Journal articles: 'Antifibrotics'

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Niitsu, Takayuki, Kiyoharu Fukushima, Sho Komukai, So Takata, Yuko Abe, Takuro Nii, Tomoki Kuge, et al. "Real-world impact of antifibrotics on prognosis in patients with progressive fibrosing interstitial lung disease." RMD Open 9, no. 1 (January 2023): e002667. http://dx.doi.org/10.1136/rmdopen-2022-002667.

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ObjectiveNo studies have demonstrated the real-world efficacy of antifibrotics for progressive fibrosing interstitial lung disease (PF-ILD). Therefore, we evaluated the efficacy of antifibrotics in patients with PF-ILD.MethodsWe retrospectively reviewed the medical records of patients with ILD from January 2012 to July 2021. Patients were diagnosed with PF-ILD if they had ≥10% fibrosis on high-resolution CT (HRCT) and a relative forced vital capacity (FVC) decline of either ≥10% or >5% to <10% with clinical deterioration or progression of fibrosis on HRCT during overlapping windows of 2 years and with a %FVC of ≥45%. We compared FVC changes and overall survival (OS) between patients with and without antifibrotics. FVC changes were analysed using generalised estimating equations. We used inverse probability weighting (IPW) and statistical matching to adjust for covariates.ResultsOf the 574 patients, 167 were diagnosed with PF-ILD (idiopathic pulmonary fibrosis (IPF), n=64; non-IPF, n=103). Antifibrotics improved the FVC decline in both IPF (p=0.002) and non-IPF (p=0.05) (IPW: IPF, p=0.015; non-IPF, p=0.031). Among patients with IPF, OS was longer in the antifibrotic group (log-rank p=0.001). However, among patients with non-IPF, OS was not longer in the antifibrotic group (p=0.3263) (IPW and statistical matching: IPF, p=0.0534 and p=0.0018; non-IPF, p=0.5663 and p=0.5618).ConclusionThis is the first real-world study to show that antifibrotics improve the FVC decline in PF-ILD. However, among patients with non-IPF, we found no significant difference in mortality between those with and without antifibrotics. Future studies must clarify whether antifibrotics improve the prognosis of non-IPF.

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Bos, Saskia, Laurens J. De Sadeleer, Arno Vanstapel, Hanne Beeckmans, Annelore Sacreas, Jonas Yserbyt, Wim A. Wuyts, and Robin Vos. "Antifibrotic drugs in lung transplantation and chronic lung allograft dysfunction: a review." European Respiratory Review 30, no. 160 (June 1, 2021): 210050. http://dx.doi.org/10.1183/16000617.0050-2021.

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This review aims to provide an overview of pre-transplant antifibrotic therapy on peri-transplant outcomes and to address the possible role of antifibrotics in lung transplant recipients with chronic lung allograft dysfunction.Lung transplantation is an established treatment modality for patients with various end-stage lung diseases, of which idiopathic pulmonary fibrosis and other progressive fibrosing interstitial lung diseases are growing indications. Theoretically, widespread use of antifibrotics prior to lung transplantation may increase the risk of bronchial anastomotic complications and impaired wound healing.Long-term graft and patient survival are still hampered by development of chronic lung allograft dysfunction, on which antifibrotics may have a beneficial impact.Antifibrotics until the moment of lung transplantation proved to be safe, without increasing peri-transplant complications. Currently, best practice is to continue antifibrotics until time of transplantation. In a large multicentre randomised trial, pirfenidone did not appear to have a beneficial effect on lung function decline in established bronchiolitis obliterans syndrome. The results of antifibrotic therapy in restrictive allograft syndrome are eagerly awaited, but nonrandomised data from small case reports/series are promising.

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Soskis, Alyssa, and Robert Hallowell. "Antifibrotic Therapy: Is There a Role in Myositis-Interstitial Lung Disease?" Respiration 100, no. 9 (2021): 923–32. http://dx.doi.org/10.1159/000515607.

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Interstitial lung disease (ILD) is a cause of substantial morbidity and mortality amongst autoimmune diseases, including myositis. Despite first-line therapy with immunosuppression, many inflammatory ILDs advance to a fibrotic stage. In such patients, progressive fibrosis may be amenable to treatment with antifibrotic medications, which were initially studied and approved for the treatment of idiopathic pulmonary fibrosis. We here review the available data that support the use of antifibrotics in connective tissue diseases and progressive fibrosing ILDs. There is now a growing body of evidence in both large randomized clinical trials and on the evolving pathophysiologic pathways to support the use of antifibrotics in select patients with autoimmune ILD and a fibrotic phenotype. Further study of antifibrotics in combination with immunosuppressive medications, and in the myositis-ILD population, is needed.

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Jegal, Yangjin, Jong Sun Park, Song Yee Kim, Hongseok Yoo, Sung Hwan Jeong, Jin Woo Song, Jae Ha Lee, et al. "Clinical Features, Diagnosis, Management, and Outcomes of Idiopathic Pulmonary Fibrosis in Korea: Analysis of the Korea IPF Cohort (KICO) Registry." Tuberculosis and Respiratory Diseases 85, no. 2 (April 1, 2022): 185–94. http://dx.doi.org/10.4046/trd.2021.0123.

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Background: The Korea Interstitial Lung Disease Study Group has made a new nationwide idiopathic pulmonary fibrosis (IPF) registry because the routine clinical practice has changed due to new guidelines and newly developed antifibrotic agents in the recent decade. The aim of this study was to describe recent clinical characteristics of Korean IPF patients.Methods: Both newly diagnosed and following IPF patients diagnosed after the previous registry in 2008 were enrolled. Survival analysis was only conducted for patients diagnosed with IPF after 2016 because antifibrotic agents started to be covered by medical insurance of Korea in October 2015.Results: A total of 2,139 patients were analyzed. Their mean age at diagnosis was 67.4±9.3 years. Of these patients, 76.1% were males, 71.0% were ever-smokers, 14.4% were asymptomatic at the time of diagnosis, and 56.9% were at gender-agephysiology stage I. Occupational toxic material exposure was reported in 534 patients. The mean forced vital capacity was 74.6% and the diffusing capacity for carbon monoxide was 63.6%. Treatment with pirfenidone was increased over time: 62.4% of IPF patients were treated with pirfenidone initially. And 79.2% of patients were treated with antifiboritics for more than three months during the course of the disease since 2016. Old age, acute exacerbation, treatment without antifibrotics, and exposure to wood and stone dust were associated with higher mortality.Conclusion: In the recent Korean IPF registry, the percentage of IPF patients treated with antifibrotics was increased compared to that in the previous IPF registry. Old age, acute exacerbation, treatment without antifibrotics, and exposure to wood and stone dust were associated with higher mortality.

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Caliskan, Canay, Benjamin Seeliger, Benedikt Jäger, Jan Fuge, Tobias Welte, Oliver Terwolbeck, Julia Freise, Coline H. M. van Moorsel, Yingze Zhang, and Antje Prasse. "Genetic Variation in CCL18 Gene Influences CCL18 Expression and Correlates with Survival in Idiopathic Pulmonary Fibrosis—Part B." Journal of Clinical Medicine 9, no. 6 (June 25, 2020): 1993. http://dx.doi.org/10.3390/jcm9061993.

