Three major causes of Kawasaki disease

Kawasaki disease is a common disease in children. It has become more and more common in recent years. There are many causes of Kawasaki disease in life. We must pay attention to it so that we can better prevent and treat Kawasaki disease. What are the three main causes of Kawasaki disease? Below is some related knowledge. Please read carefully.

In the acute phase of Kawasaki disease, T lymphocytes decrease, circulating T4 cells are activated, T8 cells decrease, and B lymphocytes are activated. These immune abnormalities may be caused by lymphotropic virus infection, and the affinity of the virus to endothelial cells may be the cause of various vasculitis. In recent years, cytokines, proliferation factors, activated cell membrane surface antigens, and intercellular adhesion factors of macrophages, T cells, B cells, and vascular endothelial cells may play an important role in the pathogenesis of Kawasaki disease. Domestic studies have found that Kawasaki disease is characterized by polyclonal activation of B cells, increased IgG1 and IgG3, significantly increased mean values ​​of B cell growth activation, molecular factors, and interleukin-6 activity, and increased tumor necrosis factor. In addition, the increase in acute coagulation and platelet activation may be related to the formation of aneurysms.

The coronary artery is the most severely damaged part, and the aorta, abdominal aorta, carotid artery, subclavian artery and pulmonary artery are the most severely damaged parts. The pathological changes are similar to those of polyarteritis nodosa in infants and young children. The vascular intima thickens, granulocytes and monocytes infiltrate, the internal elastic layer and medium rupture, the wall necrosis, and aneurysm formation. Endocarditis, myocarditis. Coronary artery thrombosis can cause myocardial infarction, often leading to death.

Kawasaki disease generally presents with fever and rash for more than 5 days, diffuse redness of the skin and mucous membranes, conjunctival congestion, transient swelling of cervical lymph nodes, stiffness and swelling of the hands and feet, and surface peeling. Due to its extensive involvement in the cardiovascular system, it has become a common acquired heart disease in Chinese children. During an attack, the heart and coronary arteries are affected for 1-6 weeks, and cardiac phlebitis, arrhythmias, and coronary phlebitis may occur. At present, the main diagnostic methods for coronary artery aneurysms are coronary angiography and two-dimensional echocardiography. The latter method is effective, non-invasive, and has good repeatability. Compared with coronary angiography, the specificity and sensitivity are 97% and 100%, respectively. Kawasaki disease combined with myocardial infarction accounts for about 1%-2%, and the course of the disease is more than one year. Clinically, it often occurs suddenly when resting, quiet or sleeping.

Kawasaki disease of the cardiovascular system is the main cause of death. If not discovered in time, it can cause myocarditis and pericarditis in the early acute stage, leading to heart failure and death. Therefore, we must be cautious. In the early stages of the disease, children often have fever and swollen lymph nodes, which will continue for one to two weeks. This time, the child must be taken to the hospital for diagnosis and treatment in time. In the later stages, there are usually symptoms such as rash, conjunctival congestion, purulent secretions and tears. Once any abnormality or precursor is found, you must go to the hospital for diagnosis and treatment in time.

The coronary artery is the most severely damaged part, and the aorta, abdominal aorta, carotid artery, subclavian artery and pulmonary artery are the most severely damaged parts. The pathological changes are similar to those of polyarteritis nodosa in infants and young children. The vascular intima thickens, granulocytes and monocytes infiltrate, the internal elastic layer and medium rupture, the wall necrosis, and aneurysm formation. Endocarditis, myocarditis. Coronary artery thrombosis can cause myocardial infarction, often leading to death.

The cause of Kawasaki disease has not been fully elucidated. Rickettsia and Propionibacterium acnes transmitted by dust mites were suspected to be the cause of Kawasaki disease, but this has not been confirmed. There are also reports that it is related to retroviruses. Retrovirus-related reverse transcriptase activity has been found in peripheral blood mononuclear cells of Kawasaki disease patients. Japanese studies have found that the frequency of HLA-BWzz in Kawasaki disease patients is about 2 times higher than that of the general population; and in the Boston area of ​​the United States, the detection rate of HLA-BW51 has increased. Therefore, genetic susceptibility and infection may be the cause of Kawasaki disease.

In the acute phase of Kawasaki disease, T lymphocytes are decreased, circulating T4 cells are activated, T8 cells are decreased, and B lymphocytes are activated. These immune abnormalities may be caused by infection with lymphotropic viruses, and the affinity of the virus for endothelial cells may be the cause of polyangiitis. Recently, it has been found that cytokines, proliferation factors, activated cell membrane surface antigens, and intercellular adhesion factors of macrophages, T cells, B cells, and vascular endothelial cells may play an important role in the pathogenesis of Kawasaki disease. Domestic studies have found that Kawasaki disease is characterized by increased IgG1 and IgG3, which is polyclonal activation of B cells. The mean values ​​of B cell growth activation, molecular factors, and interleukin-6 activity are significantly increased, and tumor necrosis factor is also increased. In addition, increased blood coagulability and platelet activation in the acute phase may be related to aneurysm formation.

Autopsy revealed that the coronary artery was the most damaged part, and the other parts included the aorta, abdominal aorta, carotid artery, subclavian artery and pulmonary artery. The pathological changes were similar to those of polyarteritis nodosa in infants and young children, showing full-thickness inflammation of the arteries; thickening of the vascular intima, infiltration of granulocytes and monocytes, rupture of the internal elastic layer and the media, necrosis of the vessel wall and formation of aneurysms. The heart had endocarditis and myocarditis. Coronary artery thrombosis can cause myocardial infarction, often leading to death.

Mucocutaneous lymphadenopathy syndrome, also known as Kawasaki disease, is an acute febrile rash disease in children with systemic vasculitis as the main pathological feature. It was first reported by Japanese doctor Tomisaku Kawasaki in 1967. Since this disease can cause serious cardiovascular lesions, it has attracted people's attention. The incidence has increased in recent years. In 1990, among the inpatients with rheumatic diseases in a children's hospital in Beijing, there were 67 cases of Kawasaki disease and 27 cases of rheumatic fever. In the same data from 11 hospitals in other provinces and cities, the number of Kawasaki disease was twice that of rheumatism. Obviously, Kawasaki disease has replaced rheumatic fever as one of the main causes of acquired heart disease in children in my country. At present, Kawasaki disease is considered to be an immune-mediated vasculitis and is temporarily included in the chapter on connective tissue diseases.

Generally, there are no prodromal symptoms, but the patient develops fever suddenly, presenting as remittent fever or persistent fever, which lasts for 1 to 2 weeks, usually 7 to 10 days, with an average maximum temperature of 39 to 39.9°C. A few days later, polymorphic red macules appear on the trunk, especially the perineum. It may also present as an urticarial rash with itching, but without blisters or scabs. Changes in the distal extremities are more typical. In the first week after the onset of the disease, the proximal end of the fingernails or toenails becomes pale (incomplete leukonychia), erythema appears on the palms and soles, the hands and feet are diffusely swollen, the skin is often tight and hard, and there is no depression when pressed. About 10 to 15 days after the onset of the disease, the periungual area, palms and soles begin to peel off; sometimes the epidermis falls off in clusters, revealing new normal skin underneath. About 2 months later, transverse grooves often appear on the fingernails and toenails. The entire course of the disease lasts for 2 to 12 weeks, and is often accompanied by non-suppurative lymphadenopathy.

After learning the above knowledge, we have a very clear understanding of the triggering factors of Kawasaki disease. Kawasaki disease is very harmful. Everyone needs to pay attention to Kawasaki disease and the causes of the disease. We can find some ways to prevent Kawasaki disease from these causes.