Allergic bronchopulmonary aspergillosis

　　Most cases of allergic bronchopulmonary aspergillosis (ABPA) are caused by high sensitivity to aspergillus, especially to smut aspergillus, but various clinical manifestations are caused by immune reactions to Candida albicans, worm spores, and other fungi such as Trichoderma mensonia.

　　ABPA is an allergic reaction of the body to aspergillus antigens, the main cause is not the direct tissue damage caused by the pathogen. In addition to allergic reactions, the inhibitory effect of aspergillus on the phagocytic function of host phagocytes and tissue invasion also plays a certain role in the pathogenesis of ABPA. The pathological changes of ABPA include exudative bronchiolitis, mucus plug, central bronchial granuloma, cystic bronchiectasis of the proximal bronchi, atelectasis, and eosinophilic pneumonia. The bronchial mucosa commonly shows infiltration of eosinophils, lymphocytes, and plasma cells. The plugs causing mucus plug are composed of condensed degenerated eosinophilic lamellae and aspergillus hyphae. The proximal bronchiectasis is plugged, while the distal part remains normal, which is different from the usual bacterial infection. In addition to eosinophilic infiltration, necrotic granuloma and obliterative bronchiolitis of the lung parenchyma are occasionally seen. Although there is obvious eosinophilic infiltration in the pathological specimens, it is rarely seen in bronchoalveolar lavage fluid, which is significantly different from chronic eosinophilic pneumonia and allergic pulmonary vasculitis (churg-straus syndrome).

　　Recurrent attacks of allergic bronchopulmonary aspergillosis can lead to complications such as pulmonary fibrosis, bronchiectasis, and emphysema in the late stage.

　　1. Pulmonary fibrosis

　　The most common symptom of pulmonary fibrosis is dyspnea. In the early stage of mild pulmonary fibrosis, dyspnea occurs only during intense activity, and when pulmonary fibrosis progresses, dyspnea also occurs at rest. Severe pulmonary fibrosis patients may experience progressive dyspnea. Other symptoms include dry cough and fatigue. 50% of patients have clubbing and cyanosis, and fine crackling sounds can be heard at the base of the lung during inspiration. Late stages of chest X-rays show diffuse reticular or nodular shadows in the middle and lower fields of both lungs, occasionally pleural effusion, thickening, or calcification.

　　2. Bronchiectasis

　　The typical symptoms are chronic cough, large amounts of purulent sputum, and recurrent hemoptysis. Bronchial iodine oil造影: It is the main basis for diagnosing bronchiectasis. It can determine the location, nature, extent, and degree of the lesion of bronchiectasis.

　　3. Emphysema

　　The severity of clinical symptoms is determined by the degree of emphysema. In the early stage, there may be no symptoms or only shortness of breath during labor or exercise, gradually becoming difficult to perform the original work, with increasing difficulty in breathing, to the extent that even slight activity or complete rest still feels short of breath. In addition, there may be fatigue, weight loss, decreased appetite, and fullness in the upper abdomen. Chronic bronchitis is the main cause of emphysema, and respiratory function tests are of great significance for the diagnosis of obstructive pulmonary emphysema, with a residual volume/total lung capacity ratio greater than 40%.

　　The symptoms of allergic bronchopulmonary aspergillosis patients are divided into typical and atypical manifestations, and the course of the disease is divided into 5 stages.

　　1. Clinical manifestations

　　1. Typical manifestations

　　The main symptoms during the acute phase include wheezing, hemoptysis, purulent sputum, fever, chest pain, and coughing up brown sputum clots. Most of the hemoptysis is sputum blood, but a small number of patients have a large amount of hemoptysis. The duration of acute phase symptoms is relatively long, often requiring hormone treatment for half a year to subside, and a few cases may evolve into a hormone-dependent phase. Due to the inconsistent definition of the acute onset phase, the reported frequency varies. Although ABPA has relatively mild asthma symptoms, nearly half of the patients require long-term local inhalation or systemic application of hormones.

　　2. Atypical manifestations

　　Occasionally, ABPA may coexist with Aspergillus ball. In a very few patients, ABPA can also cause extrapulmonary dissemination, such as brain invasion, increased cerebrospinal fluid lymphocytes, pleural effusion, etc.

