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WASOG meeting, June 2-4, Gdansk, Poland: Great Success!

włącz .

The 2016 annual meeting of WASOG was a tremendous success. It was held from June 2-4 in Gdansk, Poland, and was hosted by Professor Anna Dubaniewicz of Gdansk Medical University. Over 275 participants attended the meeting at the European Solidarity Center located at the historic Gdansk shipyards.
The attendees were treated to a visit and inspiring lecture by the founder of the Solidarity Movement, and former President of Poland, Lech Walesa.

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The content of the three-day meeting included topics in interstitial lung diseases, and sarcoidosis. A nascent tradition in recent WASOG meetings, the conference kicked off with a conjoined patient-provider conference focused on sarcoidosis. The main themes of the meeting included patient engagement, collaboration between scientists, clinicians, subspecialists, and patients, and advances in precise application of diagnostic procedures and medications for patients. Some dogmas regarding the pathogenesis and treatment of ILD and sarcoidosis were challenged by new science and evolving data from recent trials. With a broad scope of content and expertise, there was truly something for everyone!

Some highlights reported at the meeting included:

  • evidence of the usefulness of myocardial strain for cardiac sarcoidosis
  • new recommendations to consider disease behavior as a key feature in the classification of idiopathic interstitial pneumonias
  • further evidence about cryobiopsy, suggesting both safety and substantial improvements in the confidence of the multidisciplinary diagnostic discussion (MDD) for ILD
  • clinical anecdotes that implied traction bronchiectasis and honeycomb cysts may arise from identical pathologic processes in IPF; and that dysregulated iron metabolism may contribute to the pathogenesis of pulmonary fibrosis
  • a review of recent data demonstrating multiple potential prognostic biomarkers for ILD and sarcoidosis
  • New data showing a pathogenic role for deranged basal cell ontogeny as a feature of IPF, and markers of basal cells in the BAL that correspond to poor prognosis
  • the use of micro-CT to demonstrate abnormalities of airway numbers and branching in IPF patients, suggesting that airways may contribute to the pathogenesis of IPF
  • a preview of recommendations to revise the ATS/ERS/JRS/ALAT guidelines for the diagnosis of IPF, with more emphasis on the entirety of available clinical data, the course of the disease, possible drug-induced causes to eliminate some of the idiopathic cases and the use of MDD.
  • further data from recent IPF clinical trials illuminating the use of the anti-fibrotic agents—these were seen to be effective in patients with emphysema on their CT scan and those with preserved lung function. However, treatment of gastroesophageal reflux did not appear to confer added benefit in patients on antifbrotic agents in the recent trials.
  • an update on the consensus definition and outcomes of interstitial pneumonia with autoimmune features (IPAF); the designation appears to have more prognostic utility in patients with non-UIP patterns of lung disease
  • further analysis of the genetic differences between Lofgren’s syndrome (LS) and non-Lofgren’s patients in a genome wide association study; data presented suggested that the elevated CD4/CD8 ratio in LS is strongly influenced by genetic determinants in LS but not in non-LS
  • evidence for a steroid-sparing benefit of ACTHAR gel for treatment of refractory sarcoidosis with a good toxicity profile
  • corticosteroids are no longer considered to be the only option for first-line therapy. In certain cases a steroid-sparing agent might be more appropriate as monotherapy or as concomitant therapy at the time treatment is initiated

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Poster award winners:

Eva Padrao, Porto, Portugual
‘Chronic hypersensitivity pneumonitis: implications of a UIP pattern on disease severity’

Aernoud van Batenburg, Nieuwegein, Netherlands
‘Telomere shortening in Type II pneumocytes relates to idiopathic pulmonary fibrosis’

Bartlomiej Rekawiecki, Gdansk, Poland
‘Polymorphism of activating FCGR genes in an etiopathogenesis of sarcoidosis’