scholarly journals Effect of Early Initiation of Combination Therapy of Anti-Inflammatory and Anti-Fibrotic Drugs on Post COVID-19 Interstitial Lung Disease: A Case Report

2021 ◽  
Vol 7 (3) ◽  
Keyword(s):  
Case Report ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Oral Prednisone ◽  
Evidence Based ◽  
Limited Evidence ◽  
Anti Inflammatory ◽  
Short Time

The persistence of lung parenchymal changes Post COVID-19 is increasingly recognized as a vital outcome observed on some patients recovering from SARS-CoV2 infection with limited evidence-based management so far. Here we present a 64-year-old male developed extensive interstitial lung changes post SARS-CoV2 infection and was successfully managed with oral prednisone, pirfenidone, and azithromycin maintenance regimen with significant improvement in his clinical and radiographic parameters noted within a relatively short time. The role of a combined therapeutic approach with anti-inflammatory and anti-fibrotic drugs might be provocative action in patients with COVID-19 related interstitial lung disease, especially those at risk for persistent long-term abnormalities and pulmonary fibrosis development.

scholarly journals Perpetually Positive: Post-COVID Interstitial Lung Disease in an Immunocompromised Patient With Diffuse Large B-cell Lymphoma

2021 ◽  
Vol 9 ◽  
pp. 232470962110412
Author(s):  
John S. Dayco ◽  
Zeinab El-Reda ◽  
Nabeel Sumbal ◽  
Rashid Alhusain ◽  
Shaheena Raheem
Keyword(s):  
Case Report ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Medical Decision ◽  
Large B Cell Lymphoma ◽  
Large B Cell

As more patients recover from COVID-19 infection, long-term complications are beginning to arise. Our case report will explore a debilitating long-term complication, Post-COVID Interstitial Lung Disease (PC-ILD). We will introduce a patient who developed PC-ILD in the setting of diffuse large B-cell lymphoma, outlining a difficult hospital course, including a positive COVID-19 polymerase chain reaction (PCR) for more than 3 months. We will then discuss the human body’s physiological response to the virus and how our patient was not able to adequately mount an immune response. Finally, the pathophysiology of PC-ILD will be explored and correlated with the patient’s subsequent computed tomographic images obtained over a 3-month period. The difficult hospital course and complex medical decision-making outlined in this case report serve as a reminder for health care providers to maintain vigilance in protecting our most vulnerable patient population from such a devastating disease process.

scholarly journals Oxygen therapy in COPD and interstitial lung disease: navigating the knowns and unknowns

2019 ◽  
Vol 5 (3) ◽  
pp. 00118-2019 ◽  
Author(s):  
Yet H. Khor ◽  
Elisabetta A. Renzoni ◽  
Dina Visca ◽  
Christine F. McDonald ◽  
Nicole S. L. Goh
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Oxygen Therapy ◽  
Current Evidence ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Nocturnal Hypoxaemia ◽  
Long Term Oxygen Therapy

Domiciliary oxygen therapy is often prescribed for patients with hypoxaemia due to advanced lung disease, most commonly chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD). Long-term oxygen therapy (LTOT) trials conducted in patients with COPD in the 1980s remain the basis for clinical decisions and guideline recommendations regarding LTOT for patients with non-COPD conditions as there is a lack of high-quality evidence concerning its use in the non-COPD population. There is also a lack of evidence for the use of ambulatory and nocturnal oxygen therapy in patients with isolated exertional and nocturnal hypoxaemia. These deficiencies pose significant challenges in patient care, with consequent discrepancies in guideline recommendations and clinical approaches. In recent years, new studies have been and are currently being conducted to fill the gaps in our understanding and use of domiciliary oxygen therapy for other indications, including ILD. This article provides a comparison of the epidemiology and significance of hypoxaemia in patients with COPD and ILD, with an up-to-date review of current evidence regarding the role of different types of domiciliary oxygen therapy in these conditions.

Is Immune Response Relevant in Interstitial Lung Disease?

