*Read for medical professionals only
Let’s talk with experts about the pathological mechanism research and clinical diagnosis and treatment of RA-related ILD.
I believe everyone is familiar with rheumatoid arthritis (RA). It is one of the most common diseases in the Rheumatoid Immunology Department. RA patients often complain about joint swelling, pain in the joint, morning stiffness and movement disorders. However, RA is not a disease that simply involves joints, but can also involve various other organs and systems. It is a veritable systemic autoimmune disease. These extraarticular manifestations often indicate poor disease prognosis and should be given special attention in clinical practice.
Interstitial lung disease (ILD) is one of the major organ damages in RA multisystem involvement and one of its most serious comorbidities. The clinical manifestations, etiology and mechanism of RA combined with ILD have become a common concern for doctors in departments such as rheumatology, respiratory medicine, and critical care medicine. In this issue, the "medical community" was fortunate to invite Professor Ke Linhe of the Fujian Provincial Hospital Rheumatism and Immunity to share his wonderful views with us.
"Cough cough cough" -
Red signals that RA involve the lungs must not miss
Epidemiological data show that the lifetime prevalence of ILD in patients with RA is 5%-10%. According to the different ILD screening methods, the incidence rate ranges from 2.7 to 3.8/100,000 patients to [1].
Professor Lin He told us that in clinical patients with ILD may experience clinical manifestations such as active dyspnea, restricted ventilation disorders, reduced carbon monoxide diffusion function (DLCO), and hypoxemia . Among them, exertional dyspnea and dry cough are the most common. ILD has severe respiratory damage to RA patients, which can affect almost every activity in their daily life and reduce the quality of life. If it is not effectively controlled, it may cause severe breathing difficulties or even respiratory failure , which may endanger life. In addition, RA patients with ILD are prone to various respiratory infections, further aggravating ILD lesions. The infection on this basis is more difficult to treat than those without ILD, and it is also one of the reasons for life-threatening [2-3].
RA combined with ILD has a risk of death 3 times that of patients with RA alone. ILD has become the second leading cause of death in patients with RA, second only to cardiovascular disease [1, 4]. Professor Lin He therefore pointed out, "It is precisely because ILD is very clinically harmful that people are paying more and more attention to RA-related ILDs, and a lot of research has been done on its etiology and mechanism and clinical diagnosis and treatment."
Which RA patients may be high-risk groups with ILD? In this regard, Professor Lin He said that the probability of ILD in RA patients is related to many factors, including the patient's gender, age, lifestyle, disease activity and duration of RA. "In clinical practice, we observed that males and older RA patients have a higher proportion of ILD." According to clinical observations and reports of related research results, Professor Lin He told us: "Those who smoke for a long time or have a history of lung infection have poor lung conditions and are more likely to cause lung injury ." In addition, RA patients with long courses of disease and high disease activity are also high-incidence of ILD, especially those with autoantibodies , such as [4-5], who have higher levels of anti-cyclic citrulline peptide antibodies (anti-CCP antibodies). Professor Lin He suggested that patients with RA with these high-risk risk factors should be closely monitored.
Lung Lesions and joint are involved,
Who is "matching" them?
RA patients have nearly 9 times the risk of ILD than the general population [6]. How are the two seemingly unrelated manifestations of lung lesions and joint involvement linked together? Professor Lin He sorted out relevant clues for us based on some existing research data.
"At present, the exact cause and pathogenesis of RA-related ILD are not clear, and many studies have been conducted in the academic community." Professor Lin He pointed out that the occurrence of RA-related ILD is closely related to environmental factors (such as cigarette smoke, pathogens or other stimuli in the environment causing lung tissue and cell damage), genetic factors (such as the existence of susceptible genes), and immune factors (such as failure to immune tolerance, the production of autoantibodies and autoimmunity) (Figure 1) [7].
