WordNet

a pattern of symptoms indicative of some disease
a complex of concurrent things; "every word has a syndrome of meanings"
of or relating to the mucous membranes and skin

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(疾患の徴候となる一群の)症徴候,症候群 / (事件・社会的状態などのパターンを示す)徴候形態

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/04/14 03:53:59」(JST)

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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]

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

(A) Bilateral, non-exudative conjunctivitis with perilimbal sparing - "conjunctival injection". (B) Strawberry tongue and bright red, swollen lips with vertical cracking and bleeding. (C) Erythematous rash involving perineum. (D) Erythema of the palms, which is often accompanied by painful, brawny edema of the dorsa of the hands. (E) Erythema of the soles, and swelling dorsa of the feet. (F) Desquamation of the fingers. (G) Erythema and induration at the site of a previous vaccination with Bacillus Calmette-Guérin (BCG). (H) Perianal erythematous desquamation.^[4]

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]

Clinical manifestations and time course of Kawasaki disease.^[17]^[46]

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]^[47] 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]^[48] Some patients have atypical presentations and may not have the classical symptoms and this occurs in particular in young infants,^[49] and those patients are especially at higher risk for cardiac artery aneurysms.^[17]^[50]

X-ray showing aneurysmal enlargement of the coronary arteries, which is a complication in a Kawasaki syndrome

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.^[51] 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.^[47] 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.^[52]^[53]^[54] 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,^[55]^[56] 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.^[57]

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.^[58]^[59] Stenosis, which occurs as a result of the healing process of the vessel wall, often leads to significant coronary obstruction and myocardial ischemia.^[58] and eventually can lead to Myocardial infarction.^[58]

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.^[60] The highest risk of myocardial infarction occurs in the first year after the onset of the disease.^[60] 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.^[60] 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.^[58] These lesions mostly disappear with the resolution of acute illness,^[61] but a very small group of the lesions persist and progress.^[62] 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.^[63] Some of these lesions require valve replacement.^[64]

Other

Other Kawasaki disease complications have been described, such as aneurysm of other arteries: aortic aneurysm,^[65] with a higher number of reported cases involving the abdominal aorta,^[66]^[67] axillary artery aneurysm,^[68] brachiocephalic artery aneurysm,^[69] aneurysm of iliac and femoral arteries, and renal artery aneurysm.^[4]^[70] other vascular complications can occur such as increased wall thickness and decreased distensibility of carotid arteries,^[71] aorta,^[72] and brachioradial artery,^[73] this change in the vascular tone secondary to endothelial dysfunction.^[70] In addition, children with Kawasaki disease, with or without coronary artery complications, may have a more adverse cardiovascular risk profile,^[73] such as high blood pressure, obesity, and abnormal serum lipid profile.^[74]

Gastrointestinal complications in Kawasaki disease are similar to those observed in Henoch-Schönlein purpura,^[68] such as: intestinal obstruction,^[75] colon swelling,^[76] intestinal ischemia,^[77] intestinal pseudo-obstruction,^[78] and acute abdomen.^[79]

Ophthalmologic changes associated with the disease have been described since the 1980s, being found as uveitis, iridocyclitis, conjunctival hemorrhage,^[80]^[81]^[82] optic neuritis,^[68] amaurosis and ocular artery obstruction.^[83] It can also be found as necrotizing vasculitis, progressing into peripheral gangrene.^[84]

The neurological complications per central nervous system (CNS) lesion are increasingly reported.^[85] The neurological complications found are meningoencephalitis,^[86] subdural effusion,^[87]^[88] cerebral hypoperfusion,^[89] cerebral ischemia and infarct,^[90] cerebelar infarction,^[91] manifesting with seizures, chorea, hemiplegia, mental confusion, lethargy and coma,^[68] or even a cerebral infarction with no neurological manifestations.^[90] Other neurological complications from cranial nerve involvement are reported as ataxia,^[68] facial palsy,^[92] and sensorineural auditory loss.^[93]^[94] Behavioral changes, are thought to be caused by localised cerebral hypoperfusion,^[89] can include attention deficits, learning deficits, emotional disorders (emotional lability, fear of night and night terrors) and internalization problems (anxious, depressive or aggressive behavior).^[95]^[96]

