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Imaging diagnosis

Case 40

(5) all  hypersensitivity pneumonitis



【Progress】
 She was given predonine 20 mg/day and its dose gradually decreased to 5 mg for two weeks. Her symptoms were getting improved. Subsequently, the opacity of the lung on chest radiograph disappeared.

【Discussion】
 Although asthma and hypersensitivity pneumonitis (HP or extrinsic allergic alveolitis) occur by inhalation of an antigen, trachea and/or bronchi are mainly involved in case of asthma, while HP involves lung alveoli rather than bronchi. Asthma is known to often occur in children or young adults, while HP occurs mainly in forties to sixties (1, 2). Asthma causes bronchus spasm related to IgE allergic reaction, while HP causes alveolitis related IgG antibody response (1).
 The numerous antigens causing HP are known and they are classified into microbial agents, animal proteins and low-molecular weight chemicals (2). The size of antigen causing HP is the more minimum size than that causing athma (2). The repeated inhalation of the same antigen causes allergic response which is called sensitization. For sensitization, T lymphocytes are main cells in occurrence of HP. Following antigen inhalation, antigen-antibody reaction occurs and lymphocytes accumulate in alveoli follows (2). The cytokines released by T lymphocytes cause acute inflammation, chronically constant inflammation inducing the formation of granuloma and/or alveoli destruction (1, 2). IgE is usually normal in HP (1) but, in our case, the laboratory tests last year and at present were both high values. It is considered that the size of antigen caused sensitization might be the mixed sizes stimulating bronchus and alveolus, inducing the overlap of asthma and HP. HP is categorized into acute, subacute and chronic based on the duration of exposure of antigens (2). In acute HP, dry coughs, dyspnea and malaise occurs about 4 to 8 hours after exposure to the antigen and usually resolves within two days (2). Microscopically, infiltration of mononuclear cells and lymphocytes with giant cells in a broncho-vascular distribution is found (2-8). On chest CT, accumulation of patchy opacity with ground-glass density is observed (3). In subacute HP, an unknown onset of dyspnea and dry cough occur several days to weeks after exposure. Patients experience repeated attacks of antigens. Microscopically, formation of granuloma, brochiolitis with or without and interstitial fibrosis accompanied with infiltration of inflammatory cells is found (2). On chest CT, mixed pattern of ground –glass opacity plus interstitial shadow with micronodules is observed (3-8). In chronic HP, patients exposed over four months or more to antigens (2). Microscopically, dense interstitial fibrosis and alveolar destruction is found (2). On chest CT, honey comb pattern and progressive fibrotic changes with emphysema of the upper lobe are observed (3-8). This lung change process is similar as the lung change following long-standing exposure of smoking cigarettes. In our case, she lived in the 30 year-old wooden-house with auto-washing air conditioner. She experienced dry cough and dyspnea for two weeks this year and she had experienced the similar symptom on the same autumn last year. Chest CT showed patchy shadow and ground glass opacity extending from the center of pulmonary lobules. Our case is categorized subacute HP with reasonable CT findings.
 The treatment of HP is to avoid inhalation of the responsible antigen. However, the antigen is not always identified. The preventive measures are necessarily taken: personal protective mask, elimination of mold, removal of a pet. When it is difficult to remove a pet such as bird which has been kept for a long time, antigen exposures persist, resulting in chronic HP. Corticosteroids is effective to help reduce the respiratory symptoms. Long term effects of corticosteroids on pulmonary function are controversial. In our case, as the antigen was not identified, small dose of corticosteroid for short term was administered, leading to the relief of respiratory symptoms.

【Summary】
 We present a seventy four-year-old female with hypersensitivity pneumonitis (HP). She repeated to suffer from cough and dyspnea for approximately two weeks last autum and this autum. Chest CT showed ground glass opacity with accumulation of patchy shadow of pulmonary lobules, corresponded to the typical images of HP. Our case is categorized subacute HP. In pure HP, IgE is usually normal, but IgE values of our case were high, probably because overlapping of HP and asthma occurred probably due to the mixed size of antigens, namely the size to reach pulmonary alveolus and the size to stay in bronchus. We should keep in mind that ground glass opacity is the typical image of acute HP or subacute HP, and interstitial pneumonitis such as honey comb pattern as similar as CT image of long-term cigarettes smoking exposure, springs from chronic HP.

【References】
1.Bogaert P et al. Where Asthma and Hypersensitivity Pneumonitis Meet and Differ Am J Pathol. 2009 Jan; 174(1): 3–13. doi: 10.2353/ajpath.2009.071151
2.Küpeli E, et al. Clues for the differential diagnosis of hypersensitivity pneumonitis as an expectant variant of diffuse parenchymal lung disease. Postgrad MedJ 2004;80:339-345 doi:10.1136/pgmj. 2003.012435
3.Lynch DA, et al. Hypersensitivity pneumonitis: sensitivity of high-resolution CT in a population-based study. AJR Am J Roentgenol. 1992;159 (3): 469-72. AJR Am J Roentgenol (abstract) - Pubmed citation
4.Buschman DL, Gamsu G, Waldron JA et-al. Chronic hypersensitivity pneumonitis: use of CT in diagnosis. AJR Am J Roentgenol. 1992;159 (5): 957-60. AJR Am J Roentgenol (abstract) - Pubmed citation
5.Hirschmann JV, Pipavath SN, Godwin JD. Hypersensitivity pneumonitis: a historical, clinical, and radiologic review. Radiographics. 2009;29 (7): 1921-38. doi:10.1148/rg.297095707 - Pubmed citation
6.Glazer CS, Rose CS, Lynch DA. Clinical and radiologic manifestations of hypersensitivity pneumonitis. J Thorac Imaging. 2002;17 (4): 261-72. J Thorac Imaging (link) - Pubmed citation
7.Matar LD, Mcadams HP, Sporn TA. Hypersensitivity pneumonitis. AJR Am J Roentgenol. 2000;174 (4): 1061-6. AJR Am J Roentgenol (full text) - Pubmed citation
8.Lynch DA, Newell JD, Logan PM et-al. Can CT distinguish hypersensitivity pneumonitis from idiopathic pulmonary fibrosis? AJR Am J Roentgenol. 1995;165 (4): 807-11. AJR Am J Roentgenol (abstract)

2017.1.18



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