Fibromyalgia and psoriatic arthritis: Partners together

Fibromyalgia is a common condition characterized by widespread pain and tenderness, associated with elevated levels of sleep disturbance, fatigue, cognitive dysfunction and background emotional distress.¹ Prevalence rates vary according to classification criteria and range between 2% and 8% in different communities.¹ These rates increase significantly in the context of chronic illness, particularly rheumatic diseases, with the symptoms of fibromyalgia often merging with those of the underlying disease. This creates a higher symptom burden and diminished quality of life for the patient. It also greatly increases difficulties for the clinician in the assessment of response to treatment of both the rheumatic disease and the fibromyalgia.

In this issue of the Journal 2 studies address this matter in patients with psoriatic arthritis (PsA), a condition which affects up to 1% of the population.^2-4

Alsawy et al identified fibromyalgia, using the 2016 modification of the 2010/11 American College of Rheumatology (ACR) criteria,⁵ in 38.3% of 60 patients with PsA attending an outpatient department.² More PsA fibromyalgia patients were female, and more had symmetrical polyarthritis than those without fibromyalgia. There was no difference between the groups in objective measures of disease activity, such as C-reactive protein, swollen joint count and dactylitis count. However, in the fibromyalgia group there were significant increases in scores that incorporated measurements of pain and tenderness compared to those without fibromyalgia. This included standard instruments to assess PsA “disease activity”, including the psoriasis area severity index (PASI), the disease activity in psoriatic arthritis (DAPSA) index, the composite psoriatic disease index (CPDAI), tender joint count, Leeds enthesitis index, and Bath ankylosing spondylitis disease activity scores. Fibromyalgia patients also had higher fatigue and lower quality of life scores. The fibromyalgia severity scale and the fibromyalgia impact questionnaire (FIQ) each correlated with many of the disease assessment and quality of life measures.

Ulutatar et al, using the same criteria,⁵ identified fibromyalgia in 64% of 50 consecutively assessed patients with PsA, also more common in females.³ Those with fibromyalgia had significantly higher enthesopathy scores, FIQ scores, poorer sleep quality, greater fatigue, and lower quality of life. There was a moderate association between FIQ and Disease Activity Score of 28 joints (DAS28), and both enthesopathy scores, and DAS28 contributed to FIQ scores. Thus, measurements assessing fibromyalgia characteristics overlapped with those designed to assess inflammatory-related disease activity. The problem is that “disease activity” instruments incorporate measures that are common to both conditions, particularly pain and tenderness.

Both these studies add to the knowledge of the interaction between fibromyalgia and PsA. Other studies have shown fibromyalgia prevalence rates between 17% and 53.3% in different sub-types of PsA, more common in females, with variation attributed to diagnostic criteria.^6-9 These studies also highlight the disconnect between subjective patient-reported symptoms and objective measures of disease activity, with higher scores in fibromyalgia PsA patients compared to those with PsA alone. In short, PsA patients with fibromyalgia report higher levels of pain, tenderness, fatigue, and cognitive dysfunction and lower quality of life.^{6, 10}

This may result in a number of outcomes. Enthesitis assessed by tenderness will be overestimated in PsA patients with fibromyalgia.¹¹ The evaluation of synovitis and dactylitis in PsA, using standard clinical examination techniques, are also subject to the influence of the background allodynia that characterizes fibromyalgia.¹² As a consequence, PsA treatment protocols may be influenced by the presence of the symptoms of fibromyalgia.¹⁰ Patients may be inappropriately treated with disease-modifying drugs when in fact they need pain modulatory drugs and lifestyle advise. As these studies indicate, as FIQ scores increase so do the clinical and functional outcomes worsen.³

In each of the above studies the diagnosis of fibromyalgia has been defined as either present of absent. However, fibromyalgia symptoms actually exist on a spectrum and many patients have sub-criteria symptoms that will influence their self-report of pain, fatigue, sleep and cognition.⁵ These symptoms contribute to low quality of life and demand attention.

The FIQ captures fibromyalgia-related clinical items relating to everyday function and overall impact, and rates the severity of typical symptoms such as pain, energy, sleep quality, and mood,¹³ with memory, tenderness, balance and environmental sensitivity added in the latest iteration.¹⁴ The FIQ thus provides a spectrum of responses that range from mild to severe. Higher scores clearly represent more significant impact and associate with worse function. The FIQ taps into central processes that relate to emotions, distress and non-inflammatory PsA symptoms. The continuous scale derived from the widespread pain index and the symptom severity score of the 2010/2011 ACR criteria,¹⁵ modified in 2016,⁵ variously termed polysymptomatic distress scale or central sensitivity score,¹⁶ also does this. This score acts as both a clinical biomarker to identify central sensitization and also a tool that will predict outcomes to interventions, such as is seen in osteoarthritis (OA)¹⁷ and rheumatoid arthritis (RA).¹⁸ The use of these validated instruments in addition to current PsA assessment tools¹⁹ will aid the clinician in assessing the relative contribution of inflammatory disease activity, joint or soft tissue damage, and fibromyalgia symptoms to the patient's overall quality of life.

Fibromyalgia commonly associates with other inflammatory rheumatic diseases, being identified in around 20%-30% of patients with RA, spondyloarthropathy, systemic lupus erythematosus, and Sjögren's disease.^20-23 It is also similarly associated with a range of other rheumatological, neurological, gastrointestinal, infectious, endocrinological, and other internal diseases.^{24, 25} It is present in 20%-65% of patients with various other chronic pain conditions and there are increased rates of fibromyalgia in mental health disorders.^{24, 25} Furthermore, as the number of comorbidities increase so will the rate of fibromyalgia increase.²⁵

In each of these diseases/conditions the patient's fibromyalgia-related symptoms may also lead to increased investigations, modification of otherwise effective medication, or increased use of glucocorticoid medication. All of these responses may incur higher cost and morbidity, and yet still not treat the key symptoms affecting the overall quality of life of the patient.

Fibromyalgia has been traditionally considered as a comorbidity when it is present in conjunction with another disease or condition.²⁴ Another way to look at this association would be to consider fibromyalgia as part of the primary disease or condition, as it is part of the patient's response to a variety of life factors that include the effects of the disease/condition on the patient as a whole. Fibromyalgia is the clinical expression of stress-related neurobiological responses that lead to increased reactivity in a number of sensory neural systems, particularly those in the musculoskeletal system.²⁶ These systems are variably inbuilt into every person. The mechanism that results in the clinical phenotype labeled as fibromyalgia is present in all of us. Some of us are resilient with few related symptoms, some are more reactive due to genetic factors modifying neural responses, and some become more sensitive after early-life neural sensitization. Others, and perhaps the majority, are responding to the burden of having a chronic illness. This includes the symptoms of the disease, the effect on general health, the need for tests, drugs, and treatments, the disability, loss of quality of life, and modification of social and work roles, among others, as exemplified by PsA.²⁷ Psychological response to each of these issues can also feed back into the sensitization process.

In order to optimize management and achieve better outcomes, fibromyalgia, as a clinically defined phenotype reflecting activation of inbuilt stress-related neural algorithms,²⁸ needs to be identified in PsA, as it does in any chronic illness.