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This case aims to illustrate the rare occurrence of acquired LCAT deficiency and its impact on HDL-C levels.

May 25, 2026Internal Medicine0 citationsOpen Access

Severe HDL-C Deficiency Caused by Acquired LCAT Deficiency: A Case Report with Lipidomic Profiling and Anti-LCAT Autoantibody Detection

TSTetta SatoChiba University JKJunji KobayashiChiba University MKMasayuki KurodaOsaka Kaisei Hospital

Key Points

This case aims to illustrate the rare occurrence of acquired LCAT deficiency and its impact on HDL-C levels.
Lipidomic profiling was performed to analyze lipid subclasses and cholesterol accumulation.
Detection of anti-LCAT autoantibodies conducted alongside LCAT activity and protein level tests.
Genetic analysis for LCAT mutations was performed but none were identified.
Markably low HDL-C levels recorded, declining from 64 to <2 mg/dL over five years.
Lipidomic analysis indicated free cholesterol accumulation and loss of HDL subclasses.
No underlying autoimmune disease was identified, despite the presence of anti-LCAT autoantibodies.

Abstract

Acquired lecithin-cholesterol acyltransferase (LCAT) deficiency is a rare cause of a marked reduction in high-density lipoprotein cholesterol (HDL-C). We report a 75-year-old Japanese woman with a progressive decline in HDL-C from 64 to <2 mg/dL over five years. Laboratory tests showed a markedly decreased LCAT activity and protein levels with anti-LCAT autoantibodies, whereas a genetic analysis revealed no LCAT mutations. Lipidomic profiling demonstrated free cholesterol accumulation, the loss of HDL subclasses, and TG-rich LDL particles. No underlying autoimmune disease was identified. This case highlights the importance of a lipid subclass analysis and the recognition of acquired LCAT deficiency in patients with a marked HDL-C deficiency.

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