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Idiopathic pulmonary fibrosis (IPF) is a progressive disease with high mortality. CC-chemokine ligand 18 (CCL18) is predictive of survival in IPF. We described correlation of CCL18 serum levels with the genotype of rs2015086 C > T polymorphism the CCL18-gene, which was associated with survival in a pre-antifibrotic cohort (Part-A). Herein (Part-B), we aimed to validate these findings and to study the effects of antifibrotics. Two cohorts were prospectively recruited, cohort-A (n = 61, pre-antifibrotic) and cohort B (n = 101, received antifibrotics). Baseline CCL18 serum level measurement by enzyme-linked immunosorbent assay (ELISA, serially in cohort B) and genotyping of rs2015086 was performed and correlated with clinical outcomes. The CT genotype was present in 15% and 31% of patients. These patients had higher CCL18 levels compared to the TT-genotype (cohort-A: 234 vs. 115.8 ng/mL, p < 0.001; cohort B: 159.5 vs. 120 ng/mL, p = 0.0001). During antifibrotic therapy, CCL18 increased (p = 0.0036) regardless of rs2015086-genotype and antifibrotic-agent. In cohort-A, baseline CCL18-cutoff (>120 ng/mL) and CT-genotype were associated with mortality (p = 0.041 and p = 0.0051). In cohort-B, the CCL18-cutoff (>140 ng/mL) was associated with mortality (p = 0.003) and progression (p = 0.004), but not the CT/CC-genotype. In conclusion, we validated the correlation between rs2015086-genotype and CCL18 serum levels, which was predictive of (progression-free)-survival in two prospective validation cohorts.

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Dhar, Raja. "Antifibrotics in India." Lung India 36, no. 5 (2019): 445. http://dx.doi.org/10.4103/lungindia.lungindia_379_19.

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Albera, Carlo, Giulia Verri, Federico Sciarrone, Elena Sitia, Mauro Mangiapia, and Paolo Solidoro. "Progressive Fibrosing Interstitial Lung Diseases: A Current Perspective." Biomedicines 9, no. 9 (September 16, 2021): 1237. http://dx.doi.org/10.3390/biomedicines9091237.

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Interstitial lung diseases (ILDs) are a large and diverse group of rare and chronic respiratory disorders, with idiopathic pulmonary fibrosis (IPF) being the most common and best-studied member. Increasing interest in fibrosis as a therapeutic target and the appreciation that fibrotic mechanisms may be a treatable target of IPF prompted the development and subsequent approval of the antifibrotics, pirfenidone and nintedanib. The management of ILDs has changed considerably following an understanding that IPF and some ILDs share similar disease behavior of progressive fibrosis, termed “progressive fibrosing phenotype”. Indeed, antifibrotic treatment has shown to be beneficial in ILDs characterized by the progressive fibrosing phenotype. This narrative review summarizes current knowledge in the field of progressive fibrosing ILDs. Here, we discuss the clinical characteristics and pathogenesis of lung fibrosis and highlight relevant literature concerning the mechanisms underlying progressive fibrosing ILDs. We also summarize current diagnostic approaches and the available treatments of progressive fibrosing ILDs and address the optimization of treating progressive fibrosing ILDs with antifibrotics in clinical practice.

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Boleto, Gonçalo, Jérôme Avouac, and Yannick Allanore. "The role of antifibrotic therapies in the treatment of systemic sclerosis–associated interstitial lung disease." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2110666. http://dx.doi.org/10.1177/1759720x211066686.

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Systemic sclerosis (SSc) is a rare autoimmune condition with complex pathogenesis characterized by a heterogeneous presentation and different disease courses. Fibrosis of multiple organs including the lungs favored by inflammation and vasculopathy is the hallmark of SSc. SSc-associated interstitial lung disease (SSc-ILD) is common and can be associated with poor outcomes, this complication being the leading cause of death in recent series. Because of its huge heterogeneity, SSc-ILD management can be very challenging. Immunosuppressive therapy has long been used to prevent SSc-ILD progression with modest effects in clinical trials. However, thanks to a better understating of SSc pathogenesis, innovative therapies including antifibrotics are increasingly being developed. The achievement of the Safety and Efficacy of Nintedanib in Systemic SClerosIS (SENSCIS) trial has led to the approval by drug agencies of the first antifibrotic drug for SSc-ILD. In parallel, other antifibrotics are being investigated as possible beneficial therapies in SSc-ILD. An important unmet need remains to clarify the positioning of the various strategies, such as the added value of combination of immunosuppressants and antifibrotic therapies in patients at high risk of progression. Indeed, irreversible lung injury or self-perpetuated progression highlights the concept of a window of opportunity in SSc-ILD patients. Herewith, we provide an overview of the most significant clinical trials with antifibrotic drugs developed in recent years for the management of SSc-ILD and a viewpoint about their positioning in treatment algorithms.

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Cohen-Naftaly, Michal, and Scott L. Friedman. "Current status of novel antifibrotic therapies in patients with chronic liver disease." Therapeutic Advances in Gastroenterology 4, no. 6 (July 22, 2011): 391–417. http://dx.doi.org/10.1177/1756283x11413002.

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Fibrosis accumulation is a dynamic process resulting from a wound-healing response to acute or chronic liver injury of all causes. The cascade starts with hepatocyte necrosis and apoptosis, which instigate inflammatory signaling by chemokines and cytokines, recruitment of immune cell populations, and activation of fibrogenic cells, culminating in the deposition of extracellular matrix. These key elements, along with pathways of transcriptional and epigenetic regulation, represent fertile therapeutic targets. New therapies include drugs specifically designed as antifibrotics, as well as drugs already available with well-established safety profiles, whose mechanism of action may also be antifibrotic. At the same time, the development of noninvasive fibrogenic markers, and techniques (e.g. fibroscan), as well as combined scoring systems incorporating serum and clinical features will allow improved assessment of therapy response. In aggregate, the advances in the elucidation of the biology of fibrosis, combined with improved technologies for assessment will provide a comprehensive framework for design of antifibrotics and their analysis in well-designed clinical trials. These efforts may ultimately yield success in halting the progression of, or reversing, liver fibrosis.

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Tzilas, Vasilios, Argyris Tzouvelekis, Evangelos Bouros, Theodoros Karampitsakos, Maria Ntassiou, Eleni Avdoula, Athena Trachalaki, Katerina Antoniou, Ganesh Raghu, and Demosthenes Bouros. "Clinical experience with antifibrotics in fibrotic hypersensitivity pneumonitis: a 3-year real-life observational study." ERJ Open Research 6, no. 4 (October 2020): 00152–2020. http://dx.doi.org/10.1183/23120541.00152-2020.

