Pain in Psoriatic Arthritis Save

Pain is perhaps the most complex hallmark of rheumatic disease, and arguably the most important factor from a patient perspective. 

Multiple definitions of pain exist, but in reality it is used by both clinicians and patients to denote an unpleasant subjective sensation. Put simply, pain can be broadly categorised by the 3Ns: neuropathic, nociplastic or nociceptive. Classification of pain type is paramount for patient outcomes, as the management strategy for each pain type is notably different. 

Whilst we may understand that there are different types of pain theoretically, we often struggle to decipher them in the clinical setting – it is in our DNA as rheumatologists to gravitate to the inflammatory after all! 

The prioritisation of pain, and its evaluation, is especially important in those with psoriatic arthritis (PsA), when the already incredibly heterogenous nature of the condition can complicate assessment. Whilst we lean towards all pain in PsA being nociceptive in nature, evidence suggests that a significant proportion of patients with PsA also have nociplastic pain, characterised by fibromyalgia (FM).

In abstract 2256, Sunzini et al, support this by providing an objective neurobiological marker of nociplastic pain in PsA. Using functional MRI they demonstrate increased functional brain connectivity in areas involved in sensory, learning/affective and cognitive pain modulation typically associated with FM, in PsA patients fulfilling the classification for FM using the ACR 2011 FM Survey criteria.

In abstract 1218, Mease et al, also highlights the importance of remaining cognizant of different pain types in PsA patient assessment. Using the CorEvitas registry, they report the presence of chronic widespread pain (CWP) in 13.4%, and FM in 10.4% of PsA patients. Both CWP and FM were associated with female sex, obesity, depression, anxiety and also increased comorbidities. Interestingly, although perhaps not surprisingly, assessments of disease severity which included subjective measures, such as the cDAPSA, patient global and pain scores and tender joint count, were reported more severely in the FM and CWP groups. Given that these are disease outcome measures upon which we often alter our treatments, these findings really emphasise the need for thorough pain evaluation. Failing to recognise FM or CWP in this patient cohort, may result in a perceived inadequate response to disease modifying or anti-inflammatory medications, and the descent into panic over deciding the next suitable biologic agent! 

The need to recognise and adequately manage pain is a crucial step in accurately assessing inflammatory disease activity and ensuring appropriate treatment modification.

In abstract 1225, Del Rio-Guerrero and colleagues propose a screening tool for FM. They demonstrate how the elicitation of local pain during blood pressure measurement with a sphygmomanometer is strongly indicative of the presence of FM. Whilst this requires validation, it fosters promise for easily implementable and practical approaches to pain evaluation in our patients.

Pain when present is the most important element of disease for patients – they may not thank us for normalisation of their CRP levels, but we can change their life by adequately diagnosing and tackling their pain. Instead of automatically cycling to another biologic agent, remember the “3Ns” and consider pain as another domain of disease in your PsA patient.