Partial growth hormone deficiency is associated with an adverse cardiovascular risk profile and increased carotid intima-medial thickness.
OBJECTIVE
To quantify the relative prevalence of surrogate markers of vascular risk in adults with partial GH deficiency (GH insufficiency, GHI).


BACKGROUND
Hypopituitary adults with untreated GH deficiency (GHD) have an excess vascular mortality and demonstrate clustering of adverse vascular risk factors. The vascular risk profile of GHI adults has yet to be comprehensively studied.


METHODS
A cross-sectional case controlled study.


METHODS
Thirty GHD adults, 24 GHI, and 30 age- and sex-matched controls. GHI adults were defined biochemically using two GH stimulation tests (peak GH 3-7 μg/l).


METHODS
Serum lipids and apolipoproteins, plasminogen activator inhibitor type-I (PAI-I), C-reactive protein (CRP), lipoprotein (a) [Lp(a)], fibrinogen, blood pressure and carotid intima-medial thickness (IMT).


RESULTS
IGF-I levels of GHI adults were lower than controls (373 ± 123 vs 295 ± 104 μg/l; P < 0.001). Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) values were consistently between those of, but not significantly different from, GHD and control subjects. GHI adults showed significantly elevated PAI-I levels [80 (13-98) vs 50.5 (3-98) ng/ml; P = 0.01], although no there were differences in CRP, Lp(a), and fibrinogen levels compared with control subjects. No differences in systolic or diastolic blood pressure were shown between study groups. In parallel with the increased vascular risk profile of GH-insufficient adults, carotid IMT was significantly increased (0.503 ± 0.08 vs 0.578 ± 0.130 mm; P = 0.02). TC, LDL-C, Waist-Hip Ratio (WHR), truncal fat mass, and IMT correlated with IGF-I levels and GH status. TG, K(ITT), and PAI-I additionally correlated with GH status, but not with IGF-I levels.


CONCLUSIONS
GHI adults are at elevated vascular risk, reflected by adverse surrogate markers and increased carotid IMT. The surrogate risk marker profile parallels GHD adults, but is less divergent from that observed in healthy individuals. No data are yet available as to whether these anomalies will be reflected in an increased vascular mortality in GHI adults.
Murray
Robert D
RD
Department of Endocrinology, Christie Hospital NHS Trust, Manchester, UK. robert.murray@leedsth.nhs.uk
Wieringa
Gilbert
G
Lawrance
Jeremy A
JA
Adams
Judith E
JE
Shalet
Stephen M
SM
D000328:Adult; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology*; D002339:Carotid Arteries / Q000473:pathology*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D019382:Human Growth Hormone / Q000172:deficiency*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008055:Lipids / Q000097:blood; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012307:Risk Factors; D017539:Tunica Intima / Q000473:pathology*; D017540:Tunica Media / Q000473:pathology*; D049629:Waist-Hip Ratio
D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D002097:C-Reactive Protein