In order to evaluate the effect of growth hormone (GH) on erythropoiesis, red blood cell (RBC) indices (hemoglobin, Hb; hematocrit, Ht; RBC count, and mean corpuscular volume, MCV) of 19 GH-deficient children (12 with isolated GH deficiency and 7 with multiple pituitary hormone deficiencies) between 2 months and 15 years of age were compared to those of 57 sex- and age-matched short normal controls before starting treatment with recombinant human GH (rhGH). The RBC indices were expressed as standard deviation score (SDS). Moreover, the RBC indices in the GH-deficient group were analyzed after the first 3 and 6 months of GH treatment and compared to those of 9 Ullrich-Turner syndrome (UTS) patients in GH therapy. Both patients with isolated and those with multiple pituitary hormone deficiencies presented significantly lower values of Hb-SDS (-1.6 ± 1.0 and-2.0 ± 1.4, respectively; p = 0.004), Ht-SDS (-1.55 ± 0.9 and -2.5 ± 2.1, respectively; p – 0.001) and RBC-SDS (-0.6 ± 1.6 and -1.2 ± 0.9, respectively; p – 0.002) when compared to controls (Hb-SDS:-0.6 ± 1.4; Ht-SDS:-0.1 ± 1.9; RBC-SDS: 0.17 ± 1), in the presence of comparable MCV-SDS values. In contrast, RBC indices did not differ between patients with isolated and those with multiple pituitary hormone deficiencies. When the variations of RBC indices were analyzed after 3 and 6 months of rhGH therapy in the 19 GH-deficient children, an increase in the Hb-SDS (p = 0.01), Ht-SDS (p = 0.03) and RBC-SDS was observed, indicating an early stimulatory effect on RBC proliferation in these patients. However, an analysis of the RBC indices in the group of UTS patients did not reveal any significant change after both 3 and 6 months of therapy with rhGH. The increase in Hb, Ht, and RBC count observed during GH treatment confirms the in vivo erythropoietic growth-promoting effects of GH. However, this effect seems to be related only to conditions of GH deficiency. When GH deficiency is associated with multiple pituitary hormone deficiencies there are pathological influences on erythropoiesis which are not corrected until GH treatment is started, indicating a ‘permissive’ role of GH in the hematopoietic system.