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 .
Continuation of growth hormone (GH) replacement in GH-deficient patients during transition from childhood to adulthood: a two-year placebo-controlled study.
Previous studies have demonstrated beneficial effects of GH replacement , in adults with GH deficiency ( GHD ) , on body composition , physical fitness , and quality of life . These studies , however , concern patients with adult-onset GHD or childhood-onset ( CO ) patients enrolled several years after withdrawal of initial therapy . So far , the effects of continuation of GH-administration in patients with CO-GHD have not been examined . We studied a group of nineteen young adults ( 13 males + 6 females ; 16 - 26 yr old ; mean age , 20.2 + /- 0.65 yr ) with CO-GHD , in a r and omized , parallel , double-blind ,  placebo-controlled trial for 1 yr , followed by an open phase with GH for 1 yr . All patients received GH therapy  at the start of study , and trial medication ( GH/placebo ) was given in a similar dose . Patients r and omized to continued GH treatment exhibited no significant changes in any parameters tested , but intra- and interindividual variations in insulin-like growth factor (IGF)-I levels could suggest compliance problems . Discontinuation of GH for 1 yr result ed in a decrease in serum IGF-I , from 422.0 + /- 56.8 to 147.8 + /- 33.4 microg/L , in the placebo group ( P = 0.003 ) . After discontinuation of GH for 1 yr , an increase in total body fat ( TBF , kg ) , measured by dual-energy x-ray absorptiometry scan , was seen [ placebo : 22.7 + /- 2.7 to 26.5 + /- 2.5 ( P = 0.01 ) ; GH : 16.2 + /- 2.1 to 17.2 + /- 2.1 ( not significant ) ] . Resumption of GH after placebo was followed by increments in serum IGF-I ( microg/L ) [ from 147.8 + /- 33.4 to 452 + /- 76 ( P = 0.001 ) ] and IGF-binding protein 3 , as well as in fasting glucose ( mmol/L ) [ 4.9 + /- 0.2 vs. 5.3 + /- 0.2 ( P = 0.03 ) ] . After resumption of GH lean body mass ( kg ) increased [ 52.4 + /- 4.9 vs. 60.7 + /- 5.6 ( P = 0.006 ) ] . Likewise , resumption of GH therapy increased thigh muscle volume and thigh muscle/fat ratio , as assessed by computed tomography [ muscle volume ( cm2/10 mm ) : 118.2 + /- 11.7 vs. 130.0 + /- 10.9 ( P = 0.002 ) ; muscle/fat ratio : 1.33 + /- 0.24 vs. 1.69 + /- 0.36 ( P = 0.02 ) ] . In conclusion , discontinuation of GH treatment in GHD patients , during the transition from childhood to adulthood , induces significant and potentially unfavorable changes in IGF-I and body composition , both of which are reversed after resumption of GH treatment . By contrast , continuation of GH therapy results in unaltered IGF-I and body composition . We recommend continuation of GH therapy in these patients , to be undertaken in collaboration between pediatricians and adult endocrinologists
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 .