Diagnosis
Case 70
【Progress】
Both patients received corticosteroid hormone and their respiratory symptoms were recovered. During admission, respiratory symptoms of Case 1 worsened at the time of the trial over night stay at home. She was again given corticosteroid hormone for a while.
【Discussion】
Hypersensitivity disease occurs in either genetically predisposed to hypersensitive action or heavy environmental exposure beyond responsible immune ability. In other words, it occurs in case that immune system is either misguided or exaggerated. Hypersensitivity action is categorized in four types (1); Type 1 (Allergic anaphylaxis and atopy) is caused by that antigen binds IgE attached on mast cells, inducing histamine release from mast cells; Type II (anti-Body), produced IgG and/or IgM binds to self-cells, inducing damages of self-cells; Type III (Complex of antigen and antibody), complex or clumps deposits to the vessels and joints, inducing vasculitis, nephritis and arthritis: Type IV (Delayed, T cell and macrophage cell-mediated), T cell and macrophages attack self-component of a body, inducing such as contact dermatitis and multiple sclerosis. Pathological examination of histological specimen of acute hypersensitivity pneumonitis revealed alveolitis (probably due to vasculitis) and massive infiltration of lymphocytes to the alveolar wall, implying Type III and IV hypersensitivity actions (2).
Ground glass opacity of the whole lung in acute hypersensitivity pneumonitis on radiograph and chest CT (Figs 1, 2) reflect fluid due to alveolitis and thickening of alveolar wall due to lymphocytes infiltration (3 -7).
Acute hypersensitivity pneumonitis (Type III and IV reaction) is secondary to a repeated and prolonged inhalation of different types of organic dusts. Trichosporon cutaneum is known to be a kind of mold in Japanese homes, causing summer-type hypersensitivity pneumonitis (8). In our both cases, laboratory test revealed positive Trichosporon-antibody, implying that they previously sensitized to Trischoporon and hyper responsive to it.
In the past, hypersensitivity pneumonitis was categorized as acute, subacute and chronic. Subacute is termed in case of bronchiolitis. Since the differentiation of subacute from acute or chronic is unclear, it is classified to date as acute and chronic (9). Patho-histological specimen revealed; inflammation of alveolar wall with lymphocytes infiltration in the initial phase; micro-scattered granuloma occupied alveolar space (Masson body) and lumens in the respiratory or terminal bronchi in the intermediate phase; fibrosis of the central and marginal lobules and lumen of the respiratory bronchili in the late phase: interstitial inflammation and alveolar destruction (honey comb pattern) such as usual interstitial pneumonia (UIP) and non-special interstitial pneumonia (NSIP) in the final phase (5-7). As treatments, avoidance from antigens and administration of corticosteroids are listed. In our cases with acute hypersensitivity pneumonitis, corticosteroids were given.
【Summary】
We present two cases with acute hypersensitivity pneumonitis. They suffered from persistent cough for a couple of weeks. Laboratory test revealed positive Trichosporin antibody test. Chest CT showed cloudy high attenuation in the whole lung with mosaic pattern probably due to air trapping. We should keep in mind that cloudy shadow reflects alveolitis (vasculitis: infiltration of complex of antigen-antibody of IgG, IgA) and lymphocytes infiltration to alveolar wall, implying acute hypersensitivity pneumonitis belongs to allergic reaction of Type III and Type IV. Trichosporin is a kind of mold in Japanese homes, causing summer-type hypersensitivity pneumonitis. Acute phase of hypersensitivity pneumonitis can be advanced to subacute and chronic phases by continuous antigen exposure. Namely, cloudy high attenuation can be changed to bronchioritis pattern, finally honeycomb pattern on chest CT.
【References】
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2017.9.6