Lung Diseases in Inflammatory Myopathies

2019 ◽  
Vol 40 (02) ◽  
pp. 255-270 ◽  
Author(s):  
Thomas Barba ◽  
Sabine Mainbourg ◽  
Mouhamad Nasser ◽  
Jean-Christophe Lega ◽  
Vincent Cottin
Keyword(s):  
Lung Disease ◽  
Opportunistic Infections ◽  
Inflammatory Myopathy ◽  
Trna Synthetase ◽  
Pulmonary Complications ◽  
Lung Involvement ◽  
High Resolution Computed Tomography ◽  
Drug Induced ◽  
Ventilatory Failure ◽  
Nonspecific Interstitial Pneumonia

AbstractLung involvement is the leading cause of mortality in inflammatory myopathy. A careful assessment of clinical and serologic manifestations especially myositis-associated autoantibodies allows precise classification of the different phenotypes of inflammatory myopathy and stratification of the risk of lung involvement. About three out of four patients with inflammatory myopathy develop interstitial lung disease (ILD), which represents the main cause of morbidity and mortality. In patients with a confirmed diagnosis of inflammatory myopathy, the approach to the diagnosis of ILD includes assessment of clinical and functional severity, evaluation of the high-resolution computed tomography pattern of disease, which often suggests nonspecific interstitial pneumonia or organizing pneumonia. Bronchoalveolar lavage to rule out infection is often performed; however, video-assisted thoracoscopic lung biopsy is now generally discouraged, unless malignancy is suspected. The so-called antisynthetase syndrome characterized by the combination of mechanics' hands, Raynaud' phenomenon, myositis often mild or absent, and presence of one of the anti-tRNA synthetase antibodies is associated with a 70% risk of ILD, especially in subjects with antibodies other than anti-Jo1 antibodies (i.e., anti-PL7 or -PL12 antibodies). Treatment depends on both severity and progression of ILD, often including a combination of corticosteroids and immunosuppressive therapy. Rituximab-based regimen has showed promising results in retrospective studies for the management of refractory or rapidly progressive forms of ILD. Clinical trials are ongoing to evaluate the actual efficacy of this strategy on mortality related to lung disease. Secondary pulmonary complications of inflammatory myopathy include opportunistic infections, aspiration pneumonia, pneumomediastinum, ventilatory failure due to diaphragmatic muscular weakness, drug-induced pneumonitis, and rarely pulmonary hypertension.

scholarly journals Pulmonary Pathologic Manifestations of Anti-Alanyl-tRNA Synthetase (Anti–PL-12)–Related Inflammatory Myopathy

2017 ◽  
Vol 142 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Frank Schneider ◽  
Samuel A. Yousem ◽  
Chester V. Oddis ◽  
Rohit Aggarwal
Keyword(s):  
Lung Disease ◽  
Interstitial Pneumonia ◽  
Inflammatory Myopathy ◽  
Idiopathic Inflammatory Myopathy ◽  
Trna Synthetase ◽  
Raynaud Phenomenon ◽  
Nonspecific Interstitial Pneumonia ◽  
Lung Biopsies ◽  
Lymphoid Aggregates ◽  
Mechanic’S Hands

