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The effects of long‐term growth hormone and insulin‐like growth factor‐1 exposure on the development of cardiovascular, cerebrovascular and metabolic co‐morbidities in treated patients with acromegaly
Author(s) -
Jayasena C. N.,
Comninos A. N.,
Clarke H.,
Donaldson M.,
Meeran K.,
Dhillo W. S.
Publication year - 2011
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/j.1365-2265.2011.04019.x
Subject(s) - acromegaly , medicine , endocrinology , basal (medicine) , diabetes mellitus , insulin like growth factor , risk factor , biomarker , stroke (engine) , insulin , hormone , growth hormone , growth factor , biology , receptor , mechanical engineering , biochemistry , engineering
Summary Background Acromegaly is characterized by the hypersecretion of growth hormone (GH) and insulin‐like growth factor‐1 (IGF‐1). This leads to an increased cardiovascular, cerebrovascular and metabolic morbidity resulting in excess mortality. There is controversy over which biomarker, GH or IGF‐1, better predicts this increased morbidity and mortality. The relationship between the cumulative exposure to GH and IGF‐1 with co‐morbidities in acromegaly has not previously been reported. Objective To investigate the relationship between the cumulative exposure to GH and IGF‐1 with cardiovascular, cerebrovascular and metabolic co‐morbidities. Methods Records of 116 acromegalic patients were retrospectively examined. Cardiovascular and cerebrovascular histories, serum GH and IGF‐1, fasting glucose and oral glucose tolerance test results, were reviewed for the duration of follow‐up. IGF‐1 index was calculated by dividing each serum IGF‐1 value by the upper limit of reference range for IGF‐1. GH and IGF‐1 burdens were calculated for each patient by multiplying known disease duration (in years) by mean level of basal GH or IGF‐1 index recorded during the patients’ entire follow‐up. Results Patients with abnormal glucose tolerance had a significantly higher mean GH burden compared with euglycaemic patients ( P = 0·005). Ischaemic heart disease was also associated with a higher GH burden ( P = 0·009) whereas cerebrovascular disease and cardiomyopathy were associated with a significantly higher mean IGF‐1 burden ( P = 0·018, P = 0·011 respectively). Conclusion This study identifies associations of raised GH and IGF‐1 burden with cardiovascular, cerebrovascular and metabolic complications of acromegaly. Results from this study therefore suggest that consideration of the overall level of GH and IGF‐1 exposure may provide important information for the management and surveillance of patients with treated acromegaly.