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,^[97]^[98]^[99] but current theories center primarily on immunological causes for the disease. Evidence increasingly points to an infectious etiology,^[100] but debate continues on whether the cause is a conventional antigenic substance or a superantigen.^[101] 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."^[102] Other data show a clear correlation between KD and tropospheric wind patterns; winds blowing from central Asia correlate with KD cases in Japan, Hawaii and San Diego and indicate a wind-borne pathogen.^[103] Efforts are under way to identify the suspected pathogen in air-filters flown at altitude above Japan.^[104]

An association has been identified with a SNP in the ITPKC gene, which codes an enzyme that negatively regulates T-cell activation.^[105] 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.^[102] The HLA-B51 serotype has been found to be associated with endemic instances of the disease.^[106]

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,^[107] Review^[14]

Angiography showing ectatic LAD, with largest aneurysm = 6.5 mm in diameter.

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).^{[citation needed]}

Classically, five days of fever^[108] 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

Complete blood count (CBC) may reveal normocytic anemia and eventually thrombocytosis
Erythrocyte sedimentation rate (ESR) will be elevated
C-reactive protein (CRP) will be elevated
Liver function tests may show evidence of hepatic inflammation and low serum albumin

Other optional tests

Electrocardiogram may show evidence of ventricular dysfunction or, occasionally, arrhythmia due to myocarditis
Echocardiogram may show subtle coronary artery changes or, later, true aneurysms.
Ultrasound or computerized tomography may show hydrops (enlargement) of the gallbladder
Urinalysis may show white blood cells and protein in the urine (pyuria and proteinuria) without evidence of bacterial growth
Lumbar puncture may show evidence of aseptic meningitis
Angiography was historically used to detect coronary artery aneurysms and remains the gold standard for their detection, but is rarely used today unless coronary artery aneurysms have already been detected by echocardiography.
Temporal artery biopsy

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, pediatric rheumatology and pediatric infectious disease specialists (although no specific infectious agent has been identified as yet).^[102] 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^[109] 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)^[110] 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.^[111]

Corticosteroids have also been used,^[112] 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.^[113] 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.^[114]

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.^[57]^[115] 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.^[116]^[117] 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.^[59] The highest rate of progression to stenosis occurs among those who develop large aneurysms.^[4] The worst prognosis occurs in children with giant aneurysms.^[118] This severe outcome may require further treatment such as percutaneous transluminal angioplasty,^[119] coronary artery stenting,^[120] bypass grafting,^[121] and even cardiac transplantation.^[122]

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.^[102]^[123]

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.^[124] 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.^[125]

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.^[126] Later Kawasaki and colleagues were persuaded that there is definite cardiac involvement when they studied and reported 23 cases, of which 11(48%) patients had abnormalities detected by an electrocardiogram.^[127] It was not until 1974 that the first description of this disorder was published in the English language literature.^[128] in the year 1976 Melish et al., described the same illness in 16 children in Hawaii.^[129] Melish and Kawasaki had independently developed the same diagnostic criteria for the disorder, which are still used today to make the diagnosis of classic KD.

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 KD.^[130] KD 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.^[131]

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^ Newburger JW et al., Randomized trial of pulsed corticosteroid therapy for primary treatment of Kawasaki disease, N Engl J Med. 2007 February 25;356(7):663-75
^ REMICADE® Becomes First Anti-TNF Biologic Therapy to Treat One Million Patients Worldwide
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
^ 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.
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^ 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.
^ Yamamoto T, Oya T, Watanabe A, et al. Clinical features of Kawasaki disease [in Japanese] Shonika Rinsho (Jpn J Pediatr) 1968;21:291–297.
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External links

Wikimedia Commons has media related to: Kawasaki disease

Kawasaki Disease Research Program
Kawasaki Disease information from Seattle Children's Hospital Heart Center

UpToDate Contents

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1. カウデン症候群などのPTEN過誤腫症候群 pten hamartoma tumor syndrome including cowden syndrome
2. 皮膚剥脱症候群 peeling skin syndrome
3. スティーブンス・ジョンソン症候群および中毒性表皮壊死融解症：病因、臨床症状、および診断 stevens johnson syndrome and toxic epidermal necrolysis pathogenesis clinical manifestations and diagnosis
4. Peutz-Jeghers syndrome: Screening and management
5. Kindler syndrome

English Journal

Hyperreactivity of lymphocytes to streptolysin O and lack of plasma inhibitory factor (s) in patients with mucocutaneous lymphnode syndrome.

