Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 29 P53

ICEECE2012 Poster Presentations Adrenal cortex (113 abstracts)

Relationship of current glucocorticoid dose with metabolic outcomes in CAH: analysis of the United Kingdom congenital adrenal hyperplasia adult study executive (CaHASE) cohort

T. Han 5 , R. Stimson 3 , A. Rees 6 , N. Krone 4 , D. Willis 1 , S. Wild 4 , G. Conway 5 , W. Arlt 4 , B. Walker 3 , R. Ross 2 & X. CaHASE 1


1Society for Endocrinology, Bristol, UK; 2University of Sheffield, Sheffield, UK; 3University of Edinburgh, Edinburgh, UK; 4University of Birmingham, Edinburgh, UK; 5University College London, London, UK; 6Cardiff University, Cardiff, UK.


We have previously reported the following metabolic abnormalities were common in 203 adult patients with CAH: obesity (41%), hypercholesterolemia (46%), insulin resistance (29%), osteopenia (40%) and osteoporosis (7%) (Arlt et al. JCEM 2010 95 5110–21). The CAH patients were taking different glucocorticoid therapies at various doses (n=196): hydrocortisone (n=25 M, 26 W), prednisolone (n=21M,67W), dexamethasone (n=15M,22W) or combination therapy (n=4 M, 16 W). To test the hypothesis that glucocorticoid exposure mediates adverse metabolic outcomes, we converted current treatment regimens to prednisolone dose equivalents using three published models: British National Formulary (BNF), Rivkees (Pediatrics 2000 106 767–73) and Arlt (JCEM 2009 94 1059–67). The respective ratios for prednisolone:hydrocortisone:dexamethasone were 1:5:0.15, 1:4:0.057, and 1:5:0.125. The relationship of glucocorticoid dose and metabolic parameters was tested by treating dose as a continuous variable using regression analysis and as a categorised variable using ANOVA (with prednisolone dose equivalents in four categories: <2.5 mg (n=4 M, 16 W), 2.5≤5.0 mg (n=12 M, 27 W), 5.0≤7.5 mg (n=24 M, 57 W) and >7.5 mg (n=25 M, 31 W)). The mean prednisolone equivalent dose (men: 6.1:7.5:5.7, women: 5.1:6.0:5.0 mg/day) was different for the three models for both sexes (P<0.01). There was no effect of dose in any of the three models as judged by ANOVA or univariate regression analysis on; BMI, waist circumference, triglycerides, HDL-cholesterol, insulin resistance (HOMA-IR) and femoral or lumbar bone mineral density. Partial correlation analysis (age and sex adjustments) showed significant relationships between dose and systolic (BNF: r=0.188, P=0.01; Rivkees: r=0.147, P=0.04; Arlt: r=0.189, P=0.01) and diastolic blood pressure (BNF: r=0.170, P=0.02; Arlt: r=0.154, P=0.03; except Rivkees: r=0.070, P=0.37) and for Rivkees model only, between dose and HDL-cholesterol (r=0.186, P=0.02) and HOMA-IR (r=0.175, P=0.04). Confounding factors in our analysis may include variable patient compliance with drug and duration of treatment. In conclusion, no published method for comparing glucocorticoid dose equivalence is superior to another. We found little impact of dose on individual metabolic parameters in adults with CAH.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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