What are the causes of Kawasaki disease symptoms?

After the onset of Kawasaki disease, it will have a great impact on the patient's daily life, so it is necessary to slowly adjust the condition and choose appropriate methods to repair and treat it. When Kawasaki disease just occurs, the patient will have a short-term fever, faster blood flow in the body, and various functional diseases such as heart inflammation. The main cause is related to viral infection.

Symptoms and signs

Symptoms and signs of Kawasaki disease

The main symptoms are common persistent fever, 5 to 11 days or longer (2 weeks to 1 month), body temperature often reaches above 39°C, antibiotic treatment is ineffective, common bilateral conjunctival congestion, flushed lips, cracks or bleeding, bayberry-like tongue, hard edema in the hands, early flushing of the palms and soles, characteristic large flakes of peeling of the toes after 10 days, appearing at the junction of the nail bed and skin, and acute non-suppurative transient cervical lymph node swelling, which is most obvious in the front neck, with a diameter of about 1.5 cm or more, mostly appearing on one side, with slight tenderness, occurring within 3 days after the fever, and self-healing after a few days. Maculopapular or erythema multiforme-like rash appears shortly after the fever (about 1 to 4 days), and prickly heat-like rash is occasionally seen, mostly on the trunk, but without blisters and scabs, and disappears in about a week.

Other symptoms often include heart damage, symptoms of myocarditis, pericarditis and endocarditis. The patient's pulse is accelerated. Tachycardia, gallop rhythm, dull heart sounds and systolic murmurs can be heard when auscultating. Valvular regurgitation and heart failure may occur. Echocardiography and coronary angiography can show that most patients have coronary artery aneurysm, pericardial effusion, left ventricular enlargement and mitral regurgitation. Chest X-rays can show enlarged cardiac shadows. Occasionally, joint pain or swelling, cough, runny nose, abdominal pain, mild jaundice or manifestations of aseptic cerebrospinal meningitis are seen. In the acute phase, about 20% of cases experience flushing and desquamation of the perineum and perianal skin, and erythema or crusting reappears at the original site of BCG vaccination 1 to 3 years ago. Horizontal grooves can be seen on the nails during the recovery phase.

Pathological causes of Kawasaki disease

The cause of the disease is not yet clear. The disease is prevalent and local, with clinical manifestations such as fever and rash. It is speculated to be related to infection. It is generally believed that there may be multiple pathogens, including Epstein-Barr virus, retrovirus, or streptococcus and Propionibacterium infection. In 1986, it was reported that the activity of reverse transcriptase in the supernatant of peripheral blood lymphocyte culture of patients was increased, suggesting that the disease may be caused by retrovirus, but most studies have not obtained consistent results. Mycoplasma, Rickettsia, and dust mites have been proposed as pathogens of this disease in the past, but they have not been confirmed. Some people also consider that environmental pollution or chemical allergies may be the cause of the disease.

Recent studies have shown that there is obvious immune disorder in the acute phase of the disease, which plays an important role in the pathogenesis. In the acute phase, peripheral blood T cell subsets are unbalanced, CD4 increases, CD8 decreases, and the CD4/CD8 ratio increases. This change is most obvious 3 to 5 weeks after the onset of the disease and returns to normal by 8 weeks. The increased CD4/CD8 ratio activates the body's immune system, increases the secretion of lymphokines by CD4, promotes the activation of B cell polyclonal water, and promotes their proliferation and differentiation into plasma cells, leading to increased serum IgM, IgA, IgG, and IgE. Activated T cells secrete high concentrations of interleukins (1L-1, 4, 5, 6), r-interferon (IFN-r), and tumor necrosis factor (TNF). These lymphokines and active interferons can induce endothelial cells to express and produce new antigens; on the other hand, they promote B cells to secrete autoantibodies, thereby leading to endothelial cell cytotoxicity.