2020 ◽  
Vol 16 (1) ◽  
pp. 18-27
Author(s):  
Manzoor M. Khan
Keyword(s):  
Immune Response ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Lung Fibrosis ◽  
Lymphocytic Infiltration ◽  
Therapeutic Strategies ◽  
Mediators Of Inflammation ◽  
Acquired Immune Responses ◽  
Novel Therapeutic Strategies

Interstitial lung disease, a term for a group of disorders, causes lung fibrosis, is mostly refractory to treatments and has a high death rate. After diagnosis the survival is up to 3 years but in some cases the patients live much longer. It involves a heterogenous group of lung diseases that exhibit progressive and irreversible destruction of the lung due to the formation of scars. This results in lung malfunction, disruption of gas exchange, and eventual death because of respiratory failure. The etiology of lung fibrosis is mostly unknown with a few exceptions. The major characteristics of the disease are comprised of injury of epithelial type II cells, increased apoptosis, chronic inflammation, monocytic and lymphocytic infiltration, accumulation of myofibroblasts, and inability to repair damaged tissue properly. These events result in abnormal collagen deposition and scarring. The inflammation process is mild, and the disease is primarily fibrotic driven. Immunosuppressants do not treat the disease but the evidence is evolving that both innate and acquired immune responses a well as the cytokines contribute to at least early progression of the disease. Furthermore, mediators of inflammation including cytokines are involved throughout the process of lung fibrosis. The diverse clinical outcome of the disease is due to different pattern of inflammatory markers. Nonetheless, the development of novel therapeutic strategies requires better understanding of the role of the immune response. This review highlights the role of the immune response in interstitial lung disease and considers the therapeutic strategies based on these observations. For this review several literature data sources were used to assess the role of the immune response in interstitial lung disease and to evaluate the possible therapeutic strategies for the disease.

Acceleration of interstitial lung disease induced by raltitrexed

2019 ◽  
Vol 26 (5) ◽  
pp. 1241-1243 ◽  
Author(s):  
Sarah Howlett ◽  
Raminder Aul ◽  
Mark Hill ◽  
David J Pinato
Keyword(s):  
Case Report ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Thymidylate Synthase ◽  
Colorectal Adenocarcinoma ◽  
Preoperative Staging ◽  
Rapid Progression ◽  
Lung Function Tests ◽  
Clinical Pattern ◽  
Significant Acceleration

Introduction Raltitrexed is a folate analogue, which selectively inhibits thymidylate synthase, used in the treatment of colorectal carcinoma. Common side effects include asthenia and gastrointestinal and haematological toxicities. Case report We present the case of a 74-year-old gentleman with incidental mild interstitial lung disease on preoperative staging CT Chest who developed acute breathlessness whilst undergoing adjuvant raltitrexed treatment for a completely excised colorectal adenocarcinoma. Management and outcome Discontinuation of raltitrexed and a course of steroid therapy resulted in resolution of symptoms, mirrored by an improvement in lung function tests. Discussion The clinical pattern of rapid progression with steroid response highlights the potential for significant acceleration of interstitial lung disease by raltitrexed.

Is the interstitial lung disease induced by trastuzumab? Case report and literature review

2020 ◽  
Vol 45 (5) ◽  
pp. 1183-1186
Author(s):  
Ziqi Ye ◽  
Jie Chen ◽  
Ming Chen ◽  
Jiaying Wu
Keyword(s):  
Case Report ◽  
Interstitial Lung Disease ◽  
Literature Review ◽  
Lung Disease

scholarly journals AB0026 DECREASE OF ANGIOGENIC T CELLS IN CONNECTIVE TISSUE DISEASE-ASSOCIATED INTERSTITIAL LUNG DISEASE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1046.3-1047
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo Martinez ◽  
F. Genre ◽  
B. Atienza-Mateo ◽  
V. M. Mora-Cuesta ◽  
...  
Keyword(s):  
T Cells ◽  
Interstitial Lung Disease ◽  
Connective Tissue ◽  
Lung Disease ◽  
Cell Subset ◽  
Vascular Damage ◽  
Type I ◽  
Research Support ◽  
Angiogenic T Cells

