{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T19:18:23Z","timestamp":1779909503368,"version":"3.53.1"},"reference-count":25,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2007,5,30]],"date-time":"2007-05-30T00:00:00Z","timestamp":1180483200000},"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":[[2007,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Objective\u2002<\/jats:bold> Adult onset GH deficiency (GHD) is characterized by abnormalities of serum lipoprotein profiles and GH replacement results in favourable alterations in serum total and low density lipoprotein (LDL)\u2010cholesterol. Preliminary evidence has indicated that the effect of GH replacement in this respect may be additive to that of HMG CoA reductase inhibitor (statin) therapy. We have examined this possibility during prospective follow\u2010up of adult onset hypopituitary patients enrolled in KIMS (Pfizer International Metabolic Database), a pharmacoepidemiological study of GH replacement in adult hypopituitary patients.<\/jats:p><jats:p><jats:bold>Design\u2002<\/jats:bold> Lipoprotein profiles were measured centrally at baseline and after 12\u00a0months GH replacement therapy.<\/jats:p><jats:p><jats:bold>Patients\u2002<\/jats:bold> Sixty\u2010one hypopituitary patients (30 male, 31 female) on maintenance statin therapy (mean 2\u00b75\u00a0\u00b1\u00a02\u00b77 SD years before GH) (statin group \u2013 SG) and 1247 (608 male, 639 female) patients not on hypolipidaemic therapy (nonstatin group \u2013 NSG) were studied. All patients were na\u00efve or had not received GH replacement during the 6\u00a0months prior to study. Patients who developed diabetes mellitus during the first year of GH therapy or in the subsequent year and those with childhood onset GHD were excluded from this analysis. An established diagnosis of diabetes mellitus was present in 18% SG and 4\u00b74% NSG at baseline.<\/jats:p><jats:p><jats:bold>Measurements\u2002<\/jats:bold> Serum concentrations of total, high density lipoprotein (HDL)\u2010cholesterol, triglycerides and IGF\u2010I were measured centrally in all patients and LDL\u2010cholesterol was estimated using Friedewald's formula.<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> The relative frequency of various statin use was simvastatin 52% (15\u00b78\u00a0\u00b1\u00a08\u00b71\u00a0mg, mean\u00a0\u00b1\u00a0SD), atorvastatin 30% (14\u00b74\u00a0\u00b1\u00a07\u00b78\u00a0mg), pravastatin 9\u00b78% (31\u00b76\u00a0mg\u00a0\u00b1\u00a013\u00b79\u00a0mg), lovastatin 6\u00b76% (17\u00b75\u00a0\u00b1\u00a05\u00a0mg) and fluvastatin 1\u00b76% (40\u00a0mg). Baseline serum total and LDL\u2010cholesterol (mean\u00a0\u00b1\u00a0SD) were 5\u00b72\u00a0\u00b1\u00a01\u00b74 and 3\u00b71\u00a0\u00b1\u00a01\u00b73\u00a0mmol\/l in SG and 5\u00b78\u00a0\u00b1\u00a01\u00b72 and 3\u00b77\u00a0\u00b1\u00a01\u00b70\u00a0mmol\/l in NSG, respectively (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b70001, SG <jats:italic>vs<\/jats:italic>. NSG). After 12\u00a0months GH replacement (SG: 0\u00b732\u00a0\u00b1\u00a00\u00b717\u00a0mg\/day; NSG: 0\u00b738\u00a0\u00b1\u00a00\u00b71\u00a0mg\/day) serum total and LDL\u2010cholesterol decreased by a mean (\u00b1SD) of 0\u00b748 (\u00b1\u00a01\u00b725)\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b70004) and 0\u00b753 (\u00b1\u00a01\u00b708)\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b70001) in SG and by 0\u00b730 (\u00b1\u00a00\u00b789)\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b70001) and 0\u00b728 (\u00b1\u00a00\u00b780)\u00a0mmol\/l (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b70001) in NSG, respectively. There were no significant changes in HDL\u2010cholesterol or triglycerides in either group (SG <jats:italic>vs<\/jats:italic>. NSG: NS). A relationship between LDL\u2010cholesterol at baseline and the decrease in LDL\u2010cholesterol after 12\u00a0months GH was evident in both groups (SG: <jats:italic>R<\/jats:italic>\u00a0=\u00a0\u20130\u00b754, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b7001; NSG: <jats:italic>R<\/jats:italic>\u00a0=\u00a0\u20130\u00b74, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b7001) and a similar relationship for cholesterol was observed.<\/jats:p><jats:p><jats:bold>Conclusions\u2002<\/jats:bold> These data indicate that GH replacement exerts additional beneficial effects on lipoprotein profiles in patients on maintenance statin therapy, confirming that the effects of these interventions are complementary rather than exclusive.<\/jats:p>","DOI":"10.1111\/j.1365-2265.2007.02935.x","type":"journal-article","created":{"date-parts":[[2007,6,21]],"date-time":"2007-06-21T03:20:32Z","timestamp":1182396032000},"page":"623-628","source":"Crossref","is-referenced-by-count":37,"title":["Growth 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