/ml, and the amount of
Bence Jones protein synthesized was determined immunochemically. No differences in viability were apparent between untreated and
prednisone-treated cells. The type of response exhibited by an individual patient in the percent decrease of
Bence Jones protein excreted after 7 days of
prednisone treatment was comparable to the percent decrease in newly-synthesized
Bence Jones protein secreted by
tumor cells when cultured in the presence of
prednisone at a concentration of 120 mug/ml. The marked differences in the capacity of
corticosteroids to affect
Bence Jones protein synthesis appear to reflect a biochemical heterogeneity among
plasma cell neoplasms.