Kawasaki disease (KD) is an acute febrile systemic vasculitis that was first described by Kawasaki
The most commonly used definition of CAL (also known as coronary artery abnormality [CAA] or CAL) is based on the Japanese Ministryof Health criteria: maximum absolute internal diameter >3 mm in childrenyounger than 5 years of age or >4 mm in children 5 years and older,or a segmental diameter 1.5 times greater than that of an adjacent segment, orthe presence of luminal irregularity. [16-21] Coronary arteries should be corrected relative to body surface area (if available) and expressed as standard deviation units from the mean (Z scores).  Several studies analyzed CAL, including aortic root dimension,  and transient CAL (the definition of “transient” varies among studies, from 30 days to 6–8 weeks after diagnosis of disease). Thus, KD patients with coronary artery ectasia or dilatation that disappears within the first 8 weeks after disease onset are defined as having transient ectasia or dilatation (transient CAL). Kuo
Although the clinical features of KD are recognizable, its underlying immunopathogenetic mechanisms are still under investigation, particularly the agent responsible for the development of CAL. KD is regarded as an autoimmune disorder rather than an infectious disease.  Kuo
2. Allergy potential of Kawasaki disease patients
3. Clinical phenotype and presentation of Kawasaki disease
As shown in Figures 1–8, the clinical characteristics of KD patients include fever lasting longer than 5 days, diffuse mucosal inflammation, bilateral non-purulent conjunctivitis, dysmorphic skin rashes, indurative angioedema over the hands and feet, and cervical lymphadenopathy. In addition to the diagnostic criteria, there is a broad range of non-specific clinical features, including irritability, uveitis, aseptic meningitis, cough, vomiting, diarrhea, abdominal pain, gallbladder hydrops, urethritis, arthralgia, arthritis, hypoalbuminemia,  liver function impairment, and heart failure. [4, 29, 41]
3.1. Diagnosis of Kawasaki disease
To date, there is no specific diagnostic laboratory test for KD. Diagnosis is based on the clinical phenotype, i.e., presence of fever lasting longer than 5 days and fulfillment of 4 of 5 specific clinical criteria. In Japan, at least 5 of 6 criteria (fever and 5 other clinical criteria) should be fulfilled for a diagnosis of KD. However, patients with 4 of the principal clinical features can be diagnosed when coronary aneurysm or dilatation is identified.  From the Japanese Circulation Society Joint Working Groups criteria (JCS 2008, Guidelines for Diagnosis and Management of Cardiovascular Sequelae in Kawasaki Disease),  KD can be diagnosed even when fever lasts less than 5 days. However, according to the American Heart Association (AHA) criteria,  fever lasting more than 5 days is essential for the diagnosis of KD.
Some patients who do not fulfill the criteria have been diagnosed with “incomplete” or “atypical” KD, a diagnosis often based on echocardiographic identification of CAL. The term “incomplete” may be preferable to “atypical” because these patients have insufficient criteria instead of atypical presentation. 
In countries with a bacillus Calmette-Guérin (BCG) vaccine policy (i.e., Taiwan and Japan), KD with erythematous induration or even ulceration of the BCG scar has been observed in one-third to half of KD patients (the incidence of BCG site induration is higher than that of neck lymphadenopathy in these countries).  Uehara
Incomplete cases of KD are not uncommon (up to 15–20%). The incidence of CAL in patients exhibiting 4 principal symptoms of KD is slightly higher than that in patients with 5 to 6 principal symptoms.  Presentation of a small number (<4) of principal symptoms does not indicate a milder form of the disease. Patients with at least 4 principal symptoms require the same treatment as patients with complete (typical) presentation of KD, and those with 3 or fewer principal symptoms should be treated similarly when they meet the supplementary criteria. Herein, common supplementary criteria for the diagnosis of incomplete KD are introduced.
Incomplete KD is more common in young infants than in older children, making accurate diagnosis and timely treatment especially important in these young patients, who are at substantial risk of developing coronary abnormalities. [46, 47] The incidence of KD is actually higher than that previously reported worldwide, partly because earlier reports did not take incomplete forms into account. The AHA criteria (2004), which incorporate suggestions for laboratory tests and early echocardiography, are helpful for diagnosing incomplete KD. [41, 48] Consultation with an expert (cardiologist, immunologist, or rheumatologist) should be sought whenever assistance in making a diagnosis is needed. Patients with fever for 5 days or more (with 2 or 3 principal clinical features for KD) without other causes should undergo laboratory testing, and if there is evidence of systemic inflammation, an echocardiogram should be obtained even if the patient does not fully meet the clinical criteria for KD. Likewise, infants 6 months or younger with fever for 7 days or more without other causes should undergo laboratory testing, and if evidence of systemic inflammation is found, an echocardiogram should be obtained even if the infant fulfills no clinical criteria for KD. 
