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1/22. Long-term evaluation of hypersensitivity pneumonitis: a case study follow-up and literature review.

    This study reports a 3-year follow-up of a classic presentation of hypersensitivity pneumonitis (HP), originally reported elsewhere, after removal of the causative antigens. The literature is reviewed and this case is compared with outcomes of series previously reported. The patient was reevaluated by clinical, serologic, radiographic, and pulmonary function testing 3 years after removal of her home's contaminated humidifier, cleaning of the home, and administration of a course of prednisone. Repeat serologic measurements revealed positive serum precipitins only for aspergillus flavus and Phoma herbarum, significantly fewer than her original panel, which revealed precipitating antibodies to her humidifier water and 10 other specific antigens. Pulmonary function tests remained stable. Physical exam revealed bibasilar rales. Computed tomography scan revealed pulmonary fibrosis, bronchiectasis, and honeycombing that was compared with 3 years earlier. Although most of the data obtained on reevaluation suggest remission, radiographic findings have not remitted. Long-term follow-up of parameters of HP disease activity do not always reveal consistent findings. This patient appears to be in a category of HP between the classic subacute and chronic stages.
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2/22. hypersensitivity pneumonitis associated with mycobacterium avium complex and hot tub use.

    Many diseases, mainly infectious and inhalational, have been associated with the use of hot tubs. "Hot tub lung" is a recently described disease entity associated with mycobacterium avium complex (MAC) and is thought to be either an infection or a hypersensitivity pneumonitis. We describe 2 patients with progressively worsening respiratory symptoms and pulmonary function, along with diffuse radiographic changes consisting primarily of ground-glass opacities. Treatment with corticosteroids, based on lung biopsies suggesting sarcoidosis in 1 patient and eosinophilic bronchiolitis in the other, resulted in little improvement with both patients experiencing respiratory failure. Both patients continued regular and continued hot tub use despite ongoing respiratory difficulties, and MAC was identified in the hot tub water and/or lung tissue from each patient. Discontinuation of hot tub use, without antimycobacterial therapy, led to prompt improvement in symptoms, pulmonary function, and radiographic abnormalities, strongly supporting a diagnosis of hypersensitivity pneumonitis. hypersensitivity to MAC, rather than an infection, is the likely underlying mechanism in these 2 cases of hot tub lung.
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3/22. Extrinsic allergic alveolitis induced by the yeast Debaryomyces hansenii.

    A 65-yr-old female developed cough, fever and dyspnoea following repeated exposure to a home ultrasonic humidifier. High-resolution computed tomography showed ground-glass opacity in both lung fields. Arterial blood gas analysis gave an oxygen tension of 8.38 kPa (63 Torr). Pulmonary function testing revealed restrictive ventilatory impairment with a reduction in the diffusing capacity. The diagnosis of extrinsic allergic alveolitis (EAA) was confirmed by radiographic findings, pathological evidence of alveolitis and reproductive development by a provocation test to the humidifier water. The yeast Debaryomyces Hansenii was the only microorganism cultured from the water of the humidifier. The double diffusion precipitating test and lymphocyte proliferative response was positive for an extract of D. Hansenii, providing evidence to incriminate this fungus. This is the first described case of EAA caused by D. Hansenii.
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4/22. Humidifier lung: possible contribution of endotoxin-induced lung injury.

    A 56-year-old man was admitted with cough, fever, myalgia, and arthralgia. Chest computed tomography demonstrated bilateral diffuse ground-glass opacities predominantly in the upper lungs. Subpleural non-segmental consolidation was observed in the late phase. hypersensitivity pneumonitis was suspected, and an environmental provocation test with the incidental use of a home ultrasonic humidifier was positive. Unlike typical hypersensitivity pneumonitis, serum KL-6 levels were normal. Although several microorganisms were isolated from the humidifier water, there was no evidence for immune sensitization. We detected high amounts of endotoxin in the humidifier water, which may have contributed to the lung injury of this patient.
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5/22. eucalyptus as a specific irritant causing vocal cord dysfunction.