Figure 1: Development mechanism of RA-ILD [7]
RA is an autoimmune disease, and multiple autoantibodies are usually present in patients. Among them, rheumatoid factor (RF) and anti-citrulline protein antibodies (ACPA) play a very important role in the occurrence and development of RA. Compared with traditional RF, ACPA is a newly discovered important antibody related to RA disease. It is not only a high sensitivity and high specific diagnostic marker, but also a predictor of disease severity and development [8].
ACPA can cause damage to local mucosa, airway and lung interstitial body in a variety of ways, such as promoting the formation and release of inflammatory cytokines, the formation and deposition of immune complexes, etc. Studies have shown that there is a strong correlation between the increase in ACPA titer and RA-related airway diseases. In the bronchial tissue and bronchial alveolar lavage fluid of ACPA-positive RA patients, signs of immune cells [7] were found; the increase in ACPA titer is also related to the increase in the prevalence of ILD in RA patients [9]... These research results suggest that ACPA may mediate the occurrence of lung diseases in RA patients and are closely related to the progression of RA-ILD disease.
However, the specific mechanism of ACPA is not yet known, and there are many conjectures and assumptions about this in the academic community. From the perspective of joint manifestations and the time sequence of lung lesions, a considerable proportion of RA patients have ILD before joint symptoms appear, and ACPA can also exist in the body several years before RA onset, indicating that the lungs are likely to be the early organ site of ACPA-induced damage. The immune response of citrulline polypeptide in the lung may cause secondary arthritis and joint damage; and for the phenomenon that joint symptoms occur before ILD, scholars speculate that this is likely to be the result of the migration of immune response against citrulline peptides at the joints to the lungs. The higher ACPA concentration in the local and systemic systems causes significant inflammatory responses in the lungs, resulting in the occurrence of ILD [7, 9]. Regardless of the order in which joint symptoms and lung injury occur, ACPA plays an extremely important "bridge" role in it, linking lung damage to joint symptoms in RA-ILD.
Multidisciplinary joint diagnosis and treatment.
innovative drugs help control the disease of RA-ILD
RA-ILD diagnosis and treatment have always been difficult in clinical work. Early screening and diagnosis are critical for patients with high risk factors for RA-ILD. Professor Lin He said that the clinical diagnosis and treatment of RA-ILD requires multidisciplinary cooperation [10]. "Connective tissue diseases like RA are the areas that our rheumatism and immune department is good at, and connective tissue is the main tissue composition of the lungs, and many rheumatism and immune diseases may affect the lungs; at the same time, lung diseases belong to the category of diagnosis and treatment of respiratory departments. Therefore, patients with lung diseases are often first diagnosed in the respiratory department, and patients also need to undergo lung function examinations, pulmonary CT examinations, and if necessary, pathogenic examinations and pathological examinations are required." Professor Lin He also pointed out that , "In addition to the observation and judgment of clinical symptoms, the detection of serum biomarkers, imaging and histopathology evaluation are also important means of clinical diagnosis. Therefore, respiratory, radiology, pathology and laboratory departments are also key departments in multidisciplinary cooperation."
Speaking of the treatment of RA-ILD, Professor Lin He said that there are currently no specific drugs. The ideal treatment goal in clinical practice is to stabilize and improve ILD while alleviating RA and prevent the disease from progressing or worsening. Among various commonly used therapeutic drugs, traditional synthetic anti-rheumatic drugs (csDMARDs) are the first-line drugs for clinical treatment of RA. Methotrexate (MTX) is one of the classic csDMARDs drugs and is also an anchor drug recommended by many domestic and foreign guidelines. However, there are cases that MTX may induce ILD in RA patients or aggravate their condition. Although there is no high-quality evidence-based medical evidence to verify that MTX treatment will worsen the patient's prognosis, in the face of possible risks, [9, 11] should be cautious in clinical practice. "The emergence of various biological agents is a breakthrough in the field of RA treatment in recent years. As a second-line therapeutic drug for RA, biological agents can effectively improve patients' clinical symptoms and joint function."Professor Lin He said, "Although the current research results on the risk of ILD on the occurrence and progression of RA patients with large differences, overall, the use of non-TNF inhibitor biological agents has a more accurate effect on the stability and improvement of ILD in RA patients with ILD, and the risk is relatively low. "
In the relevant drug introduction, Professor Lin He focused on a novel biological agent - abacept. Abacept blocks costimulatory signals, inhibits the activation of T lymphocytes and reduces the inflammatory response in RA patients. Previous studies have shown that abacept has significant therapeutic advantages in ACPA-positive RA patients [12-15]. Combined with the possible important role of ACPA in RA-ILD mentioned above, does abacept have unique efficacy in the stability of RA-ILD patients?
