The impact of glucocorticoid replacement regimens on metabolic outcome and comorbidity in hypopituitary patients.
BACKGROUND
Hypopituitary patients with untreated GH deficiency and patients on inappropriately high doses of glucocorticoid (GC) share certain clinical features.


OBJECTIVE
The aim of the study was to examine the influence of GC substitution on clinical characteristics in hypopituitary patients before and after GH replacement therapy.


METHODS
A total of 2424 hypopituitary patients within the KIMS (Pfizer International Metabolic Database) were grouped according to ACTH status. Comparisons were performed between subjects on hydrocortisone (HC) (n = 1186), cortisone acetate (CA) (n = 487), and prednisolone/dexamethasone (n = 52), and ACTH-sufficient patients (AS) (n = 717) before and after 1 yr of GH treatment in terms of body mass index, waist and hip circumference, blood pressure, glucose, glycosylated hemoglobin (HbA1c), serum lipids, IGF-I, and comorbidity. Hydrocortisone equivalent (HCeq) doses were calculated, and measurements were adjusted for sex and age.


RESULTS
At baseline, the HC group had increased total cholesterol, triglycerides, waist circumference, and HbA1c, and the prednisolone/dexamethasone group had increased waist/hip ratio as compared with AS. After HCeq dose adjustment, the HC group retained higher HbA1c than the CA group. GC-treated patients showed a dose-related increase in serum IGF-I, body mass index, triglycerides, low-density lipoprotein cholesterol and total cholesterol levels. Subjects with HCeq doses less than 20 mg/d (n = 328) at baseline did not differ from AS in metabolic endpoints. The 1-yr metabolic response to GH was similar in all GC groups and dose categories. All new cases of diabetes (n = 12), stroke (n = 8), and myocardial infarction (n = 3) during GH treatment occurred in GC-treated subjects.


CONCLUSIONS
HCeq doses of at least 20 mg/d in adults with hypopituitarism are associated with an unfavorable metabolic profile. CA replacement may have metabolic advantages compared with other GCs.
Filipsson
Helena
H
Department of Endocrinology, Gröna Stråket 8, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden. helena.filipsson@telia.com
Monson
John P
JP
Koltowska-Häggström
Maria
M
Mattsson
Anders
A
Johannsson
Gudmundur
G
D000324:Adrenocorticotropic Hormone / Q000172:deficiency; D000328:Adult; D000368:Aged; D015992:Body Mass Index; D015897:Comorbidity; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage*; D013006:Growth Hormone / Q000627:therapeutic use*; D020249:Hormone Replacement Therapy; D006801:Humans; D007018:Hypopituitarism / Q000188:drug therapy* / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors
D005938:Glucocorticoids; D008055:Lipids; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D013006:Growth Hormone