　　Secondly, the clinical course of ABPA is divided into 5 stages

　　Not every patient has to go through a 5-stage clinical course, and some may not be obvious in one or more stages.

　　Stage I (acute stage)

　　The main characteristic is episodic symptoms, such as wheezing, fever, weight loss, etc. The level of IgE is significantly elevated, eosinophils increase, pulmonary infiltration, and serum IgE-Af and IgG-Af are positive.

　　Stage II (remission stage)

　　Symptoms can usually be controlled with bronchodilators and inhaled corticosteroids, with normal chest X-rays, no significant or mild elevation of serum IgE-Af and IgG-Af, decreased serum IgE levels but not restored to normal, and no increase in eosinophils. It can be defined as 'complete remission' if the serum IgE level decreases by 35% to 50% within 6 to 12 weeks of treatment, or if the hormone is discontinued after 6 to 9 months of oral corticosteroid treatment, and there is no deterioration for more than 3 months.

　　Stage III (exacerbation stage)

　　Most patients present with acute exacerbation symptoms, and some patients may have recurrence without symptoms, only showing a serum total IgE level more than twice as high or new infiltration shadows in the lungs, so close monitoring is needed in this stage.

　　Stage IV (hormone-dependent stage)

　　Manifested as hormone-dependent asthma, the asthma symptoms must be controlled by oral corticosteroids, and asthma worsens when the dose of hormones is reduced, even if the asthma is relieved, it is difficult to stop the medication. The level of serum IgE may be elevated or normal. Usually, X-rays do not show pulmonary infiltration, but a few patients have a variety of chest X-ray findings, which may be accompanied by central bronchiectasis. The vast majority of cases are diagnosed in this stage.

　　Stage V (fibrosis stage)

　　Patients often have widespread bronchiectasis, pulmonary fibrosis, pulmonary hypertension, fixed airway obstruction, severe irreversible pulmonary function damage, etc., and may have chest tightness, shortness of breath, dyspnea, cyanosis, and respiratory failure, and clubbing fingers. Serological examination may show or lack active phase manifestations, with poor prognosis.

　　Patients with allergic bronchopulmonary aspergillosis can lead to pulmonary cystic fibrosis. There is no good treatment method, and general corticosteroid therapy is used, but long-term hormone treatment is also harmful to the body. Therefore, preventing allergic bronchopulmonary aspergillosis is the key.

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

　　2. Prevent or reduce contact between hepatitis B patients and Aspergillus spores.

　　3. Preventive medication.

　　4. Strengthen personal hygiene and personal protection. Pay attention to frequent hand washing, gargling, and ventilation to maintain air circulation and freshness, and try to avoid crowded public places as much as possible.

　　5. Pay attention to a balanced diet, strengthen exercise, and enhance physical fitness. Avoid catching a cold, add clothes in time; pay attention to a regular lifestyle, ensure adequate sleep.

　　Laboratory tests in patients with allergic bronchopulmonary aspergillosis show an increase in serum total IgE, and the threshold generally used in the current diagnostic criteria for increased serum total IgE is 1000 IU/ml. If another threshold of 1000ug/L (equivalent to 417 IU/m1) is used, it may lead to overdiagnosis of ABPA. Positive mold precipitating antibodies, increased serum specific IgE and IgG antibodies. Increased eosinophils in peripheral blood.

　　The non-specific imaging manifestations of ABPA are recurrent and migratory pulmonary infiltration shadows, with 80% to 90% of patients showing varying degrees of pulmonary infiltration, from small to large areas of consolidation, mostly occurring at a certain stage of the disease and not always associated with acute symptoms. 30% to 40% of patients have generalized pulmonary hyperinflation or reduction in lung volume.

　　The specific imaging manifestations of ABPA are central bronchiectasis mainly in the upper lobe, with CT scans showing thickened bronchial wall, expanded lumen, double track sign, and signet ring sign. Due to the obstruction of bronchi by sputum plug, it can appear as strip-like, branching, or toothpaste-like, glove-like shadows. Mucus impaction is also a common and somewhat characteristic X-ray sign of ABPA, with 37% to 65% of patients having X-ray evidence of mucus impaction at some point in the course of the disease, accounting for nearly 1/3 of all transient lesions. The typical presentation is an opaque shadow 2-3 cm long and 5-8 mm wide, in the form of a straight strip or finger-cuff-like bifurcation, from ground-glass opacity to consolidation, and pulmonary atelectasis caused by sputum plug. In the late stage, emphysema and fibrosis may occur. Imaging changes are more common in the upper lobe, about 2-3 times that of the lower lobe.

