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Systemic lupus erythematosus (S.L.E.), commonly called lupus, is a chronic autoimmune disorder that can affect virtually any organ of the body. In lupus, the body’s immune system, which normally functions to protect against foreign invaders, becomes hyperactive, forming antibodies that attack normal tissues and organs, including the skin, joints, kidneys, brain, heart, lungs, and blood. Lupus is characterized by periods of illness, called flares, and periods of wellness, or remission.

Because its symptoms come and go and mimic those of other diseases, lupus is difficult to diagnose. There is no single laboratory test that can definitively prove that a person has the complex illness. All the anatomical heart structures can be affected, and multiple pathogenic mechanisms have been reported. Non-organ-specific auto antibodies have been implicated in immune complex formation and deposition as the initial triggers for inflammatory processes responsible for Libman–Sacks verrucous endocarditis, myocarditis and pericarditis.

Anti-phospholipid antibodies have been associated with thrombotic events in coronary arteries, heart valve involvement and intra-myocardial vasculopathy in the context of primary and secondary anti-phospholipid syndrome. Antibodies-SSA/Ro and anti-SSB/La antigens play a major pathogenic role in affecting the heart conduction tissue leading to the electrocardiographic abnormalities of the neonatal lupus syndrome and have been closely associated with endocardial fibroelastosis. In many sources lupus is said to have no cure. But recent studies have suggested that this statement might be wrong.

New research provides clues about the causes of lupus symptoms and suggests specific new targeted treatment strategies, according to Nilamadham Mishra, M.D., from Wake Forest University Baptist Medical Center, in presentations this week at the American College of Rheumatology in Boston. The studies looked at premature atherosclerosis in lupus patients as well as accelerated cell death that seems to be behind many of the diseases symptoms. Lupus is an autoimmune disorder that can involve the joints, kidneys, heart, lungs, brain and blood. An estimated two million Americans have a form of lupus.

In one study, Mishra and colleagues looked at the potential mechanisms of premature atherosclerosis, which is one of the leading causes of death and disability in lupus patients. Even when they take drugs to lower their cholesterol, lupus patients still develop fatty buildups in their vessels, which can lead to heart attack and stroke. Previous research by Mishra found that a new class of drugs being developed (histone deacetylase inhibitors) were effective at preventing atherosclerosis in mice prone to develop the disease. In the current study, Mishra and colleagues explored whether it is a specific histone deacetylase, Number 9 (HDAC9), that causes the problem.

In a separate study, scientists found a potential explanation for why cells in lupus patients die at an increased rate and accumulate in tissues. This accumulation of cells is believed to trigger the inflammation that causes symptoms. The study examined microRNAs, chains of ribonucleic acid that are involved in cell proliferation and cell death. The goal was to explore the possibility that aberrant expression of microRNAs is responsible for the abnormal cell death in lupus patients.

The scientists analyzed blood samples from five patients with lupus and seven healthy people of the same ages and sex at two points during a three-month period. A particular microRNA, miR-16, was consistently increased in lupus patients compared to the healthy participants. The scientists suspect that having too much miR-16 inhibits genes that control cell death and may also inhibit natural cell progression resulting in the accumulation in tissues.

This potential cure for lupus excites us at BoomerYearbook. We’d love to hear your thoughts on it.

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