Τομέας Παθολογίας
Library of the School of Health Sciences

2018-11-30

2018

Tomos Ioannis

Αρμαγανίδης Απόστολος, Καθηγητής, Ιατρική, ΕΚΠΑ
Παπίρης Σπυρίδων, Καθηγητής, Ιατρική, ΕΚΠΑ
Κοτανίδου Αναστασία, Καθηγήτρια, Ιατρική, ΕΚΠΑ
Μπούρος Δημοσθένης, Καθηγητής, Ιατρική, ΕΚΠΑ
Λουκίδης Στυλιανός, Αναπληρωτής Καθηγητής, Ιατρική, ΕΚΠΑ
Τσαγκάρης Ηρακλής, Αναπληρωτής Καθηγητής, Ιατρική, ΕΚΠΑ
Μάναλη Ευφροσύνη, Επίκουρη Καθηγήτρια, Ιατρική, ΕΚΠΑ

Ιδιοπαθής πνευμονική ίνωση

Greek

Idiopathic pulmonary fibrosis

Introduction: Controversy exists about the pathogenesis of acute exacerbations of idiopathic pulmonary fibrosis (AE-IPFs). According to one hypothesis AE-IPFs represent the development of any etiology diffuse alveolar damage (DAD) upon usual interstitial pneumonia (UIP), whilst other researchers argue that an accelerated phase of the intrinsic fibrotic process of unknown etiology prevails, leading to ARDS. Different cytokines might be involved in DAD pathogenesis as well as in the fibrotic process. However, little is known about the cytokine profile of AE-IPF. The aim of this study was to assess the cytokine levels in the peripheral blood from stable and exacerbated IPF patients.
Methods: Consecutive IPF patients referred to our department between October 2013 and November 2014 were included in this study. Diagnoses of IPF and AE-IPF were based on international guidelines and consensus criteria. Demographic, clinical, functional and laboratory data were recorded. The interleukins (IL) IL-4, IL-6, IL-8, IL-10, and IL-13 as well as active transforming growth factor-beta (TGF-β) were measured in blood from both stable and exacerbated patients on the day of hospital admission for deterioration. All subjects were followed for 12 months. The Mann-Whitney test as well as Tobit and logistic regression analyses were applied.
Results: Among the 41 patients studied, 23 were stable, and 18 were under exacerbation; of the latter, 12 patients survived. The IL-6 and IL-8 levels were significantly higher in exacerbated patients (p=0.002 and p=0.046, respectively). An increase in either IL-6 or IL-8 by 1 pg/ml increases the odds of death by 5.6% (p=0.021) and 6.7% (p=0.013), respectively, in all patients. No differences were detected for the other cytokines.
Conclusion: The cytokine profile in rapidly deteriorating IPF patients who develop ARDS appears to be predominantly pro-inflammatory rather than pro-fibrotic, which approximates any etiology ARDS rather than an accelerating intrinsic fibrotic process.

Health Sciences

Idiopathic pulmonary fibrosis, Acute exacerbation of idiopathic pulmonary fibrosis, Inflammatory mediators

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https://pergamos.lib.uoa.gr/uoa/dl/object/2820869