Disease relevance of Mucocutaneous Lymph Node Syndrome

• It is suggested that despite the difficulty in achieving therapeutic serum concentrations of salicylate during the febrile phase of Kawasaki disease with a dose as high as 100 mg/kg/day, this dose is potentially capable of preventing the associated coronary disease [1].
• Because parvovirus B19 occasionally causes some of the features typical of Kawasaki disease, we investigated B19 involvement in 15 children with Kawasaki disease [2].
• CONCLUSION: LPs associated with dobutamine stress testing are useful for identifying myocardial ischemia in children with Kawasaki disease, especially in those who cannot tolerate testing involving physical exercise [3].
• Although a high incidence of liver dysfunction in Japanese patients with Kawasaki disease receiving high dose aspirin (> or =80 mg/kg/day) suggests racial differences in salicylate sensitivity, the duration of fever in patients receiving high dose aspirin is shorter than that in patients receiving moderate dosages (30 to 50 mg/kg/day) [4].
• To investigate the possible role of lipopolysaccharide (LPS, endotoxin) in the pathogenesis of Kawasaki disease, neutrophils from 15 patients with the disease and 7 with sepsis (4 infected with gram-negative bacteria and 3 with gram-positive bacteria) were analyzed by flow cytometry using anti-LPS and anti-CD14 monoclonal antibodies [5].

High impact information on Mucocutaneous Lymph Node Syndrome

• The efficacy of high-dose salicylates in reducing the coronary artery involvement of Kawasaki disease was compared in 36 children who received acetylsalicylic acid, 80 to 180 mg/kg/day, and in 18 who did not receive high-dose salicylates during the febrile phase of the disease and whose fever was controlled mainly with acetaminophen [1].
• We investigated 31 individuals with Kawasaki disease, and recorded an association between expression of S100A12 and activity of Kawasaki disease [6].
• We aimed to investigate the possible role of the gene for this molecule (MBL) in white Dutch patients with Kawasaki disease [7].
• Peripheral blood mononuclear cells from ten of sixteen acute Kawasaki disease patients spontaneously secreted high levels of interleukin-1 (IL-1) [8].
• Tat and Kawasaki disease [9].

Chemical compound and disease context of Mucocutaneous Lymph Node Syndrome

• A 40-year-old black man developed the primary features of Kawasaki disease, along with a pronounced distal motor and sensory neuropathy, abnormal electromyograms, and elevated creatine kinase levels [10].
• METHODS: We assessed myocardial blood flow and flow reserve at rest and during adenosine stress with nitrogen-13 ammonia and PET in 10 children with a history of Kawasaki disease and in 10 healthy young adult volunteers [11].
• Coronary endothelial dysfunction after Kawasaki disease: evaluation by intracoronary injection of acetylcholine [12].
• Transthoracic Doppler assessment of coronary flow velocity reserve in children with Kawasaki disease: comparison with coronary angiography and thallium-201 imaging [13].
• (0.046-cm) intracoronary Doppler flow guide wire at rest and during the adenosine triphosphate-induced hyperemic response in 95 patients (75 male, 20 female, mean age 9.8+/-6.2 years) with Kawasaki disease [14].

Biological context of Mucocutaneous Lymph Node Syndrome

• The possible influence of the MBL2 genotype on the development and progression of CALs in Kawasaki disease was assessed according to age categories and MBL genotypes in univariate and multivariate analyses [15].
• It is suggested, that 201Tl ECT after dipyridamole-induced vasodilation may be used as a safe alternative to invasive coronary angiography for follow-up investigations in patients with Kawasaki disease [16].
• During the acute phase of the disease, protein binding of salicylate in 36 children with Kawasaki disease was 73 +/- 12%, significantly lower than during the subacute phase (90.4 +/- 8.7%; p less than 0.0005) [17].
• Assessment of left ventricular function in Kawasaki disease by dipyridamole-loading cineventriculography [18].
• Late diagnosis of Kawasaki disease is associated with haptoglobin phenotype [19].

Anatomical context of Mucocutaneous Lymph Node Syndrome

• Evidence that this immune activation contributes to vascular endothelial cell damage in Kawasaki disease is supported by the observation that patients in the acute phase of Kawasaki disease have circulating antibodies lytic for vascular endothelial cells activated with gamma-interferon, IL-1, or tumor necrosis factor [20].
• Induction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after Kawasaki disease [21].
• CD8 T lymphocytes do not express cytotoxic proteins in coronary artery aneurysms in acute Kawasaki disease [22].
• Safety and efficacy of intravenous adenosine for pharmacologic stress testing in children with aortic valve disease or Kawasaki disease [23].
• Here we asked whether IL-6 might be responsible for manifestations of Kawasaki disease (KD), such as immunoglobulin hypersecretion, lymphocyte activation and systemic vasculitis [24].

Gene context of Mucocutaneous Lymph Node Syndrome

• S100A12 (EN-RAGE) in monitoring Kawasaki disease [6].
• Genetic variations in the receptor-ligand pair CCR5 and CCL3L1 are important determinants of susceptibility to Kawasaki disease [25].
• Association of vascular endothelial growth factor (VEGF) and VEGF receptor gene polymorphisms with coronary artery lesions of Kawasaki disease [26].
• High levels of circulating interleukin-4 and interleukin-10 in Kawasaki disease [27].
• Evidence for RANTES, monocyte chemotactic protein-1, and macrophage inflammatory protein-1 beta expression in Kawasaki disease [28].

Analytical, diagnostic and therapeutic context of Mucocutaneous Lymph Node Syndrome

• High-dose immunoglobulin therapy, which is useful for the treatment of idiopathic thrombocytopenic purpura, autoimmune neutropenia, childhood epilepsy, and Kawasaki disease is postulated here to act by immunosuppressing the patients [29].
• To evaluate the role of tumor necrosis factor alpha (TNF-alpha) during acute Kawasaki disease, we measured p60 soluble tumor necrosis factor receptor (sT-NF-R) shedding into the circulation in 48 patients with acute Kawasaki disease, all of whom received intravenous infusions of gamma-globulin [30].
• Detection of myocardial contractile reserve by low-dose dobutamine quantitative gated single-photon emission computed tomography in patients with Kawasaki disease and severe coronary artery lesions [31].
• To examine any role of macrophage colony-stimulating factor (M-CSF), in the immune responses in Kawasaki disease (KD), we serially assayed M-CSF and several related cytokines using ELISA [32].
• A 12-month-old male infant with Kawasaki disease had an erythematous indurated plaque with prominent necrotic ulceration at the BCG vaccination site on the left upper arm [33].

References