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A case of anorexia nervosa with severe hyperlipoproteinemia
Author(s) -
Homma Yasuhiko,
Homma Koichiro,
Iizuka Shinichi,
Iigaya Kamon
Publication year - 2002
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/eat.10065
Subject(s) - endocrinology , medicine , anorexia nervosa , very low density lipoprotein , lipoprotein , apolipoprotein e , apolipoprotein b , chemistry , cholesterol , high density lipoprotein , eating disorders , disease , psychiatry
Objective The complication of severe hyperlipoproteinemia with anorexia nervosa is very rare. We investigated the mechanisms of severe hyperlipoproteinemia in a patient with anorexia nervosa. Methods The measurement of plasma levels of lipids, apolipoproteins (Apo), lipoprotein subfractions, free T 3 , and estrogen, apo (lipoprotein) E phenotyping, and the assay of lymphocyte low‐density lipoprotein (LDL)‐receptor activity were accomplished in a 40‐year‐old female patient with anorexia nervosa. Results Her body mass index was 10.3 kg/m 2 . Her plasma levels of total cholesterol (C), triglyceride (TG), apoB, apoE, very‐low‐density lipoprotein (VLDL)‐C, and intermediate‐density lipoprotein (IDL)‐C were 757 mg/dl, 526 mg/dl, 288 mg/dl, 13.6 mg/dl, 133 mg/dl, and 99 mg/dl, respectively. VLDL was cholesterol rich (C/TG ratio = 0.68; normal value = 0.2). The plasma LDL was high and skewed to less dense fractions. Her apoE phenotype was E 3/2. Her lymphocyte LDL‐receptor activity was 79% of normal subjects. The plasma level of estradiol was low and that of free T 3 was subnormal. Discussion We concluded that the plasma lipoprotein abnormality of this anorexia nervosa patient was induced by the impaired removal of TG‐rich lipoprotein remnants and less dense LDL due to apoE phenotype E 3/2,subnormal LDL‐receptor activity, subnormal plasma level of free T 3 , and diminished secretion of estrogen. © 2002 by Wiley Periodicals, Inc. Int J Eat Disord 32: 121–124, 2002.