Emerging cardiovascular risk factors/markers such as proinflammatory cytokines , C-reactive protein , and adipokines are also increased in GHD patients .
Increased cardiovascular morbidity and mortality have also been reported in GHD .
GH treatment has been shown to improve both traditional and emerging cardiovascular risk factors and markers .
The GHD population may be considered at high cardiovascular risk , and GH substitution may be expected to bring an added value to patients with hypopituitarism in terms of cardiovascular protection .
CONTEXT GH deficiency ( GHD ) of the adult is a clinical condition characterized by the presence of several traditional and emerging cardiovascular risk factors that can significantly increase cardiovascular morbidity and mortality .
It is still an open issue whether GH replacement is able not only to improve cardiovascular risk factors but also to decrease cardiovascular morbidity and mortality .
EVIDENCE SYNTHESIS In untreated GHD , cardiovascular risk is increased due to abnormal lipid profile ( increased total and low-density lipoprotein cholesterol , increased triglycerides , and reduced high-density lipoprotein cholesterol ) and impaired glucose metabolism .
Growth hormone replacement reduces C‐reactive protein and large‐artery stiffness but does not alter endothelial function in patients with adult growth hormone deficiency
Hypopituitary patients have an increased risk of vascular mortality that may relate to growth hormone deficiency ( GHD ) . We investigated the effects of 6 months of GH therapy on large‐ and small‐artery function and high‐sensitivity C‐reactive protein ( hsCRP ) in a cohort of GH‐deficient patients . Sixteen hypopituitary patients were r and omized to 6 months of GH therapy or no treatment , then vice versa . hsCRP , 24‐h blood pressure ( BP ) and pulse wave velocity ( PWV ) were measured and resistance arteries were used to construct concentration – response curves to endothelium‐dependent and ‐independent agents . GH therapy increased IGF‐1 from 60 ± 7·2 to 167 ± 16·2 µg/l [ confidence interval ( CI ) 94·9 , 138·8 , P < 0·001 ] . hsCRP declined after 6 months of GH from 3·8 ± 0·88 to 2·0 ± 0·49 mg/l ( CI 0·73 , 3·57 , P = 0·006 ) . Mean arterial BP fell from 91·7 ± 1·5 to 89·3 ± 1·2 mmHg ( CI 0·81 , 4·07 , P = 0·005 ) , as did PWV ( 8·1 ± 0·4 to 6.7 ± 0·5 m/s ) . The decline in PWV correlated with the decline in hsCRP ( r = 0·68 , P = 0·01 ) . Resistance artery function was unchanged after GH therapy . GH replacement may lead to differentially altered production of vasorelaxant agents from the endothelium of large and small arteries . Reduction in vascular inflammation may be associated with reduced vascular risk
Emerging cardiovascular risk factors/markers such as proinflammatory cytokines , C-reactive protein , and adipokines are also increased in GHD patients .
Increased cardiovascular morbidity and mortality have also been reported in GHD .
GH treatment has been shown to improve both traditional and emerging cardiovascular risk factors and markers .
The GHD population may be considered at high cardiovascular risk , and GH substitution may be expected to bring an added value to patients with hypopituitarism in terms of cardiovascular protection .
CONTEXT GH deficiency ( GHD ) of the adult is a clinical condition characterized by the presence of several traditional and emerging cardiovascular risk factors that can significantly increase cardiovascular morbidity and mortality .
It is still an open issue whether GH replacement is able not only to improve cardiovascular risk factors but also to decrease cardiovascular morbidity and mortality .
EVIDENCE SYNTHESIS In untreated GHD , cardiovascular risk is increased due to abnormal lipid profile ( increased total and low-density lipoprotein cholesterol , increased triglycerides , and reduced high-density lipoprotein cholesterol ) and impaired glucose metabolism .