Eosinophilia and related diseases Eosinophilia is defined as an absolute value of eosinophils greater than 0. 4 x 109/L (400/mm’) in the peripheral blood, often accompanied by excessive eosinophil production and accumulation in the tissues. Clinically, eosinophilia can be seen in a variety of diseases, collectively known as eosinophilic syndrome, with parasitic infections and allergic diseases being the most common. The clinical manifestations vary depending on the cause. Eosinophils are produced in the bone marrow and are regulated by IL-5, GM-CSF, and IL-3, and in the absence of these eosinophil growth factors, eosinophils will rapidly apoptosis. Among them, IL-5 specifically promotes their differentiation, development, maturation and release, and is most important in the increased eosinophil production. Normally eosinophils reside mainly in tissues, especially between epithelial cells and deep tissues of the respiratory, gastrointestinal and genitourinary tracts, where they can survive for several weeks. The morphology of eosinophils is characterized by a bilobed nucleus and a large number of specific eosinophilic granules in the cytoplasm, which determine the staining properties and functional characteristics of the cells. The exact function of eosinophils is unknown; they are involved in the immune response and are able to defend against large, non-phagocytosed pathogens. The cytotoxic effect of its basic and eosinophilic cationic proteins is used to kill multicellular pathogens, such as helminth-like larvae. These proteins also neutralize the anticoagulant activity of heparin. Eosinophils also phagocytose and kill bacteria and other microorganisms, but do not play a major role in the human body. Eosinophils synthesize a variety of cytokines to perform their functions, such as platelet-activating factor, transforming growth factor (TGF) a and beta, which promote wound healing and fibrosis, macrophage movement inhibitory factor (MIF), which is associated with the development of adult respiratory distress syndrome and asthma, and IL-12, which may be involved in Th2-mediated inflammatory responses. Eosinophils are also capable of producing and releasing a variety of inflammatory mediators. Thus, eosinophils can cause tissue cell damage while participating in normal immune defense responses. Another major protein component of eosinophils (phosphovitamin B) can form Charcot-Leyden crystals, which are found in the sputum, feces and tissues of patients with eosinophilia-related diseases and are often used as a marker of eosinophil-related diseases. Blood eosinophil counts do not always reflect the degree of tissue invasion and damage. [1] Associated diseases (a) Parasitic infections are the most common cause of eosinophilia. Unicellular protozoan infections generally do not cause eosinophilia, whereas multicellular helminth and trematode infections can cause eosinophilia, with the degree of increase paralleling the number and extent of tissue invasion by worms, especially larvae. Infections that are encapsulated within the tissues or confined to the intestinal lumen (roundworms, tapeworms) generally do not cause eosinophilia. However, parasites that can destroy the intestinal mucosa (hookworms) can cause eosinophilia. In clinical cases of unexplained eosinophilia, it is important to carefully understand the living environment and dietary history of the patient, and to examine the stool to detect eggs and larvae. However, some parasites such as Trichinella and filarial worms cannot be detected in the stool. Therefore, those with possible parasitic exposure, those with suspicion of colpus migrans such as asthma attacks, migratory pneumonia, and hepatomegaly must undergo relevant blood and histological tests to clarify the etiology. (B) Allergic diseases including allergic rhinitis, bronchial asthma, urticaria, angioneurotic edema and drug allergic reactions can present with eosinophilia. Allergic reactions to drugs can manifest only as eosinophilia, but can also cause interstitial nephritis, serum sickness, cholestatic xanthogranuloma, allergic vasculitis, and immunoblast lymphadenopathy. The drug should be discontinued as soon as drug fever and organ involvement occur. Drug-induced interstitial nephritis eosinophils are not only increased in the blood but also detected in the urine. (iii) Infectious diseases Certain acute bacterial and viral infections can cause an increase in eosinophils, which mostly return to normal during the recovery period, except for scarlet fever where eosinophils are still often increased during the recovery period. Some fungal (Aspergillus, Coccidioides) infections and individual chronic mycobacterial diseases can have eosinophilia. (D) idiopathic hypereosinophilic syndrome (idiopathichypereosinophilic syndrome) This syndrome is a myeloproliferative disease characterized by persistent and excessive eosinophil production. The diagnostic criteria are: (1) absolute blood eosinophil count >1. 5 x 109/L (1500/mm3 ) for more than six months; (2) lack of a clear cause of eosinophilia; and (3) signs and symptoms of organ involvement. The most serious and common complications are cardiac lesions with subendomyocardial thrombosis and fibrosis, leg cord fibrosis leading to atrioventricular regurgitation and eventually progressive congestive heart failure, which can be diagnosed and monitored by echocardiography. The nervous system is involved by emboli from the heart, diffuse encephalopathy and peripheral neuritis (polyneuritis mononeuritis). The skin, liver, spleen, respiratory and digestive systems are also frequently involved. The signs and symptoms of idiopathic hypereosinophilic syndrome are diverse, as the degree of damage varies with the organ it invades. Common ones include fever, cough, chest pain, palpitations, shortness of breath, neuropsychiatric symptoms, itchy skin rash, skin rash, angioneurotic edema, enlarged liver, spleen and lymph nodes, and heart murmurs. The prognosis is also poor in patients with severe involvement of major organs. However, there are patients without significant organ damage who have a benign course. Patients with angioneurotic edema and elevated IgE in this syndrome have a good prognosis and rarely have cardiac involvement even with recurrent attacks.