{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T22:51:59Z","timestamp":1772578319952,"version":"3.50.1"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,6,16]],"date-time":"2004-06-16T00:00:00Z","timestamp":1087344000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold><jats:sc>objectives\u2002<\/jats:sc><\/jats:bold> To assess effects of GH replacement therapy on cardiac structure and function, exercise capacity as well as serum lipids in elderly patients with GH deficiency (GHD).<\/jats:p><jats:p><jats:bold><jats:sc>patients and methods\u2002<\/jats:sc><\/jats:bold> Thirty\u2010one patients (six females, 25 males), aged 60\u201379\u00a0years (mean 68\u00a0years) with GHD on stable cortisone and thyroxine substitution were studied. All men with gonadotropin deficiency had testosterone and one woman had oestrogen replacement. They were randomized in a double\u2010blind manner to GH or placebo treatment for 6\u00a0months, followed by another 12\u00a0months GH (Humatrope, Eli Lilly &amp; Co, Uppsala, Sweden). GH dose was 0\u00b7017\u00a0mg\/kg\/week for 1\u00a0month and then 0\u00b7033\u00a0mg\/kg\/week divided into daily subcutaneous injections at bedtime. Echocardiography, exercise capacity tests and serum lipid measurements were performed at 0, 6, 12 and 18\u00a0months.<\/jats:p><jats:p><jats:bold><jats:sc>results\u2002<\/jats:sc><\/jats:bold> During the 6\u2010month placebo\u2010controlled period there were no significant changes in the placebo group, but in the GH\u2010treated group there was a significant increase in IGF\u2010I to normal levels for age, with median IGF\u2010I from 6\u00b79 to 18\u00b75\u00a0nmol\/l, increase in resting heart rate and maximal working capacity. During the open GH study, IGF\u2010I increased from 8\u00b77\u00a0to 19\u00b72\u00a0nmol\/l at 6\u00a0months and 18\u00b78\u00a0nmol\/l at 12\u00a0months (<jats:italic>P<\/jats:italic>\u00a0\u2264\u00a00\u00b7001). At 6\u00a0months, in the open GH study group, a minor decrease in aortic outflow tract integral (VTI) from 21\u00b78 to 20\u00b77\u00a0cm (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7031) and an increase in heart rate at rest from 63 to 67\u00a0bpm (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7017), heart rate at maximum exercise from 138 to 144 bpm (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7005) and maximum load at exercise from 142 to 151 Watts (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7014) were seen. These changes were temporary and returned at 12\u00a0months with no significant difference from baseline values. Left ventricular dimensions and blood pressure showed no significant changes. At 6\u00a0months, in the open GH study group, there was a significant decrease in serum low\u2010density lipoprotein (LDL) cholesterol from 3\u00b77 to 3\u00b74\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7006), a decrease in LDL\/HDL ratio from 3\u00b74 to 3\u00b71 (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7036) and a decrease in serum total cholesterol from 5\u00b76 to 5\u00b73\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7036). At 12\u00a0months, serum lipids showed same changes with a significant decrease in serum LDL cholesterol (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b70008), in LDL\/HDL ratio (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b70005) and in serum total cholesterol (<jats:italic>P<\/jats:italic>\u00a0= 0\u00b7049). Serum HDL cholesterol showed no significant change at 6\u00a0months, at 12\u00a0months a significant increase was seen from 1\u00b72 to 1\u00b74\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7007). There were no significant changes in serum triglycerides.<\/jats:p><jats:p><jats:bold><jats:sc>conclusions\u2002<\/jats:sc><\/jats:bold> GH substitution to elderly patients with GHD caused only a transient increase in heart rate. At the end of the 12\u00a0months there were no significant changes on cardiac noninvasive structural and functional parameters. Maximal working capacity transiently improved. Thus, the therapy was safe without negative effects on cardiac structural and functional noninvasive parameters. Lipid profiles improved with reduction of serum LDL cholesterol accompanied by significant improvement of LDL\/HDL ratio and serum HDL cholesterol after 12\u00a0months treatment.<\/jats:p>","DOI":"10.1111\/j.1365-2265.2004.02080.x","type":"journal-article","created":{"date-parts":[[2004,6,22]],"date-time":"2004-06-22T11:27:09Z","timestamp":1087903629000},"page":"113-122","source":"Crossref","is-referenced-by-count":30,"title":["The effects of GH replacement therapy on cardiac morphology and function, exercise capacity and serum lipids in elderly patients with GH 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