Tropical pulmonary eosinophilic pneumonia

　　1. Etiology

　　The onset is related to allergic reactions caused by filarial infection, which is Type I, III hypersensitivity, and may also be related to Type IV hypersensitivity.

　　2. Pathogenesis

　　The larvae enter the human body through biting and develop into mature adults. The adults settle in the lymph nodes, produce microfilariae, and then migrate to the pulmonary blood vessels. The degenerated microfilariae release antigens, causing a strong local and systemic inflammatory response, significant increases in antibodies and eosinophilic reactions, which can be found in peripheral blood and lung tissue. The total number of cells increases, and the proportion of eosinophils increases (up to 50%). The total IgE, specific IgG, IgM, and IgE in blood and BALF increase, and antibodies and eosinophils play an important role. In vitro, granulocytes and macrophages can inhibit microfilariae and cause the death of pathogens in the presence of IgG and IgE or complement. The extensive infiltration of lymphocytes and plasma cells around the microfilarial tissue indicates that lymphocytes play an important role in clearing microorganisms. In vitro, microfilarial antigens can induce the migration of lymphocytes, and the inductive products of IgE and eosinophils, mast cells, or basophils may be the cause of asthma.

　　The early stage (within 2 weeks) of the disease is characterized by alveolar, interstitial, peribronchial, and perivascular interstitial tissue cell inflammation, with normal lung tissue structure. Micro-nodules can be seen on the lung tissue. One to three months after the onset of symptoms, untreated patients may have eosinophilic granulocytes and tissue cell infiltration in the alveoli and interstitium, with eosinophilic necrotic material, and remnants of microfilariae can be found (often in the center of abscesses accompanied by alveolar wall destruction). Sometimes, there may be alveolar necrosis and eosinophilic abscesses, local bronchial edema and swelling, and epithelial cell damage. Some chronic patients who have not been treated for a long time may form nodules and pulmonary interstitial fibrosis, which may be related to the existence of chronic mixed cell inflammation. Foreign body-like granulomas are often visible, and the lymph node biopsy can show degenerated microfilariae or adults, with eosinophils and their granule products and macrophages aggregated around them.

　　Tropical pulmonary eosinophilic granulocytic pneumonia can occur at any age, with 25 to 40 years as the peak age, mostly in young women. After a long course, it can lead to pulmonary fibrosis and pulmonary heart disease.

　　It can occur at any age, with 25 to 40 years as the peak age, mostly young women. The onset is insidious, with low fever (1-2 weeks), weight loss, weakness, chest pain, muscle numbness, anorexia, and paroxysmal dry cough at night. There may be a small amount of glassy, transparent, sticky sputum, dyspnea (in severe cases, it can be in a persistent asthmatic state), and manifestations of involvement of the cardiovascular and nervous systems. Physical examination may reveal coarse moist rales, dry rales, and asthma sounds. There may be generalized lymph node and liver and spleen enlargement, and it is more common in children.

　　1. Pay attention to keeping warm and preventing colds in daily life. When there are changes in weather, change clothes in time. Those with physical weakness and susceptibility to colds can often take drugs such as Yu Ping Feng San to prevent external attacks.

　　2. Quit smoking and avoid inhaling dust and all toxic or irritating gases.

　　3. Strengthen physical exercise to enhance physical fitness.

　　4. Pay attention to concentration during eating or feeding. Patients are required to chew slowly and carefully, avoiding talking while eating to prevent food from being aspirated into the lungs.

　　Increased blood eosinophils (up to 20% to 90%, >3000/cm3) are not proportional to the severity of the clinical symptoms and X-ray findings. The serum total IgE is significantly elevated (>1000U/m1), the complement fixation test is strongly positive, the erythrocyte sedimentation rate is moderately increased, the number of eosinophils in sputum increases, and 50% of patients have abnormal electrocardiograms. High-titer specific IgE and IgG against filaria can be detected through blood coagulation tests and complement fixation tests, which are diagnostic criteria. Microfilariae can be found in lymph nodes and lungs, but not in sputum and blood. In the early stage of lung function, obstructive ventilatory dysfunction is shown, and symptoms lasting for more than 1 month or those who have not been treated for a long time may have limited ventilatory dysfunction and decreased carbon monoxide diffusion function, or be accompanied by obstructive ventilatory dysfunction.

　　X-ray manifestations: The typical case is diffuse, uniform, indistinct small nodules, network nodules, and patchy hazy shadows, with a diameter of 2-5mm, which can also merge into a sheet, mostly located in the middle and lower lung fields on both sides. After treatment, they can be resolved. Chronic cases often form fibrosis, and there are also reports of enlarged hilar lymph nodes, pleural effusion, or空洞 formation. There have been reports of concurrent bronchiectasis and normal X-rays.

       Tropical pulmonary eosinophilic granulocytosis requires attention to diet in addition to routine treatment: diet should be rich in nutrition, easy to digest, and light, with an emphasis on eating more fruits and vegetables, and drinking plenty of water. Spicy foods should be avoided, as well as greasy and heavy foods.

　　1. Treatment

　　First choice of diethylcarbamazine (Hetrazan), widely used in the treatment of filariasis, can directly kill adult worms and microfilariae, and its efficacy is better for malay filariasis than for onchocerciasis, but the adverse reactions of the former are more serious than those of the latter, 6-12mg/kg per day, taken orally in three divided doses, absorbed rapidly after oral administration, metabolized in the body, and almost all excreted in the urine. It is recommended that a course of treatment be 3 weeks, and this drug has mild adverse reactions, occasionally nausea, vomiting, dizziness, insomnia, etc. During the treatment, due to the large-scale killing of filarial worms, allergic reactions such as chills, headache, muscle pain throughout the body, rash, and even laryngeal edema should be paid special attention. Most patients can be cured after 3 weeks of treatment, but there may be an acute relapse, and continued application is still effective. If there are persistent respiratory symptoms, radiological abnormalities, blood and serological abnormalities after diethylcarbamazine treatment, it indicates that chronic inflammation persists and has developed into chronic interstitial lung disease. Follow-up for 2-5 years after standard course treatment shows that about 139 cases, including 6 cases with persistent symptoms, with a slight persistent increase in eosinophils in BALF. Chronic patients have an unsatisfactory response to treatment, and changing to other antifilarial drugs (such as ivermectin) or trying corticosteroids often works.Arsenic agents such as carbarsone can also be used, 400-600mg per day, taken in 2-3 divided doses, 10 days as a course of treatment. If necessary, stop for 10 days before starting the second course. In cases where the above treatment is ineffective, carbarsone (ethylenebisarsine) 0.75mg can be administered intramuscularly, 2 times a week, 4-8 times as a course of treatment. The initial two doses should be small. If hematuria occurs, the medication should be discontinued immediately. Other antifilarial drugs include levamisole, 150-200mg per day, taken orally in two divided doses, but it has more adverse reactions than diethylcarbamazine (Hetrazan). Furazolidone has a significant killing effect on both onchocerca and microfilariae, with a dose of 20mg/kg per day, taken orally in 2-3 divided doses, 7 days as a course of treatment. Patients who have not been treated usually have symptoms that last for several weeks to several months, which can resolve spontaneously, but often relapse after several months or years. The prognosis of this disease is good, and the vast majority can be cured. Those who have developed fibrosis have poor treatment effects.

　　2. Prognosis

　　All patients who have received treatment have a good prognosis.