Background:Interstitial lung disease (ILD) is one of the most significant complications of connective tissue diseases (CTD), leading to an increase of the morbidity and mortality in patients with CTD [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, have been involved in the pathogenesis of CTD [2-4]. However, to the best of our knowledge, no information regarding the role of TAng in CTD-ILD+ is available.Objectives:To study, for the first time, the potential role of TAng related to vascular damage in CTD-ILD+.Methods:Peripheral venous blood was collected from 40 patients with CTD-ILD+ and three comparative groups: 44 CTD-ILD- patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 20 healthy controls (HC). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4.Results:Patients with CTD-ILD+ exhibited a significantly lower TAng frequency than CTD-ILD- patients (p<0.001). Similar results were obtained when patients with CTD-ILD+ were compared with HC (p=0.004) although no difference was observed between CTD-ILD+ and IPF. In addition, a significant increase of TAng frequency was shown in patients with CTD-ILD- in relation to IPF patients (p<0.001), while no difference was observed between CTD-ILD- and HC.Conclusion:Our results reveal a decrease of TAng frequency related to vascular damage in CTD-ILD+. Furthermore, we disclose that the presence of ILD is associated with lower TAng frequency.References:[1]Expert Rev Clin Immunol 2018;14(1):69-82.[2]Circulation 2007;116(15):1671-82.[3]Ann Rheum Dis 2015 74(5):921-7.[4]PLoS One 2017;12(8):e0183102.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

scholarly journals SAT0014 ENDOTHELIAL PROGENITOR CELLS: ROLE IN ENDOTHELIAL DAMAGE OF INTERSTITIAL LUNG DISEASE ASSOCIATED TO RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 937.1-937
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo-Martínez ◽  
F. Genre ◽  
V. M. Mora-Cuesta ◽  
D. Iturbe Fernández ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Endothelial Damage ◽  
Research Support ◽  
Endothelial Progenitor

Background:Interstitial lung disease (ILD) is one of the most significant comorbidities of rheumatoid arthritis (RA), increasing the mortality in these patients [1,2]. Although the pathogenesis of ILD associated to RA (RA-ILD+) remains poorly defined [1], it is known that vascular tissue plays a crucial role in lung physiology [3]. In this context, a population of cells termed endothelial progenitor cells (EPC) are involved in vasculogenesis and endothelial tissue repair [4]. Previous reports suggest the implication of EPC in different conditions such as RA and idiopathic pulmonary fibrosis (IPF), the most common and destructive ILD [5,6]. Nevertheless, little is known about their specific role in RA-ILD+.Objectives:The purpose of this study was to shed light on the potential role of EPC in endothelial damage in RA-ILD+.Methods:Peripheral venous blood was collected from a total of 68 individuals (18 with RA-ILD+, 17 with RA-ILD-, 19 with IPF and 14 healthy controls). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by the expression of surface antigens by flow cytometry. The combination of antibodies against the stem cell marker CD34, the immature progenitor marker CD133, the endothelial marker VEGF receptor 2 (CD309) and the common leukocyte antigen CD45 was used. EPC were considered as CD34+, CD45Low, CD309+and CD133+. All statistical analyses were performed using Prism software 5 (GraphPad).Results:EPC frequency was significantly increased in patients with RA-ILD+, RA-ILD-and IPF compared to controls (p=0.001, p=0.002, p< 0.0001, respectively). Nevertheless, patients with RA, both RA-ILD+and RA-ILD-, showed a lower frequency of EPC than those with IPF (p= 0.048, p= 0.006, respectively).Conclusion:Our results provide evidence for a potential role of EPC as a reparative compensatory mechanism related to endothelial damage in RA-ILD+, RA-ILD-and IPF patients. Interestingly, EPC frequency may help to establish a differential diagnostic between patients with IPF and those who have an underlying autoimmune disease (RA-ILD+).References:[1] J Clin Med 2019; 8: 2038;[2] Arthritis Rheumatol 2015; 67: 28-38;[3] Nat Protoc 2015; 10: 1697-1708;[4] Science 1997; 275: 964-966;[5] Rheumatology (Oxford) 2012; 51: 1775-1784;[6] Angiogenesis 2013; 16: 147-157.Acknowledgments:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: PI18/00042 (ISCIII-ERDF); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo-Martínez: None declared, Fernanda Genre: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe Fernández: None declared, Sonia Fernández-Rozas: None declared, Leticia Lera-Gómez: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Belén Atienza-Mateo: None declared, Virginia Portilla: None declared, David Merino: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, Roche, Consultant of: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD, Speakers bureau: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma. MSD, Alfonso Corrales Speakers bureau: Abbvie, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD

