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 .
Serum leptin is increased in growth hormone-deficient adults: relationship to body composition and effects of placebo-controlled growth hormone therapy for 1 year.
The gene product from the ob gene , leptin , has recently been characterized in humans . The circulating level of leptin is related to body mass index ( BMI ) and more closely to estimates of total body fat , whereas visceral fat has been reported to be of minor importance . However , it is unknown if leptin is directly regulated by hormones that influence substrate metabolism and body composition . We studied leptin in adult growth hormone (GH)-deficient ( GHD ) patients substituted with GH treatment for 12 months in a parallel double-blind , placebo-controlled study . Twenty-seven GHD adults aged 44.9 + /- 1.9 years underwent  anthropometric measurements  for determination of regional and total body fat ( BMI , waist to hip ratio [ WHR ] , computed tomographic [ CT ] scan , dual-energy x-ray absorptiometry [ DEXA ] scan , and bioimpedance analysis [ BIA ] ) before and after 12 months of placebo-controlled GH substitution ( 2 IU/m2 ) in a parallel design . The same measurements were performed in 42 healthy adults aged 39.1 + /- 1.7 years . The logarithm of serum leptin levels correlated positively with abdominal subcutaneous fat and total body fat ( BIA and DEXA ) in untreated GHD patients and healthy subjects . Fasting insulin did not correlate with leptin levels in either of the groups . After 12 months of GH administration , the body composition of GHD patients was significantly changed with respect to a marked decrease in body fat . The relations of leptin to the estimates of body fat were maintained , and leptin was furthermore related to BMI and fasting insulin . In multiple linear regression analyses , additional estimates of visceral adiposity ( intraabdominal fat and maximal anterior-posterior diameter determined by CT scan ) were significant determinants of leptin in the healthy subjects . The increase in fasting insulin levels during GH substitution correlated negatively with the reduction in leptin levels ( r = -.823 , P = .003 ) . At baseline , leptin levels were increased in the patients compared with controls in both sexes ( women , 21.8 + /- 3.3 v 11.3 + /- 1.4 ng/mL , P = .002 ; men , 8.1 + /- 1.2 v 4.7 + /- 0.7 ng/mL , P = .008 ) . Leptin levels were similar in GHD patients treated for 12 months compared with healthy controls for both women and men ( women , 15.9 + /- 2.3 and 11.3 + /- 1.4 ng/mL , P = .163 ; men , 7.1 + /- 2.8 and 4.7 + /- 0.7 ng/mL , P = .759 ) . In healthy adults and in GHD patients , leptin levels were significantly higher in women than in men ( 11.3 + /- 1.4 v 4.7 + /- 0.7 ng/mL , P < .001 ; 21.8 + /- 3.3 v 8.1 + /- 1.2 ng/mL , P < .001 ) . Gender remained a significant determinant of leptin levels in several models of multiple linear regression analysis also including age , estradiol levels , insulin , and estimates of body fat . We conclude that leptin is increased but not differently regulated in GHD patients compared with normal subjects , and that leptin levels are closely related to estimates of body fat . This relationship is maintained during a decrease in body fat due to GH substitution
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 .