How to treat chronic pain in rheumatic and musculoskeletal diseases (RMDs) - A pharmacological review.

INTRODUCTION: Chronic pain is a common symptom of rheumatic diseases that impacts patients' quality of life. While non-pharmacological approaches are often recommended as first-line treatments, pharmacological interventions are important for pain management. However, the effectiveness and safety of different pharmacological treatments for chronic pain in rheumatic diseases are unclear. METHODS: This review critically synthesizes the current evidence base to guide clinicians in selecting appropriate pharmacological treatments for their patients, considering the expected benefits and potential risks and side effects. RESULTS: For osteoarthritis, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, opioids, and antidepressants are commonly used, with NSAIDs being the most recommended. In addition, topical agents, such as topical NSAIDs, are recommended for localized pain relief. For fibromyalgia, amitriptyline, serotonin and noradrenaline reuptake inhibitors (SNRIs), and gabapentinoids are commonly used, with SNRIs being the most recommended. For back pain, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, opioids are used only for acute of flare-up pain, whereas neuropathic pain drugs are only used for chronic radicular pain. For inflammatory rheumatic diseases, disease-modifying antirheumatic drugs (DMARDs) and biological agents are recommended to slow disease progression and manage symptoms. CONCLUSION: While DMARDs and biological agents are recommended for inflammatory rheumatic diseases, pharmacological treatments for other rheumatic diseases only alleviate symptoms and do not provide a cure for the underlying condition. The use of pharmacological treatments should be based on the expected benefits and evaluation of side effects, with non-pharmacological modalities also being considered, especially for fibromyalgia.

The challenge of differentiating fibromyalgia from small-fiber neuropathy in clinical practice.

Fibromyalgia and small fibre neuropathy are two diseases leading to chronic widespread pain, and it is difficult to differentiate them in order to provide appropriate care. In this review, we will describe the pathophysiological and clinical differences between fibromyalgia and small fibre neuropathy. In fibromyalgia, pain is increased by dysregulation of central pain processing while small fibre neuropathy pain is related to loss or dysfunction of intraepidermal small nerve fibres. Higher pain intensity; stabbing pain and paraesthesia; allodynia; dry eyes/mouth; changed pattern or sweating on body; skin colour alterations/modifications; reduced hair/nail growth on lower extremities; warm or cold hypoesthesia could be more common in small fibre neuropathy whereas headache or temporo-mandibular disorder point toward fibromyalgia. Length-dependent distribution of pain is common in small fibre neuropathy but can also affect the whole body. Anxiety or depression are common in these two diseases, but post-traumatic stress disorder and physical or sexual abuse in childhood or adulthood suggest fibromyalgia. Inflammatory disease or musculoskeletal disease is frequently reported with fibromyalgia whereas metabolic disorders (especially diabetes mellitus), neurotoxic exposure, Sjogren's syndrome, sarcoidosis, HIV are the main diseases associated with small fibre neuropathy. Skin biopsy, quantitative sensory testing, laser evoked potentials, confocal corneal microscopy or electrochemical skin conductance can help to discriminate between fibromyalgia and small fibre neuropathy.

Part of pain labelled neuropathic in rheumatic disease might be rather nociplastic.

Pain in rheumatic diseases is primarily due to mechanical or inflammatory mechanism, but neuropathic pain (NP) component is also occurring in many conditions and is probably underdiagnosed. The purpose of this article is to provide an overview of prevalence, pathophysiological and currently available treatment of NP in rheumatic diseases. When associated with clinical evaluation assessing neurological clinical signs and neuroanatomical distribution, Douleur Neuropathique 4 Questions, painDETECT, Leeds assessment of neuropathic symptoms and signs and Neuropathic Pain Questionnaire can detect NP component. Inflammatory or connective diseases, osteoarthritis, back pain or persistent pain after surgery are aetiologies that all may have a neuropathic component. Unlike nociceptive pain, NP does not respond to usual analgesics such as paracetamol and non-steroidal anti-inflammatory drugs. Entrapment neuropathy, peripheral neuropathy or small-fibre neuropathy are different aetiologies that can lead to NP. A part of the pain labelled neuropathic is rather nociplastic, secondary to a central sensitisation mechanism. Identifying the right component of pain (nociceptive vs neuropathic or nociplastic) could help to better manage pain in rheumatic diseases with pharmacological and non-pharmacological treatments.

Sustainability of TNF-blocker tapering in rheumatoid arthritis over 3 years: long-term follow-up of the STRASS (Spacing of TNF-blocker injections in Rheumatoid ArthritiS Study) randomised controlled trial.

INTRODUCTION: We have limited data on the sustainability of tumour necrosis factor (TNF)-blocker tapering in rheumatoid arthritis (RA) in remission over the long term in real-life settings. This study aimed to assess the probability of sustained dose reduction of TNF-blockers in an observational 3-year extended follow-up of the Spacing of TNF-blocker injections in Rheumatoid ArthritiS Study (STRASS), a randomised controlled trial comparing progressive TNF-blocker injections (spacing arm (S-arm) to maintenance arm (M-arm)) in patients with RA in stable remission. METHODS: In 2015, clinical data for the completer population were retrospectively collected at 1, 2 and 3 years after the end of the trial. The endpoints were the proportion of patients free of a biological disease-modifying antirheumatic drug (bDMARD) treatment, a sustainably spaced injection of TNF-blockers and a full-dose regimen as well as the mean dose of bDMARD intake and treatment switch rate. RESULTS: Overall, 96 patients (76.8% of the completers) had data available up to 3 years; 11.5% discontinued TNF-blockers (5.8% vs 18.2% in the M-arm and S-arm, p=0.06), 30.2% had a tapered regimen (28.8% vs 31.8%, p=0.76) and 37.5% retained a full dose (44.2% vs 29.5%, p=0.14). The mean TNF-blocker dose quotient was 66% of the full dose (74% vs 58% in the M-arm and S-arm, p=0.06); 20.8% switched to another bDMARD (21.2% vs 20.5%, p=0.94). CONCLUSION: Sustained TNF-blocker de-escalation or withdrawal is achievable in 41% of patients over 3 years with limited dose reduction. Optimal strategies remain to be determined to maintain remission after TNF-blocker tapering or discontinuation.