Kawasaki disease is an intense systemic pediatric vasculitis disease that is seen normally in childhood. Kawasaki disease is one of the most common bosom diseases. It is the inflammatory upset but the aetiology of Kawasasaki disease is unknown. It foremost appeared in 1967 by study of Tomisaku Kawasaki who was a Nipponese baby doctor. He besides called Kawasaki disease as mucocutaneous lymph node syndrome. There is no diagnostic trial ; hence, physicians are utilizing the clinical standards that were proposed by Dr. Kawasaki 45 old ages ago to name the Kawasaki disease. There are many different diagnosing of Kawasaki disease such as viral infections, familial sensitivity or environmental factors. Many research proposed that Kawasaki disease is an infective disease that may be caused by Epstein-Barr virus, rubeolas, adenovirus, enterovirus. However, there is no confirmed grounds. Normally, KD can establish more in Nipponese society but it keep spread to western states and the incidence of KD in western states are increase dramatically. There are typical symptoms that can be seen in KD such as roseola, hydrops, and mucosal membrane alterations. But there are more symptoms that are involved which are non typically found from every KD patients. Therefore, it is difficult to diagnosis patients if they have KD or non. The intervention of KD is different depends on if patients are complete or uncomplete KD and besides, the susceptibleness of IVIG will do intervention different along patients. The etiology is non certain but there are several researches shown that KD is caused by infective agents, familial factors, or immune system upset.

Current cognition on the topic

There are several symptoms that can be found in patients with Kawasaki disease. When patients have more than 5 yearss of febrility for more than 38C and have more than 4 symptoms such as bilateral nonexudative conjunctival injection, polymorphic skin eruption, nonvesicular roseola, strawberry lingua, hydrops of custodies and pess, bilateral non-suppurative cervical lymphadenopathy, and mucosal membrane alterations, patients will diagnosis as KD. Kawasaki disease can be divided into complete Kawasaki disease and uncomplete or untypical Kawasaki disease depending on the figure of symptom that are present in the patient. When patients have more than four symptoms or have developed coronary arteria abnormalcy, patients will be diagnosed as complete Kawasaki disease. In contrast, patients who have less than four of the diagnostic standards and still develop coronary arteria abnormalcy is diagnosed as untypical or uncomplete KD. Because of the cause of Kawasaki disease is unknown, diagnosing of Kawasaki disease in babies are really ambitious. Kawasaki disease can be divided into three stages. First, from one hebdomad to two hebdomads from oncoming is called acute stage. Typical symptoms are extremely feverish, cranky and the febrility approaches more than 39 Celsius. Oral alterations occurs and besides roseola can be found in perineal country. Second, from two to eight hebdomads from oncoming is called subacute stage. In this stage, fever get down to diminish easy and the perineal country, colloidal suspensions, and periungual countries start to skin off. Last, from months to old ages from oncoming, it is called recovering stage. In this stage, research lab value gets normal but there may be terrible effects. For illustration, patients who had aneurisms may continuously hold, for remainder of their life, relentless cardiac disfunction, or myocardial infarction.

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Coronary arteria aneurism can be extremely found in uncomplete Kawasaki disease patients. It is defined as coronary distension that the diameter of coronary vas gets enlarged 1.5 creases. It can be diagnosed by angiographically and it is similar to patients with coronary arteria disease. The end-diastolic force per unit area, end-diastolic volume, and expulsion fraction degrees are non normal and the left ventricular contraction is non normal. The coronary arteria aneurisms are largely caused by coronary artery disease.

There are several associated symptoms that can be seen in Kawasaki patients. Diarrhea and abdominal hurting and patients may develop arthritis. Besides, myocardial disfunction can be found in early stage of Kawasaki disease such as pancarditis which is the redness of all three beds of bosom. Another symptom is periarteritis nodosa which is disease in connective tissue that is blocked by nodules in arterias thereby doing blood to non go around decently. When Kawasaki disease shows periarteritis nodosa, other symptoms can non be found.

