Increased plasma C-reactive protein in familial hypoalphalipoproteinemia: a proinflammatory condition?

BACKGROUND: HDL molecules have an established role in the regression processes of atherosclerosis as well as a putative role as antiinflammatory agents. Our study investigated whether familial hypoalphalipoproteinemia, a genetic form of dyslipidemia characterized by very low HDL levels, might be associated with increased inflammation markers such as C-reactive protein. METHODS AND RESULTS: A total of 50 subjects with hypoalphalipoproteinemia (age, 53.1+/-16.7 years) were compared with 64 healthy controls (age, 51.9+/-12.4 years). Apart from significantly lower values of HDL cholesterol (30.2+/-4.0 versus 52.5+/-12.7 mg/dL, P<0.0001) and apolipoprotein AI (113.3+/-20.0 versus 155.4+/-24.9 mg/dL, P<0.0001) and higher levels of triglycerides (141.3+/-62.9 versus 73.5+/-39.9 mg/dL, P<0.0001), patients did not show different plasma values of total cholesterol and LDL cholesterol when compared with healthy controls (181.5+/-36.6 versus 186.3+/-32.6 mg/dL; 123.0+/-31.5 versus 119.1+/-30.3 mg/dL). CRP plasma values were significantly higher in patients than in controls (median 0.34 [range 0.02 to 4.66] versus 0.07 [0.02 to 0.85] mg/dL, P<0.0001). In the patient group, CRP values were significantly higher in subjects with angiographically documented coronary atherosclerotic disease than in those without. Moreover, CRP concentrations were inversely correlated with both HDL cholesterol (r= -0.44, P=0.0006) and apolipoprotein AI (r= -0.45, P=0.0006) values. CONCLUSIONS: Elevation of C-reactive protein values in familial hypoalphalipoproteinemia, in the absence of signs and symptoms of local or systemic inflammation or systemic or recurrent disease, may suggest an upregulation of proinflammatory mechanisms, which is further exacerbated by the presence of coronary atherosclerotic disease.