Allergic bronchopulmonary aspergillosis

Introduction to allergic bronchopulmonary aspergillosis Allergicbronchopulmonary aspergillosis (ABPA) is the most common and characteristic disease of allergic bronchial fungal disease, first reported in the United Kingdom in 1952. Its pathogenic Aspergillus is most commonly found in Aspergillus fumigatus, which is visible in Aspergillus oryzae, A. oryzae, and Aspergillus. basic knowledge Sickness ratio: 0.0004% Susceptible people: no specific population Mode of infection: non-infectious Complications: cystic fibrosis

Causes of allergic bronchopulmonary aspergillosis

(1) Causes of the disease

Most cases of ABPA are caused by high allergy to Aspergillus, especially to Fusarium oxysporum, but clinically, various clinical manifestations of Candida albicans, helminth spores, Curvularia lunata and other immune responses.

(two) pathogenesis

ABPA is an allergic reaction to Aspergillus antigen in the body. The main cause is that the pathogen directly causes tissue damage. The serum polyclonal specific Ig and total IgE of the patient are significantly increased. Compared with patients with positive Aspergillus or Aspergillosis, the number of ABPA patients is higher. The various subtypes of cloned Ig and all antigen-specific Ig tend to rise. Antibodies against antigen-specific IgA and IgE can be detected from bronchoalveolar lavage in patients, suggesting that they are locally produced in the lung; bronchoalveolar lavage fluid Although antigen-specific IgG is increased, and serum is also increased, it cannot be confirmed to be locally produced in the lung. Antigen-specific antibodies are heterogeneous. Although anti-Ag7 antibodies can be found in more than 90% of patients, different individuals are very different. In the experimental model of monkey ABPA replicated by Aspergillus fumigatus, IgE and IgG were found to cause passive transfer of pathological changes, indicating that Ig can mediate some local reactions of ABPA. In addition to elevated IgG and IgE in the acute phase of ABPA, peripheral lymphocytes of patients The cells also release antigen-specific IgE, which is different from the infection of Fusarium oxysporum. In patients with acute exacerbation of ABPA, complement activation occurs, and C1q precipitin appears in circulating blood, suggesting immunity. The presence of the compound, it is speculated that the bronchospasm of ABPA is mediated by type I allergic reaction (IgE), and the inflammatory response of the bronchus and its surroundings is mediated by type III allergic reaction (immune complex), and the cellular immune response is in the pathogenesis of ABPA. The role of the mechanism is not certain, although pathologically visible mononuclear cell infiltration and granuloma formation, but the skin delayed type hypersensitivity reaction and peripheral blood lymphocyte proliferation response to Aspergillus fumigatus antigen is absent, the pathogenicity of the normal host Aspergillus is very Weak, but some of its products can inhibit chemotaxis and opsonization, thereby weakening the phagocytic function of phagocytic cells. In the mouse Aspergillus infection model, it has been proved that the elastase produced by the pathogen is consistent with its tissue invasiveness, therefore, in addition to allergic reactions In addition, Aspergillus inhibits the phagocytosis and tissue invasion of host phagocytic cells and plays a role in the pathogenesis of ABPA.

Pathological changes in ABPA include exudative bronchiolitis, mucus impaction, bronchial central granuloma, cystic bronchiectasis of the proximal bronchi, atelectasis and eosinophilic pneumonia, common eosinophils of the bronchial mucosa, lymph Infiltration of cells and plasma cells, the emboli that causes mucus embolism consists of concentrated degraded eosinophil lamellae and Aspergillus hyphae. The proximal bronchi of the impaction is dilated, while the distal end remains normal, which is different from Common bacterial infections, in addition to eosinophil infiltration, occasionally pulmonary parenchymal necrotizing granuloma and obliterative bronchiolitis, although there is obvious eosinophil infiltration in pathological specimens, but in bronchoalveolar lavage fluid Rarely, it is significantly different from chronic eosinophilic pneumonia and allergic pulmonary vasculitis (churg-straus syndrome).

Allergic bronchopulmonary aspergillosis prevention

Main measures:

1. Treatment of the primary disease to eliminate or shorten the patient's high-risk period.

2. Prevent or reduce the contact of hepatitis B patients with Aspergillus spores.

3. Preventive medication.

Allergic bronchopulmonary aspergillosis complications Complications, pulmonary cystic fibrosis

Combined with cystic fibrosis.

Symptoms of allergic bronchopulmonary aspergillosis Common symptoms Wheezing fever with cough, slightly... hemoptysis cough out brown sputum

Typical performance

The main symptoms in the acute phase are wheezing (96%), hemoptysis (85%), pyogenic sputum (80%), fever (68%), chest pain (55%) and coughing brown sputum (54%), of which hemoptysis Most of them are blood stasis, but 4% of patients have a large amount of hemoptysis. The symptoms in the acute phase last longer. They often need hormone treatment for half a year to resolve. A few cases have evolved into hormone-dependent asthma, which is different because of the acute attack. The frequency of occurrence was different. A group of 50 patients with ABPA after 5 years of follow-up found that 29% of patients had lost more than 10 days due to respiratory symptoms; 250 cases of 1 year of observation showed 17 cases of acute infiltration on the X-ray, 66% Chronic shortness of breath in patients, although asthma symptoms are mild in ABPA, but nearly half of patients require long-term local inhalation or systemic application of hormones.

