Accordingly, further considerations have to be made. ALI/ARDS, acute interstitial pneumonia (AIP), and IPF exacerbations have common clinical, physiological, imaging, and histopathology features, and it is incon ceivable that they do not also have common etiopathogenetic mechanisms ( Figure 5 ). ALI/ARDS develops by diff erent insults to the lung, and the mainstay of its treatment is provision of excellent supportive care and etiologic manage ment of the underlying cause [46] . AIP is precisely an ARDS of 'unknown cause' , and no specifi c clinical clues to diff erentiate between 'known and unknown cause' ARDS exist [49] . Criteria for the diagnosis of AIP are the same as in IPF exacerbations with the exception of the 'incubation' time (2 months instead of 4 weeks) and the prerequisite of normal chest roent genogram. AIP, incomprehensibly, is included among the idiopathic interstitial pneumonias (IIPs) and probably should be added to the list of unknown cause ALI/ARDS, although some believe that AIP may represent a fulminant presentation of IIP secondary to imprecise autoimmune factors [1, 2] . Although there are no controlled trials of specifi c treatment, intensive immunosuppression has been the mainstay of treatment (usually under the coverage of several broad-spectrum antimicrobials, although this is not always stated) because of the inclusion of AIP among the IIPs [50] . However, AIP mortality approaches that of IPF exacerbations, and the provision of excellent suppor tive care and further search of underlying causative factors and adequate treatment seem more logical. In stable IPF (in contrast to other pneumonias), lung damage is not resolved by restitutio ad integrum. IPF exacerbations characterized by DAD upon UIP may represent the acute response of scarred and irreparably damaged lung. Epithelial cell apoptosis involves and is considered to be among the main pathogenetic mechanisms in the development of any DAD [51, 52] . Th erefore, it seems incoherent that DAD, which is the common denominator of all ALI/ARDS, AIP, and IPF exacerbations and which develops upon diff erent histology substrates (UIP in IPF exacerbations, normal lungs in AIP, and normal or diseased lungs in ARDS), presents at diff erent time intervals (7 days for ARDS [46, 53] , 4 weeks for IPF exacerbations [7] , and 2 months for AIP [1] ) and requires diff erent pharmacologic approaches, which proved certainly fatal in AIP and in IPF 'true' exacerbations.