Fatigue is, at least for SLE patients, one of the most important symptoms that interferes with daily activities or work. Apart from control of disease activity, what is your preferred treatment option? Do you use stimulants?
I have used anti-depressants, usually SSRIs; however, I have to say that even though fatigue is reported as the most important symptom in lupus, that's not my experience in dealing with these patients, unless of course they also suffer from associated fibromyalgia, not an uncommon occurrence. For the fatigue in fibromyalgia and chronic fatigue syndrome patients, on occasions I have prescribed Provigill (modafinil), a medication approved for narcolepsy/somnolence, with mixed results,
I treated fatigue caused by any case of fatigue with 5,000 up to 10,000 IU (125-250 mcg) colecalciferol, and added multiminerals, such as calcium, magnesium, potassium, sodium, zinc, selenium, mangane, chromium, and bases such as carbonate, citrate, and phosphate. I noticed that fatigue diminished and the underlying disease concomitantly had a better course and was more easy to handle. Unfortunately, meanwhile, phosphate is no longer in these so-called basic powders distributed in Germany. My clinical impression is that phosphate might be important for therapeutic success. The daily dose of elementary calcium should amount at least 1200 mg. The dose is dependent on the disease and comorbidity.
I strongly agree that checking serum vitamin D levels, and replacing as necessary is of paramount importance,
Dear collegues,
treatment of fatigue in patients with SLE is very difficult, as you known.
Checking serum vitamin D levels and replacing as necessary has no utility for this item. In SLE patients such as in patients with other diseases.
I agree that anti-depressants can be useful if fatigue is of functional genesis . S-adenosylmethionine can also be an useful approach.
Not when fatigue is a part of a flare of SLE.
In my experience, multiminerals are no effective.
As has been outlined, fatigue is incredibly common and problematic for patients with SLE. It is likely to be multifactorial in aetiology. I would say the key things I tend to do in my practice is:
1. Most importantly ensure that lupus isn't active. However, it is common for fatigue to be problematic even in those with both clinically and serologically well controlled disease
2. Ask about sleep - sleep disturbance is incredibly common in lupus (reported by at least 2/3 patients)
3. Manage pain - pain often disrupts sleep. Co-exisiting fibromyalgia is also common. Amitriptyline can help (providing tolerated)
4. Identify any underlying metabolic disorders; such as anaemia (again common), hypothyroidism and vitamin D deficiency
5. Where possible reduce steroid dose
6. Encourage a regular paced exercise regime
7. I believe a lot of the initial work on Belimumab showed an improvement in fatigue scores and this may be an option if evidence of active disease
What follow is armchair thinking from an 80% retired rheumatologist/clinical scientist..
Fatigue is a prominent symptoms of all CTDs including SLE, Sjogren and RA. It is also a confounding factors very common in healthy people of this century. So, I guess the first thing to do is to have a CHIP (Comprehensive Health Improvement Program) covering diet, sleep, exercise, alcohol, tobacco, emotions, etc.... That McGill program is for overweight people but its principles are applicable to every tired people. So, the real question for me is, when every concurrent issues have been removed or adressed: "Is there such a thing as lupic fatigue, sicca syndrome fatigue or rheumatoid fatigue?" I think so and it may be steroid responsive at small doses.
When infliximab was introduced in RA, the first thing patients insisted upon reporting, before their joints got better, was "having the impression that a heavy lead shawl had been lifted from my shoulders". That feeling was attributed to some CNS mechanism, that made them euphoric. Maybe there is more to this.
We use serum CK to measure muscle cell death and translate that in clinical weakness. Before/after weakness and before/after CK anomalies, there is months of prodromal/sequellar "fatigue". I think there is a sub-clinical muscle dysfunction maintained by a circulating low dose cytokine level. Used years ago, a measure of muscle physiology was the creatine/creatinine ratio in the urine. It was normally high during chilhood growth (more creatine, less creatinine) and stabilized at a low level at maturity (low creatine, stable creatinine related to total muscle mass). Normally, Creatine is produced in the liver, released in blood and mostly captured by striated muscle where it is used after transformation into Creatinine by CK. Cell turnover makes Creatinine appear in the urine with little untransformed Creatine left.
