Bone disease in patients receiving growth hormone.

Recent expansion of the use of recombinant growth hormone (GH) to non-GH-deficient patients demands close attention to possible complications in these patients, including effects on bone, recent studies on the use of GH in children with chronic renal failure (CRF) provide some early data. Animal models demonstrate that GH stimulates chondrocyte proliferation. Experimental data further suggest that GH can weaken the epiphyseal plate. Slipped capital femoral epiphysis (SCFE) has been reported in GH-deficient patients, having been detected before, during and after GH therapy. In CRF patients treated with GH SCFE has also been reported. As renal osteodystrophy (ROD) and hypocalcemia are risk factors for this condition, the relationship to GH therapy is unclear in this type of patient. Avascular necrosis (AVN) of the femoral head has been reported in children with congenial structural renal abnormalities and GH deficient patients treated with GH. In recent studies in over 200 children with CRF, 15 cases of AVN have been identified in treated patients. Eight were present prior to treatment; the other 7 patients were not examined radiographically prior to their treatment, and thus the relationship to GH is unknown. In several studies of GH in CRF no significant differences in radiographic osteodystrophy scores, serum calcium, phosphorus or parathyroid hormone (PTH) levels between treated and untreated groups have been found. Alkaline phosphatase increases transiently. The effect of ROD on growth response has not yet been reported. Children with CRF treated with GH should be serially monitored for AVN, SCFE and ROD with serial radiographs and serum calcium, phosphorus, alkaline phosphatase and PTH levels.