Kawasaki disease

Kawasaki disease
Classification and external resources

A child showing characteristic "strawberry tongue" seen in Kawasaki disease
ICD-10 M30.3
ICD-9 446.1
OMIM 611775
DiseasesDB 7121
MedlinePlus 000989
eMedicine ped/1236
MeSH D009080

Kawasaki disease (KD), also known as Kawasaki syndrome, lymph node syndrome and mucocutaneous lymph node syndrome,[1] is an autoimmune disease in which the medium-sized blood vessels throughout the body become inflamed. It is largely seen in children under five years of age. It affects many organ systems, mainly those including the blood vessels, skin, mucous membranes and lymph nodes; however, its rare but most serious effect is on the heart where it can cause fatal coronary artery aneurysms in untreated children. Without treatment, mortality may approach 1%, usually within six weeks of onset. With treatment, the mortality rate is less than 0.01% in the U.S.[2] There is often a pre-existing viral infection that may play a role in its pathogenesis.[3] The conjunctivae and oral mucosa, along with the epidermis (skin), become erythematous (red and inflamed). Edema is often seen in the hands and feet and one or both of the cervical lymph nodes are often enlarged. Also, a remittent fever, often 40°C (104°F) or higher, is characteristic of the acute phase of the disease.[4] In untreated children, the febrile period lasts on average approximately 10 days, but may range from five to 25 days.[4] The disorder was first described in 1967 by Tomisaku Kawasaki in Japan.[5]

Contents

Classification

Systemic vasculitis is an inflammatory condition affecting both veins and arteries throughout the body, and is usually caused by a proliferation of cells associated with an immune response to a pathogen, or autoimmunity.[6] Systemic vasculitides may be classified according to the type of cells involved in the proliferation, as well as the specific type of tissue damage occurring within the vein or arterial walls.[6] Under this classification scheme for systemic vasculitis, Kawasaki disease is considered to be a necrotizing vasculitis (also called necrotizing angeititis), which may be identified histologically by the occurrence of necrosis (tissue death), fibrosis, and proliferation of cells associated with inflammation in the inner layer of the vascular wall.[6][7] Other diseases featuring necrotizing vasculitis include Polyarteritis nodosa, Wegener's granulomatosis, Henoch-Schönlein purpura and Churg-Strauss syndrome.[6] Kawasaki disease may be further classified as a medium-sized-vessel vasculitis, affecting medium and small sized blood vessels,[8][9][10] such as the smaller cutaneous vasculature (veins and arteries in the skin) that range from 50 to 100µm in diameter.[11][12] KD is also considered to be a primary childhood vasculitis, a disorder associated with vasculitis that mainly affects children under the age of 18.[13][14] A recent, consensus-based evaluation of vasculitides occurring primarily in children resulted in a classification scheme for these disorders, to both distinguish them and suggest a more concrete set of diagnostic criteria for each.[14] Within this classification of childhood vasculitides, Kawasaki disease is, again, a predominantly medium-sized vessel vasculitis.[14]

It is also an autoimmune form of vasculitis,[4] and is not associated with ANCA antibodies, unlike other vasculitic disorders associated with them, such as wegener's granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome.[6][15] This categorization is considered essential for appropriate treatment.[16]

Signs and symptoms

Kawasaki disease often begins with a high and persistent fever that is not very responsive to normal treatment with paracetamol (acetaminophen) or ibuprofen.[17][18] it is the most prominent symptom in Kawasaki disease, which is a characteristic sign of the acute phase of the disease, is normally high (above 39-40°C), remittent and followed by extreme irritability.[18][19] recent reports says it is even present in patients with atypical or incomplete KD,[20][21] nevertheless recent reports says it is not present on 100% of cases.[22] The first day of fever is considered the first day of illness,[17] and the duration of fever is on average one to two weeks; in the absence of treatment, it may extend for three to four weeks,[4] Prolonged fever is associated with higher incidence of cardiac involvement.[23] It responds partially to antipyretic drugs and does not cease with the introduction of antibiotics.[4] However, when appropriate therapy is started – intravenous immunoglobulin (IVIG) and aspirin – the fever is gone after two days.[24]

Bilateral conjunctival injection was reported by many publications to be the most common symptom after fever,[25][26] it typically involves the bulbar conjunctivae, is not accompanied by suppuration, it is not painful.[27] It usually begins shortly after the onset of fever during the acute stage of the disease.[17] Anterior uveitis may be present on slit-lamp examination.[28][29] iritis can occur too.[30] Keratic precipitates is another eye manifestation (detectable by a slit lamp but usually too small to be seen by the unaided eye.[17][31]

Kawasaki disease presents with set of oral manifestations, the most characteristic changes are the bright red (erythema), swollen lips (edema) with vertical cracking (fissures) and bleeding.[32] The mucosa of the oropharynx may be bright red, and the tongue may have a typical "strawberry tongue" appearance (marked erythema with prominent gustative papillae).[4][12] These oral manifestations are caused by the typical necrotizing microvasculitis with fibrinoid necrosis.[32]

Cervical lymphadenopathy, is seen in approximately 50 to 75% of patients, whereas the other features are estimated to occur in 90% of patients.[17][25] But sometimes it can be the dominant presenting symptom.[31][31][33] According to the definition of the diagnostic criteria, there should be more than one impaired lymph node and > 1.5 cm in diameter.[12] Affected lymph nodes are not painful or little painful, not-fluctuating and non-suppurative; erythema of the neighboring skin may occur.[17] We should be attentive to those children with fever and neck adenitis that do not respond to antibiotics, because Kawasaki disease should be part of the differential diagnoses.[17]

Less common manifestations
System Manifestations
GIT Diarrhea, abdominal pain, vomiting, liver dysfunction, pancreatitis, Hydrops gallbladder,[34] parotitis,[25][35] cholangitis, intussusception, intestinal pseudo-obstruction, ascites, splenic infarction.
MSS Polyarthritis and arthralgia.
CVS Myocarditis, pericarditis, Tachycardia,[12] valvular heart disease.
GU Urethritis, prostatitis, cystitis, priapism, Interstitial nephritis, orchitis, nephrotic syndrome.
CNS Lethargy, semicoma,[25] Aseptic meningitis, and sensorineural deafness.
RS Shortness of breath,[12] Influenza-like illness, plural effusion, Atelectasis.
Skin Erythema and induration at BCG vaccine site, Beau's lines, and finger gangrene.
Source: review,[12] table.[36]

In the acute phase of the disease changes in the peripheral extremities can include erythema of the palms and soles, which is often striking with sharp demarcation,[17] and often accompanied by painful, brawny edema of the dorsa of the hands or feet in the acute phase of the disease, and it is why affected children frequently refuse to hold objects in their hands or to bear weight on their feet.[4][17] Later during the convalescent or the subacute phase desquamation of the fingers and toes usually begins in the periungual region within two to three weeks after the onset of fever and may extend to include the palms and soles,[37] and around 11% of children affected by the disease may continue skin peeling for many years.[38] 1 to 2 months after the onset of fever deep transverse grooves across the nails may develop (Beau’s lines),[39] And occasionally nail are shed.[39]

The most common cutaneous manifestation is a diffuse macular-papular erythematous rash, which is quite nonspecific.[40] The rash varies over time and is characteristically located on the trunk and may further spread to involve the face, extremities, and perineum.[4] many other forms of cutaneous lesions have been reported also, they may include Scarlatiniform, popular, urticariform, multiform-like erythema, and purpuric lesions, even micropustules were reported,[41][42] it can be polymorphic, non-itchy and normally observed up to the fifth day of fever.[43] however it is never bullous or vesicular[4]

