SFEBES2009 Poster Presentations Pituitary (65 abstracts)
1Leeds Teaching Hospitals NHS Trust, Leeds, UK; 2University of Manchester, Manchester, UK; 3Christie Hospital NHS Trust, Manchester, UK.
Considerable dichotomy exists in the phenotype of adults with severe GHD of childhood (CO-GHD) and adult-onset (AO-GHD). Those with CO-GHD show immaturity. Adults with partial GHD (GH insufficiency (GHI), peak GH 3.17.0 μg/l) show a similar, but milder phenotype to adults with severe GHD. Whether a similar dichotomy relating to timing of onset is observed in CO-GHI and AO-GHI adults is not known.
We studied 24 adults with GHI (CO-GHI n=13, 22.3±5.6 years; AO-GHI n=11, 42.3±11.1 years), 32 with GHD (CO-GHD n=14, 27.6±6.7 years; AO-GHD n=18, 41.0±10.4 years), and 27 age-matched controls (young normal (YN) n=17, 21.3±3.0 years and old normal (ON) n=15, 40.5±7.8 years). The study was approved by the local REC.
CO-GHI adults, compared with YN controls, were shorter (1.63±0.09 vs 1.75±0.08 m, P<0.01) and weighed less (62.1±9.5 vs 70.1±11.3 kg). DXA analysis of body composition showed reduced truncal LBM (20.1±3.7 vs 25.5±4.1 kg, P<0.01) in this group. CO-GHI adults had raised cholesterol (5.41±1.15 vs 4.61±0.59 mmol/l, P<0.05); LDL-cholesterol (3.13±1.07 vs 2.55±0.72 mmol/l, P=0.053); ApoB (94.13±25.46 vs 75.43±19.69 mg/dl, P<0.05) and PAI-1 (83.15±17.93 vs 51.94±31.31 ng/ml, P<0.05) levels. CO-GHI adults also had reduced lumbar spine DXA T-score (−1.73±0.92 vs −0.60±0.95, P<0.05).
In contrast, AO-GHI adults, compared with ON controls, were heavier (74.0±18.1 vs 69.6±12.5 kg) with increased waist circumference (89.4±17.4 vs 80.9±11.1 cm) and truncal fat mass (13.1±7.5 vs 9.0±4.1 kg). They exhibited adverse cardiovascular profile with reduced HDL-cholesterol (1.38±0.29 vs 1.60±0.25 mmol/l) and significantly increased carotid IMT (0.684±0.141 vs 0.531±0.080 mm, P<0.05). Serum leptin levels were elevated in AO-GHI compared with controls (46.89±33.10 vs 21.35±16.87 ng/ml, P<0.05). Both CO- (338±104 vs 426±117 μg/l) and AO-GHI (244±80 vs 309±89 μg/l) adults had lower IGF1 levels compared to their respective controls.
These data confirm that CO-GHI leads to adults who have failed to optimise their skeletal and somatic development, reflecting the phenotype of adults with CO-GHD. Both AO-GHI and CO-GHI adults show an adverse metabolic profile.