Evaluation of coagulation and fibrinolytic parameters in adult onset GH deficiency and the effects of GH replacement therapy: A placebo controlled study

• Published in: Growth hormone & IGF research 2012-02, Vol.22 (1), p.17-21
• Main Authors: Cakir, Ilkay, Tanriverdi, Fatih, Karaca, Zuleyha, Kaynar, Leylagul, Eser, Bulent, Unluhizarci, Kursad, Kelestimur, Fahrettin
• Format: Article
• Language: English
• Subjects: Adult; Advanced Basic Science; Blood Coagulation - physiology; Coagulation; Endocrinology & Metabolism; Female; Fibrinogen - metabolism; Fibrinogen - therapeutic use; Growth hormone deficiency; Hormone Replacement Therapy; Human Growth Hormone - deficiency; Human Growth Hormone - therapeutic use; Humans; Male; Middle Aged; Natural anticoagulants; Placebo Effect; Protein S; Prothrombin Time
• ISSN: 1096-6374; 1532-2238
• DOI: 10.1016/j.ghir.2011.12.001

Abstract Objective Increased cardiovascular mortality/morbidity observed in patients with hypopituitarism is ascribed to growth hormone deficiency (GHD) because of its unfavorable cardiovascular risk profile. Abnormalities in the coagulation system may also contribute to increased cardiovascular morbidity/mortality. To get a better insight into the role of hemostasis in GHD we assessed several hemostatic markers at baseline and after 6 months of GH replacement therapy (GHRT). Design-patients Nineteen patients with adult onset GHD were enrolled (twelve patients into the treatment and seven patients into the placebo group) into the study. Platelet count, collagen/epinephrine closure time, collagen/ADP closure time, fibrinogen, prothrombin time (PT), activated partial thromboplastin time (aPTT), antithrombin III (AT III), protein C activity, protein S activity, lupus anticoagulant, antiphospholipid antibody immunoglobulin M, and antiphospholipid antibody immunoglobulin G were measured at baseline and 6 months after treatment. Results The investigated parameters in the groups were similar at baseline except for low protein S (PS) activity. Protein S deficiency was observed in three of the patients in the GH treatment group at baseline, however the PS activity values normalized following GHRT. AT III and protein C activities decreased when compared to baseline values in the treatment group but not in the placebo group. Conclusions We observed protein S deficiency more frequent than seen in the general population and normalization of protein S activity and decreases, in other natural anticoagulants following GHRT. Further studies are required to understand the impact of these changes in cardiovascular morbidity and mortality in this patient population.