Endocrine Abstracts

Introduction: Adults with growth hormone deficiency (AGHD) have increased prevalence of hepatic steatosis (HS) that might be improved by growth hormone replacement therapy (rhGH). However, data on this topic are conflincting and scanty. Aim: to evaluate prevalence of HS, organ-specific distribution of adipose tissue and cardiovascular impairment in AGHD.

Methods: cross-sectional collection of clinical, biochemical and instrumental data (abdominal ultrasound, fibroscan, assessment of epicardial fat, supra-aortic trunks ultrasound and body composition through bio impedence) in AGHD.

Results: Fifty subjects (M/F 25/25, median age 54.5 years, IQR 46-65, median disease duration 14 years, IQR 9-21 years) were consecutively enrolled. Among them, 32/50 patients were currently on rhGH (median dose 2.4 mg/week, IQR 1.2-5.2, duration 15.6±8.2 years). In the whole cohort, 37/50 patients showed HS (74% vs around 20% in the worldwide general population), with 38% prevalence of moderate and severe forms and 6% of hepatic fibrosis. The prevalence of carotid plaques was 32% and of increased epicardial fat was 27.7%. Prevalence of hypertransaminasemia was higher in untreated than treated AGHD (27.8% vs 3.2%, P=0.02). Although not statistically significant, possibily due to sample size, untreated patients showed higher prevalence of steatosis (15/18, 83% vs 22/32, 69%), cardiovascular events (4/18, 22.2% vs 1/32, 3.1%), increased epicardial fat (41.2% vs 20%), and carotid plaques (44% vs 25%) than treated ones, with a negative association between rhGH dose and intima-media thickness (P=0.02). No difference was found in median age (P= 0.27) an sex (P=0.56) between the two groups. Lastly, AGHD with HS were compared to a cohort of 42 patients with non-alcoholic fatty liver disease (NAFLD). Despite a similar prevalence of hypertension, atherosclerosis and dyslipidemia, AGHD showed lower fat mass (33.2%, IQR 25.2-38.5% vs 40.2%, IQR 35.7-45.6, P<0.001) and lower prevalence of metabolic syndrome (36.1% vs 66.7%, P=0.01) and diabetes (5.4% vs 23.8%, P=0.02). Interestingly, AGHD were younger than NAFLD patients (53.4±15.8 years vs 64.5±12.2 years, P=0.001).

Conclusion: HS, carotid atherosclerosis and increased epicardial fat are highly prevalent in AGHD. When compared with NAFLD patients, AGHD with HS, though younger and with lower percentage of fat mass and metabolic syndrome, showed a similar prevalence of hypertension, atherosclerosis and dyslipidemia. These findings suggest a pathogenetic role of GHD in the development of metabolic complications, while the higher prevalence of hepatic derangement in untreated AGHD supports a possible impact of rhGH. We ought to confirm our findings by comparing them with age and sex- matched NAFLD patients.