Two Cases of Acquired High-Density Lipoprotein Deficiency with Immunoglobulin G4-Related Lecithin–Cholesterol Acyltransferase Autoantibody

Lecithin–cholesterol acyltransferase (LCAT) plays a significant role in the progression from premature to mature high-density lipoprotein (HDL) in circulation. Consequently, primary or secondary LCAT deletion or reduction naturally results in low serum HDL cholesterol levels. Recently, rare cases of...

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Published in:Journal of Atherosclerosis and Thrombosis 2023/08/01, Vol.30(8), pp.1070-1082
Main Authors: Komatsu, Tomohiro, Katsurada, Yuka, Miyashita, Kazuya, Abe, Satomi, Nishida, Takafumi, Endo, Yasuhiro, Teramoto, Manami, Sasaki, Kei, Arakawa, Junko, Sasaki, Makoto, Suzuki, Natsuko, kuwata, Koji, Imakiire, Toshihiko, Miyake, Takayuki, Sakurada, Masami, Matsukuma, Susumu, Hirano, Tsutomu, Uehara, Yoshinari, Ikewaki, Katsunori
Format: Article
Language:English
Subjects:
Autoantibodies
Autoantibody
Case Report
Cholesterol, HDL
High-density lipoprotein
Humans
IgG4 autoimmune disease
Immunoglobulin G
Lecithin Cholesterol Acyltransferase Deficiency
Lecithins
Lecithin–cholesterol acyltransferase
Lipoproteins, HDL
Nephrotic syndrome
Phosphatidylcholine-Sterol O-Acyltransferase
Sterol O-Acyltransferase
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Summary:Lecithin–cholesterol acyltransferase (LCAT) plays a significant role in the progression from premature to mature high-density lipoprotein (HDL) in circulation. Consequently, primary or secondary LCAT deletion or reduction naturally results in low serum HDL cholesterol levels. Recently, rare cases of acquired HDL deficiency with LCAT autoantibodies have been reported, mainly from Japan, where LCAT autoantibodies of immunoglobulin G (IgG) caused the HDL deficiency. Here to our knowledge, we report for the first time two cases of acquired HDL deficiency caused by IgG4 linked LCAT autoantibodies with or without a high serum IgG4 level. Furthermore, these cases can extend to a new concept of “IgG4 autoimmune disease” from the viewpoint of verifying the serum autoantibody and/or renal histopathology.
ISSN:1340-3478
1880-3873
DOI:10.5551/jat.63616