Metabolic Disturbances Associated with Systemic Lupus Erythematosus

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English: Common signs and symptoms of systemic...

Systemic lupus erythematosus (SLE) is an autoimmune disease and this leads to long-term (chronic) inflammation.

The underlying cause of autoimmune diseases is not fully known.

SLE is much more common in women than men. It may occur at any age, but appears most often in people between the ages of 10 and 50.

SLE may also be caused by certain drugs called Drug-induced lupus erythematosus

People with SLE have abnormal deposits in the kidney cells. This leads to a condition called lupus nephritis. Patients with this condition may eventually develop kidney failure and need dialysis or a kidney transplant.

SLE causes damage to many different parts of the body, including:

There is no cure  for SLE.

A metabolomic study was recently executed to understand the metabolic disturbances that underlie systemic lupus erythematosus (SLE).

The study compared the sera of 20 SLE patients against that of healthy controls, using LC/MS and GC/MS platforms.

Validation of key differences was performed using an independent cohort of 38 SLE patients and orthogonal assays.

The SLE metabolome exhibited profound lipid peroxidation, reflective of oxidative damage. Deficiencies were noted in the cellular anti-oxidant, glutathione, and all methyl group donors, including cysteine, methionine, and choline, as well as phosphocholines.

SLE sera showed evidence of profoundly dampened glycolysis, Krebs cycle, fatty acid β oxidation and amino acid metabolism, alluding to reduced energy biogenesis from all sources.

Whereas long-chain fatty acids, including the n3 and n6 essential fatty acids, were significantly reduced, medium chain fatty acids and serum free fatty acids were elevated.

The best discriminators of SLE included elevated lipid peroxidation products, MDA, gamma-glutamyl peptides, GGT, leukotriene B4 and 5-HETE.

Similar elevations were not observed in another chronic inflammatory autoimmune disease, rheumatoid arthritis.

Comprehensive profiling of the SLE metabolome reveals evidence of heightened oxidative stress, inflammation, reduced energy generation, altered lipid profiles and a pro-thrombotic state.

Resetting the SLE metabolome, either by targeting selected molecules or by supplementing the diet with essential fatty acids, vitamins and methyl group donors offers novel opportunities for disease modulation in this disabling systemic autoimmune ailment.

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