Most of the imaging changes occur at a certain stage of the disease. The transient X-ray changes occur on average every two years, and are not always associated with acute symptoms. The changes in the upper lobe are more common, 2 to 3 of the lower lobe. Times, the nature of the lesion includes lung consolidation, atelectasis, strip shadow (airway wall thickening), bifurcation or linear strip shadow (mucus plug) and cystic round shadow (bronchial cystic dilatation), 80% to 90% of patients have different degrees of lung infiltration, from small piece to large piece of whole leaf consolidation, in which mucus impaction is common in ABPA, and has certain characteristic X-ray signs, 37% to 65% X-ray evidence of mucus caulking at a certain time in the course of the disease, accounting for nearly 1/3 of all transient lesions, typically 2 to 3 cm long, 5 to 8 mm straight or finger-shaped bifurcation Light shadows, it is reported that half of patients after the acute infiltration period showed persistent localized changes; 80% of patients showed persistent annular shadows in the normal normal lung area after infiltration and dissipation; 30% to 40% of patients showed generalized lung Over-inflation or reduced lung volume.

Pulmonary dysfunction in patients with ABPA includes abnormalities in lung dynamics and gas exchange, but the changes are variable, depending on the degree of disease activity. ABPA is mostly obstructive in quiescent period, while acute exacerbation in pulmonary infiltration is associated with restrictive damage. Airway obstruction similar to asthma has a lower response to 2-receptor agonists than asthma, and the amount of lung diffusion is reduced, indicating gas exchange disorders. Studies have shown that ABPA reversible airway obstruction with decreased diffusion and decreased lung volume Parallel, as the disease progresses, irreversible airway obstruction and varying degrees of pulmonary fibrosis often occur, and lung function damage is further aggravated.

2. Atypical performance

Occasionally, ABPA and Aspergillus are present at the same time. ABPA can also spread outside the lung in a very small number, such as brain invasion, increased cerebrospinal fluid lymph, and thoracic exudate.

ABPA diagnosis is not easy, the individual terms of the diagnostic criteria are not specific, 54% of asthma patients have banded shadows on the chest radiograph, 20% to 28% of patients can have positive skin reactions of Aspergillus fumigatus, and 22% of patients have at least 8 Aspergillus antigens There is one type of serum precipitin positive, and the necessary diagnostic criteria for ABPA include:

1 asthma (light and heavy);

2 lung infiltration;

3 Aspergillus antigen immediately positive skin reaction;

4 serum total IgE increased (>1000ng/m1);

5 Aspergillus precipitin antibody positive;

6 serum specificity: elevated IgE and IgG antibodies;

7 The peripheral blood eosinophils increased, and the above criteria have higher diagnostic accuracy for patients with acute exacerbation.

Examination of allergic bronchopulmonary aspergillosis

Serum total IgE was elevated (>1000 ng/ml), Aspergillus precipitin antibody was positive, serum specificity: IgE and IgG antibodies were elevated, and peripheral blood eosinophils were increased.

Most of the imaging changes occur at a certain stage of the disease. The transient X-ray changes occur on average every two years, and are not always associated with acute symptoms. The changes in the upper lobe are more common, 2 to 3 of the lower lobe. Times, the nature of the lesion includes lung consolidation, atelectasis, strip shadow (airway wall thickening), bifurcation or linear strip shadow (mucus plug) and cystic round shadow (bronchial cystic dilatation), 80% to 90% of patients have different degrees of lung infiltration, from small piece to large piece of whole leaf consolidation, in which mucus impaction is common in ABPA, and has certain characteristic X-ray signs, 37% to 65% X-ray evidence of mucus caulking at a certain time in the course of the disease, accounting for nearly 1/3 of all transient lesions, typically 2 to 3 cm long, 5 to 8 mm straight or finger-shaped bifurcation Light shadows, it is reported that half of patients after the acute infiltration period showed persistent localized changes; 80% of patients showed persistent annular shadows in the normal normal lung area after infiltration and dissipation; 30% to 40% of patients showed generalized lung Over-inflation or reduced lung volume.

Diagnosis and diagnosis of allergic bronchopulmonary aspergillosis

The increase of blood eosinophils and the increase of total IgE (mean 200014000 ng/ml) in ABPA patients with pulmonary infiltration are quite significant, which can be clearly distinguished from those with aspergillus skin test positive asthma. The total IgE elevation can be earlier than acute attack. The clinical symptoms are considered to be indications for hormonal therapy. In patients with remission (spontaneous or treated), pulmonary infiltration, elevated blood eosinophils, and even skin tests and serological diagnostic indicators may be absent, difficult to diagnose, mild The diagnosis of patients with aggravating period is often delayed until the indicators of lung infiltration and serological criteria can be diagnosed. Serological diagnostic techniques, radioimmunoassay and ELASA method for the determination of specific IgE and IgG compared to convective immunoelectrophoresis and immunodiffusion The sensitivity and specificity of distinguishing between ABPA and asthma are superior, and the application value of the above technique for solitary Aspergillus is similar.

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