　　The lung function impairment in ABPA patients includes abnormalities in lung ventilation function and gas exchange function, mainly depending on the degree of disease activity. The most common reversible obstructive ventilation dysfunction is to some extent. In the late stage of chronic ABPA patients, pulmonary fibrosis can manifest as restrictive ventilation dysfunction, diffusion obstruction, and fixed airflow limitation. Some studies have shown that reversible airway obstruction in ABPA, accompanied by decreased diffusion volume, is parallel to reduced lung volume. With the progression of the disease, irreversible airway obstruction and varying degrees of pulmonary fibrosis often occur, leading to further exacerbation of lung function impairment.

　　For the dietary care of patients with allergic bronchopulmonary aspergillosis, it is encouraged to consume high-protein and high-vitamin foods. Avoid spicy, fish and shrimp, tobacco and alcohol, and other irritant foods, fried foods, and cold foods. Dietary therapy for allergic bronchopulmonary aspergillosis (the following information is for reference only, and detailed information should be consulted with a doctor):

　　1. Fritillaria pear: 5 grams of fritillaria, 1 pear, and appropriate amount of rock sugar. First, cut off the top of the pear, hollow out the core, add rock sugar and fritillaria, then cover the pear top again, and fix it with a toothpick. Place it in a bowl and steam together, serving the pear and juice together.

　　2. Three Immortals Drink: 250g of fresh radish, 250g of fresh lotus root, 2 pears. Chop and squeeze the juice with an appropriate amount of honey. For heat cough, take it raw; for cold cough, add several slices of ginger to the juice, steam and then take it.

　　3. Lily Soup: 100g of fresh lily (or 30g of dried lily), a moderate amount of sugar. Boil the lily in water, drink the soup and eat the lily, once in the morning and once in the evening.

　　4. Fritillaria and Lily Soup: 50g of fritillary bulb, 8g of lily, 25g of water caltrop, 50g of large pear, a moderate amount of rock sugar. Wash the water caltrop, peel and chop it; peel and core the large pear, wash and slice it; put the fritillary bulb, lily, and rock sugar in a pot, add an appropriate amount of water, boil for 20 minutes. Take one dose per day, eat it in two servings, for 3 to 5 days.

　　5. Silver Ear and Fresh Lotus Root Porridge: 50g of silver ear, 500g of fresh lotus root (with the joints removed), 50g of glutinous rice. After washing the lotus root, squeeze out its juice, cook the silver ear and glutinous rice into porridge as usual, add the lotus root juice when the porridge is about to thicken, and add a moderate amount of rock sugar when it is cooked. Eat it in two servings, once in the morning and once in the evening, for 3 to 5 days.

　　Glucocorticoid therapy for allergic bronchopulmonary aspergillosis can alleviate and eliminate symptoms during the acute exacerbation period, and can prevent permanent damage such as bronchiectasis, irreversible airway obstruction, and pulmonary fibrosis. The recommended dose is prednisone 0.5mg/kg daily, changed to every other day after 2 weeks, and continued for 2-3 months. The dosage reduction is determined according to clinical symptoms, X-ray findings, and total IgE levels. It is usually required that the total IgE level after treatment be reduced by more than 35%, but it is not necessarily required to return to normal. During the first year of treatment, it is necessary to regularly follow up on the total serum IgE. The efficacy of corticosteroids is not always maintained, according to a 5-year follow-up study of 40 ABPA patients, only 10% of patients were completely relieved; 19 patients became corticosteroid-dependent patients, with 41 cases of acute exacerbation; 12 cases developed pulmonary fibrosis and irreversible airway obstruction.

　　Other treatments such as inhaled antifungal drugs including amphotericin B can help alleviate acute symptoms, but there are often recurrent attacks. Some people have reported that oral ketoconazole can improve the asthma symptoms of ABPA, but this has not been repeated. Immunotherapy may be ineffective and even worsen the disease, and inhaled corticosteroids cannot prevent the acute exacerbation of ABPA.