View clinical trials related to Kawasaki Disease.
Filter by:This study evaluates the safety of defibrotide with IVIG in children with high risk Kawasaki disease.
Kawasaki disease (KD) is the leading cause of acquired heart disease in children in the developed world. Despite available treatment, 25% of children in San Diego County appropriately treated for KD develop coronary artery abnormalities that could lead to complications later in life, including heart attack. Although we can identify children with KD that have these coronary artery abnormalities, there is no approved additional treatment to decrease coronary artery inflammation and arrest or prevent damage to the coronary arteries. Statins, a class of drugs that is known for lowering cholesterol, have also been shown to decrease inflammation in general as well as at the level of the vessel wall. Anakinra, a therapy that blocks the high levels of interleukin 1 (IL1) that leads to inflammation during acute KD, has been shown in the KD mouse model to prevent the development of coronary artery damage. Both of these therapies have been demonstrated to be safe and well-tolerated in KD patients. Therefore, we propose to study the effects of combination therapy with atorvastatin and anakinra in children with acute KD and early coronary artery abnormalities.
Kawasaki disease (KD) is an acute self-limited vasculitis of infancy and early childhood. Most patients recover without sequelae although the inflammatory process causes permanent damage to the coronary arteries in 20-25% of untreated children. An infectious aetiology is suspected, but the causative agent has not been identified. The investigators aim to identify the genes underlying both susceptibility to Kawasaki disease, and the development of coronary artery aneurysms.
Kawasaki disease (KD) is an acute systemic vasculitic syndrome with coronary tropism. It has been reported worldwide, but it is ten times more common in Asian population. It is the second vasculitis of the child by its frequency after rheumatoid purpura. It occurs in 80% of cases between 1 and 5 years, with a maximal incidence around the age of 12 months. KD is not well understood and the cause is yet unknown. It may be an autoimmune disorder. The problem affects the mucous membranes, lymph nodes, walls of the blood vessels, and the heart.The clinical picture of KD associate a persistent fever and an antipyretics resistance with mucocutaneous signs and bulky cervical lymphadenopathy usually unilateral. There is currently no vaccine available against Kawasaki disease so it is extremely important to be able to recognize symptoms before they set in and become too severe. Chagas disease (CD) is caused by the parasite Trypanosoma cruzi. Acute CD occurs immediately after infection, may last up to a few weeks or months. Infection may be mild or asymptomatic. There may be fever or swelling around the site of inoculation, and acute infection may result in severe inflammation of the heart muscle. The notion that the pathology of CD has an autoimmune component was initially based on the finding of circulating antibodies binding heart tissue antigens in patients chronically infected with T. cruzi. A recent study reports a possible antigen (non-cruzi-related antibody NCRA) mimicry characterized by a serological reactivity to a well-defined T. cruzi antigen in blood samples from individuals not exposed to the parasite. The measured seroprevalence of such cross-reactivity is in favor of a highly prevalent immunogen acquired in childhood. There are similarities in mechanism of CD and KD: it could be interesting to explore the presence of NCRA in blood samples from adults with a history of KD. The objective of the study is the measurement of the biomarker NCRA in serum in adults with a history of KD compare to a control population. This measurement and the prevalence may permit to associate the NCRA to a possible pathogenic agent.