Uncoupling of cardiovascular risk markers in adolescent girls with anorexia nervosa

Objective

Cardiovascular (CV) risk begins in childhood, and low body weight should result in a favorable risk profile. However, adolescents with anorexia nervosa (AN) have alterations in many hormonal factors that mediate CV risk. We hypothesized that in AN, growth hormone (GH) resistance and hypercortisolemia would increase CV risk through effects on pro-inflammatory cytokines and lipid status despite low weight.

Study design

We examined CV risk markers (high sensitivity C-reactive protein [hsCRP], interleukin-6 [IL-6], apolipoprotein-B [Apo-B], and lipid profile) in 23 subjects with AN and in 20 control subjects 12 to 18 years of age, in whom GH, cortisol, leptin, and triiodothyronine (T3) had been previously determined.

Results

Subjects with AN had higher Apo-B (P < .0001), IL-6 (P = .03), Apo-B/high-density lipoprotien (HDL) (P = .01), and Apo-B/low-density lipoprotein (LDL) (P < .0001) and lower hsCRP (P = .01) than controls. Triglycerides were lower and HDL higher in subjects with AN. IGF-I predicted hsCRP in controls but not in AN. Log hsCRP correlated positively with GH and inversely with leptin. On regression modeling, the most significant predictor of log hsCRP was leptin; T3 predicted log IL-6, log Apo-B, log Apo-B/HDL, and Apo-B/LDL; and cortisol independently predicted log Apo-B. IL-6 decreased with weight gain.

Conclusion

CV risk markers are uncoupled in AN, with increased Apo-B and IL-6 and decreased hsCRP, related to hormonal alterations. IL-6 normalizes with weight gain.

Abbreviations: AN, Anorexia nervosa, Apo-B, Apolipoprotein-B, AUC, Area under curve, BMI, Body mass index, CV, Caridiovascular, GH, Growth hormone, HDL, High-density lipoprotein, HOMA-IR, Homeostasis model assessment-insulin resistance, HsCRP, High sensitivity C-reactive protein, IGF-I, Insulin like growth factor-I, IL-6, Interleukin-6, LDL, Low-density lipoprotein, T3, Triiodothyronine