Hi Kelly

The abstract below was the study my boys took part in.  Please bear in mind that the children who took part in the study are treated at a centre of excellence in the UK though, where minimal doses of glucocorticoid are used and patients are generally NOT overweight.  Had it been done at another centre, where they use higher doses of glucocorticoid for treating CAH, I feel the results could have been different. 

This paper was presented at the ESPE 2005 - full paper not yet out but I will send it on to you, when received. 

 

Insulin sensitivity and body composition in children with congenital adrenal hyperplasia due to 21 hydroxlyase deficiency

Deeb A, Williams RM, Murgatroyd P, Hughes IA,  & Acerini CL

 Department of Paediatrics, University of Cambridge, Addenbrookes Hospital

Wellcome Trust Clinical Research Facility, Addenbrookes Hospital

 

Children with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency are thought to be at increased risk of obesity and insulin resistance (IR).  This may be related to changes in body composition and to increased central adiposity secondary to glucocorticoid replacement treatment.  We examined relationships between indices of insulin sensitivity (HOMA-S) and body composition in a cohort of children with CAH (n 37, 16M, median (range) age 9.4y (0.5 to 15.8); daily hydrocortisone dose 11 mg/m²; puberty (Tanner) stage (PS): I n =22; II-III n =8; IV-V n =7) and in 41 (14M) matched healthy controls. Fasting blood glucose (BG), insulin, lipid profiles and body composition scans (DXA) were performed on all subjects. An oral glucose tolerance test (OGTT) was carried out in pubertal (PS II or >) subjects. 

Median (range) BMI SD scores were similar between CAH and controls [0.33 (-4.54-3.79) vs 0.27 (-2.186-2.55)]. Fasting BG was lower in CAH subjects, independent of sex, PS & BMI-SDS (mean (SD) 4.1 (0.5) vs 4.5 (0.7) mmol/l, p<0.001) but fasting insulin and HOMA S were not different. During OGTT, BG was lower at +30 min [6.5(1.3) vs 7.4(1.1) mmol/l, p<0.05] and higher at + 120min post glucose [5.5(0.8) vs 4.9(0.8), p<0.05] in CAH than controls.  There was no difference in insulin concentrations post glucose at any time point between CAH and controls. Median (range) fat/ lean ratio was also not different between groups [0.27 (0.12-1.21) vs 0.32 (0.06-0.97)].

In conclusion, no differences in insulin sensitivity were observed between CAH and controls and is likely to reflect body composition similarity between groups.  Our results do not confirm recent reports that CAH children are at risk of obesity and IR and suggest that close attention to glucocorticoid replacement therapy may be important in the avoidance of these problems.