scholarly journals SAT0304 TOFACITINIB INHIBITS TGF-Β1-INDUCED ACTIVATED CELL FUNCTIONS OF MYOFIBROBLAST IN HUMAN LUNG FIBROBLAST POPULATIONS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1097.1-1097
Author(s):  
F. Zhu ◽  
X. Zhang
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Lung Diseases ◽  
Human Lung ◽  
Interstitial Lung Diseases ◽  
Migration And Invasion ◽  
Control Group ◽  
Tgf Β1 ◽  
Invasion Assays

Background:Connective tissue disease-associated interstitial lung disease (CTD-ILD) is a class of refractory diseases.Non-specific treatment with hormone and immunosuppressive agents is mostly used at present, but the effect is limited and the long-term survival rate is not improved [1],while anti-fibrosis treatments (such as Pirfenidone and Nintedanib) have only recently been approved, the long-term efficacy is still unknown.Tofacitinib(TOFA), a JAK inhibitor, has recently been used to treat patients with severe dermatomyositis related interstitial pulmonary disease, with significantly improved survival rate [2-4].A basic study showed that TOFA improved interstitial pulmonary disease in mice by promoting the proliferation of myelogenic inhibitory cells [5].However, whether TOFA can affect the migration and invasion of human lung fibroblasts and further research to reveal the mechanism of its inhibition of pulmonary fibrosis has not been reported.Objectives:To investigate the anti - fibrosis effect of TOFA in CTD-ILD.Methods:Cell migration and invasion AssaysHLFs were incubated with TOFA for 72h, followed by TGF- β1 for 24h.DMEM serum-free medium was used to determine the cell density to 5. 0 × 107/L, 600 uL medium containing 10% fetal bovine serum was added to the lower compartment of Transwell chamber, and 200 uL cell suspension was added to the upper compartment.Incubate in incubator for 12 h.After fixation, staining and sealing, the cells were observed and counted under a microscope. At least 5 random field transmembrane cells were counted in each hole, and the mean value was taken.For the invasion assays, Transwell chamber coated with matrigel was used, and the cell incubation time was 16 h.Results:1. Effect of TOFA on HLFs migration function (Figure 1)Figure 1.Effect of TOFA on HLFs migration function(×200).Mean ± SEM. n = 5.The number of cells passing through the biofilm in the three groups was counted.It can be seen that TGF-β1 group significantly increased compared with control group (*P < 0.0001), and TOFA group significantly decreased compared with TGF- β1 group (#P < 0.0001), suggesting that TOFA can significantly inhibit TGF-β1- induced HLFs migration.2. Effect of TOFA on HLFs invasion function (Figure 2)Figure 2.Effect of TOFA on HLFs invasion function(×200).Mean ± SEM. n = 5.The number of cells passing through the matrigel in the three groups was counted.It can be seen that TGF-β1 group was significantly higher than the control group (*P < 0.0001), and TOFA group was significantly lower than TGF-β1 group(#P < 0.001), suggesting that TOFA can significantly inhibit the invasion function of HLFs induced by TGF-β1.Conclusion:TOFA can effectively inhibit the function of HLFs migration and invasion. Although further studies are needed to elucidate the mechanism by which TOFA inhibit the function of HLFs migration and invasion, our study suggests that TOFA has a potential therapeutic effect for CTD-ILD.References:[1]Aparicio, I.J. and J.S. Lee, Connective Tissue Disease-Associated Interstitial Lung Diseases: Unresolved Issues. Semin Respir Crit Care Med, 2016. 37(3): p. 468-76.[2]Kato, M., et al., Successful Treatment for Refractory Interstitial Lung Disease and Pneumomediastinum With Multidisciplinary Therapy Including Tofacitinib in a Patient With Anti-MDA5 Antibody-Positive Dermatomyositis. J Clin Rheumatol, 2019.[3]Kurasawa, K., et al., Tofacitinib for refractory interstitial lung diseases in anti-melanoma differentiation-associated 5 gene antibody-positive dermatomyositis. Rheumatology (Oxford), 2018. 57(12): p. 2114-2119.[4]Chen, Z., X. Wang, and S. Ye, Tofacitinib in Amyopathic Dermatomyositis-Associated Interstitial Lung Disease. N Engl J Med, 2019. 381(3): p. 291-293.[5]Sendo, S., et al., Tofacitinib facilitates the expansion of myeloid-derived suppressor cells and ameliorates interstitial lung disease in SKG mice. Arthritis Res Ther, 2019. 21(1): p. 184Disclosure of Interests:None declared

