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 .
Adult growth hormone (GH)-deficient patients demonstrate heterogeneity between childhood onset and adult onset before and during human GH treatment. Adult Growth Hormone Deficiency Study Group.
The onset of adult GH deficiency may be during either adulthood ( AO ) or childhood ( CO ) , but potential differences have not previously been examined . In this study the baseline and GH therapy ( 12.5 micrograms/kg per day ) data from CO ( n = 74 ; mean age 29 yr ) and AO ( n = 99 ; mean age 44 yr ) GH-deficient adult patients have been compared . The first 6 months comprised r and omized , double-blind treatment with GH or placebo , then all patients were GH-treated for a further 12 months . At baseline the height , body weight , body mass index , lean body mass , and waist/hip ratio of AO patients were significantly ( P < 0.001 ) greater than in CO patients . Serum insulin-like growth factor-I ( IGF-I ) levels were below normal but were lower in CO than AO patients ( P < 0.001 ) , and the correlation with IGF binding protein-3 was stronger in CO than in AO patients . Osteocalcin concentration in CO patients was above the normal range and significantly greater than in AO patients . Both groups had significant psychosocial distress , but the deviation from normality was greater in AO patients . Throughout GH therapy there was a significant increase in lean body mass and significant decrease in percent body fat and sum of skinfolds in each group . Wais/hip ratio was decreased by long-term therapy in AO but not CO patients . Total and low density lipoprotein cholesterol levels were decreased from baseline at 6 months in AO but not CO patients and high density lipoprotein cholesterol was increased in both groups throughout therapy . IGF-I and IGF binding protein-3 were increased into the normal range by GH therapy in both groups . Mean osteocalcin level in AO patients was increased at 6 months with no further change with GH therapy , whereas in CO patients there was a steep increase up to 12 months but then a sharp decrease . Nottingham Health Profile scores showed significant improvements in physical mobility and energy at 18 months of therapy in AO patients but no consistent effects in CO patients . GH-induced side effects were mainly reported by AO patients ; very few CO patients reported treatment-emergent adverse events . These results demonstrate significant differences in clinical and biochemical presentation and responses to therapy of the adult GH deficiency syndrome . This is consistent with the existence of two entities , developmental ( CO ) and metabolic ( AO ) , and the different functions of GH at different periods of life
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 .