| Autor: |
Komatsu T; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College.; Research Institute for Physical Activity, Fukuoka University.; Center for Preventive, Anti-aging and Regenerative Medicine, Fukuoka University Hospital., Katsurada Y; Department of Pathology and Laboratory Medicine, National Defense Medical College., Miyashita K; Immuno.Biological Laboratories (IBL) Co, Ltd., Abe S; Research Institute for Physical Activity, Fukuoka University., Nishida T; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College., Endo Y; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College., Teramoto M; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College., Sasaki K; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College.; Center for Preventive, Anti-aging and Regenerative Medicine, Fukuoka University Hospital., Arakawa J; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College., Sasaki M; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College., Suzuki N; Diabetes Center, Ebina General Hospital., Kuwata K; Department of Nephrology and Endocrinology, Department of Internal Medicine, National Defense Medical College., Imakiire T; Department of Nephrology and Endocrinology, Department of Internal Medicine, National Defense Medical College., Miyake T; Tokorozawa Heart Center., Sakurada M; Tokorozawa Heart Center., Matsukuma S; Department of Pathology and Laboratory Medicine, National Defense Medical College., Hirano T; Diabetes Center, Ebina General Hospital., Uehara Y; Research Institute for Physical Activity, Fukuoka University.; Center for Preventive, Anti-aging and Regenerative Medicine, Fukuoka University Hospital., Ikewaki K; Division of Anti-aging and Vascular Medicine, Department of Internal Medicine, National Defense Medical College. |
| Abstrakt: |
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. |