Professor Lin He pointed out that according to the monitoring after marketing Data and safety data in clinical trials, patients with RA have a lower chance of ILD in patients with RA7[16-17], and no lung damage caused by their treatment has been found in clinical practice. Moreover, relevant studies have confirmed that abacept is beneficial to the stability of patients with RA-ILD:
A single-center retrospective study in Japan showed that abacept may have a protective effect on the new occurrence or aggravation of lung diseases (including ILD and obstructive pulmonary diseases) in patients with RA, and is a significant independent protective factor for (risk odds ratio OR: 0.07, 95%CI: 0.01-0.99) [18];
Figure 2: Independent factors related to airway disease or ILD progression
Meta analysis results show that abacept can significantly reduce the ILD worsening rate in RA patients; compared with TNF inhibitors and csDMARDs, the relative risk of ILD worsening in patients treated with abacept was 90% lower than that in patients treated with abacept for 24 months of follow-up.
In a large multicenter observational study, 263 patients with RA-ILD received abacept for treatment for 6-36 months (median follow-up time was 12 months). Nearly 90% of patients with had stable lung function or improved, and 77% of patients had stable or improved radiological performance [20].
A prospective multicenter study showed that the median follow-up time for patients with RA-ILD was 27.3 (IQR) 12.2-42.8) months, 571% of patients with have stable lung function and arthritis, and have good safety. [21].
A retrospective study analysis showed that after RA-ILD patients received abacept treatment for 18 months, 88.6% of patients with ILD had stable or improved ILD. [22].
Professor Lin He believes: "Early standardized and effective treatment can well relieve the condition of RA, or slow down/stop the occurrence and development of lung disease damage. Patients can use this type of beneficial drugs as early as possible in clinical practice to better control RA-ILD. "
Finally, Professor Lin He also gave several suggestions for non-pharmaceutical intervention measures of RA-ILD: First, patients need to maintain good living habits, such as quitting smoking, which can improve lung function; perform respiratory training, exercise respiratory muscles, improve exercise ability through lung rehabilitation, and improve lung function; and for patients with severe lung damage and poor respiratory function, ventilator oxygen therapy can be given and strenuous exercise as much as possible. While following reasonable drug treatment, combined with non-pharmaceutical intervention can achieve twice the result with half the effort.
summary
ILD is a common extra-articular manifestation of RA, causing serious damage to the patient's respiratory system, affecting the quality of life and even threatening his life safety. The etiology of RA-ILD is not clear. Studies have found that ACPA may mediate the occurrence of lung diseases in RA patients and participate in the occurrence and development of ILD. A variety of DMARDs used to treat RA have been reported to increase ILD and infection risks. Abacept treatment not only has a low chance of pulmonary infection, but also has good efficacy in improving and stabilizing RA-ILD. It is a significant protective factor for RA-ILD, providing a new idea for its treatment.
*Read for medical professionals only
Let’s talk with experts about the pathological mechanism research and clinical diagnosis and treatment of RA-related ILD.
I believe everyone is familiar with rheumatoid arthritis (RA). It is one of the most common diseases in the Rheumatoid Immunology Department. RA patients often complain about joint swelling, pain in the joint, morning stiffness and movement disorders. However, RA is not a disease that simply involves joints, but can also involve various other organs and systems. It is a veritable systemic autoimmune disease. These extraarticular manifestations often indicate poor disease prognosis and should be given special attention in clinical practice.