    BACKGROUND: vocal cord dysfunction (VCD) is a well-recognized clinical entity that frequently mimics asthma and is characterized by inappropriate adduction of the vocal cords during inspiration. The pathogenesis of VCD has not yet been defined. The only previous report suggested that respiratory irritants may trigger paradoxical motion of the vocal cords. OBJECTIVE: To report the case of a 46-year-old woman with VCD precipitated by eucalyptus exposure. methods: A masked flexible fiberoptic nasolaryngoscopy was performed to confirm whether VCD occurred with eucalyptus and not with other known respiratory irritants. The patient underwent inhalation challenges consisting of water, ammonia, pine oil, and a combination of eucalyptus (dried leaves) and ammonia. Two independent observers before patient challenge could not identify eucalyptus. RESULTS: Vocal cord dysfunction occurred within minutes of exposure to eucalyptus. This is the first report to prospectively document that a specific irritant, eucalyptus, can precipitate VCD. Negative skin prick test results, total IgE level, and negative IgE eucalyptus-specific antibodies support a nonimmunologic mechanism. CONCLUSIONS: A new pathogenic mechanism for this clinical entity is supported by our observations. Furthermore, a nonimmunologic mechanism in which respiratory irritants may induce VCD is suspected. Future studies to elucidate this mechanism need to be performed in individuals with irritant-specific VCD.
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6/22. hypersensitivity pneumonitis reaction to Mycobacterium avium in household water.

    BACKGROUND: hypersensitivity pneumonitis has been described with exposure to aerosolized mycobacterium avium complex (MAC) in indoor hot tubs (hot tub lung). OBJECTIVES: To describe a case of MAC-associated hypersensitivity pneumonitis-like reaction possibly from showering and review previous hot tub lung reports. methods: For the case report, we investigated a patient with histologically diagnosed hypersensitivity pneumonitis and MAC-positive sputum culture findings. Mycobacterial cultures were obtained from his home and workplace. Isolates were typed using pulsed-field gel electrophoresis. For the review, medline and EMBASE were searched for hot tub lung reports, which were reviewed and summarized. RESULTS: A 50-year-old man had progressive dyspnea and episodic fever and myalgias. Pulmonary function testing results revealed obstruction and impaired diffusion; a chest CT scan found diffuse, centrilobular, ground-glass nodules, and air trapping, and a lymphocytic alveolitis with an elevated CD4/CD8 ratio. Transbronchial biopsy showed multiple well-formed nonnecrotizing granulomas. Multiple respiratory samples and shower and bathtub specimens grew MAC, with matching pulsed-field gel electrophoresis patterns. The patient changed from showering to tub bathing. prednisone and antimycobacterial drugs were administered for approximately 1 year. His symptoms, pulmonary function abnormalities, and CT scan findings resolved. The literature review yielded 36 cases of hot tub lung. Clinical features included dyspnea (97%), cough (78%), and fever (58%). Pulmonary function testing showed obstruction (67%), restriction (55%), and impaired diffusion (75%). A chest CT scan showed ground-glass opacification (95%) and nodules (67%). Granulomas were well-formed in 95%. Treatments included discontinuation of hot tub use and prednisone, antimycobacterial drugs, or both. Outcomes were favorable. CONCLUSIONS: A hypersensitivity pneumonitis-like reaction to mycobacteria can occur from exposures other than hot tubs. There are key differences between classic hypersensitivity pneumonitis and MAC-associated hypersensitivity pneumonitis. Antimycobacterial therapy may be required. The possibility of MAC hypersensitivity pneumonitis from showering raises potential implications in the investigation of patients with hypersensitivity pneumonitis.
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7/22. Extrinsic allergic alveolitis (hypersensitivity pneumonitis) caused by sphingobacterium spiritivorum from the water reservoir of a steam iron.

