Lipid profile in congenital adrenal hyperplasia

Glucocorticoids have been reported to exert a marked effect on lipoprotein metabolism. Several studies have shown a potential risk of hyperlipidemia in patients under long-term glucocorticoid therapy. Current management of patients with congenital adrenal hyperplasia (CAH) includes the use of glucocorticoids to attenuate the increased production of undesirable adrenal hormones. A case-control study was designed to compare the serum lipid profiles of 14 patients with CAH under glucocorticoid therapy and 14 normal controls and to determine the characteristics of the profiles. A total of 9 patients (64.3%) had serum total cholesterol (TC) greater than 4.4 mmol/L (170 mg/dL), compared with 6 individuals in the control group (42.3%). Nine patients with CAH (64.3%) had serum triglycerides (TGs) more than 1.0 mmol/L (90 mg/dL), compared with only 2 in the control group (14.3%). Similarly, the mean serum TG was higher in the CAH group versus the controls, 1.33 mmol/L (118 mg/dL) versus 0.75 mmol/L (67 mg/dL), respectively. Serum low-density lipoprotein, (LDL-C) and high-density, lipoprotein (HDL-C) cholesterol were determined in 13 children with CAH and in the 14 controls. Nine CAH patients (69.2%) and 8 controls (57%) had LDL-C greater than 2.8 mmol/L (<110 mg/dL). For HDL-C, 2 children with CAH (15.4%) and 4 controls (28.6%) had levels less than 0.9 mmol/L (35 mg/dL). There were no significant differences for the cholesterol index, 0.24 for the controls and 0.22 for the CAH group. In the CAH group, the mean serum TG level and the percentage of individuals with TGs greater than 1.0 mmol/L were statistically significant compared with the controls. The mean serum TC and LDL-C, as well as the percentage of subjects with levels over the cutoff point, although slightly higher in the CAH group, were of no statistical significance. The results of this pilot study suggest that long-term glucocorticoid therapy in patients with CAH may induce abnormalities in the serum lipid profile characterized mainly by an increment in serum TGs.