Development of Growth Hormone Deficiency after Definitive Treatment for Acromegaly

How Does GHD Effect Body Composition and Cardiovascular Risk Biomarkers?

Written by Kamiah A. Walker
Reviewed by EndocrineWeb Editorial Board

Body composition and biomarkers of cardiovascular risk are affected by both growth hormone excess and growth hormone deficiency (GHD).  While that is a known fact, it’s unknown how developing growth hormone deficiency after being treated for acromegaly affects body composition and cardiovascular risks.

A study examining this question was published in February 2012 online ahead of print.  It will be an upcoming issue of Clinical Endocrinology (Oxford), and the article is “Effects of Growth Hormone Deficiency on Body Composition and Biomarkers of Cardiovascular Risk after Definitive Therapy for Acromegaly.”

This cross-sectional study was aimed at determining if there is an association between developing GHD after definitive treatment for acromegaly and increased visceral adiposity and cardiovascular risk biomarkers.  This was compared to growth hormone sufficiency after definitive treatment for acromegaly.

All patients in the study had a history of acromegaly; there were 76 subjects included.  They were split into 3 groups:

None of the subjects were on somatostatin analogues, dopamine agonists, or human growth hormone.

Researchers measured body composition (using DXA), abdominal adipose tissue depots (by cross-sectional CT), carotid intima-media thickness (IMT), and total body water (using bioimpedance analysis).  Additionally, fasting morning serum was collected and analyzed for high-sensitivity C-reactive protein (hsCRP), lipids, and lipoprotein levels.  Subjects were also given an oral glucose tolerance test, and researchers calculated homeostasis model of assessment-insulin resistance (HOMA-IR).

The study showed that in subjects with GHD, abdominal visceral adipose tissue, total adipose tissue, and total body fat were higher than those measurements in GHS or AA (p < 0.05).

Subcutaneous abdominal fat was higher in GHD than in AA (but not in GHS) (p < 0.05); similarly, fibrinogen and IMT were lower in GHD than in AA (but not in GHS) (p < 0.05).

The following were all lower in GHD and GHS than in AA:  fasting glucose, 120-minute glucose, fasting insulin, HOMA-IR, and total body water percentage (p < 0.05).

One measurement was higher in GHS than in AA:  triglycerides (p < 0.05).

In the 3 groups, lean body mass, mean arterial pressure, total cholesterol, HDL, and LDL were comparable.

This study suggests that developing growth hormone deficiency after definitive treatment for acromegaly may have an adverse effect on body composition and inflammatory biomarkers for cardiovascular risk.  Growth hormone deficiency, though, doesn’t seem to affect glucose homestasis, lipids/lipoproteins, or other cardiovascular risk markers.



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