High-density lipoproteins (HDL) have been reported to be antiatherogenic. However, very recently the possibility that some patients with marked hyperHDLemia had developed complications caused by atherosclerosis has been reported. In this paper, atherogenicity was clinically and biologically assessed in a patient with marked HDLemia.
One 29-year-old female patient showed marked plasma hyperHDLemia (HDL-cholesterol, 105-181mg/dl, apolipoprotein AI & AII, also elevated) with almost normal levels of low or very low lipoproteins. Hepatic triglyceride lipase activity was low while lipoprotein lipase activity was rather high. Cholesterol ester transfer protein activity was normal. Incorporation of HDL into the patient lymphocytes was normal, suggesting that the HDL receptor of the patient's liver was intact. Because of these results the patient was classified as a type of hyperlipidemia characterized by marked hyperHDLemia with a low hepatic triglyceride lipase activity.
The patient had developed marked corneal opacity. However, there was no evidence of coronary atherosclerosis that could be assessed by clinical symptoms & signs, exercise-loaded electrocardiograms, or a coronary angiography. Moreover, no other complications arising from the atherosclerosis were discovered. This data indicates that the development of corneal opacity did not parallel that of atherosclerosis.
The HDL of the patient was rather more taken up by HepG2 than the control HDL, and there was normal reverse transport activity from macrophages. This data suggests that patient's HDL was at least not atherogenic.
The above results indicate that the marked hyperHDLemia was not atherogenic in spite of the development of premature corneal opacity.
