May. 01, 2010

Blood Components Help Differentiate Lupus and Antiphospholid Syndrome

Increased level of tumor necrosis factor-alpha in patients with antiphospholipid syndrome: marker not only of inflammation but also of the prothrombic state. 
Authors: Swadzba J, Iwaniec T, and Musial J. (2009). 
Rheumatology International, epub ahead of print Dec 15.  

What is the topic?

Cytokines are proteins of the immune system that work to communicate between different cells. 
Tumor necrosis factor- α (TNF-α) is a cytokine that helps to control both blood clotting and inflammation and soluble interleukin-2 receptor (sIL-2R) helps to regulate inflammation.

Although antiphospholipid syndrome and other forms of lupus can occur together in the same person, they may come about by different pathways in the immune system. Researchers hoped to learn more about important differences between antiphospholipid syndrome and lupus by studying levels of TNF-α and sIL-2R in different groups of patients. 

What did the researchers hope to learn?

Some people have antiphospholipid syndrome without other forms of lupus, called primary antiphospholipid syndrome (PAPS). The researchers hoped to learn whether people with systemic lupus or PAPS had different amounts of TNF-α and sIL-2R in their blood.  

Who was studied?

188 patients referred to a university clinic in Krakow, Poland were studied. 147 of these patients had systemic lupus (SLE), 21 had a lupus-like syndrome (SLE-LS), and 20 had PAPS. 32 healthy people were also studied.

36 patients in the SLE group also had APS, which is known as secondary antiphospholipid syndrome (SAPS).


Of the people included in the study, 66 had a history of blood clotting and 42 of the women experienced pregnancy-related complications.

How was the study conducted?

Blood levels of TNF-α and sIL-2R were measured in each study participant. 

What did the researchers find?

TNF-α was increased in all patients (SLE, SLE-LS, PAPS) compared to people without an autoimmune disease. The highest levels of TNF-α were found in the PAPS group, followed by the SAPS group. Regardless of the diagnosis of SLE or APS, increased levels of TNF-α were seen in people with antiphospholipid antibodies compared to those without them.

Blood levels of sIL-2R were increased in the SLE group compared to healthy people regardless of whether they also had a history of blot clotting or not, but this was seen only in SLE patients with antiphospholipid antibodies. 

Increased levels of TNF-α were associated with nephritis (lupus affecting the kidney), increased antibodies to double-stranded DNA, or decreased levels of C4 complement (an inflammatory protein). Increased levels of sIL-2R were associated with a wider spectrum of lupus, including skin or kidney involvement, arthritis, serositis (inflammation of the lining of the lungs, heart, or gastrointestinal tract), increased anti-Smith or anti-Ro antibodies, increased antibodies to double-stranded DNA, and decreased levels of C4 complement.

What were the limitations of the study?

This study does not provide any information about why certain groups of patients are more likely to have increased levels of TNF-α or sIL-2R, or what roles these inflammatory regulators may actually play in lupus. 

What do the results mean for you?

The results suggest that both proteins may be important clues to figuring out how lupus develops and that TNF-α, especially, may play a role in risk for blood clotting.


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