The 2004 AHA supplemental laboratory criteria include  albumin ≤ 3.0 g/dL;  anemia for age;  elevation of alanine aminotransferase (ALT);  platelets after 7 days ≥ 450,000/mm3;  white blood cell count ≥ 15,000/mm3; and  urine ≥ 10 white blood cells/high-power field.  If a patient has more than 3 supplementary criteria, incomplete KD is diagnosed and IVIG should be prescribed before performing echocardiography.  The flowchart for incomplete KD diagnosis and treatment are depicted in Figure 9.
4. Treatment for Kawasaki disease
The standard treatment for KD is IVIG (2 g/kg) infusion for 8–12 hours with high-dose aspirin (80–100 mg/ [kg day]). [20, 24, 29] The most serious complication of KD is the development of CAL, including myocardial infarction, coronary artery dilatation, coronary artery aneurysms, and coronary fistula formation. [25, 30, 49]Coronary artery aneurysms occur as a sequela of the vasculitis in 20–25% of untreated children. There are several risk factors for developing coronary arteritis, such as low serum albumin, age younger than 1 year, and long duration of the fever before treatment. Young patients with low albumin run a very high risk for CAL and IVIG treatment resistance. [5, 29] Although the introduction of IVIG therapy has greatly decreased the rate of coronary aneurysm to 3–10% of patients still develop some type of CAL. Durongpisitkul
Aspirin has been used in the treatment of KD for many years, even before the usage of IVIG. Although aspirin has important anti-inflammatory (high dose) and anti-platelet (low dose) effects, it does not appear to reduce the frequency of CAL formation. During the acute phase of the illness, aspirin is administered in 4 doses of 80–100 mg/kg per day (30–50 mg/ [kg day] in Japan)  with IVIG. High-dose aspirin and IVIG appear to possess additive anti-inflammatory effects.
Practices regarding the duration of high-dose aspirin administration vary across countries and centers, many of which reduce the aspirin dose when the patient is afebrile. When high-dose aspirin is discontinued, low-dose aspirin (3–5 mg/ [kg day]) is administered until there is no evidence of CAL and inflammatory markers (including platelets, C-reactive protein [CRP], and erythrocyte sedimentation rate [ESR]) have returned to normal levels, which usually occurs 6–8 weeks after disease onset. For children who develop CAL, low-dose aspirin (or other anti-platelet agents) is continued indefinitely until the inflammatory markers return to the normal range and the echocardiogram does not display abnormalities. Hsieh
Our recent study investigated 609 KD patients from 2 medical centers in Taiwan. The patients were divided into Group 1, receiving high-dose aspirin (N = 274), and Group 2, without high-dose aspirin (N = 335). There were no significant differences between Groups 1 and 2 in terms of gender (p = 0.51), IVIG resistance rate (34/274 vs. 26/335, p = 0.06), CAL formation rate (57/274 vs. 74/335, p = 0.64), and total hospital stay (6.3 ± 0.2 vs. 6.7 ± 0.2 days, p = 0.13). There were also no significant differences between total white blood cell counts, hemoglobin levels, platelet counts, and CRP levels before (within 1 day) and after (within 3 days) IVIG treatment of the 2 groups (p > 0.1). These results provide evidence that high-dose aspirin in the acute phase of KD does not affect the treatment results (CAL and IVIG resistance rate) or inflammatory condition. High-dose aspirin treatment in the acute phase of KD appears unnecessary, and further randomized controlled trials are needed.
