İdiyopatik pulmoner fibrozis tanılı hastalarda akciğer kanseri geliştirme risk faktörleri: Retrospektif gözlemsel çalışma
Küçük Resim Yok
Dosyalar
Tarih
2022
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Ege Üniversitesi, Tıp Fakültesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Giriş ve Amaç: İdiyopatik pulmoner fibrozis (İPF) hastalarına akciğer kanseri eşlik etmesi İPF’de kötü prognoz ve yüksek mortalite ile ilişkilidir. Bu nedenle İPF hastalarında akciğer kanseri gelişmesini önlemek ya da erken tanısı koyarak tedavi edebilmek önemlidir. Bu çalışmanın primer amacı hangi İPF hastalarının akciğer kanseri geliştirme riski altıda olduğunu belirlemektir. Çalışmanın sekonder amaçları ise; İPF hastalarında akciğer kanseri insidansı, sağkalım, tümörün patolojik tipi, evresi, anatomik lokalizasyonu ile tedavi verilerinin karşılaştırılmasıdır. Gereç ve Yöntem: Ege Üniversitesi Tıp Fakültesi Göğüs Hastalıkları Anabilim Dalı İnterstisyel Akciğer Hastalığı ve Pulmoner Hipertansiyon Bölümünde Ocak 2008-Ağustos 2021 tarihleri arasında izlenen, disiplinler arası tartışma ile İPF tanısı alan 736 hastanın verileri retrospektif olarak incelenmiştir. Bulgular: İPF hastalarının 96’sında (%13) akciğer kanseri saptanmıştır. Sadece İPF tanılı hastalar Grup 1, İPF ve akciğer kanseri olan hastalar Grup 2 olarak isimlendirilmiştir. Grup 2 hastalarda erkek oranının, Grup 1’e göre belirgin olarak daha yüksek olduğu (%94.8’e kıyasla %73.4, p<0.001), sigara kullanım oranının Grup 1 hastalarda %68.2 iken, Grup 2 hastalarda %94 olduğu saptanmıştır (p<0.001). Grup 2 hastaların %33.3’ü eş zamanlı İPF ve akciğer kanseri tanısı almış olup; %41.6’sında önce İPF, sonra akciğer kanseri, %25’inde ise önce akciğer kanseri, sonra İPF tanısı konulmuştur. Grup 2 hastalarda %28.1 adenokarsinom, %27.1 skuamöz hücreli karsinom, %18.8 küçük hücreli akciğer karsinomu, %8.3 küçük hücreli dışı akciğer karsinomu, %2.1 akciğer kanseri ve plevral karsinomatozis saptanmıştır. Histopatolojik tanısı olmayan hastalar %15.6 oranındadır. Grup 2’de yer alan hastaların büyük kısmını Evre IV akciğer kanseri olgularının oluşturduğu (%46.7); yaklaşık üçte ikisinin periferik yerleşimli (%64.1), %46.6 üst lob, %38.9 oranında alt lob yerleşimli tümör olduğu saptanmıştır. İPF hastalarında tüm grupta medyan sağkalım 47 ay (%95CI: 42.7-51.2) olarak hesaplanmıştır. Beş yılda hastaların %60’ında ölümüm gerçekleştiği; Grup 1’de medyan sağkalım 52 ay (%95CI: 47.1-56.8) iken, Grup 2’de medyan sağkalımın 18 ay (%95CI: 14.2-21.7) olduğu saptanmıştır (p<0.001). İPF hastalarına eşlik eden akciğer kanserinin mortaliteyi 2.7 kat (%95CI: 2.16-3.52) arttırdığı görülmüştür. İPF tanısından önce akciğer kanseri tanısı alan hastalar analizden çıkarıldığında; akciğer kanserinin antifibrotik alan grupta daha az görüldüğü (%7.3’e kıyasla %16.9, p<0.001), pirfenidon alan grupta nintedanibe göre daha az olduğu saptanmıştır (pirfenidon grubunda %6.2’ye kıyasla nintedanib grubunda %10.4, p=0.001). Grup 2 hastalarda pirfenidon alanlarda (medyan sağkalım 28 ay [%95CI: 17.8-38.1]), diğer hastalara göre (nintedanib alan, hiç antifibrotik almayan veya antifibrotik ilaç değişimi olan) daha az mortalite gerçekleşmiştir (p=0.002). Yarışan risk analizinde “competing risk analysis” tekli istatistiklerde İPF’de akciğer kanseri gelişimi riskini sigara içimi 9.82, erkek cinsiyet 7.8, kombine pulmoner fibrozis amfizem (KPFA) tanısının 6.48, fizyolojik ve klinik bulgusu olmayan amfizem bulunmasının 2.19 kat arttırdığı saptanmıştır (sırasıyla p=0.001, p=0.004, p<0.001 ve p=0.007). Çok değişkenli yarışan risk analizlerinde yapılan modellemelerde istatistiksel anlamlı bir birliktelik saptanmamıştır. Sonuç: İPF hasta kohortumuzda akciğer kanseri saptanan hasta sayısı 96’dır, adenokarsinom, skuamöz hücreli karsinom oranından minimal sınırlarda daha yüksektir. Tümör sıklıkla periferik ve üst lob yerleşimlidir. Sigara, erkek cinsiyet, KPFA tanısı ve subklinik amfizem varlığının İPF’de akciğer kanseri gelişimi riskini arttırdığı saptanmıştır. Pirfenidon kullanmamak akciğer kanseri gelişimi riskini arttırmıştır. İPF hastalarına eşlik eden akciğer kanserinin mortaliteyi 2.7 kat arttırdığı görülmüştür. Mortalite, akciğer kanseri gelişen, pirfenidon almakta olan hastalarda daha az gözlenmiştir.
