Effect of biological DMARDs and JAK inhibitors in pain of chronic inflammatory arthritis

Alciati, Alessandra; Carlo, Marco Di; Siragusano, Cesare; Palumbo, Antonino; Masala, Ignazio Francesco; Atzeni, Fabiola

doi:10.1080/14712598.2022.2130243

Cited by 8 publications

(4 citation statements)

References 90 publications

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“…Te lack of decrease in opioid use suggests that nonpharmacological approaches need to be incorporated into pain management. While infammation from the disease itself is a driver of pain, it is also increasingly recognised that there is a nociplastic contribution to pain in rheumatoid arthritis [20]. Pain, neuroscience education, mindfulness, cognitive behavioural therapy, and acceptance and commitment therapy have all been found to contribute to improvements in pain or function and could be trialed as strategies for improving pain and reducing opioid use in persons with rheumatoid arthritis [21][22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Use of Analgesic and Anti-Inflammatory Medicines before and after Initiation of Biological Disease-Modifying Antirheumatic Drugs for Rheumatoid Arthritis

Gadzhanova,

Roughead

2024

Journal of Clinical Pharmacy and Therapeutics

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Background. Rheumatoid arthritis (RA) is an inflammatory condition that causes joint damage and is associated with pain. The biological disease-modifying antirheumatic drugs (bDMARDs) for RA are linked to additional therapeutic benefits as they suppress the inflammatory process, which in turn prevents joint erosion and reduces pain. Thus, the use of bDMARDs has the potential to reduce the need for other analgesic and anti-inflammatory therapies for RA. The aim of this study was to examine the analgesic and anti-inflammatory use around the initiation of bDMARDs. Methods. A cohort study was conducted using a 10% random sample of the population dispensing medicines under the Australian Pharmaceutical Benefits Scheme. People who initiated the first bDMARD for RA between 2014 and 2018 were included. The proportion who received any analgesic or anti-inflammatory, including nonsteroidal anti-inflammatory drugs, opioids, or glucocorticoids, in the twelve months prior to and post-bDMARD initiation was determined and compared using regression models. Results. There were 18,360 persons in the cohort, with a mean age of 55 years, and 69% were women. The use of any analgesic or anti-inflammatory in both tumor necrosis factor inhibitor (TNFi) and non-TNF initiators increased prior to initiation of bDMARD–from 43% to 52% in TNFi and from 52% to 63% in non-TNF initiators. In both groups, overall use decreased significantly post initiation to 37% and 42% in TNFi and non-TNF initiators, respectively (p<0.0001). bDMARD initiation was associated with lower use of glucocorticoid therapy, but there was no decreasing effect on opioid use. Conclusion. While the use of any analgesic or anti-inflammatories decreased post-initiation of bDMARDs for RA, more than one-third of people were dispensed analgesic or anti-inflammatory agents twelve months post initiation. Ongoing review of the need for analgesic and glucocorticoids appears warranted, with assessment of nonpharmacological approaches to support pain management.

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Section: Discussionmentioning

confidence: 99%

Use of Analgesic and Anti-Inflammatory Medicines before and after Initiation of Biological Disease-Modifying Antirheumatic Drugs for Rheumatoid Arthritis

Gadzhanova,

Roughead

2024

Journal of Clinical Pharmacy and Therapeutics

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“…As JAKi treatment aims to IL-6 (directly) and IL-1β (indirectly), this can explain why this treatment was shown to have a good effect on pain, even more pronounced than bDMARDs. 48 …”

Section: Potential Mechanism Of Fatiguementioning

confidence: 99%

“…As JAKi treatment aims to IL-6 (directly) and IL-1β (indirectly), this can explain why this treatment was shown to have a good effect on pain, even more pronounced than bDMARDs. 48 There are also other genes like ERN1 and PRDM1 involved in fatigue regulation. ERN1 codes enzyme IRE1a important for sensing cellular stress signals, while PRDM1 encodes a transcription factor expressed by T cells and B cells and is involved in downregulation of immune responses and repression of IFN-γ expression.…”

mentioning

confidence: 99%

Potential Mechanism of Fatigue Induction and Its Management by JAK Inhibitors in Inflammatory Rheumatic Diseases