Interstitial lung disease (ILD) is one of the major organ damages in RA multisystem involvement and one of its most serious comorbidities. The clinical manifestations, etiology and mechanism of RA combined with ILD have become a common concern for doctors in departments such as rheumatology, respiratory medicine, and critical care medicine. In this issue, the "medical community" was fortunate to invite Professor Ke Linhe of the Fujian Provincial Hospital Rheumatism and Immunity to share his wonderful views with us.
"Cough cough cough" -
Red signals that RA involve the lungs must not miss
Epidemiological data show that the lifetime prevalence of ILD in patients with RA is 5%-10%. According to the different ILD screening methods, the incidence rate ranges from 2.7 to 3.8/100,000 patients to [1].
Professor Lin He told us that in clinical patients with ILD may experience clinical manifestations such as active dyspnea, restricted ventilation disorders, reduced carbon monoxide diffusion function (DLCO), and hypoxemia . Among them, exertional dyspnea and dry cough are the most common. ILD has severe respiratory damage to RA patients, which can affect almost every activity in their daily life and reduce the quality of life. If it is not effectively controlled, it may cause severe breathing difficulties or even respiratory failure , which may endanger life. In addition, RA patients with ILD are prone to various respiratory infections, further aggravating ILD lesions. The infection on this basis is more difficult to treat than those without ILD, and it is also one of the reasons for life-threatening [2-3].
RA combined with ILD has a risk of death 3 times that of patients with RA alone. ILD has become the second leading cause of death in patients with RA, second only to cardiovascular disease [1, 4]. Professor Lin He therefore pointed out, "It is precisely because ILD is very clinically harmful that people are paying more and more attention to RA-related ILDs, and a lot of research has been done on its etiology and mechanism and clinical diagnosis and treatment."
Which RA patients may be high-risk groups with ILD? In this regard, Professor Lin He said that the probability of ILD in RA patients is related to many factors, including the patient's gender, age, lifestyle, disease activity and duration of RA. "In clinical practice, we observed that males and older RA patients have a higher proportion of ILD." According to clinical observations and reports of related research results, Professor Lin He told us: "Those who smoke for a long time or have a history of lung infection have poor lung conditions and are more likely to cause lung injury ." In addition, RA patients with long courses of disease and high disease activity are also high-incidence of ILD, especially those with autoantibodies , such as [4-5], who have higher levels of anti-cyclic citrulline peptide antibodies (anti-CCP antibodies). Professor Lin He suggested that patients with RA with these high-risk risk factors should be closely monitored.
Lung Lesions and joint are involved,
Who is "matching" them?
RA patients have nearly 9 times the risk of ILD than the general population [6]. How are the two seemingly unrelated manifestations of lung lesions and joint involvement linked together? Professor Lin He sorted out relevant clues for us based on some existing research data.
"At present, the exact cause and pathogenesis of RA-related ILD are not clear, and many studies have been conducted in the academic community." Professor Lin He pointed out that the occurrence of RA-related ILD is closely related to environmental factors (such as cigarette smoke, pathogens or other stimuli in the environment causing lung tissue and cell damage), genetic factors (such as the existence of susceptible genes), and immune factors (such as failure to immune tolerance, the production of autoantibodies and autoimmunity) (Figure 1) [7].
Figure 1: Development mechanism of RA-ILD [7]
RA is an autoimmune disease, and multiple autoantibodies are usually present in patients. Among them, rheumatoid factor (RF) and anti-citrulline protein antibodies (ACPA) play a very important role in the occurrence and development of RA. Compared with traditional RF, ACPA is a newly discovered important antibody related to RA disease. It is not only a high sensitivity and high specific diagnostic marker, but also a predictor of disease severity and development [8].