scholarly journals Management of Myositis-Associated Interstitial Lung Disease

Medicina ◽  
2021 ◽  
Vol 57 (4) ◽  
pp. 347
Author(s):  
Tomoyuki Fujisawa
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Current Knowledge ◽  
Strong Predictor ◽  
Calcineurin Inhibitors ◽  
Pulmonary Involvement ◽  
Trna Synthetase ◽  
Evidence Based Guidelines ◽  
Substantial Heterogeneity

Idiopathic inflammatory myopathies, including polymyositis (PM), dermatomyositis (DM), and clinically amyopathic DM (CADM), are a diverse group of autoimmune diseases characterized by muscular involvement and extramuscular manifestations. Interstitial lung disease (ILD) has major pulmonary involvement and is associated with increased mortality in PM/DM/CADM. The management of PM-/DM-/CADM-associated ILD (PM/DM/CADM-ILD) requires careful evaluation of the disease severity and clinical subtype, including the ILD forms (acute/subacute or chronic), because of the substantial heterogeneity of their clinical courses. Recent studies have highlighted the importance of myositis-specific autoantibodies’ status, especially anti-melanoma differentiation-associated gene 5 (MDA5) and anti-aminoacyl tRNA synthetase (ARS) antibodies, in order to evaluate the clinical phenotypes and treatment of choice for PM/DM/CADM-ILD. Because the presence of the anti-MDA5 antibody is a strong predictor of a worse prognosis, combination treatment with glucocorticoids (GCs) and calcineurin inhibitors (CNIs; tacrolimus (TAC) or cyclosporin A (CsA)) is recommended for patients with anti-MDA5 antibody-positive DM/CADM-ILD. Rapidly progressive DM/CADM-ILD with the anti-MDA5 antibody is the most intractable condition, which requires immediate combined immunosuppressive therapy with GCs, CNIs, and intravenous cyclophosphamide. Additional salvage therapies (rituximab, tofacitinib, and plasma exchange) should be considered for patients with refractory ILD. Patients with anti-ARS antibody-positive ILD respond better to GC treatment, but with frequent recurrence; thus, GCs plus immunosuppressants (TAC, CsA, azathioprine, and mycophenolate mofetil) are often needed in order to achieve favorable long-term disease control. PM/DM/CADM-ILD management is still a therapeutic challenge for clinicians, as evidence-based guidelines do not exist to help with management decisions. A few prospective clinical trials have been recently reported regarding the treatment of PM/DM/CADM-ILD. Here, the current knowledge on the pharmacologic managements of PM/DM/CADM-ILD was mainly reviewed.

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