Eur J Endocrinol
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DOI: 10.1530/eje.1.02176
European Journal of Endocrinology, Vol 155, Issue 1, 109-119
Copyright © 2006 by European Society of Endocrinology
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CLINICAL STUDY

Does long-term GH replacement therapy in hypopituitary adults with GH deficiency normalise quality of life?

Maria Koltowska-Häggström1,2, Anders F Mattsson1, John P Monson3, Paul Kind4, Xavier Badia5, Felipe F Casanueva6, Jan Busschbach7, Hans P F Koppeschaar8 and Gudmundur Johannsson9

1 KIGS/KIMS/ACROSTUDY Medical Outcomes, Endocrine Care, Pfizer, Sollentuna, Sweden, 2 Department of Pharmacy, Uppsala University, Uppsala, Sweden, 3 Department of Endocrinology, St Bartholomew’s Hospital, Queen Mary University of London, London, UK, 4 Outcomes Research Group, Centre for Health Economics, University of York, York, UK, 5 Health Outcomes Research Europe, Barcelona, Spain, 6 Department of Medicine, Endocrine Section (FFC), School of Medicine and Complejo Hospitalario, University of Santiago de Compostela, Santiago de Compostela, Spain, 7 Department for Medical Psychology and Psychotherapy, Erasmus, MC, Rotterdam, The Netherlands, 8 Division of Endocrinology, Utrecht Academy, Medical Centre, Utrecht, The Netherlands and 9 Department of Endocrinology, Sahlgrenska University Hospital at Gothenburg’s University, Gothenburg, Sweden

(Correspondence should be addressed to M Koltowska-Häggström; Email: maria.koltowska-haggstrom{at}pfizer.com)

Objective: To determine whether impaired quality of life (QoL) in adults with GH deficiency (GHD) is reversible with long-term GH therapy and whether the responses in QoL dimensions differ from each other.

Methods: QoL was measured by the Quality of Life–Assessment for Growth Hormone Deficiency in Adults (QoL-AGHDA) in general population samples in England & Wales, The Netherlands, Spain and Sweden (n = 892, 1038, 868 and 1682 respectively) and compared with corresponding patients’ data from KIMS (Pfizer International Metabolic Database) (n = 758, 247, 197 and 484 respectively) for 4–6 years a follow-up. The subsets of patients from England and Wales, and Sweden with longitudinal data for 5 years’ follow-up were also analysed. The change of the total QoL-AGHDA scores and responses within dimensions were evaluated. Subanalyses were performed to identify any specificity in response pattern for gender, age, disease-onset and aetiology.

Results: Irrespective of the degree of impairment, overall QoL improved dramatically in the first 12 months, with steady progress thereafter towards the country-specific population mean. Problems with memory and tiredness were the most serious burden for untreated patients, followed by tenseness, self-confidence and problems with socialising. With treatment, these improved in the reverse order, normalising for the latter three.

Conclusions: Long-term GH replacement results in sustained improvements towards the normative country-specific values in overall QoL and in most impaired dimensions. The lasting improvement and almost identical pattern of response in each patient subgroup and independent of the level of QoL impairment support the hypothesis that GHD may cause these patients’ psychological problems.




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