In RA and PMS/DMS without elevated CK, the ratio of Creatine/Creatinine is often and still abnormally high (more creatine, same creatinine). It is the last thing to normalize when myositis goes into remission. I do not know if that abnormal ratio correlates with clinical fatigue. I have not looked at that systematically. If it does, it means that there is a sarcoplasmic membrane event (a cytokine event acting on a creatine receptor???) that prevents the muscle capture of creatine. In vitro studies should be easy to do to show that. If a membrane receptor exists, it will be easier to screen specific drugs for CTD fatigue and explain some of the effects reported using st eroids, exercise and multiminerals containing phosphates. Exercise is the new anti-inflammatory!
I hope there will be a muscle physiologist or a cell biologist reading this to correct my hypothesis and rationale.
Henri Ménard MD, FRCP (C), Emeritus Professor of Medicine, McGill U.
Interesting thoughts! The assumption here is that the accompanying fatigue these patients have is mostly muscle-based. This may be the case or perhaps, more likely the fatigue in these patients would be multi-factorial, including some muscle dysfunction, cytokine release side effects, depression, some other CNS lupus neuro dysfunction, etc. I attach below some references regarding vitamin D in lupus, previously mentioned:
Petri M, et al. A & R 2013; 65: 1865–1871
Willis R, Jajoria P, Harper BE, Gonzalez EB, Petri M, Akhter E, Fang H, Pierangeli SS, Abstract, 691, ACR Annual meeting, Washington, D.C, Nov 2012, S296.
Dr Gonzalez,
I have no argument about the multifactorial nature of most fatigue syndromes including fatigue in SLE. What I am saying is that when all other factors are removed, the residual factor that could be present in any CTD may be related to a presumed muscle dysfunction component. It would not produced weakness but would be felt as asthenia/fatigue i.e. a clinical situation that may require a metabolomic or molecular approach to document or dissect. In fact, part or all the effect of Vit D on fatigue is likely via its effect on muscle. That is the suggested explanation for the prevention of falls in elderly people given Vit D supplements.
Anyways, that is all food for thought and a fertile ground for basic and clinical research in the chronic fatigue of so-called "inactive" RA, primary SS or SLE. Best.
HM
Thank you, Dr. Ménard; my best wishes as well. Mes meilleurs voeux
on the research the possibilities of influencing PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS WITH AND WITHOUT ANTIPHOSPHOLIPID SYNDROME, I think that work colleagues from clinic "Ivan Rilski". I can give you some links to their articles.
https://www.researchgate.net/publication/311875058_Radiographic_Assessment_of_Knee_Osteoarthritis?ev=prf_pub
https://www.researchgate.net/publication/307463198_How_to_treat_patients_with_rheumatoid_arthritis_Opportunities_and_benefits_of_the_implementation_of_a_pharmacoeconomic_cost-effectiveness_analysis?ev=prf_pub
https://www.researchgate.net/publication/287284912_Hyaluronic_acid_-_Historical_data_classification_mechanism_of_action_and_recommendations?ev=prf_pub
https://www.researchgate.net/publication/301296643_Recent_trends_in_the_pathogenic_mechanism_of_osteoarthritis?ev=prf_pub
https://www.researchgate.net/publication/287264579_Biomarkers_in_osteoarthritis?ev=prf_pub
Article Radiographic Assessment of Knee Osteoarthritis
Article How to treat patients with rheumatoid arthritis? Opportuniti...
Article Hyaluronic acid - Historical data, classification, mechanism...
Article Recent trends in the pathogenic mechanism of osteoarthritis
Article Biomarkers in osteoarthritis
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