Background and Aims: Concomitant lung cancer in IPF patients is associated with a worse prognosis and higher mortality. Therefore, it is important to prevent the development of lung cancer in patients with IPF, or to diagnose and treat early. The primary aim of this study was to determine which IPF patients are at risk of developing lung cancer. The secondary aims of the study were; lung cancer incidence in IPF, comparison of survival, pathological type, stage, anatomical localization of the tumor and treatment data in IPF patients. Material and Methods: The data of 736 patients diagnosed with idiopathic pulmonary fibrosis (IPF) through multidisciplinary discussion and followed up in Ege University Faculty of Medicine, Department of Chest Diseases, Interstitial Lung Disease and Pulmonary Hypertension Section, between January 2008 and August 2021, were analyzed retrospectively Results: Lung cancer was identified in 96 (13%) of the patients with IPF. Patients with only IPF were designated as group 1, and patients with IPF and lung cancer were designated as group 2. The ratio of males was significantly higher in group 2 than in group 1 (94.8% versus 73.4%, p<0.001); the rate of smoking was 94% in group 2 versus 68.2% in group 1 (p<0.001). 33.3% of the group 2 patients were diagnosed simultaneously; 41.6% were diagnosed first with IPF; 25% were diagnosed first with lung cancer. 28.1% had adenocarcinoma, 27.1% squamous cell lung carcinoma, 18.8% small cell lung carcinoma, 8.3% non-small cell lung carcinoma NOS and 2.1% lung cancer and pleural carcinomatosis. The rate of patients without histopathological diagnosis is 15.6%. Stage IV was the most prevalent stage (46.7%); 64.1% of the cancers were located in the peripheral areas of lung, 46.6% in the upper lobe and 38.9% in the lower lobe. The median survival in the entire IPF group was 47 months (95% CI: 42.7-51.2); death occurred in 60% of the patients in 5 years. The median survival was 52 months (95% CI: 47.1-56.8) in group 1 versus 18 months (95%CI: 14.2-21.7) in group 2 (p<0.001). Lung cancer accompanying IPF was found to increase mortality 2.7 times (95%CI: 2.16-3.52). When patients who had lung cancer before the diagnosis of IPF were excluded from the analysis, lung cancer was found to be less common in the group receiving antifibrotics (16.9% compared to 7.3%, p<0.001), especially in the group receiving pirfenidone (10.4% in the nintedanib group compared to 6.2% in the pirfenidone group, p=0.001). Group 2 patients who received pirfenidone (median survival 28 months [95%CI: 17.8-38.1]) had lower mortality than other patients (who received nintedanib, no antifibrotic, or antifibrotic drug change) (p=0.002). In the competing risk analysis, it was determined that the risk of lung cancer development in IPF was increased in smokers 9.82 times, male gender 7.8 times, combined pulmonary fibrosis and emphysema (CPFE) 6.48 times, and subclinical emphysema alone 2.19 times on univariate analysis (respectively p=0.001, p=0.004, p<0.001 and p=0.007). No statistically significant association was found in the models made in multiple competing risk analyzes. Conclusions: The number of patients with lung cancer in our IPF patient cohort was 96, with a minimally higher rate of adenocarcinoma than squamous cell carcinoma. Tumors were mostly located in the peripheral lung and upper lobe. It has been determined that smoking, male gender, having CPFE or having subclinical emphysema increased the risk of developing lung cancer in IPF. Not using pirfenidone increased the risk of developing lung cancer. Lung cancer accompanying IPF was found to increase mortality 2.7 times. Mortality was lower in patients who developed lung cancer and were receiving pirfenidone.
