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Abstract Number: 2255

Apolipoprotein B Containing Lipoprotein Subclasses and Subclinical Atherosclerosis in Patients with Systemic Lupus Erythematosus (SLE)

Adnan Kiani1, Hong Fang1, Ehtisham Akhter2, Carmen Quiroga3, Nancy Simpson3, Petar Alaupovic3 and Michelle Petri1, 1Johns Hopkins University School of Medicine, Baltimore, MD, 2Div of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD, 3Oklahoma Medical Research Foundation, Oklahoma, OK

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Atherosclerosis and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus: Clinical Aspects

Session Type: Abstract Submissions (ACR)

Background/Purpose: Traditional classification in lipid biology using HDL, LDL and VLDL does not provide information on lipoprotein function.  Apolipoproteins, (which are protein components of plasma lipoproteins including A, B, C, D, E) with their different composition, metabolic and atherogenic properties provide a much detailed insight on lipoprotein functioning.  In particular ApoB/A-1 ratio is associated with atherogenic LDL and development of cardiovascular disease.  Lipoprotein function Apolipoprotein C-III and its corresponding Apolipoprotein B subclasses have been shown to be independent risk factors for cardiovascular disease in the general population (Circulation. 102:1886-92;2000 and Aterioscler Thromb Vasc Biol. 23:853-858;2003)).  We explored the association between these non-traditional risk factors with subclinical measures of atherosclerosis (coronary artery calcium) in SLE.

Methods: 58 SLE patients (97% female, 58% Caucasian, 40% African-American, 2% other, mean age 44±11 yrs) had measurement of apolipoprotein and lipoproteins measured by immunoturbidimetric procedures, electroimmunoassays and immunoprecipitation.  Coronary artery calcium was measured by helical CT.  The p-value in the table is adjusted for age, gender, and ethnicity.

Results:

Table 1:  Coronary artery calcium (CAC) and Lipoprotein Subclasses

Measures

N

Loge(CAC score+1)

Mean (SD)

P-value (adjusted)

Traditional CVRF

Normal

Abnormal

Normal

Abnormal

 

Total Cholesterol (mg/dl)

 

 

 

 

 

 

42

16

0.97 (1.64)

2.20 (2.46)

0.092

Triglycerides (mg/dl)

 

 

 

 

 

 

48

10

1.14 (1.57)

2.15 (3.23)

0.20

VLDL-C (mg/dl)

 

 

 

 

 

 

41

17

1.23 (1.61)

1.52 (2.65)

0.89

LDL-C (mg/dl)

 

 

 

 

 

 

40

14

1.02 (1.66)

2.41 (2.56)

0.083

HDL-C (mg/dl)

 

 

 

 

 

 

10

44

1.17 (1.30)

1.43 (2.14)

0.39

Cardioprotective

 

 

 

 

 

ApoA-I

 

 

 

 

 

 

21

37

0.80 (1.26)

1.60 (2.22)

0.15

LpA-I

 

 

 

 

 

 

38

20

1.18 (1.95)

1.57 (1.99)

0.41

LpA-I:A-II

 

 

 

 

 

 

15

43

1.08 (1.40)

1.39 (2.12)

0.39

Atherogenic

 

 

 

 

 

LpB:E+LpB:C:E

 

 

 

 

 

 

39

19

1.07 (1.78)

1.81 (2.25)

0.24

ApoB

 

 

 

 

 

 

46

12

1.32 (1.82)

1.28 (2.49)

0.60

LpB

 

 

 

 

 

 

55

3

1.34 (1.99)

0.80 (1.10)

0.47

LpB:C

 

 

 

 

 

 

55

3

1.38 (1.98)

0.00 (0.00)

0.24

ApoC-III

 

 

 

 

 

 

46

7

1.30 (1.90)

2.08 (2.75)

0.60

ApoC-III-HS

 

 

 

 

 

 

23

30

0.96 (1.55)

1.75 (2.28)

0.17

ApoC-III-HP

 

 

 

 

 

 

50

3

1.4 (2.0)

1.1 (1.9)

0.76

CIII-R

 

 

 

 

 

 

–

53

–

1.41 (2.02)

–

LpA-II:B:C:D:E

 

 

 

 

 

 

36

22

1.23 (1.78)

1.44 (2.25)

0.63

ApoB/ApoA-I

 

 

 

 

 

 

44

14

1.36 (1.92)

1.14 (2.12)

0.97

Conclusion: It has been shown that apoC-III containing apoB lipoproteins are risk factors for atherosclerotic progression in rheumatoid arthritis patients (Arthritis Care Res doi:10.1002.21646;2012).  In our study there was no association between any of the markers with coronary artery calcium.  However, we did show that cardioprotective components including LpA-1 and ApoA-I were decreased whereas atherogenic LpA-II:B:C:D:E was increased in our patient population compared to controls.  Further studies with larger sample size are warranted to confirm our findings.


Disclosure:

A. Kiani,
None;

H. Fang,
None;

E. Akhter,
None;

C. Quiroga,
None;

N. Simpson,
None;

P. Alaupovic,
None;

M. Petri,
None.

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