The syndrome affecting multiple organ systems, and in the acute stage of KD, systemic inflammatory changes are evident in many organs.[9] Joint pain (arthralgia) and swelling, frequently symmetrical, Also arthritis can occur.[25] Myocarditis,[44] diarrhea,[12] pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are manifested by the presence of inflammatory cells in the affected tissues.[9] If left untreated, some symptoms will eventually relent, but coronary artery aneurysms will not improve, resulting in a significant risk of death or disability due to myocardial infarction (heart attack).[12] If treated in a timely fashion, this risk can be mostly avoided and the course of illness cut short.[45]

Other reported non-specific symptoms include cough, rhinorrhea, sputum, vomiting, headache, and seizure.[25]

The course of the disease can be divided into three clinical phases.[12] The acute febrile phase, which usually lasts for 1 to 2 weeks, is characterized by fever, conjunctival injection, erythema of the oral mucosa, erythema and swelling of the hands and feet, rash, cervical adenopathy, aseptic meningitis, diarrhea, and hepatic dysfunction.[12] Myocarditis is common during this time, and a pericardial effusion may be present.[17] Coronary arteritis may be present, but aneurysms are generally not yet visible by echocardiography. The subacute phase begins when fever, rash, and lymphadenopathy resolve at about 1 to 2 weeks after the onset of fever, but irritability, anorexia, and conjunctival injection persist. Desquamation of the fingers and toes and thrombocytosis are seen during this stage, which generally lasts until about 4 weeks after the onset of fever. Coronary artery aneurysms usually develop during this time, and the risk for sudden death is highest during this stage.[17][48] The convalescent stage begins when all clinical signs of illness have disappeared and continues until the sedimentation rate returns to normal, usually at 6 to 8 weeks after the onset of illness.[12]

There is differences in clinical presentation between adults and children, as adults have more affection of neck lymph nodes (93% of adults versus 15% of children); hepatitis (65% versus 10%), and arthralgia (61% versus 24-38%).[12][49] Some patients have atypical presentations and may not have the classical symptoms and this occurs in particular in young infants,[50] and those patients are especially at higher risk for cardiac artery aneurysms.[17][51]

Complications

Cardiac

The cardiac complications are the most important aspect of the disease. It is the main cause of heart disease acquired in childhood in the USA and in Japan.[12] In the United States and other developed nations, it appears to have replaced acute rheumatic fever as the most common cause of acquired heart disease in children.[17] Coronary artery aneurysms occur as a sequela of the vasculitis in 20-25% of untreated children.[52] it is first detected at a mean of 10 days of illness and that the peak frequency of coronary dilatation or aneurysms occurs within 4 weeks of onset.[48] aneurysms are classified into small (internal diameter of vessel wall <5mm), medium (diameter ranging from 5-8mm), and giant (diameter > 8mm).[12] Saccular and fusiform aneurysms usually develop between 18 and 25 days after the onset of illness.[17] Even when treated with high-dose IVIG regimens within the first ten days of illness, 5% of children with Kawasaki disease develop at the least transient coronary artery dilation and 1% develop giant aneurysms.[53][54][55] Death can occur due either to myocardial infarction secondary to thrombosis of a coronary artery aneurysm or to rupture of a large coronary artery aneurysm. Death is most common 2 to 12 weeks after the onset of illness.[17]

Many risk factors predicting coronary artery aneurysms have been identified.[23] include persistent fever after IVIG therapy,[56][57] low hemoglobin concentrations, low albumin concentrations, high white-blood-cell count, high band count, high CRP concentrations, male sex, and age less than one year.[58]

Coronary artery lesions resulting from Kawasaki disease change dynamically with time.[4] Resolution one to two years after the onset of the disease has been observed in half of vessels with coronary aneurysms.[59][60] Stenosis, which occurs as a result of the healing process of the vessel wall, often leads to significant coronary obstruction and myocardial ischemia.[59] and eventually can lead to Myocardial infarction.[59]

Myocardial infarction caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the principal cause of death from Kawasaki disease.[61] The highest risk of myocardial infarction occurs in the first year after the onset of the disease.[61] Myocardial infarction in children presents with different symptoms from that in adults. The main symptoms were shock, unrest, vomiting, and abdominal pain; chest pain was most common in older children.[61] most of these children, had the attack occurring during sleep or at rest, and around one third of attacks were asymptomatic.[17]

Valvular insufficiencies, particularly of mitral or tricuspid valves, are often observed in the acute phase of Kawasaki disease due to valvulitis or myocarditis-induced myocardial dysfunction, regardless of coronary involvement.[59] These lesions mostly disappear with the resolution of acute illness,[62] but a very small group of the lesions persist and progress.[63] There is also late-onset aortic or mitral insufficiency caused by thickening or deformation of fibrosed valves, with the timing ranging from several months to years after the onset of Kawasaki disease.[64] Some of these lesions require valve replacement.[65]

Other

Other Kawasaki disease complications have been described, such as aneurysm of other arteries: aortic aneurysm,[66] with a higher number of reported cases involving the abdominal aorta,[67][68] axillary artery aneurysm,[69] brachiocephalic artery aneurysm,[70] aneurysm of iliac and femoral arteries, and renal artery aneurysm.[4][71] other vascular complications can occur such as increased wall thickness and decreased distensibility of carotid arteries,[72] aorta,[73] and brachioradial artery,[74] this change in the vascular tone secondary to endothelial dysfunction.[71] In addition, children with Kawasaki disease, with or without coronary artery complications, may have a more adverse cardiovascular risk profile,[74] such as high blood pressure, obesity, and abnormal serum lipid profile.[75]

Gastrointestinal complications in Kawasaki disease are similar to those observed in Henoch-Schönlein purpura,[69] such as: intestinal obstruction,[76] colon swelling,[77] intestinal ischemia,[78] intestinal pseudo-obstruction,[79] and acute abdomen.[80]

Ophthalmologic changes associated with the disease have been described since the 1980s, being found as uveitis, iridocyclitis, conjunctival hemorrhage,[81][82][83] optic neuritis,[69] amaurosis and ocular artery obstruction.[84] It can also be found as necrotizing vasculitis, progressing into peripheral gangrene.[85]

The neurological complications per central nervous system (CNS) lesion are increasingly reported.[86] The neurological complications found are meningoencephalitis,[87] subdural effusion,[88][89] cerebral hypoperfusion,[90] cerebral ischemia and infarct,[91] cerebelar infarction,[92] manifesting with seizures, chorea, hemiplegia, mental confusion, lethargy and coma,[69] or even a cerebral infarction with no neurological manifestations.[91] Other neurological complications from cranial nerve involvement are reported as ataxia,[69] facial palsy,[93] and sensorineural auditory loss.[94][95] Behavioral changes, are thought to be caused by localised cerebral hypoperfusion,[90] can include attention deficits, learning deficits, emotional disorders (emotional lability, fear of night and night terrors) and internalization problems (anxious, depressive or aggressive behavior).[96][97]

Causes

Like all autoimmune diseases, the cause of Kawasaki disease is presumably the interaction of genetic and environmental factors, possibly including an infection. The specific cause is unknown,[98][99][100] but current theories center primarily on immunological causes for the disease. Evidence increasingly points to an infectious etiology,[101] but debate continues on whether the cause is a conventional antigenic substance or a superantigen.[102] Children's Hospital Boston reported that "some studies have found associations between the occurrence of Kawasaki disease and recent exposure to carpet cleaning or residence near a body of stagnant water; however, cause and effect have not been established."[103] Other data suggests possible correlation of KD with tropospheric wind patterns

An association has been identified with a SNP in the ITPKC gene, which codes an enzyme that negatively regulates T-cell activation.[104] An additional factor that suggests genetic susceptibility is the fact that regardless of where they are living, Japanese children are more likely than other children to contract the disease.[103] The HLA-B51 serotype has been found to be associated with endemic instances of the disease.[105]