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BackgroundFibrotic hypersensitivity pneumonitis (f-HP) can exhibit a progressive course similar to idiopathic pulmonary fibrosis (IPF). The lack of diagnostic guidelines and randomised controlled trials in this population represent a significant unmet need.ObjectivesTo describe our clinical experience with antifibrotics in patients with f-HP.Material and methodsRetrospective study of 30 patients diagnosed with f-HP upon re-evaluation within a multidisciplinary team discussion of 295 consecutive patients (January 2012 to December 2017) who had been diagnosed initially with IPF at outside facilities and were referred to our centres.ResultsPirfenidone was initially administered to 14 (46.7%) patients and nintedanib to 16 (53.3%) patients. There were 26 (86.7%) males, with mean±sd age 70.2±8.4 years. The annual rate of decline in forced vital capacity (FVC) % predicted over the 3-year treatment period adjusted for baseline FVC % pred measurement was 4.2% (95% CI 1.9–6.6%, p=0.001) and 7.5% (95% CI 3.3–11.7%; p=0.001) in imputation analysis. The annual rate of decline in diffusing capacity of the lung for carbon monoxide (DLCO) % predicted throughout the 3-year treatment period adjusted for baseline DLCO % pred was 5.7% (95% CI 3.1–8.4%, p<0.001) and 5.8% (95% CI 3.4–8.1%, p<0.001) in imputation analysis. The nature of adverse events was related to the type of antifibrotic agent administered.ConclusionIn patients with f-HP receiving antifibrotics there is a statistically significant annual decline in FVC % pred and DLCO % pred over a period of 3 years. Prospective randomised trials exceeding 1 year are warranted to determine the long-term efficacy of antifibrotics.

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Majewski, Sebastian, Maria Królikowska, Ulrich Costabel, Wojciech J. Piotrowski, and Marek Ochman. "Double Lung Transplantation for Idiopathic Pulmonary Fibrosis in a Patient with a History of Liver Transplantation and Prolonged Journey for Disease-Specific Antifibrotic Therapy." Case Reports in Pulmonology 2022 (August 13, 2022): 1–5. http://dx.doi.org/10.1155/2022/4054339.

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Idiopathic pulmonary fibrosis (IPF) is characterized by uncontrolled progressive lung fibrosis with a median survival of 3 to 5 years. Although currently available pharmacotherapy cannot cure the disease, antifibrotics including pirfenidone and nintedanib were shown to slow disease progression and improve survival in IPF. Nevertheless, there is a knowledge gap on the safety of antifibrotics in patients after liver transplantation receiving concomitant immunosuppressive therapy. This case report of a 68-year-old male patient with IPF illustrates how a complex medical history has led to diagnostic and therapeutic challenges considerably affecting clinical decisions and impacting the patient’s journey. The increasing severity of lung function impairment due to the progressive natural history of IPF ultimately led to severe respiratory failure. Double lung transplantation (LTx) was performed as the only therapeutic option in end-stage disease with the potential to improve quality of life and survival. To the best of our knowledge, this is the first case report describing the feasibility and safety of antifibrotic therapy with pirfenidone for IPF in a 68-year-old patient with a history of liver transplantation receiving concomitant immunosuppressive therapy with tacrolimus who underwent successful double lung transplantation when alternative medical interventions had been exhausted.

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Pockros, Paul J. "Antifibrotics for Chronic Hepatitis C." Clinics in Liver Disease 13, no. 3 (August 2009): 365–73. http://dx.doi.org/10.1016/j.cld.2009.05.005.

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Wright, William Alexander, Louise E. Crowley, Dhruv Parekh, Anjali Crawshaw, Davinder P. Dosanjh, Peter Nightingale, and David R. Thickett. "Real-world retrospective observational study exploring the effectiveness and safety of antifibrotics in idiopathic pulmonary fibrosis." BMJ Open Respiratory Research 8, no. 1 (March 2021): e000782. http://dx.doi.org/10.1136/bmjresp-2020-000782.

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BackgroundPirfenidone and nintedanib are the only disease-modifying treatments available for idiopathic pulmonary fibrosis (IPF). Our aim was to test their effectiveness and safety in clinical practice.MethodsThis is a single-centre retrospective observational study undertaken at a specialised interstitial lung disease centre in England. Data including progression-free survival (PFS), mortality and drug tolerability were compared between patients with IPF on antifibrotic therapies and an untreated control group who had a forced vital capacity percentage (FVC %) predicted within the licensed antifibrotic treatment range.Results104 patients received antifibrotic therapies and 64 control patients were identified. PFS at 6 months was significantly greater in the antifibrotic group (75.0%) compared with the control group (56.3%) (p=0.012). PFS was not significant at 12 or 18 months when comparing the antifibrotic group with the control group. The 12-month post-treatment mean decline in FVC % predicted (−4.6±6.2%) was significantly less than the 12-month pretreatment decline (−10.4±11.8%) (p=0.039). The 12-month mortality rate was not significantly different between the antifibrotic group (25.3%) and the control group (35.5%) (p=0.132). Baseline Body Mass Index of≤25, baseline diffusion capacity for carbon monoxide percentage predicted of ≤35 and antifibrotic discontinuation within 3 months were independent predictors of 12-month mortality. Antifibrotic discontinuation was significantly higher by 3 and 6 months for patients on pirfenidone than those on nintedanib (p=0.006 and p=0.044, respectively). Discontinuation at 12 months was not significantly different (p=0.381).ConclusionsThis real-world study revealed that antifibrotics are having promising effects on PFS, lung function and mortality. These findings may favour commencement of nintedanib as first-line antifibrotic therapy, given the lower rates of early treatment discontinuation, although further studies are required to investigate this.

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Iftikhar, Imran H. "Antifibrotics and All-Cause Mortality Rates." Chest 161, no. 5 (May 2022): e330-e331. http://dx.doi.org/10.1016/j.chest.2021.12.660.

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Fallowfield, Jonathan A. "Therapeutic targets in liver fibrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 5 (May 2011): G709—G715. http://dx.doi.org/10.1152/ajpgi.00451.2010.

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Detailed analysis of the cellular and molecular mechanisms that mediate liver fibrosis has provided a framework for therapeutic approaches to prevent, slow down, or even reverse fibrosis and cirrhosis. A pivotal event in the development of liver fibrosis is the activation of quiescent hepatic stellate cells (HSCs) to scar-forming myofibroblast-like cells. Consequently, HSCs and the factors that regulate HSC activation, proliferation, and function represent important antifibrotic targets. Drugs currently licensed in the US and Europe for other indications target HSC-related components of the fibrotic cascade. Their deployment in the near future looks likely. Ultimately, treatment strategies for liver fibrosis may vary on an individual basis according to etiology, risk of fibrosis progression, and the prevailing pathogenic milieu, meaning that a multiagent approach could be required. The field continues to develop rapidly and starts to identify exciting potential targets in proof-of-concept preclinical studies. Despite this, no antifibrotics are currently licensed for use in humans. With epidemiological predictions for the future prevalence of viral, obesity-related, and alcohol-related cirrhosis painting an increasingly gloomy picture, and a shortfall in donors for liver transplantation, the clinical urgency for new therapies is high. There is growing interest from stakeholders keen to exploit the market potential for antifibrotics. However, the design of future trials for agents in the developmental pipeline will depend on strategies that enable equal patient stratification, techniques to reliably monitor changes in fibrosis over time, and the definition of clinically meaningful end points.

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Taweesedt, Pahnwat, Ploypin Lertjitbanjong, Dararat Eksombatchai, Prangthip Charoenpong, Teng Moua, Charat Thongprayoon, Supawit Tangpanithandee, and Tananchai Petnak. "Impact of Antifibrotic Treatment on Postoperative Complications in Patients with Interstitial Lung Diseases Undergoing Lung Transplantation: A Systematic Review and Meta-Analysis." Journal of Clinical Medicine 12, no. 2 (January 13, 2023): 655. http://dx.doi.org/10.3390/jcm12020655.

