Premium
Growth hormone replacement does not increase mortality in patients with childhood‐onset growth hormone deficiency
Author(s) -
Berglund Agnethe,
Gravholt Claus Højbjerg,
Olsen Morten Smærup,
Christiansen Jens Sandahl,
Stochholm Kirstine
Publication year - 2015
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.12848
Subject(s) - medicine , short stature , hazard ratio , population , proportional hazards model , endocrinology , growth hormone deficiency , confounding , growth hormone treatment , pediatrics , hormone , growth hormone , confidence interval , environmental health
Summary Context Long‐term safety of growth hormone ( GH ) treatment is an area of much debate. Studies including children treated with GH not only due to GHD , but also due to non‐ GHD causes like idiopathic short stature or like short stature in children born small for gestational age have suggested that GH treatment is associated with increased mortality or stroke. Objective To study the impact of GH replacement on overall and cause‐specific mortality in childhood‐onset GHD ( CO GHD ) patients. Design A nationwide population‐based registry study on patients with CO GHD and general population controls matched on age and gender. Mortality hazard ratios ( HR s) were computed comparing patients and controls, and comparing GH ‐replaced patients and non‐ GH ‐replaced patients, using C ox regression. Comparing GH ‐ and non‐ GH ‐replaced patients HR s were adjusted for birth year, year of diagnosis, gender, irradiation, ACTH insufficiency and primary disease. Patients and controls A total of 494 patients with CO GHD each matched with 100 general population controls were included. Results Mortality was substantially increased comparing patients with CO GHD and general population controls, HR = 7·51 (95% CI = 6·06–9·31). Comparing GH ‐replaced patients with non‐ GH ‐replaced patients mortality was significantly decreased in total ( HR = 0·27, CI = 0·17–0·43) and due to malignancy ( HR = 0·14, CI = 0·07–0·28) in GH ‐replaced patients. Adjusting for relevant confounders, this decrease remained significant both in total ( HR = 0·56, CI = 0·32–0·96) and due to malignancy ( HR = 0·33, CI = 0·16–0·69). Overall and cause‐specific mortality was increased in both GH ‐replaced and non‐ GH ‐replaced patients compared to general population controls, but mortality was generally highest in non‐ GH ‐replaced patients. Conclusion The present data from a national cohort of patients with CO GHD do not support the suggestion that GH replacement is associated with increased mortality.