Context.— Patients with anti–aminoacyl-tRNA synthetase syndrome (ARS), a subset of idiopathic inflammatory myopathy, have a high prevalence of lung involvement. Autoantibodies directed against alanyl-tRNA synthetase (anti–PL-12 Abs) represent 1 of the 8 autoantibodies currently described under the rubric of ARS. Objective.— To describe the clinical, radiographic, and pulmonary histopathologic findings in patients possessing anti–PL-12 autoantibodies. Design.— Patients with anti–PL-12 ARS were identified in the University of Pittsburgh Idiopathic Inflammatory Myopathy registry. Lung biopsies from 10 patients and lung explants from 2 patients with anti–PL-12 ARS were reviewed, together with chest computed tomography and clinical records. Results.— Patients primarily presented with dyspnea and variable combinations of cough, fever, mechanic's hands, Raynaud phenomenon, and skin and muscle involvement. Chest computed tomography most commonly showed lower lung zone-predominant reticular infiltrates and traction bronchiectasis, with or without honeycomb change. Surgical lung biopsies and pneumonectomies for lung transplantation revealed usual interstitial pneumonia in 8 of 12 cases (67%), nonspecific interstitial pneumonia in 2 of 12 cases (17%), and organizing pneumonia in 2 of 12 cases (17%). Lymphoplasmacytic interstitial inflammation with lymphoid aggregates was common. Conclusions.— Lung disease is often the first manifestation of anti–PL-12 ARS. There are no pathognomonic histopathologic features to distinguish anti–PL-12 ARS-related lung disease from idiopathic variants of diffuse interstitial lung disease. Increased inflammation, lymphoid aggregates, and nonspecific interstitial pneumonia–like areas in a biopsy, as well as clinical features of mechanic's hands, Raynaud phenomenon, arthritis, and fever, should prompt pathologists to suggest involvement by ARS.

scholarly journals Nonspecific interstitial pneumonia: A rare adverse reaction of atorvastatin

2018 ◽  
Vol 5 (4) ◽  
pp. 16
Author(s):  
Jack Xu ◽  
Steven Verga ◽  
Jonathan Stoll ◽  
Lauren Pioppo ◽  
Eileen Shanahan ◽  
...  
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Statin Therapy ◽  
Interstitial Pneumonia ◽  
Case Series ◽  
Pulmonary Complications ◽  
Drug Induced ◽  
Cardiovascular Morbidity And Mortality ◽  
Nonspecific Interstitial Pneumonia ◽  
Coa Reductase

Introduction: Statins have been shown to effectively prevent both cardiovascular morbidity and mortality by inhibiting the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase enzyme. Pulmonary complications are very rare, and can include pneumonitis, pleural effusion, and nonspecific interstitial pneumonia (NSIP). There have been very few previously documented cases of statin-induced fibrotic NSIP.Case report: We present a female with a history of hyperlipidemia on atorvastatin who presented with shortness of breath. Computed tomography scan of the chest revealed interstitial infiltrates with bilateral ground-glass opacities. She underwent a surgical lung biopsy which showed uniform fibrous alveolar septal thickening, scattered collections of alveolar macrophages and inflammation, along with areas of fibrosis. The findings were most suggestive of fibrotic NSIP. Atorvastatin was stopped and she was started on mycophenolic acid with improvement of her symptoms.Discussion: Although rare, the clinician should be aware of possible pulmonary complications of statin therapy. The exact mechanism of injury is unclear, however immunological or toxicological mechanisms are implicated. One case series of statin induced interstitial lung disease showed some improvement of dyspnea with systemic glucocorticoids and termination of statin therapy. Statins, specifically pravastatin, lovastatin, and simvastatin have been associated with drug induced pneumonitis and interstitial lung disease.

scholarly journals FRI0056 LUNG COMPROMISE SCREENING IN PATIENTS WITH EARLY RA. A MULTICENTRIC CROSS SECTIONAL STUDY

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 604.1-604
Author(s):  
F. Benavidez ◽  
G. Rodriguez ◽  
A. Riopedre ◽  
D. Mata ◽  
A. Benitez ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Physical Examination ◽  
Lung Disease ◽  
Lung Involvement ◽  
High Resolution Computed Tomography ◽  
Cross Sectional ◽  
Multicentric Study ◽  
Link Type ◽  
Immunological Tests ◽  
Pulmonary Manifestations