Wakiguchi H, Fujieda M, Matsumoto K, Ohara Y, Wakiguchi A, Shiraishi T, Kurashige T, Kitamura I.AbstractLymphocyte activation by streptolysin O (SLO) and factors in the plasma which inhibit the response to SLO were examined in 19 patients with mucocutaneous lymphnode syndrome (MCLS), 54 age-matched (6 months-6 years) normal children, 41 normal children older than 6 years and 10 normal adults. In normal children younger than 6 years, the response to SLO was weak and in many cases no response was seen. On the other hand, in the patients with MCLS, the response of lymphocytes to SLO was high and comparable to the response in adults and children older than 6 years. The DNA synthesis of lymphocytes stimulated by SLO was inhibited almost completely by autologous or allogeneic plasma of many of the normal children and adults. The plasma of patients with MCLS did not inhibit, but rather enhanced the response to SLO. These results suggest that the increased response of lymphocytes to SLO and the lack of plasma inhibitory factors in patients with MCLS may be due to the immune response to the pathogen of MCLS, as yet undiscovered.
Acta medica Okayama.Acta Med Okayama.1986 Dec;40(6):285-9.
Lymphocyte activation by streptolysin O (SLO) and factors in the plasma which inhibit the response to SLO were examined in 19 patients with mucocutaneous lymphnode syndrome (MCLS), 54 age-matched (6 months-6 years) normal children, 41 normal children older than 6 years and 10 normal adults. In norma
PMID 3825591

Kidney pathology in muco-cutaneous lymphnode syndrome.

Ogawa H.
Nihon Jinzo Gakkai shi.Nihon Jinzo Gakkai Shi.1985 Sep;27(9):1229-37.
PMID 4087543

Mucocutaneous lymphnode syndrome or Kawasaki disease.

[No authors listed]
Boletín de la Asociación Médica de Puerto Rico.Bol Asoc Med P R.1985 Jun;77(6):245.
PMID 3863629

Japanese Journal

川崎病全国調査からみた川崎病疫学の特徴とその変遷

中村好一,屋代真弓,上原里程
日本小児循環器学会雑誌 = Acta cardiologica paediatrica Japonica 28(3), 148-156, 2012-05-01
1970年に第1回全国調査が実施されて以来, わが国では21回に渡ってほぼ2年に一度の頻度で川崎病全国調査が実施され, 2011年には第21回調査を実施した. 過去3回(1979年, 1982年, 1986年)以降, 全国規模の流行はないが, 1990年代後半より患者数および罹患率は徐々に上昇し, 2010年の罹患率は1982年の罹患率よりも高かった. 1月に患者が多く, 夏場にも小さな山がみられ …
NAID 10031121934

急性熱性皮膚粘膜リンパ節症候群(MCLS)におけるプロテインCおよびプロテインSの推移について

今中康文
奈良医学雑誌 41(5), 571-584, 1990-10-31
… Plasma levels of protein C (PC) and protein S (PS) were investigated in 34 children with mucocutaneous lymphnode syndrome (MCLS). …
NAID 80005706142

川崎病(MCLS:Mucocutaneous Lymphnode Syndrome)における白血球産生Leukotriene B_4(LTB_4)の意義について

浜崎雄平,宮崎澄雄
アレルギー 39(3), 354-360, 1990-03-30
多核白血球は, 強力な白血球走化因子であるロイコトリエンB_4(LTB_4)を大量に産生する.川崎病の血管炎の進展にこの走化因子がなんらかの役割を果たしている可能性を検討する目的で, 19人の川崎病患児より, 急性期(0-12日), 回復期(13-29日), 治癒期(30日以上)の3期に計55回の採血をおこない, 多核白血球を分離, 培養し, Ca ionophore刺激によるLTB_4産生量をH …
NAID 110002416495

「川崎病」

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

　　[★]

英: Kawasaki disease, Kawasaki's disease
同: Kawasaki病。皮膚粘膜リンパ節症候群, 粘膜皮膚リンパ節症候群, mucocutaneous lymph node syndrome, mucocutaneous lymphnode syndrome, MCLS, 急性熱性皮膚粘膜リンパ節症候群, acute febrile MCLS,(小児)急性熱性皮膚粘膜リンパ節症候群, acute febrile mucocutaneous lymphnode syndrome

HIM.2130

概念

乳児～幼児(0-4歳、0歳半～1歳が最多)に後発する熱性疾患(全身性の心血管炎)
原因不明の急性熱性発疹性疾患。リンパ節腫脹と粘膜病変が特徴(SPE.370)