However, Reye syndrome is a risk in children who receive salicylates while they are experiencing active infection with varicella or influenza and has been reported in patients receiving high-dose aspirin for a prolonged period after KD.  Taken together, it seems unnecessary to expose children to high-dose aspirin in acute KD, especially those with G6PD deficiency.However, as reported in the literature, due to the anti-platelet effect, low-dose aspirin has been prescribed for at least 6–8 weeks to prevent thrombocytosis in KD patients.  If patients are allergic or intolerant to a particular drug, clinicians must avoid using it and look for alternatives.Aspirin is used in most patients, often in conjunction with dipyridamole. Dipyridamole has been widely used to treat patients with a coronary aneurysm resulting from KD. [43, 53] The relationship between aspirin therapy and hemolytic disorder in G6PD-deficient patients is unclear. There are also no literature regarding usage of low-dose aspirin and the outcome of KD. G6PD deficiency, an X-linked disorder, is the most common enzymatic disorder of red blood cells in humans. The clinical expression of G6PD deficiency encompasses a spectrum of hemolytic syndromes. While affected patients are usually asymptomatic, some have episodic anemia, while a few have chronic hemolysis. With the most prevalent G6PD variants (G6PD A- and G6PD Mediterranean), severe hemolysis is induced by the sudden destruction of older, more deficient erythrocytes after exposure to drugs with a high redox potential or to fava beans, selected infections, or metabolic abnormalities. The likelihood of developing hemolysis and the severity of disease are determined by the magnitude of the enzyme deficiency, which in turn is determined by the biochemical characteristics of the G6PD variant. The World Health Organization has classified the different G6PD variants according to the magnitude of the enzyme deficiency and the severity of hemolysis.  Class I variants have severe enzyme deficiency (less than 10% of normal) and are associated with chronic hemolytic anemia. Class II variants also have severe enzyme deficiency, but are usually only intermittently associated with hemolysis. Class III variants have moderate enzyme deficiency (10–60% of normal), with intermittent hemolysis usually associated with infection or drugs. Class IV variants have no enzyme deficiency or hemolysis. Class V variants have increased enzyme activity, and classes IV and V are of no clinical significance. The incidence of hemolysis development in a patient with G6PD deficiency after taking aspirin is dosage-related.  G6PD deficiency is commonly considered a contraindication to aspirin intake. However, just few studies  have suggested that aspirin can be safely administered in therapeutic doses to G6PD-deficient subjects without nonspherocytic hemolytic anemia. Anti-platelet therapy is most commonly used to prevent thrombotic events for adults with atherosclerotic vascular disease, children with certain types of congenital heart disease, stroke, and KD.  Unfortunately, very little data on the efficacy and safety of anti-platelet therapy for pediatric patients, or even G6PD patients, are available. No prospective data exist to guide clinicians in selecting an optimal regimen. Therapeutic regimens used in patients with KD depend on the severity of CAL and include anti-platelet therapy with aspirin, with or without dipyridamole or clopidogrel; anticoagulant therapy with warfarin or low-molecular-weight heparin; or a combination of anticoagulant and anti-platelet therapy. 
A few articles have reported G6PD-deficient patients with sustained KD.  However, the question of whether aspirin is suitable for KD patients with G6PD deficiency remains
4.2. Intravenous immunoglobulin (IVIG or IVGG)responsiveness
The efficacy of IVIG administered in the acute phase of KD for reducing the incidence of coronary artery abnormalities is well established.  The mechanism of IVIG action is still under investigation. IVIG appears to have a generalized anti-inflammatory effect. Possible mechanisms of action include modulation of cytokine production, neutralization of bacterial super-antigens or other etiologic agents, augmentation of regulatory T cell activity (TGF-), [23, 26] suppression of antibody synthesis and inflammatory markers (CD40-CD40L, nitric oxide, and iNOS expression), [60-62]provision of anti-idiotypic antibodies, Fc-gamma receptor,  and balancing Th1/Th2 responses. [28-30]
KD patients should be treated with a single 12-hour infusion of 2 g/kg IVIG together with aspirin in the acute phase with fever or inflammation progression without fever. [3, 4, 15] This therapy should be administered within 10 days of illness onset, and if this is not possible, within 7 days of illness onset. Treatment of KD before day 5 of illness appears no more likely to prevent cardiac sequelae than treatment on days 5–9. However, it may be associated with an increased need for repeat IVIG treatment. [64, 65] In the presence of 4 of 5 classic criteria for KD, US and Japanese experts agree that only 4 days of fever are necessary before initiating treatment with IVIG. [15, 66]
The efficacy of treating patients using IVIG after 10 days of illness is unknown; therefore, early diagnosis and treatment is desired. IVIG should be administered to children presenting after day 10 of illness (i.e., children with delayed diagnosis or incomplete KD) if they have either persistent fever without explanation or aneurysms and ongoing systemic inflammation, as manifested by elevated ESR or CRP. [4, 67-69] Burns
4.3. IVIG resistance (or IVIG unresponsiveness, initial IVIG treatment failure)
The incidence of IVIG resistance varies from 9.4% to 23% between centers (but it can be as high as 38%, as reported in one US cohort).  Recent studies have identified demographic and laboratory characteristics as predictors of IVIG resistance, including age, illness day, platelet count, ESR, hemoglobin concentration, CRP, eosinophils, lactate dehydrogenase, albumin, and ALT. [5, 29, 71-73] As IVIG-resistant patients are at a higher risk for CAL formation, it is important to identify those who may benefit from more aggressive therapy. As shown in Figure 1 (modified from Newburger
4.4. Methylprednisolone pulse therapy
At present, the usefulness of steroids in the initial treatment of KD is not well established. Newburger
The safety of IVMP therapy in patients with KD is uncertain. Miura
4.5. Tumor necrosis factor- blockade
TNF- levels are elevated in children with KD,  and the TNF- (–308) genetic polymorphism is associated with KD susceptibility, suggesting a role for TNF- receptor blocking in the treatment of KD, especially for those patients/cases refractory to IVIG. The early administration of TNF- receptor antagonists in KD may provide effective adjunctive therapy. Infliximab, which binds the pro-inflammatory cytokine TNF-, has been evaluated in several studies and shown to have a significant effect in KD patients with IVIG resistance. [91-93] Recently, etanercept, a more suitable TNF- receptor blocker for children with refractory juvenile idiopathic arthritis, [94, 95] was reported to benefit the treatment of IVIG-resistant KD as an adjuvant therapy to initial IVIG. [96, 97]A TNF- receptor blocker may be administered after initial IVIG treatment failure or after a second dose of IVIG therapy.