Background:Rheumatoid arthritis (RA) affects 0.4-1.3% of general population (1). It can affect lungs in different ways, with interstitial lung disease (ILD) as the most severe. Clinically evident ILD has been reported in 10-42% of patients, with a great impact in prognosis (2).Objectives:Toidentify the prevalence of lung involvement in early rheumatoid arthritis patients (ERA) without previous known lung disease and describe the association between high resolution computed tomography (HRCT), lung functional tests (LFT) and clinical findings.Methods:Cross sectional multicentric study. We included ERA patients (1 year or less since diagnose) consecutively. Patients with previous RA related lung disease or biologic/targeted synthetic Dmard treatment were excluded. HRCT, immunological tests (rheumatoid factor, anti-CCP, ANA), LFT and clinical evaluation were performed.Results:We included 74 patients, 63 (85,1%) woman, mean (SD) of 47 (17,7) years. Thirty-seven patients (50%) were current or former smokers. Abnormal findings in HRCT were found in 62 patients (88,6%): ILD in 6 (8,6%), airway involvement in 40 (70%) and emphysema in 7 (10%). Ten patients (13,5%) had abnormal auscultation (2 sibilances, 2 roncus, and 6 crackles). Six patients (8,1%) had digital clubbing. Regarding immunological tests, 54/61 (88,5%) patients were positive for Anti CCP, and 53/61 (86,9%) were positive for FR. We compared features of patients with findings related to RA in HRCT (interstitial and/or airway) with those without them. We found no differences in the mean (SD) of DAS-28 [4,74 (1,38) vs 4,32 (1,39); p= 0,27]. The prevalence of anti- CCP was not higher in patients with abnormal HRCT [38/44 (86,3%) vs 16/17 (94,1%); p=0,39]. Patients with abnormal HRCT were older [median (IQR) 50,5 years (44,5-59,5) vs 43 years (32-51); p=0,008) and showed higher VSG values [mean (SD) 39,09 (24,03) vs 27,38 (17,6); p= 0,043]. Abnormal physical examination or dyspnea (class 2 mMRC or higher) was significantly associated with HRCT abnormalities [26 (50%) vs 3 (13,6%); p=0.003) and the presence of ILD on HRCT was significantly associated with crackles on the auscultation [4/68(6,25%) vs 2/6 (33,33%); p 0,023].Conclusion:This study shows a high prevalence of lung involvement in ERA patients of less 1 year from diagnosis. Also, we showed a significant association between HRCT and physical examination findings. This data highlights the importance of the clinical examination in Rheumatoid Arthritis patients. More studies with bigger samples and longitudinal follow up are needed to confirm and complete our results.References:[1]Rooney BK, Silman AJ. Epidemiology of the rheumatic diseases. Curr Opin Rheumatol [Internet]. 1999 Mar [cited 2016 Jul 19];11(2):91–7. Available from:http://www.ncbi.nlm.nih.gov/pubmed/10319210.[2]Antin-Ozerkis D, Evans J, Rubinowitz A, Homer RJ, Matthay RA. Pulmonary Manifestations of Rheumatoid Arthritis. Clin Chest Med [Internet]. 2010;31(3):451–78. Available from:http://dx.doi.org/10.1016/j.ccm.2010.04.003.Disclosure of Interests:None declared

Prognosis of adult idiopathic inflammatory myopathy-associated interstitial lung disease: a retrospective study of 679 adult cases

Rheumatology ◽  
2020 ◽  
Author(s):  
Shan Li ◽  
Yuxin Sun ◽  
Chi Shao ◽  
Hui Huang ◽  
Qian Wang ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Retrospective Study ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Inflammatory Myopathy ◽  
Idiopathic Inflammatory Myopathy ◽  
Mortality Rates ◽  
Trna Synthetase ◽  
Significant Difference ◽  
All Cause Mortality

