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Race disparity in blood sphingolipidomics associated with lupus cardiovascular comorbidity. |
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Race disparity in blood sphingolipidomics associated with lupus cardiovascular comorbidity.
eMediNexus Editorial,  28 November 2019
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#Allergy and Immunology #Rheumatology

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Systemic lupus erythematous (SLE) is a chronic multi-organ autoimmune disease. Genetic and environmental factors contribute to the disease onset and severity. Sphingolipids are signaling molecules involved in regulating cell functions and have been associated with multiple genetic disease processes.

A new study published in PLoS One examined the influence of race on plasma sphingolipid profiles in SLE patients, as well as the association of sphingolipid levels with comorbid atherosclerosis and SLE disease activity.

Here, mass spectrometry was used to ascertain sphingomyelin and sphingomyelin levels in participants.

The results revealed that healthy African-Americans had higher sphingomyelin levels and lower lactosylcermide levels compared to healthy Whites. Additionally, SLE patients, irrespective of race, had higher levels of ceramides and sphingoid bases – sphingosine and dihydrosphingosine and their phosphates, compared to healthy subjects. When compared to African-American controls, African-American SLE patients had higher levels of ceramides, hexosylceramides, sphingosine and dihydrosphingosine 1-phosphate. Whereas, White SLE patients exhibited higher levels of sphingoid bases and their phosphates, but lower ratios of C16:0 ceramide/sphingosine 1-phosphate and C24:1 ceramide/sphingosine 1-phosphate than the White controls. Furthermore, White SLE patients with atherosclerosis exhibited lower levels of sphingoid bases compared to White SLE patients without atherosclerosis. On the contrary, African-American SLE patients with atherosclerosis had higher levels of sphingoid bases and sphingomyelins compared to African-American SLE patients without atherosclerosis.

Hence, it was noted thatAfrican-American SLE patients with atherosclerosis had higher levels of select sphingolipids than White SLE patients with atherosclerosis. While plasma levels of sphingosine, C16:0 ceramide/sphingosine 1-phosphate ratio and C24:1 ceramide/sphingosine 1-phosphate ratio significantly correlated with the SLE disease activity index in the African-American, but not in White SLE patients. In inference, it was stated that C16:0 ceramide/sphingosine 1-phosphate ratio in SLE patients and levels of C18:1 and C26:1 lactosylcermides, C20:0 hexosylceramide and sphingoid bases in SLE patients with atherosclerosis could be dependent on race. Further ethnic studies in SLE cohorts are necessary to verify the use of sphingolipidomics as a complementary diagnostic tool.

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