ACPA can cause damage to local mucosa, airway and lung interstitial body in a variety of ways, such as promoting the formation and release of inflammatory cytokines, the formation and deposition of immune complexes, etc. Studies have shown that there is a strong correlation between the increase in ACPA titer and RA-related airway diseases. In the bronchial tissue and bronchial alveolar lavage fluid of ACPA-positive RA patients, signs of immune cells [7] were found; the increase in ACPA titer is also related to the increase in the prevalence of ILD in RA patients [9]... These research results suggest that ACPA may mediate the occurrence of lung diseases in RA patients and are closely related to the progression of RA-ILD disease.
However, the specific mechanism of ACPA is not yet known, and there are many conjectures and assumptions about this in the academic community. From the perspective of joint manifestations and the time sequence of lung lesions, a considerable proportion of RA patients have ILD before joint symptoms appear, and ACPA can also exist in the body several years before RA onset, indicating that the lungs are likely to be the early organ site of ACPA-induced damage. The immune response of citrulline polypeptide in the lung may cause secondary arthritis and joint damage; and for the phenomenon that joint symptoms occur before ILD, scholars speculate that this is likely to be the result of the migration of immune response against citrulline peptides at the joints to the lungs. The higher ACPA concentration in the local and systemic systems causes significant inflammatory responses in the lungs, resulting in the occurrence of ILD [7, 9]. Regardless of the order in which joint symptoms and lung injury occur, ACPA plays an extremely important "bridge" role in it, linking lung damage to joint symptoms in RA-ILD.
Multidisciplinary joint diagnosis and treatment.
innovative drugs help control the disease of RA-ILD
RA-ILD diagnosis and treatment have always been difficult in clinical work. Early screening and diagnosis are critical for patients with high risk factors for RA-ILD. Professor Lin He said that the clinical diagnosis and treatment of RA-ILD requires multidisciplinary cooperation [10]. "Connective tissue diseases like RA are the areas that our rheumatism and immune department is good at, and connective tissue is the main tissue composition of the lungs, and many rheumatism and immune diseases may affect the lungs; at the same time, lung diseases belong to the category of diagnosis and treatment of respiratory departments. Therefore, patients with lung diseases are often first diagnosed in the respiratory department, and patients also need to undergo lung function examinations, pulmonary CT examinations, and if necessary, pathogenic examinations and pathological examinations are required." Professor Lin He also pointed out that , "In addition to the observation and judgment of clinical symptoms, the detection of serum biomarkers, imaging and histopathology evaluation are also important means of clinical diagnosis. Therefore, respiratory, radiology, pathology and laboratory departments are also key departments in multidisciplinary cooperation."
Speaking of the treatment of RA-ILD, Professor Lin He said that there are currently no specific drugs. The ideal treatment goal in clinical practice is to stabilize and improve ILD while alleviating RA and prevent the disease from progressing or worsening. Among various commonly used therapeutic drugs, traditional synthetic anti-rheumatic drugs (csDMARDs) are the first-line drugs for clinical treatment of RA. Methotrexate (MTX) is one of the classic csDMARDs drugs and is also an anchor drug recommended by many domestic and foreign guidelines. However, there are cases that MTX may induce ILD in RA patients or aggravate their condition. Although there is no high-quality evidence-based medical evidence to verify that MTX treatment will worsen the patient's prognosis, in the face of possible risks, [9, 11] should be cautious in clinical practice. "The emergence of various biological agents is a breakthrough in the field of RA treatment in recent years. As a second-line therapeutic drug for RA, biological agents can effectively improve patients' clinical symptoms and joint function."Professor Lin He said, "Although the current research results on the risk of ILD on the occurrence and progression of RA patients with large differences, overall, the use of non-TNF inhibitor biological agents has a more accurate effect on the stability and improvement of ILD in RA patients with ILD, and the risk is relatively low. "
In the relevant drug introduction, Professor Lin He focused on a novel biological agent - abacept. Abacept blocks costimulatory signals, inhibits the activation of T lymphocytes and reduces the inflammatory response in RA patients. Previous studies have shown that abacept has significant therapeutic advantages in ACPA-positive RA patients [12-15]. Combined with the possible important role of ACPA in RA-ILD mentioned above, does abacept have unique efficacy in the stability of RA-ILD patients?
