The effect of disease modifying drugs on the lung in patients with rheumatoid arthritis

doi:10.12746/swrccc2016.0413.166

Cited by 3 publications

(5 citation statements)

References 27 publications

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“…Multiple environmental factors including gastroesophageal reflux disease (GERD), infections (7,65), environmental chemicals, toxic substances, drugs (66)(67)(68), and tobacco smoke are associated with inflammatory lung injury (8,69,70). The prevalence of GERD in ILD can be as high as 94% (71)(72)(73).…”

Section: Environmental Factorsmentioning

confidence: 99%

Interstitial Lung Disease in Connective Tissue Disease: A Common Lesion With Heterogeneous Mechanisms and Treatment Considerations

et al. 2021

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Connective tissue disease (CTD) related interstitial lung disease (CTD-ILD) is one of the leading causes of morbidity and mortality of CTD. Clinically, CTD-ILD is highly heterogenous and involves rheumatic immunity and multiple manifestations of respiratory complications affecting the airways, vessels, lung parenchyma, pleura, and respiratory muscles. The major pathological features of CTD are chronic inflammation of blood vessels and connective tissues, which can affect any organ leading to multi-system damage. The human lung is particularly vulnerable to such damage because anatomically it is abundant with collagen and blood vessels. The complex etiology of CTD-ILD includes genetic risks, epigenetic changes, and dysregulated immunity, which interact leading to disease under various ill-defined environmental triggers. CTD-ILD exhibits a broad spectra of clinical manifestations: from asymptomatic to severe dyspnea; from single-organ respiratory system involvement to multi-organ involvement. The disease course is also featured by remissions and relapses. It can range from stability or slow progression over several years to rapid deterioration. It can also present clinically as highly progressive from the initial onset of disease. Currently, the diagnosis of CTD-ILD is primarily based on distinct pathology subtype(s), imaging, as well as related CTD and autoantibodies profiles. Meticulous comprehensive clinical and laboratory assessment to improve the diagnostic process and management strategies are much needed. In this review, we focus on examining the pathogenesis of CTD-ILD with respect to genetics, environmental factors, and immunological factors. We also discuss the current state of knowledge and elaborate on the clinical characteristics of CTD-ILD, distinct pathohistological subtypes, imaging features, and related autoantibodies. Furthermore, we comment on the identification of high-risk patients and address how to stratify patients for precision medicine management approaches.

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Section: Environmental Factorsmentioning

confidence: 99%

Interstitial Lung Disease in Connective Tissue Disease: A Common Lesion With Heterogeneous Mechanisms and Treatment Considerations

et al. 2021

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“…Rheumatoid nodules may cavitate in approximately one-third of cases, presumably due to ongoing vasculitis with ischemic necrosis [ 6 ]. We know that drugs used to treat the joint activity of RA can result in lung disease [ 7 ]. Progression and acceleration of rheumatoid nodule formation are well-known following MTX and LEF therapy in RA patients.…”

Section: Discussionmentioning

confidence: 99%

Outcome of solid and cavitary pulmonary nodules in rheumatoid arthritis patients? case series

Aksoy¹,

Kocakaya²,

Yalçınkaya³

et al. 2022

Turkish Journal of Medical Sciences

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Background/aim Rheumatoid pulmonary nodule can be detected in up to 32% of rheumatoid arthritis (RA) patients and approximately one-third of nodules may cavitate. We aimed to evaluate characteristics of patients with RA developing cavitary pulmonary nodular (CPN) lesions under disease-modifying antirheumatic drugs (DMARDs), follow-up of both cavitary and solid nodules, and their outcome with the treatment. Materials and methods RA patients who presented with CPN lesions during follow-up were recruited retrospectively in this case series analysis. Total numbers and mean diameters of cavitary and solid nodules in each thorax computed tomography (CT) have been determined and followed up by two experienced pulmonary physicians. Moreover, changes in treatment after the development of the CPN lesions and characteristics of cavitary nodules were collected. Results Eleven patients with CPN lesions were reported. At the time of CPN diagnosis, more patients were taking leflunomide than methotrexate (81% vs 19%). Half of the patients were receiving biologic therapy and only 18% were taking anti-TNF drugs. After a median of 24 (3–65) months of follow-up, the regression of CPN lesions was determined in 45% (5/11) of patients. Four of these 5 (80%) patients were switched to a treatment regimen without leflunomide and three of them to nonanti-TNF biologic treatment or targeted synthetic DMARDs (tocilizumab, tofacitinib, and rituximab). Conclusion CPN lesions seen in RA patients are often pulmonary manifestations of the underlying disease; however, one must rule out malignancies or infections. If lesions progress under DMARDs, it is advised to discontinue synthetic DMARDs (LEF/MTX) and switch to another biological DMARD with different modes of action