Kawasaki disease can be diagnosis by physical test but besides it can be diagnose by research lab test and imagination technique. First, complete blood count trial should be performed to look at the sum of white blood cell in blood. Complete blood count is the computation of white blood cells, ruddy blood cells, and thrombocyte. The figure of white blood cell increased to more than 15,000. Besides, the erythrocyte deposit rate and C-reactive protein addition. After 2 hebdomads from oncoming of disease, the thrombocytes ‘ degree dramatically increases up to 1 to 2*106. There are other abnormalcies such as unfertile pyuria, additions of hepatic aminotransferases, hypoalbuminemia. In patients who have KD will hold higher degree of aminotransferase than normal individual. Besides, they will hold higher degree of ALAT and GGT than other patients who have other feverish diseases. When ALAT degree additions, it will take to coronary arteria disease. Research proposed that about 50 % of uncomplete KD patients had pyuria in vesica piss. Pyuria can do different diseases depends on where it is. When pyuria is in vesica, it can do tubulointerstitial Bright’s diseases but when it is in voided piss, it will do urethral redness. Another symptom to diagnosis uncomplete KD is to look at acute anterior uveitis after the oncoming. Patients who have anterior uveitis do non hold hurting, photophobia, nor ocular damage. By utilizing ophthalmological rating, it can observe if patients have different disease which have similar symptoms with anterior uveitis. One of the research in 2006 showed that there were 40 % of KD patients had hyponatromia. It is caused by wrong endocrine secernment by intellectual vasculitis, desiccation, or cannular dysfuction. It is difficult to diagnosis KD since there is no diagnosing trial. To handle uncomplete KD, the rule clinical standards should be renewed in order non to lose out some patients who did non hold rule symptoms. By losing out patients will develop terrible other diseases and will non be able to give proper interventions.

KD besides can be found out by utilizing imaging technique. At acute stage, chest X ray or echocardiography ( ECG ) are used to look at bosom job. Patients may develop coronary arteria abnormalcies in acute stage and this can be showed by ECG. When patients are really terrible, bosom specializers sometimes use individual photon emanation computed imaging to look into blood stream of patients. SPECT will supply an image in 3D by utilizing gamma beams.


Kawasaki disease is new disease that is preponderantly found among Asiatic children1,2,3. It was foremost found in Japan by Dr.Kawasaki in 1961. In early 1970s, Pathologist Eunice Larson and Benjamin Landing at Los Angeles recognized it as a new disease. Still today, there is no grounds of how Kawasaki disease emerged but some research workers proposed that Kawasaki disease emerged from Japan and spread to Western states through Hawaii after World War II. Kawasaki disease was countrywide epidemics but now it is more likely a regional eruption. The average one-year incidence rate is different in assortment of states and districts3. There are 90 to 112 per 100,000 in Japan, 8.0 to 47.7 per 100000 in US, and 3.6 to 3.7 per 100000 in the United Kingdom and Australia for kids who are less than 5 old ages old. Research in China indicates that the incidence rate is 18.2 to 18.6 per 1000003. The statistics shows that Japan preponderantly has highest incidence rate among Asiatic. Kawasaki disease can be found normally in males than females and the reoccurrence rate is less than 1 % 3. The incidence of Kawasaki disease has been increasing yearly. In 2000, the incidence rate was 73.7 per 100000 but in 2002, the figure of happening increased to 95.5 per 1000003.

There are relationships between season and happening of Kawasaki disease3. But there are fluctuations among different states. From Nipponese studies, there were more patients in winter but in American information shows that patients will develop KD more in the spring and winter. For female the happening appeared to be high in March, and highest in July. For male childs, the highest happening rate was in May and the lowest happening rate was in February. As the research indicated, the season and climes have relationship with the susceptibleness to Kawasaki disease3.


Patients with Kawasaki disease may develop coronary arteria abnormalcies ( CAAs ) if patients are non treated early. Normally patients are treated with high sums of endovenous gamma-globulin ( IVGG ) every bit good as acetylsalicylic acid which are used to cut down the possibility of developing CAAs2. However, 10-20 % of Kawasaki patients do non response to bring on endovenous gamma-globulin. Coronary arteria abnormalcy will develop more often to patients who are non reacting good to IVGG than patients who respond good to IVGG. Recent research reported that matrix metalloproteinase-9 ( MMP-9 ) is involved in formation of CAA in acute stage of Kawasaki disease patients2. From research, the degree of MMP-9 in serum who have Kawasaki disease have much higher than serum from kids who does non hold KD and patients who have other sorts of feverish diseases2. Using MMP-9 inhibitors might forestall the formation of CAA. However, MMP-9 inhibitors are non used clinically. MMP-9 is endopeptidase that depends on Zn that has zinc at the active site. MMP-9 have major function in tissue remodelling of extracellular membrane ( ECM ) 2. It can be seen in cardiac remodelling after myocardial infarction, plaque destabilization of atherosclerotic lesion. The mechanism of angiotensin-converting enzyme ( ACE ) inhibitors is involve with the bind Zn to the active site and stabilise by H bonds and hydrophobic interactions in the active site. The ACE inhibitor can suppress the activity of MMP-9 and MMP-2, which have major function in neointimal formation and angiogenesis. The consequence of the ACE inhibitor on MMP-9 can be measure by utilizing Capoten to the enzyme2.

