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 (GH) replacement reduces total body fat and normalizes insulin sensitivity in GH-deficient adults: a report of one-year clinical experience.
The effects of GH replacement on body fat composition and insulin sensitivity were assessed in GH-deficient adults . The patients were r and omized into a double-blind , placebo-controlled study of human recombinant GH replacement therapy for 6 months ( period 1 ) , followed by an open phase of GH for another 6 months ( period 2 ) . Anthropometric variables , body fat composition ( fat % ) , and biochemical parameters were measured during the trial . Measurements of in vivo insulin sensitivity were carried out at the commencement of the study and on completion of the trial by modified insulin suppression test . The modified insulin suppression test was performed both in the morning ( AM ) and in the afternoon ( PM ) to further evaluate the PM-AM steady-state plasma glucose ( SSPG ) pattern . We found that the GH-deficient adults had more body fat and were insulin resistant . Significant reduction in fat % and total body fat mass was found in the active arm of period 1 without alteration of body weight . Besides , we demonstrated , for the first time , the GH replacement for 6 months did not alter the insulin sensitivity , but replacement for a longer period ( 12 months ) normalized not only the AM SSPG level but also the PM-AM SSPG pattern . We also found a positive correlation between SSPG ( regardless of AM vs. PM ) and fat % and total body fat mass . In conclusion , normalization of insulin sensitivity in GH-deficient adults after replacement of GH may be related to the reduction of total body fat
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 .