Andrea F. Attanasio, Daojun Mo, Eva Marie Erfurth, Meng Tan, Ken Y. Ho, David Kleinberg, Alan G. Zimmermann, Philippe Chanson*, and on behalf of the International Hypopituitary Control and Complications Study Advisory Board
Cascina del Rosone (A.F.A.), 14041 Agliano Terme, Italy; Lilly Research Laboratories (D.M., A.G.Z., M.T.), Eli Lilly & Co., Indianapolis, Indiana 46285; Department of Endocrinology (E.M.E.), Lund University Hospital, SE 221 85 Lund, Sweden; Pituitary Research Unit (K.Y.H.), Garvan Institute of Medical Research, Sydney, New South Wales 2010, Australia; Neuroendocrine Unit (D.K.), New York University School of Medicine, New York, New York 10016; Assistance Publique-Hôpitaux de Paris, Service d'Endocrinologie et des Maladies de la Reproduction, Centre de Référence des Maladies Rares de la Croissance (P.C.), Hôpital de Bicêtre, Le Kremlin-Bicêtre F-94275, France; and Université Paris-Sud 11 (P.C.) and Institut National de la Santé et de la Recherche Médicale Unité 693 (P.C.), Le Kremlin-Bicêtre, F-94276, France
* To whom correspondence should be addressed. E-mail: email@example.com.
Context and Objective: Metabolic and body compositional consequences of GH deficiency (GHD) in adults are associated with a phenotype similar to the metabolic syndrome (MetS).
Patients: We assessed MetS prevalence in adult GHD patients (n = 2531) enrolled in the Hypopituitary Control and Complications Study. Prevalence was assessed at baseline and after 3 yr of GH replacement in a subset of 346 adult-onset patients.
Results: Baseline MetS crude prevalence was 42.3%; age-adjusted prevalence in the United States and Europe was 51.8 and 28.6% (P < 0.001), respectively. In the United States, age-adjusted prevalence was significantly higher (P < 0.001) than in a general population survey. Increased MetS risk at baseline was observed for age 40 yr or older (adjusted relative risk 1.34, 95% confidence interval 1.17–1.53, P < 0.001), females (1.15, 1.05–1.25, P = 0.002), and adult onset (1.77, 1.44–2.18, P < 0.001). In GH-treated adult-onset patients, MetS prevalence was not changed after 3 yr (42.5–45.7%, P = 0.172), but significant changes were seen for waist circumference (62.1–56.9%, P = 0.008), fasting glucose (26.0–32.4%, P < 0.001), and blood pressure (59.8–69.7%, P < 0.001). Significantly increased risk of MetS at yr 3 was associated with baseline MetS (adjusted relative risk 4.09, 95% confidence interval 3.02–5.53, P < 0.001) and body mass index 30 kg/m2 or greater (1.53, 1.17–1.99, P = 0.002) and increased risk (with a P value < 0.1) for GH dose 600 ?g/d or greater (1.18, 95% confidence interval 0.98–1.44, P = 0.088).
Conclusion: MetS prevalence in GHD patients was higher than in the general population in the United States and higher in the United States than Europe. Prevalence was unaffected by GH replacement, but baseline MetS status and obesity were strong predictors of MetS after GH treatment.