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Antifibrotic treatment has been approved for reducing disease progression in fibrotic interstitial lung disease (ILD). As a result of increased bleeding risk, some experts suggest cessation of antifibrotics prior to lung transplantation (LT). However, extensive knowledge regarding the impact of antifibrotic treatment on postoperative complications remains unclear. We performed a comprehensive search of several databases from their inception through to 30 September 2021. Original studies were included in the final analysis if they compared postoperative complications, including surgical wound dehiscence, anastomosis complication, bleeding complications, and primary graft dysfunction, between those with and without antifibrotic treatment undergoing LT. Of 563 retrieved studies, 6 studies were included in the final analysis. A total of 543 ILD patients completing LT were included, with 161 patients continuing antifibrotic treatment up to the time of LT and 382 without prior treatment. Antifibrotic treatment was not significantly associated with surgical wound dehiscence (RR 1.05; 95% CI, 0.31–3.60; I2 = 0%), anastomotic complications (RR 0.88; 95% CI, 0.37–2.12; I2 = 31%), bleeding complications (RR 0.76; 95% CI, 0.33–1.76; I2 = 0%), or primary graft dysfunction (RR 0.87; 95% CI, 0.59–1.29; I2 = 0%). Finally, continuing antifibrotic treatment prior to LT was not significantly associated with decreased 1-year mortality (RR 0.80; 95% CI, 0.41–1.58; I2 = 0%). Our study suggests a similar risk of postoperative complications in ILD patients undergoing LT who received antifibrotic treatment compared to those not on antifibrotic therapy.

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LaCamera, Peter P., Susan L. Limb, Tmirah Haselkorn, Elizabeth A. Morgenthien, John L. Stauffer, and Mark L. Wencel. "Physician characteristics associated with treatment initiation patterns in idiopathic pulmonary fibrosis." Chronic Respiratory Disease 16 (January 1, 2019): 147997311987967. http://dx.doi.org/10.1177/1479973119879678.

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Pirfenidone and nintedanib are oral antifibrotic agents approved for the treatment of idiopathic pulmonary fibrosis (IPF). Real-world data on factors that influence IPF treatment decisions are limited. Physician characteristics associated with antifibrotic therapy initiation following an IPF diagnosis were examined in a sample of US pulmonologists. An online, self-administered survey was fielded to pulmonologists between April 10, 2017, and May 17, 2017. Pulmonologists were included if they spent >20% of their time in direct patient care and had ≥5 patients with IPF receiving antifibrotics. Participants answered questions regarding timing and reasons for considering the initiation of antifibrotic therapy after an IPF diagnosis. A total of 169 pulmonologists participated. The majority (81.7%) considered initiating antifibrotic therapy immediately after IPF diagnosis all or most of the time (immediate group), while 18.3% considered it only some of the time or not at all (delayed group). Pulmonologists in the immediate group were more likely to work in private practice (26.1%), have a greater mean percentage of patients receiving antifibrotic therapy (60.8%), and decide to initiate treatment themselves (31.2%) versus those in the delayed group (16.1%, 30.5%, and 16.1%, respectively). Most pulmonologists consider initiating antifibrotic treatment immediately after establishing an IPF diagnosis all or most of the time versus using a “watch-and-wait” approach. Distinguishing characteristics between pulmonologists in the immediate group versus the delayed group included practice setting, percentage of patients receiving antifibrotic therapy, and the decision-making dynamics between the patient and the pulmonologist.

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Guler, Sabina A., and Manuela Funke-Chambour. "Antifibrotics: Shrinking the Box of Therapeutic Uncertainty." Respiration 97, no. 3 (November 19, 2018): 202–4. http://dx.doi.org/10.1159/000494275.

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Lama, Paul J., and Robert D. Fechtner. "Antifibrotics and Wound Healing in Glaucoma Surgery." Survey of Ophthalmology 48, no. 3 (May 2003): 314–46. http://dx.doi.org/10.1016/s0039-6257(03)00038-9.

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Cheng, Shih-Lung, Chau-Chyun Sheu, Chih-Feng Chian, Jeng-Yuan Hsu, Kuo-Chin Kao, Liang-Wen Hang, Ching-Hsiung Lin, Wen-Feng Fang, Hao-Chien Wang, and Diahn-Warng Perng. "NICEFIT—A Prospective, Non-Interventional, and Multicentric Study for the Management of Idiopathic Pulmonary Fibrosis with Antifibrotic Therapy in Taiwan." Biomedicines 10, no. 10 (September 22, 2022): 2362. http://dx.doi.org/10.3390/biomedicines10102362.

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Idiopathic pulmonary fibrosis (IPF) causes progressive lung fibrosis with subsequent fatality and has limited treatment options. NICEFIT is the first Taiwan-based prospective, observational, and non-interventional registry for IPF progression under routine clinical practice in Taiwan. Data on 101 patients (aged 74.6 ± 9.1 years and 83.2% men) with IPF were collected over 2 years (2018−2020) from medical centers in Taiwan at baseline, 1 month, and subsequent 3-month intervals. Treated patients (n = 88) received the antifibrotics nintedanib or pirfenidone, compared with the untreated group (n = 13). The 2-year assessment revealed overall preserved lung functionality in the treated patients, with insignificant changes from baseline for percent predicted forced vital capacity or FVC (±1.7%). The presence of respiratory comorbidities significantly increased the risk of both AE and death (with or without AE) over the full study duration. Furthermore, the decline of predicted FVC significantly increased with the risk of acute exacerbations (AE) in the second year. Overall, antifibrotic medication was beneficial in stalling IPF progression, reducing AEs, and delaying mortality in the treated cohort, despite their lower baseline lung functions. Further, no new safety concerns over antifibrotic treatments were observed for the Taiwanese population.

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Iommi, Marica, Andrea Faragalli, Martina Bonifazi, Federico Mei, Lara Letizia Latini, Marco Pompili, Flavia Carle, and Rosaria Gesuita. "Prognosis and Survival in Idiopathic Pulmonary Fibrosis in the Era of Antifibrotic Therapy in Italy: Evidence from a Longitudinal Population Study Based on Healthcare Utilization Databases." International Journal of Environmental Research and Public Health 19, no. 24 (December 12, 2022): 16689. http://dx.doi.org/10.3390/ijerph192416689.

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The aim was to evaluate the determinants of acute exacerbation (AE) and death in new cases of idiopathic pulmonary fibrosis (IPF) using administrative databases in the Marche Region. Adults at their first prescription of antifibrotics or hospitalization with a diagnosis of IPF occurring in 2014–2019 were considered as new cases. Multiple Cox regression was used to estimate the risk of AE and of all-cause mortality adjusted by demographic and clinical characteristics, stratifying patients according to antifibrotic treatment. Overall, 676 new cases of IPF were identified and 276 deaths and 248 AE events occurred. In never-treated patients, the risk of AE was higher in patients with poor health conditions at diagnosis; the risk of death was higher in males, in patients aged ≥75 and in those with poor health conditions at baseline. The increasing number of AEs increased the risk of death in treated and never-treated patients. Within the limits of an observational study based on secondary data, the combined use of healthcare administrative databases allows the accurate analysis of progression and survival of IPF from the beginning of the antifibrotic therapy era, suggesting that timely and early diagnosis is critical to prescribing the most suitable treatment to increase survival and maintain a healthy life expectancy.

