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Endocrine Abstracts (2016) 41 EP700 | DOI: 10.1530/endoabs.41.EP700

1Division of Endocrinology, Manchester, UK; 2Endocrine Care, Pfizer Health AB, Pfizer Health AB, Sollentuna, Sweden; 3Global Health and Value, Pfizer Inc., La Jolla, USA; 4Endocrine Care, Pfizer, Inc., New York, USA; 5Antwerp Centre for Endocrinology, Antwerp, Belgium.


Introduction: In adult patients with pituitary disease no relationship has been established between the biochemical severity of GHD and the degree of QoL impairment. Reasons may include heterogeneity of underlying pathologies, and the type of therapies received by GHD patients.

Methods: The KIMS (Pfizer International Metabolic Database) database was used to focus solely on patients with non-functioning pituitary adenomas and prolactinomas treated by surgery alone. Entry criteria include peak GH of less than 3 ng/ml to an ITT and at least 2 other pituitary hormone deficits. IGF-I was measured centrally and IGF-I SDS calculated using normal range for age and gender. Health-related QoL was measured using QoL-AGHDA, a disease-specific validated questionnaire for which higher scores (0-25) indicate worse QoL. In the UK, QoL-AGHDA scores alone are used to determine treatment eligibility.

Results: The analysis was performed separately for UK data versus the collective other European countries (Belgium, Germany, Sweden, France, Holland, Spain) data. Median AGHDA score at baseline for UK (n=68) was 15.5 and for Europe (n=299) 7.0 (P<0.0001) whilst median IGF-I SDS for UK (n=54) was −0.87 and for Europe (n=178) -1.53 (P=0.0042). The UK cohort have much greater impairment of QoL but are less severely GHD than the Europe cohort, implying a significant component of impaired QoL in the UK cohort is unrelated exclusively to their GH status.

Conclusions: The literature indicates that QoL improves significantly in UK GHD adults in response to GH replacement, however our results question a treatment strategy focused on QoL alone, a medical endpoint not shown to be related to the degree of GHD, and affected by multiple factors; for all other endocrine deficits the classical approach is to treat those with biochemical evidence of the severest deficit first.

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