WordNet

used to express refusal or denial or disagreement etc or especially to emphasize a negative statement; "no, you are wrong"
a negative; "his no was loud and clear"
referring to the degree to which a certain quality is present; "he was no heavier than a child" (同)no more
not in any degree or manner; not at all; "he is no better today"
quantifier; used with either mass nouns or plural count nouns for indicating a complete or almost complete lack or zero quantity of; "we have no bananas"; "no eggs left and no money to buy any"; "have you no decency?"; "did it with no help"; "Ill get you there in no time"
sway gently back and forth, as in a nodding motion; "the flowers were nodding in the breeze"
be almost asleep; "The old man sat nodding by the fireplace"
let the head fall forward through drowsiness; "The old man was nodding in his chair"
the act of nodding the head
a sign of assent or salutation or command
express or signify by nodding; "He nodded his approval"
lower and raise the head, as to indicate assent or agreement or confirmation; "The teacher nodded when the student gave the right answer"
any thickened enlargement (同)knob, thickening
(botany) the small swelling that is the part of a plant stem from which one or more leaves emerge (同)leaf node
a connecting point at which several lines come together
(computer science) any computer that is hooked up to a computer network (同)client, guest
(astronomy) a point where an orbit crosses a plane
(physics) the point of minimum displacement in a periodic system
any bulge or swelling of an anatomical structure or part
a pattern of symptoms indicative of some disease
a complex of concurrent things; "every word has a syndrome of meanings"
a thin coagulable fluid (similar to plasma but) containing white blood cells (lymphocytes) and chyle; is conveyed to the blood stream by lymphatic vessels

PrepTutorEJDIC

《名詞の前に置いて》『一つも』(『一人も,少しも』)・・・『ない』 / 《補語につけて》『決して・・・でない』 / 《省略文で》・・・なし;・・・お断り / 《話》少ししか(あまり)・・・ない / (肯定の問いに対して)『いいえ』;(否定の問いに対して)はい,ええ / 《not, norの前に挿入して》『いや』,否 / 《形容詞の前に置その形容詞を否定して》…どころではない / 《比較級の前に置いて》ちっとも…でない,…と全く同じ / 《… or no の形で》…であってもなくても / 《驚き・困惑・不信などを表して》とんでもない / 《単数形で》『拒否』,「『いいえ』」という返事 / 《複数形で》反対[投]票
(承諾・あいさつ・合図などで)『うなずく』,会釈する / (眠くて)『こっくりする』,(油断して)うとうとする《+off》 / 〈草木・穂などが〉揺れる / (承諾・あいさつなどで)〈頭〉‘を'『うなずかせる』 / …‘を'うなずいて示す / 《副詞[句]を伴って》〈人〉‘に'うなずいて示す / 《同意・承諾・あいさつ・命令など,また時には拒絶を表して》(…に対する)『うなずき』,『会釈』《+『to』+『名』》;(眠気による)こっくり
(茎・幹の)節(ふし) / (体組織にできた)結節,こぶ(リンパ瘤(りゅう)など) / (天体の軌道の)交点 / (物事の)中心点
(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
リンパ[液]

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/11/19 08:54:50」(JST)

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For other uses see Kawasaki

Kawasaki disease, also known as Kawasaki syndrome, lymph node syndrome, and mucocutaneous lymph node syndrome,^{[note 1]}^[1] is an immune^[2] 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. Its rarest 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 0.17% in the U.S.^[3]

Often, a pre-existing viral infection may play a role in its pathogenesis.^[4] The skin, the conjunctivae of the eyes, and the mucus membranes of the mouth become red and inflamed. Swelling of the hands and feet is often seen and lymph nodes in the neck are often enlarged. A recurrent fever, often 37.8°C (100.0°F) or higher, is characteristic of the acute phase of the disease.^[5] In untreated children, the fever lasts about 10 days but may range from five to 25 days.^[5] The disorder was first described in 1967 by Tomisaku Kawasaki in Japan.^[6]

Classification

Systemic vasculitis is an inflammatory condition affecting arteries and veins throughout the body, and is usually caused by a proliferation of cells associated with an immune response to a pathogen, or autoimmunity.^[7] 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.^[7] 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.^[7]^[8] (Other diseases featuring necrotizing vasculitis include polyarteritis nodosa, granulomatosis with polyangiitis, Henoch-Schönlein purpura, and Churg-Strauss syndrome.^[7])