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Iswandana, Raditya, Bao Tung Pham, Su Suriguga, Theerut Luangmonkong, Louise A. van Wijk, Yvette J. M. Jansen, Dorenda Oosterhuis, Henricus Antonius Maria Mutsaers, and Peter Olinga. "Murine Precision-cut Intestinal Slices as a Potential Screening Tool for Antifibrotic Drugs." Inflammatory Bowel Diseases 26, no. 5 (January 14, 2020): 678–86. http://dx.doi.org/10.1093/ibd/izz329.

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Abstract Background Intestinal fibrosis is a hallmark of Crohn’s disease. Here, we investigated the impact of several putative antifibrotic compounds on the expression of fibrosis markers using murine precision-cut intestinal slices. Methods Murine precision-cut intestinal slices were cultured for 48 hours in the presence of profibrotic and/or antifibrotic compounds. The fibrotic process was studied on gene and protein level using procollagen 1a1 (Col1α1), heat shock protein 47 (Hsp47), fibronectin (Fn2), and plasminogen activator inhibitor-1 (Pai-1). The effects of potential antifibrotic drugs mainly inhibiting the transforming growth factor β (TGF-β) pathway (eg, valproic acid, tetrandrine, pirfenidone, SB203580, and LY2109761) and compounds mainly acting on the platelet-derived growth factor (PDGF) pathway (eg, imatinib, sorafenib, and sunitinib) were assessed in the model at nontoxic concentrations. Results Murine precision-cut intestinal slices remained viable for 48 hours, and an increased expression of fibrosis markers was observed during culture, including Hsp47, Fn2, and Pai-1. Furthermore, TGF-β1 stimulated fibrogenesis, whereas PDGF did not have an effect. Regarding the tested antifibrotics, pirfenidone, LY2109761, and sunitinib had the most pronounced impact on the expression of fibrosis markers, both in the absence and presence of profibrotic factors, as illustrated by reduced levels of Col1α1, Hsp47, Fn2, and Pai-1 after treatment. Moreover, sunitinib significantly reduced Hsp47 and Fn2 protein expression and the excretion of procollagen 1. Conclusions Precision-cut intestinal slices can successfully be used as a potential preclinical screening tool for antifibrotic drugs. We demonstrated that sunitinib reduced the expression of several fibrosis markers, warranting further evaluation of this compound for the treatment of intestinal fibrosis.

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Albrecht, Katinka, Anja Strangfeld, Ursula Marschall, and Johanna Callhoff. "Interstitial lung disease in rheumatoid arthritis: incidence, prevalence and related drug prescriptions between 2007 and 2020." RMD Open 9, no. 1 (January 2023): e002777. http://dx.doi.org/10.1136/rmdopen-2022-002777.

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ObjectiveTo investigate prevalence, incidence and medication of interstitial lung disease (ILD) among German individuals with rheumatoid arthritis (RA).MethodsNationwide BARMER claims data from 2007 to 2020 were used. RA-ILD was identified by diagnosis codes, prescription of disease-modifying antirheumatic drugs (DMARDs) and lung diagnostics. ILD was assigned as incident or prevalent relative to the year of the first diagnosis. We identified prescriptions of glucocorticoids, conventional synthetic (cs), biological (b) and targeted synthetic (ts)DMARDs, antifibrotics and rheumatology and/or pulmonology care.ResultsAmong all persons with RA (40 686 in 2007 to 85 175 in 2020), 1.7%–2.2%/year had ILD with a slight decline since 2013. Incident ILD was 0.13%–0.21% per year and remained stable over time. ILD was more common in seropositive RA, in men and in the elderly (mean age 72 years in 2020). Glucocorticoids (84% to 68%), csDMARD (83% to 55%) and non-steroidal anti-inflammatory drug use (62% to 38%) declined, while bDMARDs (16% to 24%) rose. In 2020, 7% received tsDMARDs, 3% antifibrotics, 44% analgesics and 30% opioids. DMARD therapy was more common if a rheumatologist was involved and antifibrotics if a pulmonologist was involved. Opioid use was highest if no specialist was involved (39%) but also common in rheumatology care (32%) and less frequent in pulmonology care (21%).ConclusionsRA-ILD is rare and mainly affects elderly persons. No trend in incidence was observed but treatment strategies have enlarged. Specialist care is necessary to provide disease-specific therapies. The continuing high analgesic and opioid demand shows unmet needs in these patients.

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Mishra, Mayank, and Girish Sindhwani. "Antifibrotics for COVID-19 related lung fibrosis: Agents with benefits?" Advances in Respiratory Medicine 89, no. 2 (April 30, 2021): 231–33. http://dx.doi.org/10.5603/arm.a2021.0023.

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Ramachandran, Prakash, and Neil C. Henderson. "Antifibrotics in chronic liver disease: tractable targets and translational challenges." Lancet Gastroenterology & Hepatology 1, no. 4 (December 2016): 328–40. http://dx.doi.org/10.1016/s2468-1253(16)30110-8.

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Antoniou, Katerina M., Athina Trachalaki, Argyris Tzouvelekis, Venerino Poletti, Eirini Vasarmidi, Petros Sfikakis, and Demosthenes Bouros. "A role of antifibrotics in the treatment of Scleroderma-ILD?" Pulmonology 26, no. 1 (January 2020): 1–2. http://dx.doi.org/10.1016/j.pulmoe.2019.08.004.

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Wilfong, Erin M., and Rohit Aggarwal. "Role of antifibrotics in the management of idiopathic inflammatory myopathy associated interstitial lung disease." Therapeutic Advances in Musculoskeletal Disease 13 (January 2021): 1759720X2110609. http://dx.doi.org/10.1177/1759720x211060907.

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The antifibrotic therapies nintedanib and pirfenidone were first approved by the United States for the treatment of idiopathic pulmonary fibrosis in 2014. In 2020, nintedanib received U.S. Food and Drug Administration (FDA) approval for the treatment of all progressive fibrosing interstitial lung disease (ILD). Given that a major cause of mortality and morbidity in the idiopathic inflammatory myopathies (IIM) is progressive interstitial lung disease and respiratory failure, antifibrotic therapies may be useful as adjuvant to traditional immunosuppression. However, randomized controlled trials of antifibrotic therapies in IIM are lacking. The purpose of this review is to (1) summarize the mechanism of action of nintedanib and pirfenidone in ILD with possible role in IIM-ILD, (2) review the clinical data supporting their use in interstitial lung disease in general, and more specifically in connective tissue disease associated ILD, and (3) discuss the evidence and remaining challenges for using antifibrotic therapies in IIM-ILD.

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Rockey, Don C. "New Therapies in Hepatitis C Virus and Chronic Liver Disease: Antifibrotics." Clinics in Liver Disease 10, no. 4 (November 2006): 881–900. http://dx.doi.org/10.1016/j.cld.2006.08.019.

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Bansal, Meena B., and Naichaya Chamroonkul. "Antifibrotics in liver disease: are we getting closer to clinical use?" Hepatology International 13, no. 1 (October 9, 2018): 25–39. http://dx.doi.org/10.1007/s12072-018-9897-3.

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Torrisi, Sebastiano Emanuele, Mauro Pavone, Ada Vancheri, and Carlo Vancheri. "When to start and when to stop antifibrotic therapies." European Respiratory Review 26, no. 145 (September 30, 2017): 170053. http://dx.doi.org/10.1183/16000617.0053-2017.