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“…Paradoxically however, these agents themselves may be associated with new-onset ILD, as well as exacerbations of pre-existing ILD. [21,22] The predominant pattern of ILD involvement is a usual interstitial pneumonia (UIP) pattern, which has a high mortality in patients with prior UIP. [23] Other patterns that have been described include organising pneumonia, nonspecific interstitial pneumonia (NSIP), diffuse alveolar haemorrhage (DAH) and lymphocytic interstitial pneumonitis (LIP).…”

Section: Tumour Necrosis Factor Inhibitorsmentioning

confidence: 99%

“…[23] Other patterns that have been described include organising pneumonia, nonspecific interstitial pneumonia (NSIP), diffuse alveolar haemorrhage (DAH) and lymphocytic interstitial pneumonitis (LIP). [21,23] Studies describing these findings have however been criticised for not conclusively demonstrating an absence of ILD prior to initiation of TNF inhibitors and many patients using these agents did so in conjunction with other disease-modifying antirheumatic drugs (DMARDs) known to produce similar effects in the lung. [23] According to data obtained from the British Society of Rheumatology Biologics Register, the mortality rate from ILD in patients with rheumatoid arthritis (RA) treated with TNF-α inhibitors was similar to those treated with conventional DMARDs.…”

Section: Tumour Necrosis Factor Inhibitorsmentioning

confidence: 99%

“…[24] While TNF-α inhibition has been used successfully to treat noninfectious granulomatous diseases, paradoxically TNF-α antagonism has also been associated with the development of a granulomatous, sarcoid-like disease, which may have both pulmonary and extra-pulmonary effects. [21,23,25] In almost all instances, the disease resolves on withdrawal of therapy, providing compelling evidence of causality. [23,25] The presence of pulmonary granulomas could also be explained by the development of sarcoidosis, hypersensitivity pneumonitis or an unidentified infectious agent, although the latter is unlikely given the continued resolution of disease despite initiation of replacement immunosuppressive regimens after withdrawal of TNF-α inhibitors.…”

Section: Tumour Necrosis Factor Inhibitorsmentioning

confidence: 99%

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Adverse effects of biologic anti-inflammatory agents on the respiratory system: A review

Joseph

Tintinger

Ker

et al. 2021

Afr J Thorac Crit Care Med

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The therapy of autoimmune rheumatological conditions has undergone significant changes with the introduction of biologic antiinflammatory agents including cytokine antagonists and agents that interfere with the function of T and B cells or those that inhibit intracellular enzymes such as Janus kinase (JAK). Although useful to control inflammation, these agents may be associated with druginduced lung disease, which may be difficult to differentiate from pulmonary disorders caused by the underlying autoimmune diseases. This review aims to provide a description of lung disease, both infectious and non-infectious, that may be induced by the administration of biologic anti-inflammatory agents with emphasis on inhibitors of tumour necrosis factor, interleukin-1, interleukin-6 and JAK.

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The effect of disease modifying drugs on the lung in patients with rheumatoid arthritis

Cited by 3 publications

References 27 publications

Interstitial Lung Disease in Connective Tissue Disease: A Common Lesion With Heterogeneous Mechanisms and Treatment Considerations

Interstitial Lung Disease in Connective Tissue Disease: A Common Lesion With Heterogeneous Mechanisms and Treatment Considerations

Outcome of solid and cavitary pulmonary nodules in rheumatoid arthritis patients? case series

Adverse effects of biologic anti-inflammatory agents on the respiratory system: A review

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