Endocrine Abstracts (2003) 5 P184

Differential effects of the route of testosterone administration on GH sensitivity and bone mineral density in hypopituitarism

AM Brooke, PV Carroll, D Walker, GM Besser & JP Monson


Department of Endocrinology, St. Bartholomew's and the Royal London, Queen Mary, UL, London, UK.


The route of oestrogen replacement has an important influence on growth hormone (GH) sensitivity, but it remains unclear whether the route of testosterone treatment in hypopituitarism influences the response to GH replacement. We have compared IGF-I levels, body composition and BMD in hypopituitary male patients with severe GH-deficiency receiving either oral testosterone undecanoate (T.U.)(80-160 milligrams per day) or intramuscular testosterone (I.M.) (250-500 milligrams per 3 - 4 weeks) prior to and after titrated GH replacement. 13 patients received T.U. (59 plus/minus 9 years (mean plus/minus SD)) and 22 I.M. testosterone (57 plus/minus 9 years). Prior to commencement of GH, IGF-I (113 plus/minus 49 nanogram per millilitre vs. 97 plus/minus 57 nanogram per millilitre, TU vs. IM), BMI, and waist:hip ratio were similar in both groups. Similarly no differences were recorded in BMD Z scores at the lumbar spine (LS) or femoral neck (FN) (LS; 0.58 plus/minus 1.33 vs 0.53 plus/minus 1.85, TU vs IM); (FN;-0.3 plus/minus 1.03 vs. -0.27 plus/minus 1.06 TU vs IM). Following 3 years GH titrated to achieve IGF-I levels in the upper part of the age matched range the percentage change in serum IGF-I per milligram of GH administered was higher in the TU group compared to IM group (792 plus/minus 711 vs 397 plus/minus 331 I.M. (p = 0.03)). After GH therapy BMD-Z score increased by 0.4 plus/minus 0.91 (p=0.05) at L2-4 and 0.3 plus/minus 0.66 (p=0.05) at the femoral neck in IM patients. Changes in the TU group were confined to an increase at the femoral neck (0.6 plus/minus 0.8, p=0.06) but no change was recorded at L2-4.
The discordant effects of TU and IM on sensitivity to GH (IGF-I generation) and change in BMD may be explained by differences in aromatisation to oestrogen between preparations.

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