Kawasaki disease, or “lymphocyte syndrome mucocutaneous” or “syndrome adeno-mucocutaneous,” is a childhood disease, immune-mediated, consisting of febrile vasculitis affecting arteries of medium and small size.
The prevailing hypothesis is that it is an infectious disease may be secondary to co-infection with several bacteria, resulting in inflammation of the arteries. This is an emerging disease in Europe.
This syndrome was described in 1967 in Japan, where the disease is common.
Asian countries are the most affected, particularly Japan (+ / – 175 cases per 100 000 children under five each year).
The disease affects children between 6 months and 5 years of age in more than three quarters of the cases. It is much more common in Japan, where the incidence is slightly less than 200 cases per 100 000 children under 5 years. This impact is less than 5 per 100 000 children in Europe.
Its causes had remained completely unknown until the 1990s. The hypothesis of its infectious nature has been raised due to the group of cases geography. A multi-bacterial infection could explain this syndrome: the intestinal flora of patients contains 10 to 100 times more than two pathogenic bacteria, staphylococci produce superantigens, on which the patient’s immune system responds with fever and possible edema, and bacteria characterized by a protein called “HSP 60,” which also stimulate the production of this protein in the blood vessel walls, which are then attacked by the patient’s immune system.
The disease develops most often favorably 2 to 3 weeks (only 0.5% to 2.8% of patients die), but some patients develop cardiac complications (coronary aneurysms). The risk of cardiac complications including myocarditis, pericarditis, or coronary artery disease may cause infarction, acute heart failure, and arrhythmias.
Dilation of the coronary arteries can be objectified in a little less than half of the cases from the second week of illness. In four-fifths of cases, this dilation regresses, but aneurysms can occur in the last fifth. In these cases, the healing is to the formation of fibrosis of the artery with formation of strictures of the latter (stenosis) manifested by a lack of oxygen supply to the heart muscle (ischemia), which may be complicated with angina or myocardial infarction. These complications occur most often less than a year after onset of the disease. Other arteries may have the same pattern of rare manner. In the long term, the risk of myocardial infarction persists, though less.
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