Hypersensitivity pneumonitis is a group of non-asthmatic allergic lung diseases caused by various sensitizing agents, characterized pathologically by diffuse interstitial inflammation. It results from an allergic reaction to the inhalation of organic dust particles (diameter <10μ) containing fungal spores, bacterial products, animal proteins, or insect antigens, hence also known as extrinsic allergic alveolitis.

bubble_chart Pathogenesis

It is generally considered to be a type III hypersensitivity reaction (due to the deposition of immune complexes), but lung biopsies have not revealed the pulmonary vasculitis characteristic of tissue damage in type II hypersensitivity. Therefore, some support the view of type IV hypersensitivity (delayed reaction), as its histological damage in the acute phase is primarily lymphocyte infiltration of the alveolar walls, followed by mononuclear cell infiltration and scattered non-caseating giant cell granulomas. The late stage [third stage] involves pulmonary tissue fibrosis and organizing obstructive bronchiolitis, consistent with type IV hypersensitivity. However, there are also reports suggesting that type II hypersensitivity and non-immunological mechanisms are involved in the pathogenesis of this condition. The disease often manifests symptoms 3–6 hours after inhaling the antigen, peaks at 6–8 hours, and resolves within about 24 hours. Examples include "farmer's lung," caused by exposure to moldy hay, and "pigeon breeder's lung," resulting from hypersensitivity to avian proteins in bird droppings. Some reports indicate an association between the patient's histocompatibility antigen (HLA) system and the occurrence of hypersensitivity pneumonitis. For instance, "pigeon breeder's lung" is more common in individuals with leukocytes carrying HLA-A_1,1

bubble_chart Pathological Changes

The findings show subacute granulomatous inflammation with infiltration of lymphocytes, plasma cells, epithelioid cells, and Langhans giant cells, leading to widened interstitium. Following a chronic sexually transmitted disease course, interstitial fibrosis and lung parenchymal destruction occur, with bronchioles obliterated by collagen deposition and granulation tissue obstruction. Persistent exposure to sensitizing antigens may result in pulmonary fibrosis, and in severe cases, the lungs may develop a cystic honeycomb appearance.

bubble_chart Clinical Manifestations

The first episode of hypersensitivity pneumonitis is easily confused with viral pneumonia, with symptoms appearing several hours after antigen exposure: fever, dry cough, dyspnea, chest pain, and cyanosis. A few atopic patients may initially exhibit immediate allergic reactions such as wheezing and rhinorrhea upon antigen exposure, followed by a type III reaction manifesting as hypersensitivity pneumonitis 4–6 hours later. Physical examination reveals moist rales in the lungs, usually without wheezing, and no signs of consolidation or airway obstruction. Chest X-rays show diffuse interstitial infiltrates, with millet-sized or small nodular shadows, more pronounced in the mid and lower lung fields, later progressing to patchy dense shadows.

During acute episodes, peripheral blood tests reveal leukocytosis (15×10⁹–25×10⁹/L or 15,000–25,000) with neutrophilia but usually no eosinophilia. Gamma globulin levels rise to 20–30 g/L (2–3 g/dL), accompanied by elevated IgG, IgM, and IgA. Blood moistening and tonifying levels are normal, and wind-dampness factors may test positive. Pulmonary function tests demonstrate restrictive ventilatory impairment, reduced vital capacity, decreased diffusion capacity, and regional ventilation-perfusion mismatch, without significant airway obstruction or increased vascular resistance.

The diagnosis relies on medical history (including environmental factors, lifestyle habits, and hobbies), symptoms, signs, and changes in pulmonary function. X-ray findings and immunological tests, particularly the detection of specific precipitating antibodies to sensitizing antigens in serum, are helpful for diagnosis.

bubble_chart Treatment Measures

Immediate avoidance of allergens is necessary. If pulmonary lesions are extensive, corticosteroid therapy (prednisone 1-2 mg/(kg·d) continued for 1-2 months) can rapidly resolve symptoms, signs, and X-ray abnormalities.