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Idiopathic pulmonary fibrosis (IPF) is characterised by progressive changes of the lung architecture causing cough and dyspnoea and ultimately leading to lung failure and death. Today, for the first time, two drugs that may reduce the inexorable progression of the disease are available, suggesting that treatment with specific drugs for IPF should be started as soon as diagnosis is made. This applies to any disease and particularly to IPF, which is marked by a 5-year survival comparable or even worse than many cancers. However, despite common sense and even worse, in spite of scientific data coming from clinical trials, post hoc analysis, long-term safety studies and real-life experiences, the question of when to start and when to stop treatment with antifibrotics is still debated. In IPF, particularly when the disease is diagnosed at an early stage, “wait and watch” behaviour is not rare to observe. This is largely due to the lack of awareness of both patients and clinicians regarding the progression of the disease and its prognosis. Another important issue is when treatment should be stopped. In general, there are two main reasons to stop a therapy: unbearable side-effects and/or lack of efficacy. According to current (although preliminary) evidence, antifibrotic drugs should not be discontinued except for safety issues.

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Bansal, Ruchi, Beata Nagórniewicz, and Jai Prakash. "Clinical Advancements in the Targeted Therapies against Liver Fibrosis." Mediators of Inflammation 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/7629724.

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Hepatic fibrosis, characterized by excessive accumulation of extracellular matrix (ECM) proteins leading to liver dysfunction, is a growing cause of mortality worldwide. Hepatocellular damage owing to liver injury leads to the release of profibrotic factors from infiltrating inflammatory cells that results in the activation of hepatic stellate cells (HSCs). Upon activation, HSCs undergo characteristic morphological and functional changes and are transformed into proliferative and contractile ECM-producing myofibroblasts. Over recent years, a number of therapeutic strategies have been developed to inhibit hepatocyte apoptosis, inflammatory responses, and HSCs proliferation and activation. Preclinical studies have yielded numerous targets for the development of antifibrotic therapies, some of which have entered clinical trials and showed improved therapeutic efficacy and desirable safety profiles. Furthermore, advancements have been made in the development of noninvasive markers and techniques for the accurate disease assessment and therapy responses. Here, we focus on the clinical developments attained in the field of targeted antifibrotics for the treatment of liver fibrosis, for example, small molecule drugs, antibodies, and targeted drug conjugate. We further briefly highlight different noninvasive diagnostic technologies and will provide an overview about different therapeutic targets, clinical trials, endpoints, and translational efforts that have been made to halt or reverse the progression of liver fibrosis.

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Liang, Minrui, Eric L. Matteson, Andy Abril, and Jörg H. W. Distler. "The role of antifibrotics in the treatment of rheumatoid arthritis–associated interstitial lung disease." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2210744. http://dx.doi.org/10.1177/1759720x221074457.

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The major pulmonary complication of rheumatoid arthritis (RA) is interstitial lung disease (ILD), which causes significant morbidity and mortality and influences the natural course of disease. Recent advances in the management of arthritis have improved patient outcomes. However, exceptionally high medical needs still remain for effective therapies for the patients with ILD in RA. Better understanding of the shared and distinct pathophysiology of fibrotic diseases led to the development of novel antifibrotic agents such as nintedanib and pirfenidone. The further stratification analysis of the phase III INBUILD trial demonstrated beneficial effects of nintedanib in RA-ILD with a progressive phenotype by reducing the rate of decline in forced vital capacity (FVC) over 52 weeks by 60%. Pirfenidone is another antifibrotic agent currently under phase II clinical study (TRAIL1) aiming to evaluate its effects for RA-ILD. This review provides an overview of state-of-the-art pathogenesis and the current therapeutic options for RA-ILD, with a focus on antifibrotic strategies.

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Rohner, Nathan A., Dung Nguyen, and Horst A. von Recum. "Affinity Effects on the Release of Non-Conventional Antifibrotics from Polymer Depots." Pharmaceutics 12, no. 3 (March 17, 2020): 275. http://dx.doi.org/10.3390/pharmaceutics12030275.

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For many chronic fibrotic conditions, there is a need for local, sustained antifibrotic drug delivery. A recent trend in the pharmaceutical industry is the repurposing of approved drugs. This paper investigates drugs that are classically used for anthelmintic activity (pyrvinium pamoate (PYR)), inhibition of adrenal steroidgenesis (metyrapone (MTP)), bactericidal effect (rifampicin (RIF), and treating iron/aluminum toxicity (deferoxamine mesylate (DFOA)), but are also under investigation for their potential positive effect in wound healing. In this role, they have not previously been tested in a localized delivery system suitable for obtaining the release for the weeks-to-months timecourse needed for wound resolution. Herein, two cyclodextrin-based polymer systems, disks and microparticles, are demonstrated to provide the long-term release of all four tested non-conventional wound-healing drugs for up to 30 days. Higher drug affinity binding, as determined from PyRx binding simulations and surface plasmon resonance in vitro, corresponded with extended release amounts, while drug molecular weight and solubility correlated with the improved drug loading efficiency of cyclodextrin polymers. These results, combined, demonstrate that leveraging affinity interactions, in combination with drug choice, can extend the sustained release of drugs with an alternative, complimentary action to resolve wound-healing and reduce fibrotic processes.

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Ali, Mohamed, Ashley M. Egan, Gaja F. Shaughnessy, Harika Dasari, Virginia P. Van Keulen, Marie Christine Aubry, Andrew H. Limper, Tobias Peikert, and Eva M. Carmona. "Antifibrotics Modify B-cell Induced Fibroblast Migration and Activation in IPF Patients." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 234.18. http://dx.doi.org/10.4049/jimmunol.204.supp.234.18.

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Abstract Background Acute respiratory exacerbations in idiopathic pulmonary fibrosis (IPF), often triggered by infection, are life threatening events characterized by rapid deterioration of lung function and associated with poor prognosis. Since microbial antigens modulate immunity by activating different pattern recognition receptors (PRR) expressed by innate immune cells (including B-cells), we sought to investigate how the activation of human B-cells through PRR stimulation by different microbial (CpG and β-glucan) and non-microbial (Mitochondrial DAMPs; MTDs) antigens resulted in the release of an inflammatory/fibrotic milieu that contributed to the pathogenesis of fibrosis in patients with IPF. Results Our results show that an inflammatory milieu is induced by stimulating circulating B-cells with both noninfectious (MTDs) and infectious antigens (CpG and β-glucan) commonly found in bacteria and fungi. Moreover, we show that the inflammatory milieu produced was specific to the inducing antigen, and that the microbial antigens (CpG and β-glucan) triggered distinct signaling pathways in B-cells. Specifically, CpG induced mTOR-activation while β-glucan was mTOR-independent and activated Src and p38. Furthermore, our results also show that B-cell aggregates are present within fibrotic areas of the lung in IPF patients and activated B-cells induce fibroblast migration, which was modified by antifibrotics (nintedanib and pirfenidone). Conclusion Our results highlight the potential contribution of activated B-cells through PRRs to the proinflammatory and profibrotic milieu seen in patients with idiopathic pulmonary fibrosis.

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Suissa, Samy, and Deborah Assayag. "Mortality benefit with antifibrotics in idiopathic pulmonary fibrosis: real world evidence or bias?" European Respiratory Journal 57, no. 3 (March 2021): 2004562. http://dx.doi.org/10.1183/13993003.04562-2020.

