Chest
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Bullous pemphigoid, the most common autoimmune blistering disease, is characterized by an autoimmune response to a component of hemidesmosomes within the dermal-epidermal junction. Immunofluorescence examination of skin biopsies demonstrates linear deposition of IgG and C3 in the basement membrane zone. ⋯ Direct immunofluorescence showed linear deposition of IgG and C3 along the basement membranes of the lung and skin specimens. Lung disorders associated with bullous pemphigoid are extremely rare, and, to our knowledge, this is the first report of an immunologically confirmed case of interstitial pneumonia.
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Two central challenges in the field of occupational and environmental epidemiology include accurately measuring biologic responses to exposure and preventing subsequent disease. As exposure-related lung diseases continue to be identified, advances in exposure biology have introduced toxicogenomic approaches that detect biomarkers of exposure at the gene, protein, and metabolite levels. Moreover, genetic epidemiology research has focused more recently on common, low-penetrant (ie, low-relative-risk) genetic variants that may interact with commonly encountered exposures. ⋯ Exhaled breath condensate analysis has provided another noninvasive means of assessing toxicant exposures and systemic effects. As these technologies become more refined, clinicians and public health practitioners will need to appreciate the social implications of the individual- and population-level risks conferred by certain genetic polymorphisms or by biomarker evidence of exposure. At present, the primary approach to occupational and environmental lung disease prevention remains elimination or reduction of known hazardous exposures and requires continued application of local and international resources toward exposure control.
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Editorial Comment
Obstructive sleep apnea: the elephant in the cardiovascular room.
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Pulmonary arterial hypertension (PAH) is a progressive angioproliferative disease with high morbidity and mortality. Although the histopathology is well described, its pathogenesis is largely unknown. We previously identified the increased presence of mast cells and their markers in a rat model of flow-associated PAH. The aim of this study was to test the effect of mast cell stabilization on pulmonary vascular remodeling in experimental PAH. ⋯ We showed in rats with PAH that mast cell stabilization attenuated pulmonary vascular remodeling and that a lower chymase activity correlated with more favorable hemodynamics and pulmonary vascular remodeling. The results of this experimental study support the concept of the use of antiinflammatory therapy by mast cell stabilizers, a group of drugs already licensed for clinical use, to attenuate disease progression in PAH.