Abstract Objectives Few studies have investigated the prognostic factors for idiopathic inflammatory myopathy-associated interstitial lung disease (IIM-ILD) across different clinical/serological phenotypes. Methods We conducted a retrospective analysis of patients diagnosed with IIM between January 2012 and December 2017. Results Of the 760 IIM cases registered, 679 adult cases were included in this study. ILD was present in 508 cases, and the presence of ILD in the clinically amyopathic DM, DM and PM groups was 92.7, 73.6 and 55.1%, respectively (P < 0.01). The prevalence of ILD in the anti-synthetase antibody (ASA)+-IIM group was higher than that in ASA–-IIM group (95.2 vs 72.4%, P < 0.01); no such difference was found between the anti-histidyl-tRNA synthetase (Jo-1)+-IIM and Jo-1–ASA+-IIM groups (93.0 vs 98.5%, P > 0.05). The prevalence of ILD in the melanoma differentiation-associated protein-5 (MDA-5)+-IIM group was higher than that in MDA-5–-IIM group (97.8 vs 72.1%, P < 0.01). Among adults with IIM, men with concurrent ILD, who were older than 50 years, were most likely to die. No significant difference was found in the all-cause mortality rates between DM-ILD and clinically amyopathic DM-ILD groups (33.3 vs 23%, P > 0.05), although both were higher than that in PM group (13.2%, P = 0.01 and P < 0.05, respectively). No difference was found in the all-cause mortality rates between MDA5–ASA–-IM-ILD and MDA5–ASA+-IM-ILD groups (17.2 vs 12.8%, P > 0.05), and both were lower than that in MDA5+ASA–-IM-ILD group (33.7%, P < 0.05). Conclusion The prevalence of ILD in IIM and the prognosis of IIM-ILD patients may vary depending on the statuses of the ASA and MDA-5 antibodies.

SAT0288 CHARACTERIZATION OF ANTI-AMINOACYL TRNA SYNTHETASE AUTOANTIBODIES IN PATIENTS WITH IDIOPATHIC INFLAMMATORY MYOPATHIES

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1088.1-1089
Author(s):  
C. Preger ◽  
A. Notarnicola ◽  
C. Hellström ◽  
E. Wigren ◽  
C. Cerqueira ◽  
...  
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Inflammatory Myopathy ◽  
Clinical Manifestations ◽  
Trna Synthetase ◽  
University Hospital ◽  
Idiopathic Inflammatory Myopathies ◽  
Inflammatory Myopathies ◽  
Research Support ◽  
Mortality And Morbidity

Background:Idiopathic inflammatory myopathies (IIM) are rare chronic inflammatory diseases associated with high mortality and morbidity [1]. One sub-group of IIM, anti-synthetase syndrome (ASS), is characterized by the presence of autoantibodies that target aminoacyl transfer(t) RNA synthetases (aaRS), together with specific clinical manifestations such as myositis, interstitial lung disease (ILD), arthritis, mechanic’s hand, Raynaud’s syndrome and fever [2]. The most common anti-aaRS autoantibody, anti-Jo1 targeting histidyl tRNA synthetase (HisRS), is present in up to 20-30% of patients with IIM, and up to 90% of patients with myositis and ILD [3, 4]. Besides Jo1, there are today seven other identified autoantigens within the aaRS family.Objectives:A large part of patients with IIM, including individuals with clinical manifestations indicating