Background and Aims: Concomitant lung cancer in IPF patients is associated with a worse prognosis and higher mortality. Therefore, it is important to prevent the development of lung cancer in patients with IPF, or to diagnose and treat early. The primary aim of this study was to determine which IPF patients are at risk of developing lung cancer. The secondary aims of the study were; lung cancer incidence in IPF, comparison of survival, pathological type, stage, anatomical localization of the tumor and treatment data in IPF patients. Material and Methods: The data of 736 patients diagnosed with idiopathic pulmonary fibrosis (IPF) through multidisciplinary discussion and followed up in Ege University Faculty of Medicine, Department of Chest Diseases, Interstitial Lung Disease and Pulmonary Hypertension Section, between January 2008 and August 2021, were analyzed retrospectively Results: Lung cancer was identified in 96 (13%) of the patients with IPF. Patients with only IPF were designated as group 1, and patients with IPF and lung cancer were designated as group 2. The ratio of males was significantly higher in group 2 than in group 1 (94.8% versus 73.4%, p<0.001); the rate of smoking was 94% in group 2 versus 68.2% in group 1 (p<0.001). 33.3% of the group 2 patients were diagnosed simultaneously; 41.6% were diagnosed first with IPF; 25% were diagnosed first with lung cancer. 28.1% had adenocarcinoma, 27.1% squamous cell lung carcinoma, 18.8% small cell lung carcinoma, 8.3% non-small cell lung carcinoma NOS and 2.1% lung cancer and pleural carcinomatosis. The rate of patients without histopathological diagnosis is 15.6%. Stage IV was the most prevalent stage (46.7%); 64.1% of the cancers were located in the peripheral areas of lung, 46.6% in the upper lobe and 38.9% in the lower lobe. The median survival in the entire IPF group was 47 months (95% CI: 42.7-51.2); death occurred in 60% of the patients in 5 years. The median survival was 52 months (95% CI: 47.1-56.8) in group 1 versus 18 months (95%CI: 14.2-21.7) in group 2 (p<0.001). Lung cancer accompanying IPF was found to increase mortality 2.7 times (95%CI: 2.16-3.52). When patients who had lung cancer before the diagnosis of IPF were excluded from the analysis, lung cancer was found to be less common in the group receiving antifibrotics (16.9% compared to 7.3%, p<0.001), especially in the group receiving pirfenidone (10.4% in the nintedanib group compared to 6.2% in the pirfenidone group, p=0.001). Group 2 patients who received pirfenidone (median survival 28 months [95%CI: 17.8-38.1]) had lower mortality than other patients (who received nintedanib, no antifibrotic, or antifibrotic drug change) (p=0.002). In the competing risk analysis, it was determined that the risk of lung cancer development in IPF was increased in smokers 9.82 times, male gender 7.8 times, combined pulmonary fibrosis and emphysema (CPFE) 6.48 times, and subclinical emphysema alone 2.19 times on univariate analysis (respectively p=0.001, p=0.004, p<0.001 and p=0.007). No statistically significant association was found in the models made in multiple competing risk analyzes. Conclusions: The number of patients with lung cancer in our IPF patient cohort was 96, with a minimally higher rate of adenocarcinoma than squamous cell carcinoma. Tumors were mostly located in the peripheral lung and upper lobe. It has been determined that smoking, male gender, having CPFE or having subclinical emphysema increased the risk of developing lung cancer in IPF. Not using pirfenidone increased the risk of developing lung cancer. Lung cancer accompanying IPF was found to increase mortality 2.7 times. Mortality was lower in patients who developed lung cancer and were receiving pirfenidone.
Açıklama
Anahtar Kelimeler
İdiyopatik Pulmoner Fibrozis, Akciğer Kanseri, Sağkalım, Pirfenidon, Nintedanib, Risk Faktörleri, Idiopathic Pulmonary Fibrosis, Lung Cancer, Survival, Pirfenidone, Nintedanib, Risk Factors