検査

[show details]

診断基準

参考1より引用

本症は、主として4歳以下の乳幼児に好発する原因不明の疾患で、その症候は以下の主要症状と参考条項とに分けられる。

A 主要症状

1．5日以上続く発熱(ただし、治療により5日未満で解熱した場合も含む)
2．両側眼球結膜の充血
3．口唇、口腔所見：口唇の紅潮、いちご舌、口腔咽頭粘膜のびまん性発赤
4．不定形発疹
5．四肢末端の変化：

(急性期)手足の硬性浮腫、掌蹠ないしは指趾先端の紅斑
(回復期)指先からの膜様落屑

6．急性期における非化膿性頸部リンパ節腫脹

6つの主要症状のうち5つ以上の症状を伴うものを本症とする。

ただし、上記6主要症状のうち、4つの症状しか認められなくても、経過中に断層心エコー法もしくは、

心血管造影法で、冠動脈瘤(いわゆる拡大を含む)が確認され、他の疾患が除外されれば本症とする。

B参考条項

以下の症候および所見は、本症の臨床上、留意すべきものである。

1. 心血管：聴診所見(心雑音、奔馬調律、微弱心音)、心電図の変化(PR・QTの延長、異常Q波、低電位差、ST-Tの変化、不整脈)、胸部X線所見(心陰影拡大)、断層心エコー図所見(心膜液貯留、*冠動脈瘤)、狭心症状、末梢動脈瘤(腋窩など)
2. 消化器：下痢、嘔吐、腹痛、胆嚢腫大、麻痺性イレウス、軽度の黄疸、血清トランスアミナーゼ値上昇
3. 血液：核左方移動を伴う白血球増多、血小板増多、赤沈値の促進、CRP陽性、低アルブミン血症、α2グロブリンの増加、軽度の貧血
4. 尿：蛋白尿、沈査の白血球増多
5. 皮膚：BCG接種部位の発赤・痂皮形成、小膿疱、爪の横溝
6. 呼吸器：咳嗽、鼻汁、肺野の異常陰影
7. 関節：疼痛、腫脹
8. 神経：髄液の単核球増多、けいれん、意識障害、顔面神経麻痺、四肢麻痺

備考

1. 主要症状Aの5は、回復期所見が重要視される。
2. 急性期における非化膿性頸部リンパ節腫脹は他の主要症状に比べて発現頻度が低い(約65%)
3. 本症の性比は、1.3～1.5：1で男児に多く、年齢分布は4歳以下が80～85%を占め、致命率は0.1%前後である。
4. 再発例は2～3%に、同胞例は1～2%にみられる。
5. 主要症状を満たさなくても、他の疾患が否定され、本症が疑われる容疑例が約10%存在する。この中には冠動脈瘤(いわゆる拡大を含む)が確認される例がある。

鑑別診断

IMD

溶連菌感染症、麻疹、多形滲出性紅斑、ブドウ球菌性熱傷様皮膚症候群

参考

1. 川崎病関連情報

診断の手引き、治療ガイドラインなど

http://www.kawasaki-disease.org/tebiki/index.html

uptodate

1. [charged] 川崎病：臨床的特徴および診断 - uptodate [1]
2. [charged] 川崎病：初期治療および予後 - uptodate [2]
3. [charged] 川崎病：疫学および病因 - uptodate [3]
4. [charged] 不完全（非定型）川崎病 - uptodate [4]
5. [charged] 川崎病：合併症 - uptodate [5]
6. [charged] 難治性川崎病の治療 - uptodate [6]
7. [charged] 川崎病の心血管後遺症 - uptodate [7]

国試

103D039

「MCLS」

　　[★] 川崎病。mucocutaneous lymphnode syndrome 粘膜皮膚リンパ節症候群

「acute febrile mucocutaneous lymphnode syndrome」

　　[★] 川崎病。急性熱性皮膚粘膜リンパ節症候群

「syndrome」

　　[★]

n.

症候群

「mucocutaneous」

　　[★]

adj.

粘膜皮膚の

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リンク元	「川崎病」「MCLS」
拡張検索	「acute febrile mucocutaneous lymphnode syndrome」
関連記事	「syndrome」「mucocutaneous」

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

匿名

検索

案内

mucocutaneous lymphnode syndrome