Engagement of the immune system

From the surveies by Satoshi Sato, Kawasaki disease is normally found from patients who are younger than 5 old ages old1. The mean age of happening of this disease is 2 old ages. Kawasaki disease does non happen often from kids who is less than 6 months and can barely happen patients who are less than 3 months1. Kawasaki disease normally does non happen for grownups who have unsusceptibility to common infective disease. This consequence explains that kids are more susceptible to Kawasaki disease because they might non bring forth antibodies to common infective viruses, and bacteria1. Mannose bind lectin ( MBL ) is an of import constituent of the innate unsusceptibility and is a reactant for hepatic beginning which can adhere to multiple lectin domains1. MBL has really of import function in complement activation and opsonisation. Complement activation refers to as the biochemical activity that helps to acquire rid of pathogen from animate being and opsonisation have similar activity to complement activation that plays function of pathogens to acquire rid of the being by consumption and devastation by phagocyte1. It is normally found in bacterial cells, fungus cells, and viruses. It has reiterating form of mannose and N-acetylglucosamine sugar. There are three individual polymorphisms in chromosome 10 for MBL cistron at codon 52 ( CGT to TCT ) , codon 54 ( GGC to GAC ) , and codon 57 ( GGA to GAA ) . This mutant will take to decrease of the degree of MBL concentration but polymorphism of the booster part of MBL will take to increase the degree of MBL concentration in the serum1. When the base alterations from glycine to aspartic acid in codon 54, it will deflect the interaction between MBL and MBL-associated serine peptidase. The interaction between MBL and MBL-associated serine peptidase defend against infection when patients are immature. But when patients become older, the interaction of these two molecules will non hold impact on the innate immunity1. Because, the patients will develop the mature lymphocytes and Igs and they will steep the invaded pathogen. Therefore, this research proposes the susceptibleness of the Kawasaki disease will be influenced by the MBL polymorphism1.

Childs who have Kawasaki disease develop endothelial dysfuntion in early stage after oncoming of disease and this will caused by the production of azotic oxide ( NO ) 5. As described earlier, the primary innate immune system is really of import characteristic for Kawasaki disease. Tumour mortification factor alpha, IL-1, 6, 8, monocyte, chemoattractant protein-1 ( MCP-1 ) , and vascular endothelial growing factor ( VEGF ) will be activated to bring forth cytokine storm5. After cytokines are produced, it will let go of iNOS ( inducible azotic oxide synthase ) in neutrophils, endothelial cells, and smooth musculus cells. Nitric oxide is produced by two enzymes which are endothelial NOS and iNOS5. Recent research found out that patients who developed Kawasaki disease have higher degree of iNOS concentration in neutrophils in acute stage. Besides, kids have high degree of azotic oxide metabolites such as NOx, NO3- , and NO2- . After production of Nitric Oxide, it will respond with Reactive Oxygen Species ( ROS ) to give more biochemical reactions. This will be measured by new device called fluorescent indicators5. There are new devices used to mensurate the concentration of NO and ROS. First, Hydroxyphenyl fluorescence ( HPF ) was used to mensurate the concentration of ROS. Another device is called Diaminofluorescin-Flu Diacetate ( DAF-FM DA ) which is used to mensurate the concentration of intracellular Nitric Oxide5.

There are important groundss that the production of ROS and NO by neutrophils were much higher in Kawasaki disease patients in comparison to people who have non-KD feverish kids or non-febrile children5. By handling with IVIG, NO degree will diminish. But, the production of NO can be good or harmful. Normally, NO is cytotoxic but sometimes, it can protect cells from toxic stuffs. No may respond with hydroxyl groups to bring forth much higher toxicity. To command the influence of NO, the continuance, the sum of NO synthesis should be controlled. Therefore, in acute stage of Kawasaki disease, NO and ROS is extremely produced and will do harm to endothelial cells5.

