Pulmonary eosinophilic infiltration

　　Firstly, etiology

　　The etiology of this group of diseases has not been fully understood.

　　Secondly, pathogenesis

　　However, it is generally believed that its pathogenesis is related to allergy. In recent years, with the development of eosinophil biology, people have gained more and more understanding of the biological behavior of eosinophils. Now it is known that eosinophils are usually controlled by T helper cells, which can not only release many mediators, but also release a large amount of cytokines, oxygen free radicals, and arachidonic acid metabolites, all of which participate in the process of lung tissue injury. However, in pulmonary eosinophilic infiltration, whether eosinophils are the initiators of inflammation or the result of inflammation has not been fully clarified, and its role in the pathogenesis needs to be further elucidated.

　　Itchiness may occur with a rash. In severe cases, life-threatening conditions may occasionally occur due to bronchial, bronchiolar obstruction, and heart failure. Therefore, once detected, active treatment is needed, and preventive measures should also be taken in daily life.

　　There are symptoms such as chest tightness, shortness of breath, fatigue, low fever, cough, and wheezing, which can be acute, subacute, or chronic in onset, with a great difference in the course of the disease. In addition to acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP).

　　Currently, there are three main criteria used for the diagnosis of such diseases:

　　1. Hypereosinophilia of peripheral blood and pulmonary X-ray showing infiltrative changes.

　　2. The proportion of eosinophils in bronchoalveolar lavage fluid (BALF) is significantly increased.

　　3. Bronchopulmonary tissue biopsy (TBLB), with common pathological changes of widespread infiltration of eosinophils in the lung parenchyma, interstitium, and peribronchial tissue, BAL and TBLB also have great value in excluding infections caused by various microorganisms and tumors.

　　There is currently no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease. The main treatment is to treat the primary disease and should not revolve around the killing of eosinophils. Primary hyper eosinophilic syndrome can be treated with adrenal cortical hormones to reduce the infiltration of eosinophils. Hydroxyurea, vincristine, or busulfan may be added when necessary. Alpha interferon may be effective for refractory or intolerant cases to the above treatment.

　　1. Eosinophils in peripheral blood are significantly increased.

　　2. Changes in lung X-rays are often transient.

　　3. Increased total serum IgE, except for parasites.

　　4. Bronchoalveolar lavage: significantly increased eosinophil counts in lavage fluid.

　　5. Bronchopulmonary tissue biopsy: widespread infiltration of eosinophils in the lung parenchyma, interstitium, and peribronchial tissue.

　　What foods are good for the body when eating pulmonary eosinophilic infiltration syndrome:

　　1. Eat more foods rich in high-quality protein

　　2. Eat more foods rich in vitamins

　　3. Eat more foods rich in trace elements

　　(The above information is for reference only, please consult a doctor for details)

　　Treatment:

　　Diethylcarbamazine (Hetrazan) is the first-line drug for this condition, with a dose of 6-8mg/(kg·d) taken orally in three divided doses for a continuous period of 3 weeks. Clinical symptoms, increased peripheral blood and BALF eosinophil counts, and abnormal changes in lung X-rays are often relieved within 7-10 days after the start of treatment. About 20% of cases may experience recurrence, in which case the dose of diethylcarbamazine can be increased and the treatment duration appropriately extended to 3-4 weeks. Patients who are ineffective to DEC treatment can choose antihelminthic drugs such as carbendazime ethylacetylarsenate.