Diagnosis

Criteria for Diagnosis of Kawasaki Disease
Fever of ≥5 days' duration associated with at least 4† of the following 5 changes
Bilateral nonsuppurative conjunctivitis
One of more changes of the mucous membranes of the upper respiratory tract, including pharyngeal injection, dry fissured lips, injected lips, and "strawberry" tongue
One or more changes of the extremities, including peripheral erythema, peripheral edema, periungual desquamation, and generalized desquamation
Polymorphous rash, primarily truncal
Cervical lymphadenopathy >1.5 cm in diameter
Disease cannot be explained by some other known disease process
†A diagnosis of Kawasaki disease can be made if fever and only 3 changes are present in conjunction with coronary artery disease documented by two-dimensional echocardiography or coronary angiography.
Source: Nelson's essentials of pediatrics,[106] Review[14]

Kawasaki disease can only be diagnosed clinically (i.e. by medical signs and symptoms). There exists no specific laboratory test for this condition. It is difficult to establish the diagnosis, especially early in the course of the illness, and frequently children are not diagnosed until they have seen several health care providers. Many other serious illnesses can cause similar symptoms, and must be considered in the differential diagnosis, including scarlet fever, toxic shock syndrome, juvenile idiopathic arthritis, and childhood mercury poisoning (infantile acrodynia).

Classically, five days of fever[107] plus four of five diagnostic criteria must be met in order to establish the diagnosis. The criteria are: (1) erythema of the lips or oral cavity or cracking of the lips; (2) rash on the trunk; (3) swelling or erythema of the hands or feet; (4) red eyes (conjunctival injection) (5) swollen lymph node in the neck of at least 15 millimeters.

Many children, especially infants, eventually diagnosed with Kawasaki disease do not exhibit all of the above criteria. In fact, many experts now recommend treating for Kawasaki disease even if only three days of fever have passed and at least three diagnostic criteria are present, especially if other tests reveal abnormalities consistent with Kawasaki disease. In addition, the diagnosis can be made purely by the detection of coronary artery aneurysms in the proper clinical setting.

Investigations

A physical examination will demonstrate many of the features listed above.

Blood tests

Other optional tests

Treatment

Children with Kawasaki disease should be hospitalized and cared for by a physician who has experience with this disease. When in an academic medical center, care is often shared between pediatric cardiology and pediatric infectious disease specialists (although no specific infectious agent has been identified as yet).[103] It is imperative that treatment be started as soon as the diagnosis is made to prevent damage to the coronary arteries.

Intravenous immunoglobulin (IVIG) is the standard treatment for Kawasaki disease[108] and is administered in high doses with marked improvement usually noted within 24 hours. If the fever does not respond, an additional dose may have to be considered. In rare cases, a third dose may be given to the child. IVIG by itself is most useful within the first seven days of onset of fever, in terms of preventing coronary artery aneurysm.

Salicylate therapy, particularly aspirin, remains an important part of the treatment (though questioned by some)[109] but salicylates alone are not as effective as IVIG. Aspirin therapy is started at high doses until the fever subsides, and then is continued at a low dose when the patient returns home, usually for two months to prevent blood clots from forming. Except for Kawasaki disease and a few other indications, aspirin is otherwise normally not recommended for children due to its association with Reye's syndrome. Because children with Kawasaki disease will be taking aspirin for up to several months, vaccination against varicella and influenza is required, as these infections are most likely to cause Reye's syndrome.[110]

Corticosteroids have also been used,[111] especially when other treatments fail or symptoms recur, but in a randomized controlled trial, the addition of corticosteroid to immune globulin and aspirin did not improve outcome.[112] Additionally, corticosteroid use in the setting of Kawasaki disease is associated with increased risk of coronary artery aneurysm, and so its use is generally contraindicated in this setting. In cases of kawasaki disease refractory to IVIG, cyclophosphamide and plasma exchange have been investigated as possible treatments, with variable outcomes.

There are also treatments for iritis and other eye symptoms. Another treatment may include the use of Infliximab (Remicade). Infliximab works by binding tumour necrosis factor alpha.[113]

Prognosis

With early treatment, rapid recovery from the acute symptoms can be expected and the risk of coronary artery aneurysms greatly reduced. Untreated, the acute symptoms of Kawasaki disease are self-limited (i.e. the patient will recover eventually), but the risk of coronary artery involvement is much greater. Overall, about 2% of patients die from complications of coronary vasculitis. Patients who have had Kawasaki disease should have an echocardiogram initially every few weeks, and then every one or two years to screen for progression of cardiac involvement.

Laboratory evidence of increased inflammation combined with demographic features (male sex, age less than six months or greater than eight years) and incomplete response to IVIG therapy create a profile of a high-risk patient with Kawasaki disease.[58][114] The likelihood that an aneurysm will resolve appears to be determined in large measure by the initial size of the aneurysm, in which the smaller aneurysms have a greater likelihood of regression.[115][116] Other factors that are positively associated with the regression of aneurysms include being younger than a year old at the onset of Kawasaki disease, fusiform rather than saccular aneurysm morphology, and an aneurysm location in a distal coronary segment.[60] The highest rate of progression to stenosis occurs among those who develop large aneurysms.[4] The worst prognosis occurs in children with giant aneurysms.[117] This severe outcome may require further treatment such as percutaneous transluminal angioplasty,[118] coronary artery stenting,[119] bypass grafting,[120] and even cardiac transplantation.[121]

It is also not uncommon that a relapse of symptoms may occur soon after initial treatment with IVIG. This usually requires re-hospitalization and re-treatment. Treatment with IVIG can cause allergic and non-allergic acute reactions, aseptic meningitis, fluid overload and, rarely, other serious reactions. Overall, life-threatening complications resulting from therapy for Kawasaki disease are exceedingly rare, especially compared with the risk of non-treatment. There is also evidence that Kawasaki disease produces altered lipid metabolism that persists beyond clinical resolution of the disease.

Epidemiology

Kawasaki disease affects boys more than girls with people of Asian ethnicity, particularly Japanese and Korean people are most susceptible as well as people of Afro-Caribbean ethnicity. The disease was rare in Caucasians until the last few decades and incidence rate fluctuates from country to country.

Currently, Kawasaki disease is the most commonly diagnosed pediatric vasculitis in the world. By far the highest incidence of Kawasaki disease occurs in Japan, with the most recent study placing the attack rate at 218.6 per 100,000 children <5 years of age (~1 in 450 children). At this present attack rate, more than 1 in 150 children in Japan will develop Kawasaki disease during their lifetime.

However, its incidence in the United States is increasing. Kawasaki disease is predominantly a disease of young children, with 80% of patients younger than five years of age. Approximately 2,000-4,000 cases are identified in the United States each year.[103][122]

In the United Kingdom, estimates of incidence rate vary because of the rarity of Kawasaki disease. However, Kawasaki disease is believed to affect fewer than 1 in every 25,000 people.[123] Incidence of the disease doubled from 1991 to 2000 however, with 4 cases in per 100,000 children in 1991 compared with a rise of 8 cases per 100,000 in 2000.[124]

History

The disease was first reported by Tomisaku Kawasaki in a four-year-old child with a rash and fever at the Red Cross Hospital in Tokyo, Japan in January 1961, and later published a report on 50 similar cases.[125] Later Yamamoto and colleagues were persuade that there is definite cardiac involvement when they studied and reported 23 cases, of which 11(48%) patients had abnormalities detected by an electrocardiogram.[126] It was not until 1974 that the first description of this disorder was published in the English language literature.[127] in the year 1976 Melish et al., described the same illness in 16 children in Hawaii.[128] Melish and Kawasaki had independently developed the same diagnostic criteria for the disorder, which are still used today to make the diagnosis of classic KS.