Professor Lin He pointed out that according to the monitoring after marketing Data and safety data in clinical trials, patients with RA have a lower chance of ILD in patients with RA7[16-17], and no lung damage caused by their treatment has been found in clinical practice. Moreover, relevant studies have confirmed that abacept is beneficial to the stability of patients with RA-ILD:
A single-center retrospective study in Japan showed that abacept may have a protective effect on the new occurrence or aggravation of lung diseases (including ILD and obstructive pulmonary diseases) in patients with RA, and is a significant independent protective factor for (risk odds ratio OR: 0.07, 95%CI: 0.01-0.99) [18];
Figure 2: Independent factors related to airway disease or ILD progression
Meta analysis results show that abacept can significantly reduce the ILD worsening rate in RA patients; compared with TNF inhibitors and csDMARDs, the relative risk of ILD worsening in patients treated with abacept was 90% lower than that in patients treated with abacept for 24 months of follow-up.
In a large multicenter observational study, 263 patients with RA-ILD received abacept for treatment for 6-36 months (median follow-up time was 12 months). Nearly 90% of patients with had stable lung function or improved, and 77% of patients had stable or improved radiological performance [20].
A prospective multicenter study showed that the median follow-up time for patients with RA-ILD was 27.3 (IQR) 12.2-42.8) months, 571% of patients with have stable lung function and arthritis, and have good safety. [21].
A retrospective study analysis showed that after RA-ILD patients received abacept treatment for 18 months, 88.6% of patients with ILD had stable or improved ILD. [22].
Professor Lin He believes: "Early standardized and effective treatment can well relieve the condition of RA, or slow down/stop the occurrence and development of lung disease damage. Patients can use this type of beneficial drugs as early as possible in clinical practice to better control RA-ILD. "
Finally, Professor Lin He also gave several suggestions for non-pharmaceutical intervention measures of RA-ILD: First, patients need to maintain good living habits, such as quitting smoking, which can improve lung function; perform respiratory training, exercise respiratory muscles, improve exercise ability through lung rehabilitation, and improve lung function; and for patients with severe lung damage and poor respiratory function, ventilator oxygen therapy can be given and strenuous exercise as much as possible. While following reasonable drug treatment, combined with non-pharmaceutical intervention can achieve twice the result with half the effort.
summary
ILD is a common extra-articular manifestation of RA, causing serious damage to the patient's respiratory system, affecting the quality of life and even threatening his life safety. The etiology of RA-ILD is not clear. Studies have found that ACPA may mediate the occurrence of lung diseases in RA patients and participate in the occurrence and development of ILD. A variety of DMARDs used to treat RA have been reported to increase ILD and infection risks. Abacept treatment not only has a low chance of pulmonary infection, but also has good efficacy in improving and stabilizing RA-ILD. It is a significant protective factor for RA-ILD, providing a new idea for its treatment.
Expert Profile
Linhe Professor
Department of Rheumatology and Immunology, Fujian Provincial Hospital, Chief Physician
Chairman of Fujian Rheumatology Society
Director of Fujian Rheumatology Specialties Alliance
Member of Chinese Medical Association Rheumatology Society
China Executive Director of Rheumatology and Immune Disease Medical Alliance
First member of the National Clinical Medical Research Center for Skin and Immune Diseases
Standing Committee Member of the China Rheumatology and Immune Disease Reproductive and Pregnancy Research Committee
References:
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[2] Spagnolo P, Lee JS, Sverzellati N, et al. The Lung in Rheumatoid Arthritis: Focus on Interstitial Lung Disease[J]. Arthritis Rheumatol, 2018, 70(10):1544-1554.