ASS, test seronegative to all known myositis specific autoantibodies. However, these patients could potentially harbor autoantibodies against targets not tested for in clinic. In this study, we aimed at extending the detection of autoantibodies by including all cytoplasmic aaRS in the analysis of patients with IIM. We hypothesized the existence of new potential autoantigens within this protein family.Methods:The presence of anti-aaRS autoantibodies was determined using a multiplex suspension bead array assay on 242 IIM patients from the Karolinska University Hospital myositis cohort. A panel of 186 recombinant constructs, representing 57 proteins that included full-length or partial sequence overlaps between constructs of all cytoplasmic aaRS as well as other myositis related proteins, were coupled to magnetic color-coded beads and each plasma sample was tested against the complete antigen panel.Results:By the use of this multiplex method we identified patients with autoantibodies against many of the tested aaRS. Autoantibodies binding to HisRS have previously been shown to bind with higher reactivity to the WHEP domain of HisRS and this was also confirmed in this study. We confirmed reactivity against three of the other aaRS tested for in the clinic (PL-12, PL-7, and EJ). In addition, we identified patients positive for anti-Zo, -KS and -HA, autoantibodies usually not screened for in routine. Finally, our data indicates that there are autoantibodies binding to other aaRS than the previously known eight autoantigens, which will be presented.Conclusion:In this study, we could detect autoantibodies in plasma from patients with IIM, both against the most common aaRS autoantigens, but also against other aaRS that are usually not tested for in clinic. We conclude that it is important to continue the studies of anti-aaRS autoantibodies, and their correlation to clinical manifestations, and in the long run also include more aaRS autoantigens in clinical practice.References:[1]Dobloug, G.C., et al., Mortality in idiopathic inflammatory myopathy: results from a Swedish nationwide population-based cohort study. Ann Rheum Dis, 2018. 77(1): p. 40-47.[2]Barsotti, S. and I.E. Lundberg, Myositis an evolving spectrum of disease. Immunol Med, 2018. 41(2): p. 46-54.[3]Vencovsky, J., H. Alexanderson, and I.E. Lundberg, Idiopathic Inflammatory Myopathies. Rheum Dis Clin North Am, 2019. 45(4): p. 569-581.[4]Richards, T.J., et al., Characterization and peripheral blood biomarker assessment of anti-Jo-1 antibody-positive interstitial lung disease. Arthritis Rheum, 2009. 60(7): p. 2183-92.Disclosure of Interests:Charlotta Preger: None declared, Antonella Notarnicola: None declared, Cecilia Hellström: None declared, Edvard Wigren: None declared, Catia Cerqueira: None declared, Peter Nilsson: None declared, Ingrid E. Lundberg Grant/research support from: Bristol Meyer Squibb, Corbus Pharmaceuticals, Inc and Astra Zeneca, Helena Persson: None declared, Susanne Gräslund: None declared, Per-Johan Jakobsson Shareholder of: Gesynta Pharma, Grant/research support from: Gesynta Pharma, AstraZeneca,

