LAUSR

Pulmonologists treating patients with interstitial lung disease (ILD) know that there is some chance that the diagnosis will be hypersensitivity pneumonitis (HP). To arrive at that diagnosis, we must remember that HP patients are usually non-smokers, younger than 60 years of age, almost always without nail clubbing, normal auscultation, or else auscultation with non-velcro crackles, and occasionally, a few high-pitched, end-inspiratory wheezes, known as chirping rales.1,2 In the acute form, high-resolution computed tomography (HRCT) will reveal the characteristic centrilobular nodules and ground glass opacities, particularly in the upper lobes and in the middle lobe and lingula, or a mosaic attenuation pattern with ground glass opacities combined with other clear/hyperlucent areas indicating hyperinflation from inflammatory centrilobular bronchiolar involvement. In the chronic form, mosaic attenuation patterns and centrilobular nodules, already indicating some degree of fibrosis, will be visualized, along with honeycombing areas, also in the lung bases. HP cannot be ruled out if HRCT shows images of usual interstitial pneumonia, non-specific interstitial pneumonia, or organizing pneumonia, and even if a combination of emphysema and fibrosis is revealed. A meticulous case history must be obtained, looking for evidence of previous contact with birds, feathers (down comforters, etc.), or fungi (damp environments, aerosols with contaminated water, spas, steam iron, moldy walls, etc.). Other etiologies, such as isocyanates, cutting fluids, inhaled proteins, hard metals, etc., are less common. Specific immunoglobulin G (sIgG) against the serum (but not the droppings) of various birds and some fungi will be determined. This will help clarify if there has been contact with these antigens, inducing an immunological response. Bronchoalveolar lavage (BAL) and cryobiopsy should be performed, since a lymphocyte concentration of greater than 20% in