A question was raised whether the disease only started during the period between 1960 and 1970, but later a preserved heart of a 7 year old boy who died in 1870 was examined and showed three aneurysms of the coronary arteries with clots, as well as pathologic changes consistent with KS.[129] KS is now recognized worldwide. In the United States and other developed nations, it appears to have replaced acute rheumatic fever as the most common cause of acquired heart disease in children.[130]

References

  1. ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. pp. 1232–4. ISBN 1-4160-2999-0. 
  2. ^ "Merck Manual, Online edition: Kawasaki Disease". http://www.merck.com/mmpe/sec19/ch286/ch286d.html. Retrieved May 9, 2010. 
  3. ^ Okano M, Luka J, Thiele GM, Sakiyama Y, Matsumoto S, Purtilo DT (October 1989). "Human herpesvirus 6 infection and Kawasaki disease". Journal of Clinical Microbiology 27 (10): 2379–80. PMC 267029. PMID 2555393. http://jcm.asm.org/cgi/pmidlookup?view=long&pmid=2555393. 
  4. ^ a b c d e f g h i j k l m Kim DS (December 2006). "Kawasaki Disease". Yonsei Medical Journal 47 (6): 759–72. doi:10.3349/ymj.2006.47.6.759. PMC 2687814. PMID 17191303. http://www.eymj.org/DOIx.php?id=10.3349/ymj.2006.47.6.759. 
  5. ^ Kawasaki T (1967). "[Acute febrile mucocutaneous syndrome with lymphoid involvement with specific desquamation of the fingers and toes in children]". Arerugi 16 (3): 178–222. PMID 6062087. 
  6. ^ a b c d e Guillevin L, Pagnoux C (Mar 2008). "[Classification of systemic vasculitides]" (in French). La Revue Du Praticien 58 (5): 480–6. PMID 18524103. 
  7. ^ "necrotizing vasculitis - definition of necrotizing vasculitis". Free Online Medical Dictionary, Thesaurus and Encyclopedia. http://medical-dictionary.thefreedictionary.com/necrotizing+vasculitis. Retrieved 2010-05-19. 
  8. ^ Dillon MJ, Eleftheriou D, Brogan PA (Nov 2009). "Medium-size-vessel vasculitis". Pediatric Nephrology (Berlin, Germany) 25 (9): 1641–52. doi:10.1007/s00467-009-1336-1. ISBN 0046700913361. PMC 2908435. PMID 19946711. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2908435. 
  9. ^ a b c Fujiwara H, Fujiwara T, Kao TC, Ohshio G, Hamashima Y (Jun 1986). "Pathology of Kawasaki disease in the healed stage. Relationships between typical and atypical cases of Kawasaki disease". Acta Pathologica Japonica 36 (6): 857–67. PMID 3766134. 
  10. ^ Rigante D (2006). "Clinical overview of vasculitic syndromes in the pediatric age". European Review for Medical and Pharmacological Sciences 10 (6): 337–45. PMID 17274537. 
  11. ^ Brandt HR, Arnone M, Valente NY, Sotto MN, Criado PR (2009). "[Medium and large vessel vasculitis"] (in Portuguese). An Bras Dermatol 84 (1): 55–67. PMID 19377760. http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0365-05962009000100008&lng=en&nrm=iso&tlng=en. 
  12. ^ a b c d e f g h i j k l m n Castro PA, Urbano LM, Costa IM (Aug 2009). "[Kawasaki disease"] (in Portuguese). Anais Brasileiros De Dermatologia 84 (4): 317–29. doi:10.1590/S0365-05962009000400002. PMID 19851663. http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0365-05962009000400002&lng=en&nrm=iso&tlng=en. 
  13. ^ Herlin T, Nielsen S (Sep 2008). "[Primary childhood vasculitis--new classification criteria]". Ugeskr Laeger 170 (36): 2784–2787. PMID 18761873. 
  14. ^ a b c d Ozen S, Ruperto N, Dillon MJ, et al. (July 2006). "EULAR/PReS endorsed consensus criteria* for the classification of childhood vasculitides". Ann. Rheum. Dis. 65 (7): 936–41. doi:10.1136/ard.2005.046300. PMC 1798210. PMID 16322081. http://ard.bmj.com/cgi/pmidlookup?view=long&pmid=16322081. 
  15. ^ Guillevin L, Pagnoux C, Guilpain P (May 2007). "[Classification of systemic vasculatides"] (in French). Presse Med 36 (5 Pt 2): 845–53. doi:10.1016/j.lpm.2007.01.035. PMID 17408915. http://www.masson.fr/masson/S0755-4982(07)00189-3. 
  16. ^ Jennette JC, Falk RJ (Oct 2000). "Do vasculitis categorization systems really matter?". Curr Rheumatol Rep 2 (5): 430–8. doi:10.1007/s11926-000-0044-4. PMID 11123094. 
  17. ^ a b c d e f g h i j k l m n o p Rowley AH, Shulman ST (Jul 1998). "Kawasaki Syndrome". Clinical Microbiology Reviews 11 (3): 405–14. PMC 88887. PMID 9665974. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=9665974. 
  18. ^ a b Kawasaki T (Jan 1995). "General review and problems in Kawasaki disease". Japanese Heart Journal 36 (1): 1–12. doi:10.1536/ihj.36.1. PMID 7760506. 
  19. ^ Cassidy JT, Petty RE. Vasculitis. In: Cassidy JT, Petty RE, eds. Textbook of pediatric rheumatology. 3rd ed. Philadelphia, W.B: Saunders Company; 1995. p. 365-422
  20. ^ Fukushige J, Takahashi N, Ueda Y, Ueda K (October 1994). "Incidence and clinical features of incomplete Kawasaki disease". Acta Paediatrica (Oslo, Norway : 1992) 83 (10): 1057–60. doi:10.1111/j.1651-2227.1994.tb12985.x. PMID 7841704. 
  21. ^ Rowley AH, Gonzalez-Crussi F, Gidding SS, Duffy CE, Shulman ST (March 1987). "Incomplete Kawasaki disease with coronary artery involvement". The Journal of Pediatrics 110 (3): 409–13. doi:10.1016/S0022-3476(87)80503-6. PMID 3819942. 
  22. ^ Rodriguez-Lozano AL, Rivas-Larrauri FE, Hernandez-Bautista VM, Yamazaki-Nakashimada MA (September 2011). "Fever is not always present in Kawasaki disease". Rheumatology International. doi:10.1007/s00296-011-2123-4. PMID 21881982. 
  23. ^ a b Mori M, Imagawa T, Yasui K, Kanaya A, Yokota S (August 2000). "Predictors of coronary artery lesions after intravenous gamma-globulin treatment in Kawasaki disease". The Journal of Pediatrics 137 (2): 177–80. doi:10.1067/mpd.2000.107890. PMID 10931408. 
  24. ^ Newburger JW, Takahashi M, Beiser AS, et al. (June 1991). "A single intravenous infusion of gamma globulin as compared with four infusions in the treatment of acute Kawasaki syndrome". The New England Journal of Medicine 324 (23): 1633–9. doi:10.1056/NEJM199106063242305. PMID 1709446. 
  25. ^ a b c d e f Yun SH, Yang NR, Park SA (July 2011). "Associated Symptoms of Kawasaki Disease". Korean Circulation Journal 41 (7): 394–8. doi:10.4070/kcj.2011.41.7.394. PMC 3152734. PMID 21860641. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3152734. 
  26. ^ Martínez Ruiz M, del Castillo Martín F, Borque Andrés C, et al. (October 2003). "[Incidence and clinical characteristics of Kawasaki's disease]" (in Spanish; Castilian). Anales De Pediatría (Barcelona, Spain : 2003) 59 (4): 323–7. PMID 14519302. 