High-resolution computed tomography of drug-induced lung disease

1992 ◽  
Vol 46 (4) ◽  
pp. 232-236 ◽  
Author(s):  
S.P.G. Padley ◽  
B. Adler ◽  
D.M. Hansell ◽  
N.L. Müller
Keyword(s):  
Computed Tomography ◽  
High Resolution ◽  
Lung Disease ◽  
High Resolution Computed Tomography ◽  
Drug Induced

Pulmonary pathologic manifestations of anti-glycyl-tRNA synthetase (anti-EJ)-related inflammatory myopathy

2014 ◽  
Vol 67 (8) ◽  
pp. 678-683 ◽  
Author(s):  
Frank Schneider ◽  
Samuel A Yousem ◽  
David Bi ◽  
Kevin F Gibson ◽  
Chester V Oddis ◽  
...  
Keyword(s):  
Lung Disease ◽  
Immunosuppressive Therapy ◽  
Diffuse Alveolar Damage ◽  
Inflammatory Myopathy ◽  
Usual Interstitial Pneumonia ◽  
Trna Synthetase ◽  
Raynaud Phenomenon ◽  
University Of Pittsburgh ◽  
Lung Biopsies ◽  
Mechanic’S Hands

AimsAntisynthetase syndromes are a subset of the idiopathic inflammatory myopathies characterised by the presence of autoantibodies to aminoacyl transfer-RNA synthetases (ARS) and monotypic clinical features including Raynaud phenomenon, fever, non-erosive inflammatory arthritis and hyperkeratotic skin changes (‘mechanic's hands’). Interstitial lung disease (ILD) is particularly common in ARS syndromes, affecting up to 90% of patients.MethodsFour patients with ARS syndrome who possessed anti-glycyl-tRNA synthetase (anti-EJ) autoantibodies were retrieved from the University of Pittsburgh database. We report their clinical, radiographic and histopathologic findings.ResultsPatients presented with dyspnoea accompanied by Raynaud phenomenon and ‘mechanic's hands’. Lung disease was the first manifestation in all four patients (100%) who were all amyopathic. High-resolution CT of the chest showed patchy opacities and consolidations in two patients (50%) whose surgical lung biopsies revealed organising diffuse alveolar damage (DAD), and lower lung zone predominant reticular infiltrates and traction bronchiectasis without honeycomb change in two patients (50%) whose surgical lung biopsies revealed usual interstitial pneumonia (UIP). Mild lymphoplasmacytic inflammation and few scattered lymphoid aggregates were present, but we found no pathognomonic histopathologic features of anti-EJ ARS syndrome. Serologic testing revealed no other autoantibodies. All patients responded to immunosuppressive therapy.ConclusionsIdentifying ARS-associated autoantibodies in ILD patients with or without myopathy is desirable because patients may respond well to immunosuppressive therapy, and their prognosis is better than that of patients with idiopathic forms of DAD or UIP.

scholarly journals Clinical profile of unclassifiable interstitial lung disease: Comparison with chronic fibrosing idiopathic interstitial pneumonias

2017 ◽  
Vol 46 (1) ◽  
pp. 448-456 ◽  
Author(s):  
Daniel Traila ◽  
Cristian Oancea ◽  
Emanuela Tudorache ◽  
Ovidiu Fira Mladinescu ◽  
Bogdan Timar ◽  
...  
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Clinical Features ◽  
Clinical Profile ◽  
Diffusing Capacity ◽  
High Resolution Computed Tomography ◽  
Risk Of Mortality ◽  
Point Increase ◽  
Nonspecific Interstitial Pneumonia ◽  
Lower Carbon

Objective Unclassifiable interstitial lung disease (ILD) is a common problem in clinical practice. These patients pose a distinct challenge with regard to appropriate evaluation and management. We investigated the clinical features and prognosis of unclassifiable ILD and compared its clinical profile with that of idiopathic pulmonary fibrosis (IPF) and idiopathic nonspecific interstitial pneumonia (NSIP). Methods Patients with IPF (n = 40), NSIP (n = 14), and unclassifiable ILD (n = 27) were selected from an ongoing database. Baseline clinical features, pulmonary function, and the extent of fibrosis on high-resolution computed tomography (HRCT) were evaluated. Mortality was estimated based on the ILD–Gender, Age, Physiology (ILD-GAP) index and composite physiologic index (CPI). Results IPF was associated with the worst survival (hazard ratio [HR] = 4.361 compared with NSIP), followed by unclassifiable cases (HR = 1.251 compared with NSIP). Increasing mortality was significantly impacted by age (HR = 1.04 per 1-year increase), lower carbon monoxide diffusing capacity of the lung (HR = 0.97), HRCT interstitial score (HR = 1.119 per 1-point increase), ILD-GAP score (HR = 1.570 per 1-point increase), and CPI (HR = 1.039 per 1-point increase). Conclusions Patients with unclassifiable ILD had an intermediate prognosis between that of IPF and NSIP. Patients at high risk of mortality can be identified using baseline clinical, physiological, and radiological features.

scholarly journals Clinical features of anti-synthetase syndrome associated interstitial lung disease: a retrospective cohort in China

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xi Zhan ◽  
Wei Yan ◽  
Ying Wang ◽  
Qing Li ◽  
Xuhua Shi ◽  
...  
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Clinical Features ◽  
Retrospective Cohort ◽  
Positive Response ◽  
Inflammatory Myopathy ◽  
Trna Synthetase ◽  
Response To Therapy ◽  
The Other

