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 therapy induces insulin resistance by activating the glucose-fatty acid cycle.
The effects of GH replacement therapy on energy metabolism are still uncertain , and long-term benefits of increased muscle mass are thought to outweigh short-term negative metabolic effects . This study was design ed to address this issue by examining both short-term ( 1 wk ) and long-term ( 6 months ) effects of a low-dose ( 9.6 micro g/kg body weight.d ) GH replacement therapy or placebo on whole-body glucose and lipid metabolism ( oral glucose tolerance test and euglycemic hyperinsulinemic clamp combined with indirect calorimetry and infusion of 3-[(3)H]glucose ) and on muscle composition and muscle enzymes/metabolites , as determined from biopsies obtained at the end of the clamp in 19 GH-deficient adult subjects . GH therapy result ed in impaired insulin-stimulated glucose uptake at 1 wk ( -52 % ; P = 0.008 ) and 6 months ( -39 % ; P = 0.008 ) , which correlated with deterioration of glucose tolerance ( r = -0.481 ; P = 0.003 ) . The decrease in glucose uptake was associated with an increase in lipid oxidation at 1 wk ( 60 % ; P = 0.008 ) and 6 months ( 60 % ; P = 0.008 ) and a concomitant decrease in glucose oxidation . The deterioration of glucose metabolism during GH therapy also correlated with the enhanced rate of lipid oxidation ( r = -0.508 ; P = 0.0002 ) . In addition , there was a shift toward more glycolytic type II fibers during GH therapy . In conclusion , replacement therapy with a low-dose GH in GH-deficient adult subjects is associated with a sustained deterioration of glucose metabolism as a consequence of the lipolytic effect of GH , result ing in enhanced oxidation of lipid substrates . Also , a shift toward more insulin-resistant type II X fibers is seen in muscle . Glucose metabolism should be carefully monitored during long-term GH replacement therapy
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 .