  27. ^ Svobodová D, Slaný J, Pískovský T (2008). "[Kawasaki disease and its ocular manifestations]" (in Czech). Casopís Lékar̆ů C̆eských 147 (3): 162–4. PMID 18401983. 
  28. ^ Burns JC, Joffe L, Sargent RA, Glode MP (1985). "Anterior uveitis associated with Kawasaki syndrome". Pediatric Infectious Disease 4 (3): 258–61. doi:10.1097/00006454-198505000-00010. PMID 4039819. 
  29. ^ Bachmeyer C, Turc Y, Curan D, Duval-Arnould M (Jan 2000). "Anterior uveitis as the initial sign of adult Kawasaki syndrome (mucocutaneous lymph node syndrome)". American Journal of Ophthalmology 129 (1): 101–2. doi:10.1016/S0002-9394(99)00285-8. PMID 10653425. http://linkinghub.elsevier.com/retrieve/pii/S0002939499002858. 
  30. ^ Smith LB, Newburger JW, Burns JC (Feb 1989). "Kawasaki syndrome and the eye". The Pediatric Infectious Disease Journal 8 (2): 116–8. PMID 2468129. 
  31. ^ a b c Kubota M, Usami I, Yamakawa M, Tomita Y, Haruta T (Jun 2008). "Kawasaki disease with lymphadenopathy and fever as sole initial manifestations". Journal of Paediatrics and Child Health 44 (6): 359–62. doi:10.1111/j.1440-1754.2008.01310.x. PMID 18476929. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1034-4810&date=2008&volume=44&issue=6&spage=359. 
  32. ^ a b Scardina GA, Fucà G, Carini F, et al. (December 2007). "Oral necrotizing microvasculitis in a patient affected by Kawasaki disease". Medicina Oral, Patología Oral Y Cirugía Bucal 12 (8): E560–4. PMID 18059239. 
  33. ^ Stamos JK, Corydon K, Donaldson J, Shulman ST (March 1994). "Lymphadenitis as the dominant manifestation of Kawasaki disease". Pediatrics 93 (3): 525–8. PMID 8115224. 
  34. ^ Suddleson EA, Reid B, Woolley MM, Takahashi M (October 1987). "Hydrops of the gallbladder associated with Kawasaki syndrome". Journal of Pediatric Surgery 22 (10): 956–9. doi:10.1016/S0022-3468(87)80600-0. PMID 3316594. 
  35. ^ Do HJ, Baek JG, Kim HJ, et al. (November 2009). "Kawasaki Disease Presenting as Parotitis in a 3-Month-Old Infant". Korean Circulation Journal 39 (11): 502–4. doi:10.4070/kcj.2009.39.11.502. PMC 2790127. PMID 19997548. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2790127. 
  36. ^ http://www.scielo.br/img/revistas/abd/v84n4/en_4a02qua03.jpg
  37. ^ Wang S, Best BM, Burns JC (June 2009). "Periungual Desquamation in Patients with Kawasaki Disease". The Pediatric Infectious Disease Journal 28 (6): 538–9. doi:10.1097/INF.0b013e3181945984. PMC 2738931. PMID 19483521. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2738931. 
  38. ^ Michie C, Kinsler V, Tulloh R, Davidson S (October 2000). "Recurrent skin peeling following Kawasaki disease". Archives of Disease in Childhood 83 (4): 353–5. doi:10.1136/adc.83.4.353. PMC 1718513. PMID 10999876. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1718513. 
  39. ^ a b López Neyra A, Alvarez-Coca González J, Pérez Suárez E, Martínez Pérez J, Rubio Villanueva JL (December 2007). "[Beau's lines and Kawasaki disease]" (in Spanish; Castilian). Anales De Pediatría (Barcelona, Spain : 2003) 67 (6): 610–1. PMID 18053534. 
  40. ^ González Pascual E, Villanueva Lamas J, Ros Viladoms J, Pons Odena M, Ruiz García-Diego S (January 1999). "[Kawasaki disease. A report of 50 cases]" (in Spanish; Castilian). Anales Españoles De Pediatría 50 (1): 39–43. PMID 10083641. 
  41. ^ Kwan YW, Leung CW (December 2005). "Pustulo-vesicular skin eruption in a child with probable Kawasaki disease". European Journal of Pediatrics 164 (12): 770–1. doi:10.1007/s00431-005-1715-y. PMID 16010565. 
  42. ^ Ulloa-Gutierrez R, Acón-Rojas F, Camacho-Badilla K, Soriano-Fallas A (December 2007). "Pustular rash in Kawasaki syndrome". The Pediatric Infectious Disease Journal 26 (12): 1163–5. doi:10.1097/INF.0b013e31814619ec. PMID 18043462. 
  43. ^ Dajani AS, Taubert KA, Gerber MA, et al. (May 1993). "Diagnosis and therapy of Kawasaki disease in children". Circulation 87 (5): 1776–80. doi:10.1161/01.CIR.87.5.1776. PMID 8491037. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8491037. 
  44. ^ Dahdah N (Apr 2010). "Not just coronary arteritis, Kawasaki disease is a myocarditis, too". Journal of the American College of Cardiology 55 (14): 1507; author reply 1507–8. doi:10.1016/j.jacc.2009.11.067. PMID 20359606. http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(10)00398-0. 
  45. ^ Tse SM, Silverman ED, McCrindle BW, Yeung RS (Apr 2002). "Early treatment with intravenous immunoglobulin in patients with Kawasaki disease". J. Pediatr. 140 (4): 450–5. doi:10.1067/mpd.2002.122469. PMID 12006960. http://linkinghub.elsevier.com/retrieve/pii/S0022-3476(02)76010-1. 
  46. ^ Full text at PMC: 88887 / 88887
    Citation will be completed automatically in a few minutes.Jump the queue or expand by hand
  47. ^ http://img.medscape.com/pi/emed/ckb/pediatrics_general/1331341-1331368-965367-2063095.jpg
  48. ^ a b Hirose O, Misawa H, Kijima Y, et al. (March 1981). "[Two-dimensional echocardiography of coronary artery in Kawasaki disease (MCLS): detection, changes in acute phase, and follow-up observation of the aneurysm (author's transl)]" (in Japanese). Journal of Cardiography 11 (1): 89–104. PMID 7264399. 
  49. ^ Wolff AE, Hansen KE, Zakowski L (May 2007). "Acute Kawasaki Disease: Not Just for Kids". Journal of General Internal Medicine 22 (5): 681–4. doi:10.1007/s11606-006-0100-5. PMC 1852903. PMID 17443379. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1852903. 
  50. ^ Burns JC, Wiggins JW, Toews WH, et al. (November 1986). "Clinical spectrum of Kawasaki disease in infants younger than 6 months of age". The Journal of Pediatrics 109 (5): 759–63. doi:10.1016/S0022-3476(86)80689-8. PMID 3772656. 
  51. ^ Boven K, De Graeff-Meeder ER, Spliet W, Kuis W (August 1992). "Atypical Kawasaki disease: an often missed diagnosis". European Journal of Pediatrics 151 (8): 577–80. doi:10.1007/BF01957725. PMID 1505575. 
  52. ^ Suzuki A, Kamiya T, Kuwahara N, et al. (1986). "Coronary arterial lesions of Kawasaki disease: cardiac catheterization findings of 1100 cases". Pediatric Cardiology 7 (1): 3–9. doi:10.1007/BF02315475. PMID 3774580. 
  53. ^ Durongpisitkul K, Gururaj VJ, Park JM, Martin CF (December 1995). "The prevention of coronary artery aneurysm in Kawasaki disease: a meta-analysis on the efficacy of aspirin and immunoglobulin treatment". Pediatrics 96 (6): 1057–61. PMID 7491221. 
