Focus on Fatigue? Save

Pain is the most common complaint and cause of debility in most arthritis patients. Fatigue is not far behind as the complaint that affects the quality of life in numerous rheumatic and autoimmune disorders.

Fatigue can have multiple origins outside of musculoskeletal disease, and may lead to consideration or evaluations for anemia, endocrine or metabolic disorders, heart failure, hypoxia and neoplastic conditions. However, in my clinic the primary cause of fatigue is: 1) poor sleep, 2) depression, 3) uncontrolled pain, 4) inflammation, and 5) deconditioning. While fatigue is a common accompaniment to rheumatoid arthritis, lupus, Sjogren's syndrome, PMR – predominant fatigue is more likely to be from fibromyalgia, poor sleep and depression.

Unfortunately, patients and referring physicians often approach fatigue as a symptom remediable by iron, B12 shots, liver pills or vitamins, when what they really need is better sleep, a good rheumatologist and medication compliance.

Clinical trialists have tried to employ measures that reflect the impact of fatigue, but these measures are not as revealing as the core variables gathered by the ACR20 response or SLEDAI criteria. My view is that this need is driven to better quantify the dramatic feeling of wellbeing seen in those initiating TNF inhibitor therapy. This “born again” feeling is unique in TNF inhibitors, seldom seen with other biologics or DMARDs, and represents a response that often precedes measureable improvements in joint swelling or tenderness. This response is not identified by the SF-36, HAQ or even numerous fatigue scales. Yet trialists continue to call for FACIT and other fatigue scales.

Research shows physicians don’t give fatigue the same priority that patients do. At EULAR 2015, physician estimates were often below patient’s scores for fatigue in RA, OA, and fibromyalgia patients (http://url.ie/z1lb). While fatigue scores were higher in the presence of high disease activity in RA, OA and SLE, disease activity did not correlate with fatigue in patients with fibromyalgia. Fatigue changes when the patient's outcome changes and is a surrogate for overall benefit. Dr. Barry Bresnihan's group examined fatigue and disease activity in a rheumatoid arthritis cohort initiating aggressive therapies and found that fatigue was inconsistently explained by ACR Core variables over 6 months. Hence at baseline fatigue accounted for 28% of patient status and this changed to 38% and 46% at 3 and 6 months respectively (http://buff.ly/1zK1hiy).

Population-based statistics say fatigue is more likely to be from poor sleep and fibromyalgia, than lupus or RA. Secondary fibromyalgia occurs in 13% of lupus patients, 6.6% of RA patients, 12.6% in AS, 10% in OA, and 12-50% of Sjogren’s syndrome patients(http://t.co/MDuQP0aHrS). While the prevalence of RA is 1.3% of the population, the prevalence of fibromyalgia is estimated to be 2.1-6.4% (http://t.co/K2NWFmdRn3 http://t.co/lGpFWeFR2l).

I’m very concerned about my patients’ complaints of fatigue. But I am confident that identifying and managing the most likely cause will lead to substantial relief of this complaint. I don’t have a good “fatigue” drug. I prefer to use my many proven therapies that will alleviate sleep, depression, pain, and if necessary, inflammation. Fatigue surveys, metric tools and clinical trials assessing fatigue are focusing on the symptom instead of the disease and cause of fatigue.