Nintedanib in the management of pulmonary fibrosis after COVID-19: a case report

Chakrabortty, Rajashish; Rahman, Samia; Jahan, Rawnak; Dip, A.; Rahman, Mohammed Mirazur

doi:10.3329/birdem.v11i2.53139

Cited by 5 publications

(5 citation statements)

References 15 publications

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“…looked at the efficacy and safety of nintedanib 150 mg twice daily against placebo in patients with IPF. In these investigations, nintedanib slowed the fall in FVC in patients with IPF, which is consistent with a slowing of disease progression (17). Nintedanib has an inhibitory action on profibrotic mediators such as platelet-derived growth factor (PDGF).…”

Section: Treatment Managementsupporting

confidence: 63%

Post Covid-19 pulmonary fibrosis: A review article

Patel¹,

Patel²,

Raval³

et al. 2022

Int. J. Biol. Pharm. Sci. Arch.

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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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Section: Treatment Managementsupporting

confidence: 63%

Post Covid-19 pulmonary fibrosis: A review article

Patel¹,

Patel²,

Raval³

et al. 2022

Int. J. Biol. Pharm. Sci. Arch.

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“…[42] A few case reports documented that antifibrotic agents, for example, pirfenidone and nintedanib, were effective in treating post-COVID-19 pulmonary fibrosis. [43][44][45] At present, there is no approved treatment for the management of post-COVID-19 pulmonary fibrosis. Thus, more clinical trials are warranted to identify the most suitable treatment approach to this disease.…”

Section: Discussionmentioning

confidence: 99%

“…Early treatment with corticosteroids is well-tolerated in patients with post-COVID-19 pulmonary fibrosis and is associated with a rapid and significant improvement in well-being [42] . A few case reports documented that antifibrotic agents, for example, pirfenidone and nintedanib, were effective in treating post-COVID-19 pulmonary fibrosis [43–45] . At present, there is no approved treatment for the management of post-COVID-19 pulmonary fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics and outcomes of post-COVID-19 pulmonary fibrosis

et al. 2022

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The development of pulmonary fibrosis is a rare complication of the novel coronavirus disease 2019 (COVID-19). Limited information is available in the literature about that, and the present study aimed to address this gap. This case-control study included 64 patients with post-COVID-19 pulmonary fibrosis who were hospitalized for COVID-19. The percentage of patients aged ≥65 years (44%) who demised was higher than those who survived (25%). Male patients (62%) had higher mortality than female patients (37%). The most frequently reported clinical symptoms were shortness of breath (98%), cough (91%), and fever (70%). Most COVID-19 patients with pulmonary fibrosis (81%) were admitted to an intensive care unit (ICU), and 63% required mechanical ventilation. Bilateral lung infiltrates (94%), “ground glass” opacity (91%), “honeycomb” lung (25%), and pulmonary consolidation (9%) were commonly identified in COVID-19 patients with pulmonary fibrosis who survived. The findings for computed tomography and dyspnea scale were significantly higher in severe cases admitted to the ICU who required mechanical ventilation. A higher computerized tomography score also correlated significantly with a longer duration of stay in hospital and a higher degree of dyspnea. Half of the COVID-19 patients with pulmonary fibrosis (50%) who survived required oxygen therapy, and those with “honeycomb” lung required long-term oxygen therapy to a far greater extent than others. Cox regression revealed that smoking and asthma were significantly associated with ICU admission and the risk of mortality. Post-COVID-19 pulmonary fibrosis is a severe complication that leads to permanent lung damage or death.

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“…This interplay between oxidative stress and inflammation can induce cumulative oxidative damage and changes in various macromolecules and cellular components [152]. On the one hand, a spike in ROS levels initiates cellular damage and disrupts mitochondrial dynamics [120], and on the other hand, the accumulation of dysfunctional mitochondria creates a prerequisite for the formation of free mROS and intermediate ROS products [89,97,156]. In response, there is a disruption of the intracellular redox balance and activation of redox-sensitive effector pathways, followed by a strong immune response, apoptosis, and necrosis [117,130,157].…”

Section: Oxidative Stress and Endothelial Dysfunction In Post-acute S...mentioning

confidence: 99%

COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction

Georgieva,

Ananiev,

Yovchev

et al. 2023

IJMS

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SARS-CoV-2 infection, discovered and isolated in Wuhan City, Hubei Province, China, causes acute atypical respiratory symptoms and has led to profound changes in our lives. COVID-19 is characterized by a wide range of complications, which include pulmonary embolism, thromboembolism and arterial clot formation, arrhythmias, cardiomyopathy, multiorgan failure, and more. The disease has caused a worldwide pandemic, and despite various measures such as social distancing, various preventive strategies, and therapeutic approaches, and the creation of vaccines, the novel coronavirus infection (COVID-19) still hides many mysteries for the scientific community. Oxidative stress has been suggested to play an essential role in the pathogenesis of COVID-19, and determining free radical levels in patients with coronavirus infection may provide an insight into disease severity. The generation of abnormal levels of oxidants under a COVID-19-induced cytokine storm causes the irreversible oxidation of a wide range of macromolecules and subsequent damage to cells, tissues, and organs. Clinical studies have shown that oxidative stress initiates endothelial damage, which increases the risk of complications in COVID-19 and post-COVID-19 or long-COVID-19 cases. This review describes the role of oxidative stress and free radicals in the mediation of COVID-19-induced mitochondrial and endothelial dysfunction.

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Nintedanib in the management of pulmonary fibrosis after COVID-19: a case report

Cited by 5 publications

References 15 publications

Post Covid-19 pulmonary fibrosis: A review article

Post Covid-19 pulmonary fibrosis: A review article

Clinical characteristics and outcomes of post-COVID-19 pulmonary fibrosis

COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction

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