  54. ^ Terai M, Shulman ST (December 1997). "Prevalence of coronary artery abnormalities in Kawasaki disease is highly dependent on gamma globulin dose but independent of salicylate dose". The Journal of Pediatrics 131 (6): 888–93. doi:10.1016/S0022-3476(97)70038-6. PMID 9427895. http://linkinghub.elsevier.com/retrieve/pii/S0022-3476(97)70038-6. Retrieved 2011-12-08. 
  55. ^ Dajani AS, Taubert KA, Takahashi M, et al. (February 1994). "Guidelines for long-term management of patients with Kawasaki disease. Report from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association". Circulation 89 (2): 916–22. PMID 8313588. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8313588. Retrieved 2011-12-08. 
  56. ^ Kobayashi T, Inoue Y, Morikawa A (February 2008). "[Risk stratification and prediction of resistance to intravenous immunoglobulin in Kawasaki disease]" (in Japanese). Nihon Rinsho. Japanese Journal of Clinical Medicine 66 (2): 332–7. PMID 18260333. 
  57. ^ Harada K (December 1991). "Intravenous gamma-globulin treatment in Kawasaki disease". Acta Paediatrica Japonica; Overseas Edition 33 (6): 805–10. PMID 1801561. 
  58. ^ a b Koren G, Lavi S, Rose V, Rowe R (March 1986). "Kawasaki disease: review of risk factors for coronary aneurysms". The Journal of Pediatrics 108 (3): 388–92. doi:10.1016/S0022-3476(86)80878-2. PMID 3950818. 
  59. ^ a b c d Kato H, Sugimura T, Akagi T, et al. (September 1996). "Long-term consequences of Kawasaki disease. A 10- to 21-year follow-up study of 594 patients". Circulation 94 (6): 1379–85. PMID 8822996. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8822996. Retrieved 2011-12-08. 
  60. ^ a b Takahashi M, Mason W, Lewis AB (February 1987). "Regression of coronary aneurysms in patients with Kawasaki syndrome". Circulation 75 (2): 387–94. doi:10.1161/01.CIR.75.2.387. PMID 3802442. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=3802442. Retrieved 2011-12-08. 
  61. ^ a b c Kato H, Ichinose E, Kawasaki T (June 1986). "Myocardial infarction in Kawasaki disease: clinical analyses in 195 cases". The Journal of Pediatrics 108 (6): 923–7. doi:10.1016/S0022-3476(86)80928-3. PMID 3712157. 
  62. ^ Suzuki A, Kamiya T, Tsuchiya K, et al. (February 1988). "Tricuspid and mitral regurgitation detected by color flow Doppler in the acute phase of Kawasaki disease". The American Journal of Cardiology 61 (4): 386–90. doi:10.1016/0002-9149(88)90950-2. PMID 3341217. http://linkinghub.elsevier.com/retrieve/pii/0002-9149(88)90950-2. Retrieved 2011-12-02. 
  63. ^ Akagi T, Kato H, Inoue O, Sato N, Imamura K (August 1990). "Valvular heart disease in Kawasaki syndrome: incidence and natural history". American Heart Journal 120 (2): 366–72. doi:10.1016/0002-8703(90)90081-8. PMID 2382613. 
  64. ^ Gidding SS, Shulman ST, Ilbawi M, Crussi F, Duffy CE (April 1986). "Mucocutaneous lymph node syndrome (Kawasaki disease): delayed aortic and mitral insufficiency secondary to active valvulitis". Journal of the American College of Cardiology 7 (4): 894–7. doi:10.1016/S0735-1097(86)80354-0. PMID 3958349. 
  65. ^ Fukunaga S, Egashira A, Arinaga K, et al. (March 1996). "Aortic valve replacement for aortic regurgitation due to Kawasaki disease. Report of two cases". The Journal of Heart Valve Disease 5 (2): 231–4. PMID 8665019. 
  66. ^ Ravekes WJ, Colan SD, Gauvreau K, et al. (April 2001). "Aortic root dilation in Kawasaki disease". The American Journal of Cardiology 87 (7): 919–22. doi:10.1016/S0002-9149(00)01541-1. PMID 11274955. 
  67. ^ Fuyama Y, Hamada R, Uehara R, et al. (June 1996). "Long-term follow up of abdominal aortic aneurysm complicating Kawasaki disease: comparison of the effectiveness of different imaging methods". Acta Paediatrica Japonica; Overseas Edition 38 (3): 252–5. PMID 8741316. 
  68. ^ Miyake T, Yokoyama T, Shinohara T, Seto S, Oiki M (August 1995). "Transient dilatation of the abdominal aorta in an infant with Kawasaki disease associated with thrombocytopenia". Acta Paediatrica Japonica; Overseas Edition 37 (4): 521–5. PMID 7572158. 
  69. ^ a b c d e Alves NR, Magalhães CM, Almeida Rde F, Santos RC, Gandolfi L, Pratesi R (June 2011). "Prospective study of Kawasaki disease complications: review of 115 cases". Revista Da Associação Médica Brasileira (1992) 57 (3): 295–300. PMID 21691693. 
  70. ^ Yang G, Thompson D, Warren A (February 2009). "Late-appearing brachiocephalic aneurysm: an atypical vascular sequella of Kawasaki disease". Pediatric Cardiology 30 (2): 197–9. doi:10.1007/s00246-008-9296-y. PMID 18704549. 
  71. ^ a b Dhillon R, Clarkson P, Donald AE, et al. (November 1996). "Endothelial dysfunction late after Kawasaki disease". Circulation 94 (9): 2103–6. PMID 8901658. 
  72. ^ Cheung YF, Wong SJ, Ho MH (January 2007). "Relationship between carotid intima‐media thickness and arterial stiffness in children after Kawasaki disease". Archives of Disease in Childhood 92 (1): 43–7. doi:10.1136/adc.2006.096628. PMC 2083125. PMID 16820386. http://adc.bmj.com/cgi/pmidlookup?view=long&pmid=16820386. Retrieved 2011-12-02. 
  73. ^ Ooyanagi R, Fuse S, Tomita H, et al. (August 2004). "Pulse wave velocity and ankle brachial index in patients with Kawasaki disease". Pediatrics International : Official Journal of the Japan Pediatric Society 46 (4): 398–402. doi:10.1111/j.1442-200x.2004.01929.x. PMID 15310302. http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1328-8067&date=2004&volume=46&issue=4&spage=398. Retrieved 2011-12-02. 
  74. ^ a b Cheung YF, Yung TC, Tam SC, Ho MH, Chau AK (January 2004). "Novel and traditional cardiovascular risk factors in children after Kawasaki disease: implications for premature atherosclerosis". Journal of the American College of Cardiology 43 (1): 120–4. doi:10.1016/j.jacc.2003.08.030. PMID 14715193. http://linkinghub.elsevier.com/retrieve/pii/S073510970301369X. Retrieved 2011-12-02. 
  75. ^ Senzaki H, Chen CH, Ishido H, et al. (April 2005). "Arterial hemodynamics in patients after Kawasaki disease". Circulation 111 (16): 2119–25. doi:10.1161/01.CIR.0000162483.51132.25. PMID 15851619. http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15851619. Retrieved 2011-12-02. 
  76. ^ Yaniv L, Jaffe M, Shaoul R (September 2005). "The surgical manifestations of the intestinal tract in Kawasaki disease". Journal of Pediatric Surgery 40 (9): e1–4. doi:10.1016/j.jpedsurg.2005.05.063. PMID 16150324. 
