Practical Insights in SLE: Fatigue and Homocysteine Levels

We all know that fatigue is often multifactorial and in SLE it may be related to active disease (possibly including residual inflammation), medications, treatment, concomitant fibromyalgia, and altered sleep and stress. As rheumatologists, we are still looking for something effective treatments for fatigue since this is a common and miserable symptom for our patients.

A study presented by I. Carrion-Barbera, et al (THU0273) showed that fatigue in SLE was associated with increasing age, function (modified HAQ), damage (SDI SLICC score) and low vitamin D (and slightly with photosensitivity). What we still don't know is: Will supplementation with vitamin D improve fatigue, especially since many of our patients avoid the sun due to photosensitivity?

There has been an ongoing debate about homocysteine levels and CV risk. In the general population, the presumed association has been debunked. However, there have been consistent data in SLE that abnormal levels of homocysteine are associated with increased CV risk. The Hopkins cohort (G Stojan et al, THU0270) looked at elevated levels of homocysteine, antiphospholipid antibodies, and thrombosis in SLE. When hyper-homocysteinemia was present, there were fewer APS antibodies. Any elevation of homocysteine with APS increased the rate of myocardial infarction more than 2-fold and DVTs by 1.5-fold.

What is the take home? You can measure homocysteine levels and treat CV risks more aggressively in these patients or just remember that there are other factors that increase clotting risk. Traditional risk factors need to be aggressively sought and treated, including: hypertension, smoking, diabetes, lipids, lack of exercise, and steroids. Remember that if antibodies to phospholipids are present, they are even more apt to be clinically relevant if the patient also has high homocysteine levels.

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