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 .
Alterations of monocyte function in patients with growth hormone (GH) deficiency: effect of substitutive GH therapy.
GH deficiency ( GHD ) is associated with increased prevalence of atherosclerosis and cardiovascular morbidity . Because monocytes play a crucial role in the development of atherosclerosis , we investigated in the present study the effect of GH deficiency and subsequent GH replacement on monocytic function in hypopituitary subjects . Twelve patients were r and omized to receive GH replacement therapy ( either 3 or 6 microg/kg x day , s.c . ) for 3 months . Plasma levels and monocyte production of cytokines and monocyte adhesion to endothelium were determined in controls and patients with GHD before and after GH treatment . Before GH therapy , patients with GHD had increased basal plasma tumor necrosis factor-alpha ( TNF alpha ; 220 % over control values ; P = 0.004 ) and interleukin-6 ( IL-6 ; 340 % over control values ; P 0.0009 ) levels . Basal monocyte production of both cytokines was also significantly higher in patients with GHD [ 484 % over control values for TNF alpha ( P = 0.0007 ) ; 1479 % over control values for IL-6 ( P = 0.035 ) ] . GH treatment for 3 months led to a reduction in plasma TNF alpha ( 135 % over control values ; P = 0.03 , pre- vs. post-GH therapy ) , monocyte TNF alpha production ( 204 % over control values ; P = 0.01 ) , plasma IL-6 ( 219 % over control values ; P = 0.07 ) , and monocyte IL-6 production ( 448 % over control values ; P = 0.01 ) . Plasma TNF alpha levels positively correlated with monocyte TNF alpha production in patients with GHD both before and after GH therapy ( P = 0.003 and P = 0.049 , respectively ) . A positive correlation ( P = 0.0003 ) was also observed between monocyte TNF alpha production and monocyte IL-6 production . There were no correlations between these plasma cytokine levels or monocyte cytokine production and parameters of body composition , lipid profile , or IGF-I and IGF-binding protein-3 levels . Before GH treatment , adhesiveness of monocytes to cultured aortic endothelial cells was also enhanced . This alteration was not reversed by GH administration . In conclusion , our results demonstrate that markers of monocyte activation are increased in patients with GHD and that GH replacement partly reduces these abnormalities . Reduction of cellular activation of monocytes by GH therapy could potentially contribute to reduce the risk of cardiovascular events in patients with GHD
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 .