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Ko, Audrey C. "Ablative laser assisted topical delivery of antifibrotics in the management of cicatricial ectropion." World Journal of Ophthalmology 4, no. 2 (2014): 7. http://dx.doi.org/10.5318/wjo.v4.i2.7.

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Cilli, Aykut, Fatih Uzer, Can Sevinç, Funda Coşkun, Ahmet Ursavaş, Şükriye Öner, and Fırat Kose. "Tolerability and efficacy of second-line antifibrotics in patients with idiopathic pulmonary fibrosis." Pulmonary Pharmacology & Therapeutics 71 (December 2021): 102099. http://dx.doi.org/10.1016/j.pupt.2021.102099.

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Bansal, Meena B., and Naichaya Chamroonkul. "Correction to: Antifibrotics in liver disease: are we getting closer to clinical use?" Hepatology International 13, no. 1 (January 2019): 40–41. http://dx.doi.org/10.1007/s12072-018-09924-1.

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Kuzubova, N. A., O. N. Titova, E. S. Lebedeva, and E. V. Volchkova. "Pulmonary fibrosis associated with COVID-19." Russian Medical Inquiry 5, no. 7 (2021): 492–96. http://dx.doi.org/10.32364/2587-6821-2021-5-7-492-496.

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An analysis of scientific publications based on the study results conducted during the COVID-19 pandemic indicates a possible risk of pulmonary fibrosis or progression of existing interstitial lung disease with the pulmonary fibrosis development in patients with the SARS-CoV-2 virus. A fibrous histological pattern was detected in about 22% of COVID-19 cases, starting from the third week of the disease. The molecular basis of the pulmonary fibrosis progression after infection with the SARS-CoV-2 virus remains unclear, but it is considered multifactorial, including direct viral effects, immune dysregulation, cytokine storm and increased oxidative stress. The question needs to be answered why a certain part of patients undergo a transition to uncontrolled cell proliferation with the accumulation of fibroblasts and myofibroblasts, excessive deposition of collagen and extracellular matrix, which leads to progressive pulmonary fibrosis, a more severe disease course and increases the risk of severe complications and mortality. There is no regulated therapeutic approach to the treatment of pulmonary fibrosis associated with a new coronavirus infection. Along with the approved antifibrotics for the treatment of idiopathic pulmonary fibrosis, nintedanib and pirfenidone, new means of preventing the fibrosis process are being investigated. An important research area is a search for biomarkers for early identification of patients with a high risk of severe COVID-19, burdened by the development of interstitial fibrotic lung lesions. KEYWORDS: pulmonary fibrosis, COVID-19, SARS-CoV-2, pneumonia, angiotensin-converting enzyme 2, immune dysregulation, antifibrotics. FOR CITATION: Kuzubova N.A., Titova O.N., Lebedeva E.S., Volchkova E.V. Pulmonary fibrosis associated with COVID-19. Russian Medical Inquiry. 2021;5(7):492–496 (in Russ.). DOI: 10.32364/2587-6821-2021-5-7-492-496.

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Kumar, Naresh. "Post-COVID-19 Pulmonary Fibrosis: An Update." Journal of Advanced Research in Medicine 08, no. 02 (June 30, 2021): 16–26. http://dx.doi.org/10.24321/2349.7181.202109.

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Coronavirus disease 2019 (COVID-19) is caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The most common cause of hospitalisation for COVID-19 is interstitial pneumonia that may be complicated by Acute Respiratory Distress Syndrome (ARDS). With an increasing magnitude of COVID-19 survivors, post-COVID interstitial lung disease and pulmonary vascular disease are likely to be the most important long term respiratory complications. Data from previous coronavirus infections such as Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS), as well as emerging data from the COVID-19 pandemic, suggest that there could be substantial pulmonary fibrotic consequences following SARS-CoV-2 infection. Thus, the long-term consequences of COVID-19 appear crucial. Here, we have discussed the pathogenesis, natural history, and radiological aspects of such patients and the possible predictors which might lead to the development of lung fibrosis. Older age, severity of illness, prolonged ICU stay, history of smoking and alcoholism are few of the risk factors for the development of post-COVID-19 pulmonary fibrosis. Therapeutic options like antifibrotic drugs such as pirfenidone, nintedanib, pulmonary rehabilitation, SARS-COV-2 vaccine etc. have been described. The role of steroids and antifibrotics in the prevention of post-COVID fibrosis is still controversial. Careful longitudinal follow-up of multiple cohorts of post-COVID-19 survivors with serial lung function testing and imaging is required to complete the knowledge about natural history of the disease and the response to various therapies.

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Hage, René, and Macé M. Schuurmans. "COVID-19-Associated Lung Fibrosis: Two Pathways and Two Phenotypes, Lung Transplantation, and Antifibrotics." Transplantology 3, no. 3 (July 6, 2022): 230–40. http://dx.doi.org/10.3390/transplantology3030024.

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COVID-19 can be associated with lung fibrosis. Although lung fibrosis after COVID-19 is a relatively rare finding, the mere fact that globally a very large number of patients have had COVID-19 leads to a significant burden of disease. However, patients with COVID-19-associated lung fibrosis have different clinical and radiological features. The aim of this review is to define the different phenotypes of COVID-19-associated lung fibrosis, based on the medical literature. We found that two phenotypes have emerged. One phenotype is COVID-19-related acute respiratory distress syndrome (CARDS); the other phenotype is post-COVID-19 pulmonary fibrosis (PCPF). Both phenotypes have different risk factors, clinical, and radiological features, and differ in their pathophysiological mechanisms and prognoses. A long-term follow-up of patients with pulmonary complications after COVID-19 is warranted, even in patients with only discrete fibrosis. Further studies are needed to determine the optimal treatment because currently the literature is scarce, and evidence is only based on small case series or case reports.

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Assayag, Deborah. "Broad Adoption of Antifibrotics in Idiopathic Pulmonary Fibrosis: Still a Long Way to Go." Annals of the American Thoracic Society 18, no. 7 (July 2021): 1115–16. http://dx.doi.org/10.1513/annalsats.202102-123ed.

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Lambers, Christopher, Panja M. Boehm, Silvia Lee, Fabio Ius, Peter Jaksch, Walter Klepetko, Igor Tudorache, Robin Ristl, Tobias Welte, and Jens Gottlieb. "Effect of antifibrotics on short-term outcome after bilateral lung transplantation: a multicentre analysis." European Respiratory Journal 51, no. 6 (April 20, 2018): 1800503. http://dx.doi.org/10.1183/13993003.00503-2018.

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Dhwani Patel, Prutha Patel, Neel Raval, and Jagdish Kakadiya. "Post Covid-19 pulmonary fibrosis: A review article." International Journal of Biological and Pharmaceutical Sciences Archive 4, no. 1 (September 30, 2022): 040–45. http://dx.doi.org/10.53771/ijbpsa.2022.4.1.0048.

