We investigated the effects of various steroids on erythroid colony formation by normal human bone marrow and peripheral blood, and by marrow and peripheral blood from 18 patients with primary hypoproliferative anemia. These agents were variously found to enhance both CFU-E and BFU-E derived colony growth by normal human cells. Fluoxymesterone and dexamethasone were the most active inducers of CFU-E proliferation, and etiocholanolone and dexamethasone were the most potent burst augmenters. Androsterone did not significantly influence BFU-E proliferation in 66% of the marrow cultures from hematologically normal donors. Colony formation by erythroid progenitor cells of the patients with hypoproliferative anemia was reduce (20 +/- 10 CFU-E derived colonies/6 X 10(4) marrow cells; 12 +/- 5 BFU-E derived colonies/1 X 10(5) blood cells) when compared to growth by normal cells (65 +/- 14 CFU-E derived colonies/6 X 10(4) marrow cells; 21 +/- 9 BFU-E derived colonies/1 X 10(5) blood cells). Colony formation by marrow or peripheral blood cells of eight patients with steroid-responsive anemia was only moderately reduced (26 +/- 11 CFU-E derived colonies/6 +/- 10(4) marrow cells; 17 +/- 3 BFU-E derived colonies/1 X 10(5) blood cells) when compared to growth by marrow cells of three steroid-unresponsive patients (3 +/- 1.5 CFU-E derived colonies/6 X 10(4) cells). Whereas the addition of steroids of the same class to marrow and peripheral blood cultures of the steroid-responsive patients enhanced colony growth by 60-300%, their addition to marrow cultures of the steroid-unresponsive patients increased colony growth by less than 60%. It appears that further investigations using in vitro culture techniques as predictors of response to steroid therapy in patients with hypoproliferative anemia may be warranted.