    A case of extrinsic allergic alveolitis (EAA) caused by sphingobacterium spiritivorum is described. The symptoms were associated with the use of a steam iron. The water reservoir was heavily contaminated with S. spiritivorum (10(6) CFU ml(-1)). This is the first report of S. spiritivorum as a causative agent of EAA.
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8/22. Fatal hypersensitivity pneumonitis.

    BACKGROUND: hypersensitivity pneumonitis (HP) is an uncommon, non-IgE-mediated interstitial lung disease caused by the inhalation of a variety of organic dusts, most commonly from exposure at work or in the pursuit of hobbies. Typically, after the disease is recognized, the causative allergen or environment is identified and treatment initiated through avoidance measures and corticosteroids. Progression of the disease is then usually halted and even reversed. Fatal cases of HP are unusual. OBJECTIVE: To report a case of progressive and deadly HP in a 40-year-old printer who developed subacute bird fancier's disease with its clinical characteristics and positive precipitins to pigeon proteins. methods: Chest x-ray examinations and tests of lung function were performed in the patient. Two months after initial consultation, when the diagnosis was still elusive, an open lung biopsy was performed and the patient was treated with prednisone for 3 months. A subsequent chest x-ray examination was performed 4 months after the biopsy. RESULTS: With avoidance of birds and treatment with corticosteroids, the patient's symptoms resolved and lung function normalized. He was subsequently diagnosed as having asthma followed by bronchitis and 2 episodes of pneumonia. He did not fully recover from these but developed progressive dyspnea. After linking his symptoms to work by history, he underwent lung biopsy with findings consistent with chronic HP. serum antibody titers were positive for Aspergillus but not pigeon proteins. Based on exposure to water-based coolants, he was suspected of having chronic occupational HP, although this could not be confirmed. Despite aggressive treatment, he developed a progressive course that was ultimately fatal. CONCLUSIONS: This report details the progressive disease course in an individual who presented initially with subacute HP. Unfortunately, even after appropriate diagnosis and management, the course of the disease can be fatal.
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9/22. Extrinsic allergic alveolitis caused by a cold water humidifier.

    Three workers developed classical extrinsic allergic alveolitis while working in a printing works that had a contaminated cold water humidifier. All had nodular shadows on their chest radiographs, reduced gas transfer measurements, and lung biopsy specimens that showed an alveolitis with giant cells and cholesterol clefts. In two subjects bronchoalveolar lavage was performed and the lavage fluid contained more than 70% lymphocytes in each case. bronchial provocation tests with the humidifier antigen in these two workers reproduced their symptoms. Unlike previously reported cases, where exposure was to humidifiers working at generally higher temperatures, challenge with thermophilic actinomycetes in our two patients produced no reaction. Tests for precipitins to the humidifier antigen gave strongly positive reactions in the three workers but no single organism isolated from the humidifier produced a significantly positive reaction.
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10/22. Allergic alveolitis caused by home humidifiers. Unusual clinical features and electron microscopic findings.

    Allergic alveolitis (hypersensitivity pneumonitis) developed in two patients who were exposed to home humidifiers contaminated by thermophilic actinomycetes. diagnosis was difficult because severe dyspnea was chronic and not easily associated with specific environmental exposure. Furthermore, chest roentgenograms were normal for long periods despite severe physiologic abnormalities. After several years of disabling symptoms, open lung biopsy findings suggested allergic alveolitis rather than sarcoidosis because a mononuclear interstitial infiltrate overshadowed the granulomas. Also, plasma cells were prominent and there was an intense bronchiolitis. Cultures of the humidifier water grew thermophilic organisms to which the patient's sera formed precipitins. Both patients experienced notable subjective and objective improvement following removal of the contaminated appliances. The ultrastructure of alveolar macrophages and basement membranes was similar to that described in animal models, suggesting cell-mediated hypersensitivity in the patients.
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