Marked reduction in serum high-density lipoprotein cholesterol concentrations in a woman with acute inflammation due to diabetic gangrene.
BACKGROUND
C-reactive protein (CRP) is a well-established, sensitive marker of systemic inflammation and the risk of cardiovascular disease. High-density lipoprotein (HDL) is an anti-atherogenic lipoprotein known to be regulated by genetic and acquired factors.


METHODS
The patient was a 77-year-old Japanese woman, who was diagnosed with type 2 diabetes mellitus (DM), with a body height of 152 cm and a weight of 65 kg (body mass index 28.1 kg/m2). She suffered from diabetic foot gangrene in her right foot with high-grade fever when she visited our hospital. Her plasma glucose (PG) concentration and serum CRP were markedly elevated being 21.6 mmol/l and 370 mg/l, respectively, while her serum HDL-C concentrations were markedly low being 0.13 mmol/l. She was immediately admitted to our hospital and received intensive insulin treatment, along with intravenous-administration of antibiotics. Her general conditions were gradually improved and the high-grade fever disappeared, with concentrations of plasma PG and serum CRP being reduced, and concurrent reciprocal increase in her serum HDL-C concentrations.


RESULTS
To determine the potential causative factors responsible for the drastic change in serum HDL-C concentrations, we investigated the relationship of serum HDL-C to serum CRP, serum total protein (TP) and PG. Serum CRP and PG showed inverse relationships with serum HDL-C, while serum TP concentrations showed a positive association with HDL-C. After multivariate analyses with CRP, TP and PG as independent variables and serum HDL-C as dependent variable, CRP maintained its independent association with serum HDL-C. CRP also showed inverse correlations with lipoprotein lipase (LPL) mass and cholesteryl ester transfer protein mass.


CONCLUSIONS
In acute inflammation and poorly controlled diabetes, CRP is suggested to be inversely associated with serum HDL-C, independent of PG and TP.
Kobayashi
Junji
J
Department of Internal Medicine, Shimotsuga General Hospital, 5-32 Fujimicho, Tochigi City, Tochigi 328-8505, Japan. maryland95@angel.ne.jp
Tateishi
Sumiko
S
Maruyama
Tokiko
T
Kudoh
Akito
A
Murano
Shunichi
S
D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D001798:Blood Proteins / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D008076:Cholesterol, HDL / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000473:pathology; D017719:Diabetic Foot / Q000097:blood* / Q000473:pathology; D005260:Female; D005734:Gangrene / Q000097:blood / Q000150:complications / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology; D008071:Lipoprotein Lipase / Q000032:analysis
D015415:Biomarkers; D001786:Blood Glucose; D001798:Blood Proteins; D008076:Cholesterol, HDL; D002097:C-Reactive Protein; D008071:Lipoprotein Lipase