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Abstract Number: 2653

Low Vitamin D Is Associated With Increased Risk of Venous Thrombosis in Systemic Lupus Erythematosus, Regardless of Lupus Anticoagulant Status

Michelle Petri and Hong Fang, Johns Hopkins University School of Medicine, Baltimore, MD

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: systemic lupus erythematosus (SLE) and thrombosis, Vitamin D

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Session Information

Session Title: Antiphospholipid Syndrome

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Vitamin D deficiency is common in SLE. Vitamin D deficiency is also associated with activation of Tissue Factor. In cross-sectional studies, vitamin D deficiency is more common with APS and thrombosis. We determined whether vitamin D deficiency was associated with thrombosis in SLE.

Methods: 1131 SLE patients had a measure of 25-OH vitamin D. Twenty-seven% had a history of any thrombosis, 15% arterial thrombosis (defined as stroke, myocardial infarction, digital gangrene or other arterial thrombosis), and 17% venous thrombosis (defined as DVT or PE, or other venous thrombosis).

Results:

Table 1 shows that low 25-OH vitamin D (<32 ng/ml) was associated with all thrombosis and with venous thrombosis, but not with arterial thrombosis.

               Table 1. Association of 25-OH vitamin D level with thrombosis.

 

Variable

Number (%) with the characteristic

Vitamin D <32 (n=667)               Vitamin D ≥32 (n=464)

Adjusted p-value

All thrombosis

199 (30%)

105 (23%)

0.0017*

Arterial thrombosis

107 (16%)

63 (14%)

0.43**

Venous thrombosis

130 (19%)

59 (13%)

0.0004*

Same-day lupus anticoagulant

111 (17%)

62 (14%)

0.089§

*Adjusted for age at last assessment, ethnicity, gender, and history of lupus anticoagulant (LAC).

**Adjusted for age at last assessment, ethnicity, gender, history of LAC, history of hypertension, and history of hypercholesterolemia.

§Adjusted for age at last assessment, ethnicity, and gender.

Vitamin D deficiency was not associated with any gene signature (interferon, BAFF, neutrophil, or plasma cell).

Conclusion: Vitamin D deficiency in SLE is associated with venous (but not arterial thrombosis) in adjusted analyses that controlled for other risk factors, including lupus anticoagulant. Vitamin D deficiency is not associated with the interferon gene signature. Given that vitamin D deficiency is associated with Tissue Factor expression and that it is already known to be associated with thrombosis in antiphospholipid patients, this is another rationale for vitamin D measurement and supplementation in SLE. Clinical trials, already underway, in the general population may shed further light on the anti-thrombotic potential of vitamin D.


Disclosure:

M. Petri,
None;

H. Fang,
None.

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