Neumonitis por hipersensibilidad (hp)

Notas del editor

• #3: Loscalzo J. MD, phD. (2013). Hypersensivity Pneumonitis and Infiltrates with Eosinophilia. En Harrison's Pulmonary and Critical Care Medicine(79-85). United States: Mc Graw Hill.
• #4: Loscalzo J. MD, phD. (2013). Hypersensivity Pneumonitis and Infiltrates with Eosinophilia. En Harrison's Pulmonary and Critical Care Medicine(79-85). United States: Mc Graw Hill.
• #8: Laurell noto, en su laboratorio en suecia, pues era químico clínico
• #9: Laurell noto, en su laboratorio en suecia, pues era químico clínico
• #24: Two small genetic susceptibility studies in Mexican8 and Dutch36 patients with bird fancier’s disease found protective polymorphisms in the tissue inhibitor of metalloproteinase-3 (TIMP-3) gene, which is involved in the inhibition of metalloproteinases associated with extracellular matrix turnover. TIMP-3 has also been identified recently as the primary inhibitor of TNF-α–converting enzyme (TACE/ADAM-17), and this enzyme is responsible for processing TNF-α to its soluble form, which is intensely proinflammatory. The TIMP-3 polymorphism was not found in patients with IPF or NSIP.8 It is therefore reasonable to speculate that the expression and/or proteolytic processing of TNF-α is important in the pathogenesis of HP, though clearly this leaves much to be explained concerning the varying clinical pictures of the disease
• #26: Proposed mechanisms in the pathogenesis of hypersensitivity pneumonitis. Most exposed individuals develop an immune tolerance, and the antigen inhalation may result at most in a mild increase of local lymphocytes, without clinical consequences. The coexistence of genetic or environmental promoting factors provokes the development of an exaggerated immune reaction that results in marked lung inflammation. The generation of the granulomatous inflammation requires, among others, the expression of Th1 cytokines, including tumor necrosis factor-a, IL-12, and interferon-g, as well as a toll-like receptor 9–mediated dendritic cell response, which is believed to promote Th1 skewing and prevent Th2 skewing during the development of the adaptive immune response. Subsequently, in the presence of progressing factors (i.e., further exposure) or genetic predisposition, critical immunopathological changes occur in the lung microenvironment inducing the expansion and activation of the fibroblast population and the accumulation of extracellular matrix.
• #34: his is most clearly demonstrated in HP due to bird exposure. Long-term exposure to low amounts of bird antigens is associated with chronic HP. Pigeon breeder’s disease has different presentations in different geographic areas, manifesting as an acute HP in some and chronic HP in others. Intermittent exposure of pigeon breeders to large amounts of pigeon antigens in the United States and Europe is associated with acute disease and a good prognosis, whereas chronic exposure to a few household pigeons in Mexico is associated with chronic disease and a much poorer prognosis. In the United States and Europe, pigeon breeders keep their animals in an enclosure separate from their living areas, which they visit periodically so that exposure is intermittent. In Mexico, birds are often kept in living quarters so that exposure is constant. It is of interest that bird antigens can persist in a room for substantial lengths of time (>18 months) after removal of the birds,12 so that Mexicans with pigeon breeder’s disease might be exposed to pigeon antigens for prolonged periods even after removal of the pigeons. Therefore, pigeon breeder’s disease in Mexico resembles bird fancier’s disease in the United States and Europe in type of exposure, clinical presentation, and prognosis. It differs greatly from the acute HP that characterizes the pigeon breeder’s disease in the United States and Europe. 
• #37:  There is typically no fever, but tachypnea and bibasilar dry rales are usually present.