  77. ^ Kim MY, Noh JH (August 2008). "A Case of Kawasaki Disease with Colonic Edema". Journal of Korean Medical Science 23 (4): 723–6. doi:10.3346/jkms.2008.23.4.723. PMC 2526417. PMID 18756065. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2526417. 
  78. ^ Beiler HA, Schmidt KG, von Herbay A, Löffler W, Daum R (April 2001). "Ischemic small bowel strictures in a case of incomplete Kawasaki disease". Journal of Pediatric Surgery 36 (4): 648–50. doi:10.1053/jpsu.2001.22311. PMID 11283899. 
  79. ^ Akikusa JD, Laxer RM, Friedman JN (May 2004). "Intestinal pseudoobstruction in Kawasaki disease". Pediatrics 113 (5): e504–6. doi:10.1542/peds.113.5.e504. PMID 15121996. 
  80. ^ Zulian F, Falcini F, Zancan L, et al. (June 2003). "Acute surgical abdomen as presenting manifestation of Kawasaki disease". The Journal of Pediatrics 142 (6): 731–5. doi:10.1067/mpd.2003.232. PMID 12838207. 
  81. ^ Ohno S, Miyajima T, Higuchi M, et al. (June 1982). "Ocular manifestations of Kawasaki's disease (mucocutaneous lymph node syndrome)". American Journal of Ophthalmology 93 (6): 713–7. PMID 7201245. 
  82. ^ Burke MJ, Rennebohm RM (1981). "Eye involvement in Kawasaki disease". Journal of Pediatric Ophthalmology and Strabismus 18 (5): 7–11. PMID 7299613. 
  83. ^ Anand S, Yang YC (2004). "Optic disc changes in Kawasaki disease". Journal of Pediatric Ophthalmology and Strabismus 41 (3): 177–9. PMID 15206604. 
  84. ^ Farvardin M, Kashef S, Aleyasin S, Nabavizadeh SH, Sajjadi M, Safari M (2007). "Sudden unilateral blindness in a girl with Kawasaki disease". Journal of Pediatric Ophthalmology and Strabismus 44 (5): 303–4. PMID 17913174. 
  85. ^ Tomita S, Chung K, Mas M, Gidding S, Shulman ST (January 1992). "Peripheral gangrene associated with Kawasaki disease". Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America 14 (1): 121–6. doi:10.1093/clinids/14.1.121. PMID 1571415. 
  86. ^ Tabarki B, Mahdhaoui A, Selmi H, Yacoub M, Essoussi AS (September 2001). "Kawasaki disease with predominant central nervous system involvement". Pediatric Neurology 25 (3): 239–41. doi:10.1016/S0887-8994(01)00290-9. PMID 11587880. 
  87. ^ Takagi K, Umezawa T, Saji T, Morooka K, Matsuo N (September 1990). "[Meningoencephalitis in Kawasaki disease]" (in Japanese). No to Hattatsu. Brain and Development 22 (5): 429–35. PMID 2223179. 
  88. ^ Aoki N (March 1988). "Subdural effusion in the acute stage of Kawasaki disease (Mucocutaneous lymph node syndrome)". Surgical Neurology 29 (3): 216–7. doi:10.1016/0090-3019(88)90009-2. PMID 3344468. 
  89. ^ Bailie NM, Hensey OJ, Ryan S, Allcut D, King MD (2001). "Bilateral subdural collections--an unusual feature of possible Kawasaki disease". European Journal of Paediatric Neurology : EJPN : Official Journal of the European Paediatric Neurology Society 5 (2): 79–81. doi:10.1053/ejpn.2001.0469. PMID 11589317. 
  90. ^ a b Ichiyama T, Nishikawa M, Hayashi T, Koga M, Tashiro N, Furukawa S (July 1998). "Cerebral hypoperfusion during acute Kawasaki disease". Stroke; a Journal of Cerebral Circulation 29 (7): 1320–1. doi:10.1161/01.STR.29.7.1320. PMID 9660380. 
  91. ^ a b Fujiwara S, Yamano T, Hattori M, Fujiseki Y, Shimada M (1992). "Asymptomatic cerebral infarction in Kawasaki disease". Pediatric Neurology 8 (3): 235–6. doi:10.1016/0887-8994(92)90077-C. PMID 1622525. 
  92. ^ Muneuchi J, Kusuhara K, Kanaya Y, et al. (January 2006). "Magnetic resonance studies of brain lesions in patients with Kawasaki disease". Brain & Development 28 (1): 30–3. doi:10.1016/j.braindev.2005.04.003. PMID 15967620. 
  93. ^ Wright H, Waddington C, Geddes J, Newburger JW, Burgner D (September 2008). "Facial nerve palsy complicating Kawasaki disease". Pediatrics 122 (3): e783–5. doi:10.1542/peds.2007-3238. PMID 18678602. 
  94. ^ Knott PD, Orloff LA, Harris JP, Novak RE, Burns JC (2001). "Sensorineural hearing loss and Kawasaki disease: a prospective study". American Journal of Otolaryngology 22 (5): 343–8. doi:10.1053/ajot.2001.26495. PMID 11562886. 
  95. ^ Silva CH, Roscoe IC, Fernandes KP, Novaes RM, Lázari CS (2002). "[Sensorineural hearing loss associated to Kawasaki Disease"] (in Portuguese). Jornal De Pediatria 78 (1): 71–4. PMID 14647816. http://www.jped.com.br/conteudo/02-78-01-71/ing.asp. Retrieved 2011-12-01. 
  96. ^ Carlton-Conway D, Ahluwalia R, Henry L, Michie C, Wood L, Tulloh R (2005). "Behaviour sequelae following acute Kawasaki disease". BMC Pediatrics 5: 14. doi:10.1186/1471-2431-5-14. PMC 1156909. PMID 15916701. http://www.biomedcentral.com/1471-2431/5/14. Retrieved 2011-12-02. 
  97. ^ King WJ, Schlieper A, Birdi N, Cappelli M, Korneluk Y, Rowe PC (May 2000). "The effect of Kawasaki disease on cognition and behavior". Archives of Pediatrics & Adolescent Medicine 154 (5): 463–8. PMID 10807296. http://archpedi.ama-assn.org/cgi/pmidlookup?view=long&pmid=10807296. Retrieved 2011-12-02. 
  98. ^ Rowley AH, Baker SC, Orenstein JM, Shulman ST (May 2008). "Searching for the cause of Kawasaki disease--cytoplasmic inclusion bodies provide new insight". Nat. Rev. Microbiol. 6 (5): 394–401. doi:10.1038/nrmicro1853. PMID 18364728. 
  99. ^ "Kawasaki Disease". American Heart Association. http://www.americanheart.org/presenter.jhtml?identifier=4634. Retrieved 3 January 2009. 
  100. ^ "Kawasaki Disease: Causes". Mayo Clinic. http://www.mayoclinic.com/health/kawasaki-disease/DS00576/DSECTION=causes. Retrieved 3 January 2009. 
  101. ^ Nakamura Y, Yashiro M, Uehara R, Oki I, Watanabe M, Yanagawa H (2008). "Monthly observation of the number of patients with Kawasaki disease and its incidence rates in Japan: chronological and geographical observation from nationwide surveys". J Epidemiol 18 (6): 273–9. doi:10.2188/jea.JE2008030. PMID 19075496. 
  102. ^ Freeman AF, Shulman ST (June 2001). "Recent developments in Kawasaki disease". Curr Opin Infect Dis 14 (3): 357–61. doi:10.1097/00001432-200106000-00017. PMID 11964855. 
  103. ^ a b c d "Who Kawasaki Disease Affects". Children's Hospital Boston. http://www.childrenshospital.org/clinicalservices/Site468/mainpageS468P5.html. Retrieved 2009-01-04. 
  104. ^ Onouchi Y, Gunji T, Burns JC, et al. (January 2008). "ITPKC functional polymorphism associated with Kawasaki disease susceptibility and formation of coronary artery aneurysms". Nat. Genet. 40 (1): 35–42. doi:10.1038/ng.2007.59. PMC 2876982. PMID 18084290. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2876982. 