Felis-Giemza,

Massalska,

Roszkowski

et al. 2023

JIR

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It is well known that fatigue is a highly disabling symptom commonly observed in inflammatory rheumatic diseases (IRDs). Fatigue is strongly associated with a poor quality of life and seems to be an independent predictor of job loss and disability in patients with different rheumatic diseases. Although the pathogenesis of fatigue remains unclear, indirect data suggest the cooperation of the immune system, the central and autonomic nervous system, and the neuroendocrine system in the induction and sustainment of fatigue in chronic diseases. Fatigue does not correspond with disease activity and its mechanism in IRDs. It is suggested that it may change over time and vary between individuals. Abnormal production of pro-inflammatory cytokines such as interleukin-6 (IL-6), interferons (IFNs), granulocyte-macrophage colony-stimulating factor (GM-CSF), TNF, IL-15, IL-17 play a role in both IRDs and subsequent fatigue development. Some of these cytokines such as IL-6, IFNs, GM-CSF, and common gamma-chain cytokines (IL-15, IL-2, and IL-7) activate the Janus Kinases (JAKs) family of intracellular tyrosine kinases. Therapy blocking JAKs (JAK inhibitors -JAKi) has been recently proven to be an effective approach for IRDs treatment, more efficient in pain reduction than anti-TNF. Therefore, the administration of JAKi to IRDs patients experiencing fatigue may find rational implications as a therapeutic modulator not only of disease inflammatory symptoms but also fatigue with its components like pain and neuropsychiatric features as well. In this review, we demonstrate the latest information on the mechanisms of fatigue in rheumatic diseases and the potential effect of JAKi on fatigue reduction. Plain Language Summary• JAKi block pro-inflammatory cytokines, decrease activation of IDO, diminish the effects of genetic polymorphism (particularly mediated by IL-6 and IL-1β) as well as sickness behavior also connected with IL-1β expression, which result in fatigue and pain inhibition. • In patients treated with JAKi, it was observed that there was significantly greater improvement compared to placebo and MTX in fatigue and pain reduction measured using PROs. • Administration of JAKi (BARI+UPA) benefits over TNFi treatment in pain and fatigue reduction assessed by PtGA in RA patients. • The effectiveness of fatigue reduction in PROs under recently approved JAKi still needs to be proven in clinical practice, especially in selective and nonselective groups of JAKi.

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“…Ее «базис» (морфологическую основу) составляют воспалительные и дегенеративные изменения, связанные с аутоиммунными и иммуновоспалительными процессами, механическим или метаболическим стрессом, поражающими структуры скелетно-мышечной системы. Но появление истинной хронической боли как самостоятельной патологии определяет, условно говоря, «надстройка» -нейропластические процессы (центральная сенситизация), психоэмоциональные нарушения и негативные поведенческие реакции [27][28][29].…”

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Do not say or write: “pain syndrome”! You say “pain”!

Karateev

2024

Naučno-praktičeskaâ revmatologiâ

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Effect of biological DMARDs and JAK inhibitors in pain of chronic inflammatory arthritis

Cited by 8 publications

References 90 publications

Use of Analgesic and Anti-Inflammatory Medicines before and after Initiation of Biological Disease-Modifying Antirheumatic Drugs for Rheumatoid Arthritis

Use of Analgesic and Anti-Inflammatory Medicines before and after Initiation of Biological Disease-Modifying Antirheumatic Drugs for Rheumatoid Arthritis

Potential Mechanism of Fatigue Induction and Its Management by JAK Inhibitors in Inflammatory Rheumatic Diseases

Do not say or write: “pain syndrome”! You say “pain”!

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