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COVID-19 also known as Coronavirus disease 2019 is an infectious disease caused by the highly contagious pathogen SARS-CoV-2.Various studies have found that 70–80% of patients who recovered from COVID-19 continue to have at least one or more symptoms even after being pronounced COVID-free. Pulmonary fibrosis is a severe respiratory illness consequence. It is defined by the lungs' failure to repair the injured alveolar epithelium, the persistence of fibroblasts, and the excessive deposition of collagen and other extracellular matrix components. An initial phase of lung injury is followed by acute inflammation and an effort at healing. Oxygen toxicity and ventilator-induced lung injury are two iatrogenic variables that may contribute to the fibrosis seen in survivors of severe COVID19 pneumonia. Based on scientific evidence and demographic findings, Pirfenidone and Nintedanib, used alone or in combination with anti-inflammatory agents and this combination is effective in preventing serious complications during COVID-19 infection. Pirfenidone inhibits TGF-β stimulated collagen synthesis and the synthesis of tumor necrosis factor, interferon-gamma, interleukin- 1beta, and interleukin-6 resulting in anti-inflammatory action. Depending on the concentration, pirfenidone has been demonstrated to have antioxidant capabilities. Nintedanib saw inhibitory action on pro-fibrotic mediators like platelet-derived growth factor and fibroblast growth factor, transforming growth factor-beta, and vascular endothelial growth factor. Who were already taking antifibrotic therapy saw a reduction in the number of acute exacerbations of IPF. Thus, Nintedanib and Pirfenidone both drugs slowed down the progression of Lung Fibrosis in patients over 18yr of age. However, more studies are required for usage of antifibrotics in Non- IPF patients.

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Ali, Mohamed F., Ashley M. Egan, Gaja F. Shaughnessy, Dagny K. Anderson, Theodore J. Kottom, Harika Dasari, Virginia P. Van Keulen, et al. "Antifibrotics Modify B-Cell–induced Fibroblast Migration and Activation in Patients with Idiopathic Pulmonary Fibrosis." American Journal of Respiratory Cell and Molecular Biology 64, no. 6 (June 2021): 722–33. http://dx.doi.org/10.1165/rcmb.2020-0387oc.

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Naibey, Rosdiana, Widya Wasityastuti, Nungki Anggorowati, and Nur Arfian. "Antifibrotics and Antioxidants of Chlorogenic Acid Inhibits Toll- Like Receptors-4 as Liver Fibrotic Marker." Green Medical Journal 3, no. 2 (August 31, 2021): 91–99. http://dx.doi.org/10.33096/gmj.v3i2.86.

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Introduction: Chlorogenic Acid (CGA) is an antifibrotic and antioxidant for fibrotic tissues. These double roles be able to inhibit or fibrotic tissues chains because of internal and external issues. For example, virus, bacteria or other pathogens and also by drugs, alcohol, cigarettes, etc. as external factor that affect quality of body tissues. Toll-Like Receptor-4 (TLR-4) as a marker fibrotic tissues. It is a key for researcher could be find out by expression performance. The aim of this study is to reveal the CGA as a candidate of antifibrotic & antioxidant in liver fibrosis that induced by CCL4. Methods: This is a pure experimental research with a simple experimental design or post-test only control group design. The total 29 mices of 2.5-month-old male Swiss mices with weigh 35-40 gram divided into 6 group: 3 groups of controls (injected by natrium chloride, CGA, and CCL4) and 3 groups of treated (injected by CGA doses 42 mg/kg, 63 mg/kg or 84 mg/kg). Liver organ was used to examine the expression of TLR-4 by rt-PCR. This research revealed that expression of TLR-4 lower than the CCL4 control group (respectively, p=0.042; p=0.005; p=0.006; and p=0.001). Higher dose of CGA showed greater ability as anti-fibrotic through inhibit the expression of TLR-4. Some research found the expression of TLR-4 has been decreased by treatment of Clorogenic Acid (CGA). Conclusion: To sum up, CGA has double roles to repair liver fibrotic tissues. The greater doses of CGA, the stronger inhibition of TLR-4 expression.

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Bendstrup, Elisabeth, and Meena Kalluri. "Real-World Data on Bleeding Risk and Anticoagulation in Patients with IPF Treated with Antifibrotics." Drug Safety 43, no. 10 (August 20, 2020): 953–55. http://dx.doi.org/10.1007/s40264-020-00991-8.

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Iswandana, Raditya, Bao Tung Pham, Theerut Luangmonkon, Henricus A. M. Mutsaers, and Peter Olinga. "ID2033 Precision-cut tissue slices as a novel ex-vivo model for evaluating the efficacy of potential drugs." Biomedical Research and Therapy 4, S (September 5, 2017): 63. http://dx.doi.org/10.15419/bmrat.v4is.272.

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Background: Recently, we developed a novel model for drug screening by culturing ex-vivo precision-cut tissue slices (PCTS). The tissue slice consists of multiple cell types still in their normal matrix environment and structure provides numerous advantages compare to other models. Our objective was to use this model to investigate the effect of various potential compounds. In this study precision-cut intestinal slices (PCIS) were used to evaluate some transforming growth factor (TGF- β) and platelet-derived growth factor (PDGF) pathway inhibitors. TGF-β and PDGF are key cytokines in fibrotic and cancer diseases and are the main targets for treatment. Methods: Murine PCIS were cultured for 48 h in the presence of profibrotic and/or antifibrotic compounds. The fibrotic process was studied on gene and protein level using a variety of markers including (pro)collagen 1a1 (Col1a1), heat shock protein 47 (Hsp47), fibronectin (Fn2) and plasminogen activator inhibitor-1 (PAI-1). The effects of potential drugs mainly inhibiting the TGFb pathway i.e. valproic acid, tetrandrine, pirfenidone, SB203580 and LY2109761 as well as compounds mainly acting on the PDGF pathway i.e. imatinib, sorafenib and sunitinib were assessed in the model at maximum non-toxic concentrations. Results: Murine PCIS remained viable for 48 h and the onset of fibrosis was observed during culture, as demonstrated by an increased expression of, amongst others, Hsp47, Fn2 and Pai-1. Furthermore, TGFb1 stimulated fibrogenesis while PDGF had no effect. Regarding the tested antifibrotics, pirfenidone, LY2109761 and sunitinib had the most pronounced impact on fibrogenesis, both in the absence and presence of profibrotic factors, as illustrated by reduced levels of Col1a1, Hsp47, Fn2 and Pai-1 following treatment. Moreover, LY2109761 significantly reduced fibronectin protein expression in the presence of TGFb1. Conclusion: PCIS can successfully be used to test drug efficacy. Using the model we demonstrated that tetrandrine, pirfenidone, LY2109761 and sunitinib showed potential antifibrotic effects on a gene level, warranting further evaluation of these compounds for the treatment of fibrosis disease. By using tissue extracted from patient, PCIS could also be a promising model to screen drug for personalized treatment in fibrotic and cancer disease.

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Joannes, A., C. Morzadec, F. Llamas Gutierrez, B. Richard De Latour, L. Wollin, S. Jouneau, and L. Vernhet. "Antifibrotics effects of nintedanib on lung fibroblasts derived from patients with progressive fibrosing intertitial lung diseases." Revue des Maladies Respiratoires 39, no. 2 (February 2022): 128–29. http://dx.doi.org/10.1016/j.rmr.2022.02.048.

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Tezel, G??lg??n, Allan E. Kolker, Michael A. Kass, and Martin B. Wax. "Late Removal of Releasable Sutures After Trabeculectomy or Combined Trabeculectomy With Cataract Extraction Supplemented With Antifibrotics." Journal of Glaucoma 7, no. 2 (April 1998): 75???81. http://dx.doi.org/10.1097/00061198-199804000-00002.

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Journal articles on the topic 'Antifibrotics'

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