  105. ^ Keren G, Danon YL, Orgad S, Kalt R, Gazit E (August 1982). "HLA Bw51 is increased in mucocutaneous lymph node syndrome in Israeli patients". Tissue Antigens 20 (2): 144–6. doi:10.1111/j.1399-0039.1982.tb00337.x. PMID 6958087. 
  106. ^ Behrman, Richard E.; Kliegman, Robert; Karen Marcdante; Jenson, Hal B. (2006). Nelson essentials of pediatrics. St. Louis, Mo: Elsevier Saunders. ISBN 1-4160-0159-X. 
  107. ^ "Kawasaki Disease - June 1999 - American Academy of Family Physicians". http://www.aafp.org/afp/990600ap/3093.html. 
  108. ^ Oates-Whitehead RM, Baumer JH, Haines L, et al. (2003). Intravenous immunoglobulin for the treatment of Kawasaki disease in children. In Baumer, J Harry. "Cochrane Database of Systematic Reviews". Cochrane Database Syst Rev (4): CD004000. doi:10.1002/14651858.CD004000. PMID 14584002. 
  109. ^ Hsieh KS, Weng KP, Lin CC, Huang TC, Lee CL, Huang SM (December 2004). "Treatment of acute Kawasaki disease: aspirin's role in the febrile stage revisited". Pediatrics 114 (6): e689–93. doi:10.1542/peds.2004-1037. PMID 15545617. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=15545617. 
  110. ^ "Pediatrics, Kawasaki Disease: Treatment & Medication - eMedicine Emergency Medicine". Emedicine.medscape.com. 2010-03-18. http://emedicine.medscape.com/article/804960-treatment. Retrieved 2010-05-19. 
  111. ^ Sundel RP, Baker AL, Fulton DR, Newburger JW (June 2003). "Corticosteroids in the initial treatment of Kawasaki disease: report of a randomized trial". J. Pediatr. 142 (6): 611–6. doi:10.1067/mpd.2003.191. PMID 12838187. http://linkinghub.elsevijer.com/retrieve/pii/S0022347603001173. 
  112. ^ Newburger JW et al., Randomized trial of pulsed corticosteroid therapy for primary treatment of Kawasaki disease, N Engl J Med. 2007 Feb 25;356(7):663-75
  113. ^ REMICADE® Becomes First Anti-TNF Biologic Therapy to Treat One Million Patients Worldwide
  114. ^ Beiser AS, Takahashi M, Baker AL, Sundel RP, Newburger JW (May 1998). "A predictive instrument for coronary artery aneurysms in Kawasaki disease. US Multicenter Kawasaki Disease Study Group". The American Journal of Cardiology 81 (9): 1116–20. doi:10.1016/S0002-9149(98)00116-7. PMID 9605052. http://linkinghub.elsevier.com/retrieve/pii/S0002914998001167. Retrieved 2011-12-08. 
  115. ^ Fujiwara T, Fujiwara H, Hamashima Y (1987). "Size of coronary aneurysm as a determinant factor of the prognosis in Kawasaki disease: clinicopathologic study of coronary aneurysms". Progress in Clinical and Biological Research 250: 519–20. PMID 3423060. 
  116. ^ Nakano H, Ueda K, Saito A, Nojima K (November 1985). "Repeated quantitative angiograms in coronary arterial aneurysm in Kawasaki disease". The American Journal of Cardiology 56 (13): 846–51. doi:10.1016/0002-9149(85)90767-2. PMID 4061324. http://linkinghub.elsevier.com/retrieve/pii/0002-9149(85)90767-2. Retrieved 2011-12-08. 
  117. ^ Tatara K, Kusakawa S (November 1987). "Long-term prognosis of giant coronary aneurysm in Kawasaki disease: an angiographic study". The Journal of Pediatrics 111 (5): 705–10. doi:10.1016/S0022-3476(87)80246-9. PMID 3668739. 
  118. ^ Ishii M, Ueno T, Akagi T, et al. (October 2001). "Guidelines for catheter intervention in coronary artery lesion in Kawasaki disease". Pediatrics International : Official Journal of the Japan Pediatric Society 43 (5): 558–62. doi:10.1046/j.1442-200X.2001.01464.x. PMID 11737728. http://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1328-8067&date=2001&volume=43&issue=5&spage=558. Retrieved 2011-12-08. 
  119. ^ Akagi T, Ogawa S, Ino T, et al. (August 2000). "Catheter interventional treatment in Kawasaki disease: A report from the Japanese Pediatric Interventional Cardiology Investigation group". The Journal of Pediatrics 137 (2): 181–6. doi:10.1067/mpd.2000.107164. PMID 10931409. http://linkinghub.elsevier.com/retrieve/pii/S0022-3476(00)76097-5. Retrieved 2011-12-08. 
  120. ^ Kitamura S (December 2002). "The role of coronary bypass operation on children with Kawasaki disease". Coronary Artery Disease 13 (8): 437–47. doi:10.1097/00019501-200212000-00009. PMID 12544719. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0954-6928&volume=13&issue=8&spage=437. Retrieved 2011-12-08. 
  121. ^ Checchia PA, Pahl E, Shaddy RE, Shulman ST (October 1997). "Cardiac transplantation for Kawasaki disease". Pediatrics 100 (4): 695–9. doi:10.1542/peds.100.4.695. PMID 9310527. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=9310527. Retrieved 2011-12-08. 
  122. ^ "Kawasaki Disease - Signs and Symptoms". http://www.ucsfchildrenshospital.org/conditions/kawasaki_disease/signs_and_symptoms.html. 
  123. ^ "BBC - Health: Kawasaki Disease". 31 March 2009. http://www.bbc.co.uk/health/physical_health/conditions/kawasaki2.shtml. 
  124. ^ "Rare heart disease rate doubles". BBC. 17 June 2002. http://news.bbc.co.uk/1/hi/health/2043402.stm. 
  125. ^ Kawasaki T (March 1967). "[Acute febrile mucocutaneous syndrome with lymphoid involvement with specific desquamation of the fingers and toes in children]" (in Japanese). [[Arerugī = [Allergy]]] 16 (3): 178–222. PMID 6062087. 
  126. ^ Yamamoto T, Oya T, Watanabe A, et al. Clinical features of Kawasaki disease [in Japanese] Shonika Rinsho (Jpn J Pediatr) 1968;21:291–297.
  127. ^ Kawasaki T, Kosaki F, Okawa S, Shigematsu I, Yanagawa H (September 1974). "A new infantile acute febrile mucocutaneous lymph node syndrome (MLNS) prevailing in Japan". Pediatrics 54 (3): 271–6. PMID 4153258. 
  128. ^ Melish ME, Hicks RM, Larson EJ (June 1976). "Mucocutaneous lymph node syndrome in the United States". American Journal of Diseases of Children (1960) 130 (6): 599–607. PMID 7134. 
  129. ^ Gee S J. Cases of morbid anatomy. St Bartholomew’s Hosp Rep. 1871;7:141–148.
  130. ^ Taubert K A, Rowley A H, Shulman S T. A 10 year (1984–1993) United States hospital survey of Kawasaki disease. In: Kato H, editor. Kawasaki disease. Amsterdam, The Netherlands: Elsevier Science B. V.; 1995. pp. 34–38.

External links

Large vessel
Medium vessel
Small vessel
Ungrouped
Other

M: VAS

anat(a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot

noco/syva/cong/lyvd/tumr, sysi/epon, injr

proc, drug(C2s+n/3/4/5/7/8/9)