Abstract Background Anti-synthetase syndrome (ASSD) is a chronic autoimmune condition characterized by antibodies directed against an aminoacycl transfer RNA synthetase (ARS) along with a group of clinical features including the classical clinical triad: inflammatory myopathy, arthritis, and interstitial lung disease (ILD). ASSD is highly heterogenous due to different organ involvement, and ILD is the main cause of mortality and function loss, which presents as different patterns when diagnosed. We designed this retrospective cohort to describe the clinical features and disease behaviour of ASSD associated ILD. Methods Data of 108 cases of ASSD associated ILD were retrospectively collected in Beijing Chaoyang Hospital from December 2017 to March 2019. Data were obtained from the Electronic Medical Record system. Patients were divided into 5 groups according to distinct aminoacyl tRNA synthetase (ARS) antibodies. Results Overall, 108 consecutive patients were recruited. 33 were JO-1 positive, 30 were PL-7 positive, 23 were EJ positive, 13 were PL-12 positive and 9 were OJ positive. The JO-1 (+) group had a significant higher rate of mechanic’s hand (57.6%) than other 4 groups. Polymyositis/dermatomyositis (PM/DM) was diagnosed in 25 (23.1%) patients and no difference was observed among the 5 groups. The PL-7 (+) group had a higher frequency of UIP pattern (13.3%) than the other 4 groups but the difference was not significant, and the EJ (+) group had the most frequent OP pattern (78.2%), which was significantly higher than the PL-7 (+) (P < 0.001) and PL-12 (+) groups (P = 0.025). The median follow-up time was 10.7 months, during which no patients died. All received prednisone treatment, with or without immunosuppressants. At the 6-month follow-up, 96.3% of all patients (104/108) had a positive response to therapy, the JO-1 (+) and EJ (+) groups had a significantly higher improvement of forced vital capacity than the other 3 groups (P < 0.05), and the PL-7 group had the lowest FVC improvement (P < 0.05). The JO-1 (+) group and EJ (+) group had significantly higher anti-Ro-52 positive occurrence than the other 3 groups (P < 0.05). Conclusion Anti PL-7 antibody had the same frequency as anti-JO-1 in ASSD-ILD, in which the ILD pattern was different with distinct anti-ARS antibodies. Most ASSD-ILD had a positive response to steroid therapies, with or without immunosuppressants. The PL-7 (+) group had the highest occurrence of UIP pattern, and a significantly lower response to therapy.

scholarly journals Drug induced lung disease - amiodarone in focus

2014 ◽  
Vol 67 (9-10) ◽  
pp. 334-337 ◽  
Author(s):  
Nada Vasic ◽  
Branislava Milenkovic ◽  
Dragica Pesut ◽  
Ruza Stevic ◽  
Dragana Jovanovic
Keyword(s):  
Lung Disease ◽  
Pulmonary Toxicity ◽  
Illicit Drugs ◽  
Clinical Laboratory ◽  
Vascular System ◽  
Clinical Findings ◽  
Rapid Improvement ◽  
High Resolution Computed Tomography ◽  
Drug Induced ◽  
Computed Tomography Scanning

More than 380 medications are known to cause pulmonary toxicity. Selected drugs that are important causes of pulmonary toxicity fall into the following classes: cytotoxic, cardiovascular, anti-inflammatory, antimicrobial, illicit drugs, miscellaneous. The adverse reactions can involve the pulmonary parenchyma, pleura, the airways, pulmonary vascular system, and mediastinum. Drug-induced lung diseases have no pathognomonic clinical, laboratory, physical, radiographic or histological findings. A drug-induced lung disease is usually considered a diagnosis of exclusion of other diseases. The diagnosis of drug-mediated pulmonary toxicity is usually made based on clinical findings. In general, laboratory analyses do not help in establishing the diagnosis. High-resolution computed tomography scanning is more sensitive than chest radiography for defining radiographic abnormalities. The treatment of drug-induced lung disease consists of immediate discontinuation of the offending drug and appropriate management of the pulmonary symptoms. Glucocorticoids have been associated with rapid improvement in gas exchange and reversal of radiographic abnormalities. Before starting any medication, patients should be educated about the potential adverse effects of the drug. Amiodarone is an antiarrhythmic agent used in the treatment of many types of tachyarrhythmia. Amiodarone-caused pulmonary toxicity is a well-known side effect (complication) of this medication. The incidence of amiodarone-induced lung disease is approximately 5-7%.

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