Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P301

SFEBES2009 Poster Presentations Pituitary (65 abstracts)

Adults with partial GH deficiency (GHD) show phenotypic dichotomy related to the timing of onset of the deficiency

Haliza Haniff 1 , Judith Adams 2 , Stephen Shalet 3 & Robert Murray 1,

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 3.1–7.0 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.

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