[3] Manfredi A, Cassone G, Luppi F, et al. Rheumatoid arthritis related interstitial lung disease[J]. Expert Rev Clin Immunol. 2021, 17(5):485-497.
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[6] Nermeen Samy, Haitham Salah, Rasha M. Hammoda, et al. Rheumatoid arthritis patients with interstitial lung disease: Clinical, radiological and laboratory characteristics[J]. The Egyptian Rheumatologist, 2021, 43: 29-34.
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[10] Kadura S, Raghu G. Rheumatoid arthritis-interstitial lung disease: manifestations and current concepts in pathogenesis and management[J]. Eur Respir Rev. 2021, 30(160):210011.
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[12] Gottenberg JE, Courvoisier DS, Hernandez MV, et al. Brief Report:Association of Rheumatoid Factor and Anti-Citrullinated Protein Antibody Positivity With Better Effectiveness of Abatacept: Results From the Pan-European Registry Analysis[J]. Arthritis Rheumatol, 2016, 68(6): 1346-52.
[13] Schiff M, Weinblatt ME, Valente R, et al. Head-to-head comparison of subcutaneous abatacept versus adalimumab for rheumatoid arthritis:two-year efficiency and safety findings from AMPLE trial[J]. Ann Rheum Dis, 2014, 73(1): 86-94.
[14] Fleischmann R, Weinblatt M, Ahmad H, et al. Efficacy of Abatacept and Adalimumab in Patients with Early Rheumatoid Arthritis With Multiple Poor Prognostic Factors:Post Hoc Analysis of a Randomized Controlled Clinical Trial(AMPLE)[J]. Rheumatol Ther, 2019, 6(4): 559-571.
[15] Harrold LR, Litman HJ, Connolly SE, et al. Effect of Anticitrullinated Protein Antibody Status on Response to Abatacept or Antitumor Necrosis Factor-αTherapy in Patients with Rheumatoid Arthritis: A US National Observational Study[J]. J Rheumatol, 2018, 45(1): 32-39.
[16] Harigai M, Ishiguro N, Inokuma S, et al. Postmarketing survey of the safety and effectiveness of abatacept in Japanese patients with rheumatoid arthritis[J]. Mod Rheumatol 2016, 26: 491–8.
[17] Weinblatt ME, Moreland LW, Westhovens R, et al. Safety of abatacept Administered intravenously in treatment of rheumatoid arthritis: integrated analysis of up to 8 years of treatment from the abatacept clinical trial program[J]. J Rheumatol. 2013, 40:787–97.[18] Kurata I,Tsuboi H,Terasaki M,et al. Effect of biological disease-modifying anti-rheumatoid drugs on airway and interstitial lung disease in patients with rheumatoid arthritis[J].Int Med, 2019, 58:1703–12.
[19] Vicente-Rabaneda EF, Atienza-Mateo B, Blanco R, et al. Efficacy and safety of abatacept in interstitial lung disease of rheumatoid arthritis: A systemic literature review[J]. Autoimmun Rev. 2021, 20(6):102830.
[20] Fernández-Díaz C, Castañeda S, Melero-González RB, et al. Abatacept in interstitial lung disease associated with rheumatoid arthritis: national multicenter study of 263 patients[J]. Rheumatology(Oxford), 2020,59(12): 3906-3916.
[21] Mena-Vázquez N, Rojas-Gimenez M, Fuego-Varela C, et al. Safety and Effectiveness of Abatacept in a Prospective Cohort of Patients with Rheumatoid Arthritis-Associated Interstitial Lung Disease. Biomedicines. 2022, 10(7):1480.
[22] Tardella M, Di Carlo M, Carotti M, et al. A retrospective study of the efficiency of JAK inhibitors or abatacept on rheumatoid arthritis-interstitial lung disease[J]. Inflammopharmacology. 2022, 30(3):705-712.
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