{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T21:12:29Z","timestamp":1790975549907,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2012,8,14]],"date-time":"2012-08-14T00:00:00Z","timestamp":1344902400000},"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":[[2012,9]]},"abstract":"Summary<\/jats:title>Background<\/jats:title>Both growth hormone (GH<\/jats:styled-content>) excess and GH<\/jats:styled-content> deficiency are associated with abnormalities in body composition and biomarkers of cardiovascular risk in patients with pituitary disorders. However, the effects of developing GH<\/jats:styled-content> deficiency after definitive treatment of acromegaly are largely unknown.<\/jats:p><\/jats:sec>Objective<\/jats:title>To determine whether development of GH<\/jats:styled-content> deficiency after definitive therapy for acromegaly is associated with increased visceral adiposity and biomarkers of cardiovascular risk compared with GH<\/jats:styled-content> sufficiency after definitive therapy for acromegaly.<\/jats:p><\/jats:sec>Design<\/jats:title>Cross\u2010sectional.<\/jats:p><\/jats:sec>Patients<\/jats:title>We studied three groups of subjects, all with a history of acromegaly (n<\/jats:italic>\u00a0=\u00a076): subjects with subsequent GH<\/jats:styled-content> deficiency (GHD<\/jats:styled-content>; n<\/jats:italic>\u00a0=\u00a031), subjects with subsequent GH<\/jats:styled-content> sufficiency (GHS<\/jats:styled-content>; n<\/jats:italic>\u00a0=\u00a025) and subjects with active acromegaly (AA<\/jats:styled-content>; n<\/jats:italic>\u00a0=\u00a020). No study subjects were receiving somatostatin analogues, dopamine agonists or hGH<\/jats:styled-content>.<\/jats:p><\/jats:sec>Measurements<\/jats:title>Body composition (by DXA<\/jats:styled-content>), abdominal adipose tissue depots (by cross\u2010sectional CT<\/jats:styled-content>), total body water (by bioimpedance analysis) and carotid intima\u2010media thickness (IMT<\/jats:styled-content>) were measured. Fasting morning serum was collected for high\u2010sensitivity C<\/jats:styled-content>\u2010reactive protein (hsCRP<\/jats:styled-content>), lipids and lipoprotein levels. An oral glucose tolerance test was performed, and homoeostasis model of assessment\u2010insulin resistance (HOMA<\/jats:styled-content>\u2010IR<\/jats:styled-content>) was calculated.<\/jats:p><\/jats:sec>Results<\/jats:title>Abdominal visceral adipose tissue, total adipose tissue and total body fat were higher in subjects with GHD<\/jats:styled-content> than GHS<\/jats:styled-content> or AA<\/jats:styled-content> (P<\/jats:styled-content>\u00a0<\/jats:italic><\u00a0<\/jats:italic>0\u00b705). Subcutaneous abdominal fat was higher, and fibrinogen and IMT<\/jats:styled-content> were lower in GHD<\/jats:styled-content> (but not GHS<\/jats:styled-content>) than AA<\/jats:styled-content> (P<\/jats:styled-content>\u00a0<\/jats:italic><\u00a0<\/jats:italic>0\u00b705). Patients with GHD<\/jats:styled-content> had the highest hsCRP<\/jats:styled-content>, followed by GHS<\/jats:styled-content>, and hsCRP<\/jats:styled-content> was lowest in AA<\/jats:styled-content> (P<\/jats:styled-content>\u00a0<\/jats:italic><\u00a0<\/jats:italic>0\u00b705). Fasting glucose, 120\u2010min glucose, fasting insulin, HOMA<\/jats:styled-content>\u2010IR<\/jats:styled-content> and per cent total body water were lower in GHD<\/jats:styled-content> and GHS<\/jats:styled-content> than AA<\/jats:styled-content> (P<\/jats:styled-content>\u00a0<\/jats:italic><\u00a0<\/jats:italic>0\u00b705). Triglycerides were higher in GHS<\/jats:styled-content> than AA<\/jats:styled-content> (P<\/jats:styled-content>\u00a0<\/jats:italic><\u00a0<\/jats:italic>0\u00b705). Lean body mass, mean arterial pressure, total cholesterol, HDL<\/jats:styled-content> and LDL<\/jats:styled-content> were comparable among groups.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Development of GHD<\/jats:styled-content> after definitive treatment of acromegaly may adversely affect body composition and inflammatory biomarkers of cardiovascular risk but does not appear to adversely affect glucose homoeostasis, lipids and lipoproteins, or other cardiovascular risk markers.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2265.2012.04361.x","type":"journal-article","created":{"date-parts":[[2012,2,9]],"date-time":"2012-02-09T01:55:31Z","timestamp":1328752531000},"page":"430-438","source":"Crossref","is-referenced-by-count":33,"title":["Effects of growth hormone deficiency on body composition and biomarkers of cardiovascular risk after definitive therapy for acromegaly"],"prefix":"10.1111","volume":"77","author":[{"given":"E.","family":"Lin","sequence":"first","affiliation":[{"name":"Department of Neuroendocrine Unit Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. L.","family":"Wexler","sequence":"additional","affiliation":[{"name":"Department of Neuroendocrine Unit Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Nachtigall","sequence":"additional","affiliation":[{"name":"Department of Neuroendocrine Unit Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Tritos","sequence":"additional","affiliation":[{"name":"Department of Neuroendocrine Unit Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.","family":"Swearingen","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Hemphill","sequence":"additional","affiliation":[{"name":"Division of Cardiology Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Loeffler","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology Massachusetts General Hospital and Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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