Chronic vascular inflammation and endothelial dysfunction persists in KD patients with CAL, even long after the acute stage. [98, 99] There is currently no specific treatment for ongoing vascular inflammation and endothelial dysfunction. Low-dose aspirin can be prescribed until CAL normalizes, but it does not have an effect on inflammation or endothelial dysfunction. Lipid abnormalities in the acute phase of KD, with decreased triglycerides and high-density lipoprotein cholesterol (HDL-C) levels have been reported in previous studies. [100, 101]
Statins, hydroxymethylglutaryl coenzyme A reductase inhibitors, have been shown to reduce cholesterol levels as well as improve surrogate markers of atherosclerosis and cardiovascular disease.  Huang
4.7. Other treatments
Acute KD can lead to the development of large coronary artery aneurysms that may persist for years. Abciximab, a platelet glycoprotein IIb/IIIa receptor inhibitor, is associated with resolution of thrombi and vascular remodeling in adults with acute coronary syndromes. Williams
There are still no well-defined treatments for refractory KD. Suzuki
Specific changes in inflammatory markers (such as white blood cell count, neutrophil count, CRP, IL-6, soluble IL-2 receptor [sIL-2R] , Th17/regulatory T-cell imbalance , and IL-1 pathway ) have been reported to disrupt immunological functions and result in KD with IVIG resistance and CAL formation. This indicates the possible treatment role of plasma exchange (PE) for KD with IVIG resistance. Mori
5. Genetic association study in Kawasaki disease
The higher incidence of KD in Asia, in conjunction with a higher incidence of the disease in Asian descendants compared with other ethnic populations in the United States and Europe, suggests that genetic predisposition might play an important role in the susceptibility to this disease. [3, 4, 9, 15] There is also evidence that the incidence of KD is higher among siblings than in the general population. A growing number of research reports provide evidence that genetic polymorphisms contribute to the susceptibility to KD. For example, single-nucleotide polymorphisms (SNPs) in the monocyte chemoattractant protein 1 (
6. Genetic polymorphisms of the ITPKC signaling pathway in Kawasaki disease
A major advancement in the genetic study of KD was made by the discovery of
In the non-excitable cells such as T and B cells, calcium entry is mainly through store-operated calcium channels (SOC). The activation of SOC can be controlled by the expression level of IP3, which is the substrate of ITPKC protein. AsITPKCis involved in the Ca2+-dependent NFAT signaling in T cells, genetic association studies between calcium pathways and susceptibility of KD were performed. The calcium-dependent downstream gene CASP3 is a good example. Onouchi
7. Genetic polymorphisms of the TGF- signaling pathway in Kawasaki disease
TGF- is an important molecule that is involved in the regulation of cytokine expression and immune response. It has been shown that TGF--mediated signaling pathways are mainly via transcription factors, Smads, which include at least 3 common proteins: Smad2, Smad3, and Smad4. The binding of TGF- to its receptor results in the phosphorylation of Smad2 or Smad3, which heterodimerizes with Smad4. The formation of the Smad complex further translocates to the nulclus to regulate activation of the target genes. In the cardiovascular system, which is an important target of KD, TGF- signaling is involved in the pathogenesis of multiple cardiovascular diseases via aberrant vascular remodeling. Low expression levels of endogenous TGF- activity in the blood may contribute to the development of atherosclerotic cardiovascular disease. In 2011, a large genetic study revealed a significant association between the polymorphisms in TGF- pathways and KD susceptibility or CAL formation in the European and US populations. In this study, Shimizu
8. Genome-wide association study (GWAS) in Kawasaki disease
In 2009, Burgner
Several major advances have been made in understanding the genetic effects of the susceptibility and clinical status of KD over the past decade. Very recently, genome-wide association led 2 groups (Lee
We thank Siou-Jin Chiu (Kaohsiung Medical University) for help with the figure and the National Science Council (Taiwan) for their research support.
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