Treatment and future research

When patients are diagnosis as complete or uncomplete KD, intervention should be induced right off. Because when patients have more than 10 yearss of febrility will develop CAA. Major intervention that physicians use to handle KD is endovenous Ig ( IVIG ) . Intravenous immuglobulin induced into blood stream which contains Ig antibody G that is brought from other control blood givers. IVIG is still a major recommended intervention but some patients do non response to this intervention. The effects of IVIG last for 2 hebdomads up to 3 months. The typical sum of IVIG is a dosage of 1000mg per kilogram of patient ‘s bodyweight. High sum of IVIG with acetylsalicylic acid will cut down the rate of coronary arteria abnormalcies ( CAA ) which includes coronary arteria distension or aneurisms from 20 % to 3 to 5 % . Besides, depends of patients, IVIG can besides used with acetylsalicylic acid to handle KD.

There is one illustration about the wrong intervention will do terrible disease. When IVIG was induced, patients could non bring around coronary arteria lesion. When patients induced with corticoid, they developed more coronary arteria lesion3.

There are two therapies which are antiinflammatory and antithrombotic therapy which are to handle Kawasaki disease alternatively of utilizing IVIG. In antiinflammatory therapy, methylprenisolone, Orasone, Pediapred, and Remicade are used to handle Kawasaki disease. For antithrombotic therapy, Aspirin, Lipo-Hepin, Coumadin, exoxaparin, tissue plasminogen activator, clopidogrel, and abciximab are used. Recently, Remicade proved by US Food and Drug disposal to bring around non merely Crohn disease but besides used to handle Kawasaki disease patients. It was non used at all in 2001 but today, the disposal of infliximab use increased up to 2.3 % of entire figure of therapies used. It became favorable because of two grounds. First, it merely administer to patients merely one clip. Second, by non utilizing infliximab more than one time, it cut down the complication as seen in other therapies which are used more than one time. Infliximab is an antibody to tumour mortification factor alpha, and cytokine in inflammatory response. It binds to tumour mortification factor alpha and blocks the T-cell receptors to barricade the biochemical cascade. It will diminish the coronary arteria abnormalcies in patients who developed Kawasaki disease in early ague stage.

To handle KD much better manner, there should be more research. First, there should be more research lab and echocardiographic informations. Second, more development of clinical standards and symptoms should be proposed. Even today, there is no perfect grounds that can explicate the cause of KD ; hence, there should be more research on familial factors by looking at KD patients ‘ household. Last, after intervention of KD in childhood, complication may be developed after several decennaries and there is non much information about complication. Therefore, by monitoring and maintain in touch with KD patients are good manner to happen out more about complication after initial intervention.


  1. Sato, S. , H. Kawashima, Y. Kashiwagi, T. Fujioka, K Takekuma, and A. Hoshika. 2009. Association of mannose-binding lectin cistron polymorphisms with Kawasaki disease in the Japanese. I. Jour. R. Dis. 12:307-310.
  2. Inoue, N. , S. Takai, D. Jin, K. Okumura, N. Okamura, M. Kajiura, S. Yoshikawa, N. Kawamura, H. Tamai, M. Miyazaki. 2010. Consequence of angiotensin-converting enzyme inhibitor on matrix metalloproteinase-9 activity in patients with Kawasaki disease. Clinica Chimica Acta. 411:267-269.
  3. Huang, G.Y. , Ma, X.J. , Huang, M. , Chen, S.B. , Huang, M.R. , Gui, Y.H. , Ning, S.B. , Zhang, T.H. , Du, Z.D. , Yanagawa H. , and Kawasaki T. 2006. Epidemiologic Pictures of Kawasaki disease in Shanghai from 1998 through 2002. Journal of Epidemiology. 16: No. 1.
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  7. Son, M.B.F. , Gauvreau, K. , Ma, L. , Baker, A.L. , Sundel, R.P. , Fulton, D.R. , Newburger, J.W. 2009. Treatment of Kawasaki Disease: Anlaysis of 27 US Pediatric Hospitals From 2001 to 2006. Pediatrics. 124:1-8.
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