While QST is a well-researched method for the detection and characterization of sensory disorders, it is fully dependent on the subjective input from the participants. In previous studies with RA patients, only single elements of QST have been applied e.g., the RA disease resulted in higher baseline pain levels in those patients who reported lower pressure pain thresholds (PPTs). Moreover, QST may allow predictions and reflections of treatment responses. One method to detect sensory disorders and neuropathic pain is quantitative sensory testing (QST), which can provide valuable information about the underlying pathophysiological mechanisms of pain. Recent survey-based research emphasized that certain groups of RA patients even suffer from a neuropathic pain component, which would require treatment adjustment according to different treatment strategies than immunosuppressive drugs. However, a significant number of patients continue to experience pain despite adapted treatment. Further options in case the basic therapy is insufficient are topical capsaicin, weak opioids, and treatments such as joint infiltrations or surgical management. Disease-modifying antirheumatic drugs (DMARDs) usually represent the basic treatment for RA, while nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids (GCs) are used for symptomatic treatment. Nevertheless, RA patients show disease-associated pain problems even in the absence of inflammatory signs or low disease activity scores. RA patients report pain as one of the most important factors for those negative effects, which serves as a substitute marker for impairment and is often associated with disease activity. Rheumatoid arthritis (RA) is an immune-mediated joint disease that can severely reduce function and quality of life. Further studies are needed to prove if our proposed method can act as a marker for the success of anti-inflammatory treatment. The effect of topical capsaicin on HPTs and CHEPs can act as a marker for the extent of sensitization and the development of neuropathic symptoms. The effect in CHEPs probably uncovers neuropathic symptoms. ConclusionĪs the overall effect of topical capsaicin application was higher in HS for QST, we suggest the existence of a sensitization of TRPV1 channels in RA patients caused by long-time chronical inflammation, despite a lack of clinical signs of inflammation due to adequate treatment. We observed contrary effects regarding changes in CHEPs (HS: g*max = − 0.65 RA patients: g*max = 0.72). The application of capsaicin cream on the thigh provoked a stronger effect in HS for both mechanical and heat pain thresholds (MPT and HPT, resp.), according to the area under the receiver operation characteristic (AUROC) (HS: HPT: 0.8965, MPT: 0.7402 RA: HPT: 0.7012, MPT: 0.6113). We recruited 16 RA patients in remission or low disease activity state (mean age: 59.38 years ) and 16 healthy subjects (mean age: 56.69 years ). We used the quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain and Electroencephalography (EEG)–based contact heat evoked potentials (CHEPs) before and after topical capsaicin application. Our study aimed at examining the long-time inflammatory effects of rheumatoid arthritis (RA) as chronic immune-mediated disease on pain sensation and neuropathy development compared to healthy subjects (HS).
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