Kawasaki disease may be further classified as a medium-sized-vessel vasculitis, affecting medium- and small-sized blood vessels,^[9]^[10]^[11] such as the smaller cutaneous vasculature (veins and arteries in the skin) that range from 50 to 100 µm in diameter.^[12]^[13] Kawasaki disease is also considered to be a primary childhood vasculitis, a disorder associated with vasculitis that mainly affects children under the age of 18.^[14]^[15] A recent, consensus-based evaluation of vasculitides occurring primarily in children resulted in a classification scheme for these disorders, to distinguish them and suggest a more concrete set of diagnostic criteria for each.^[15] Within this classification of childhood vasculitides, Kawasaki disease is, again, a predominantly medium-sized vessel vasculitis.^[15]

It is also an autoimmune form of vasculitis,^[5] and is not associated with ANCA antibodies, unlike other vasculitic disorders associated with them (such as granulomatosis with polyangiitis, microscopic polyangiitis, and Churg-Strauss syndrome).^[7]^[16] This categorization is considered essential for appropriate treatment.^[17]

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.^[18]^[19] It is the most prominent symptom in Kawasaki disease, is a characteristic sign of the acute phase of the disease, is normally high (above 39-40°C), remittent, and is followed by extreme irritability.^[19]^[20] Recently, it is reported to be present in patients with atypical or incomplete Kawasaki disease;^[21]^[22] nevertheless, it is not present in 100% of cases.^[23] The first day of fever is considered the first day of illness,^[18] 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.^[5] Prolonged fever is associated with higher incidence of cardiac involvement.^[24] It responds partially to antipyretic drugs and does not cease with the introduction of antibiotics.^[5] However, when appropriate therapy is started – intravenous immunoglobulin and aspirin – the fever is gone after two days.^[25]

Bilateral conjunctival inflammation was reported to be the most common symptom after fever.^[26]^[27] It typically involves the bulbar conjunctivae, is not accompanied by suppuration, and is not painful.^[28] It usually begins shortly after the onset of fever during the acute stage of the disease.^[18] Anterior uveitis may be present on slit-lamp examination.^[29]^[30] Iritis can occur, too.^[31] Keratic precipitates are another eye manifestation (detectable by a slit lamp but are usually too small to be seen by the unaided eye).^[18]^[32]

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.^[33] 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).^[5]^[13] These oral manifestations are caused by the typical necrotizing microvasculitis with fibrinoid necrosis.^[33]

Cervical lymphadenopathy is seen in 50% to 75% of patients, whereas the other features are estimated to occur in 90% of patients,^[18]^[26] but sometimes it can be the dominant presenting symptom.^[32]^[34] According to the definition of the diagnostic criteria, at least one impaired lymph node ≥ 1.5 cm in diameter should be involved.^[13] Affected lymph nodes are painless or minimally painful, nonfluctuant, and nonsuppurative; erythema of the neighboring skin may occur.^[18] Children with fever and neck adenitis who do not respond to antibiotics should have Kawasaki disease considered as part of the differential diagnoses.^[18]

Less common manifestations
System	Manifestations
GIT	Diarrhea, abdominal pain, vomiting, liver dysfunction, pancreatitis, Hydrops gallbladder,^[35] parotitis,^[26]^[36] cholangitis, intussusception, intestinal pseudo-obstruction, ascites, splenic infarction
MSS	Polyarthritis and arthralgia
CVS	Myocarditis, pericarditis, tachycardia,^[13] valvular heart disease
GU	Urethritis, prostatitis, cystitis, priapism, interstitial nephritis, orchitis, nephrotic syndrome
CNS	Lethargy, semicoma,^[26] aseptic meningitis, and sensorineural deafness
RS	Shortness of breath,^[13] influenza-like illness, pleural effusion, atelectasis
Skin	Erythema and induration at BCG vaccination site, Beau's lines, and finger gangrene
Source: review,^[13] table.^[37]

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^[18] and often accompanied by painful, brawny edema of the dorsa of the hands or feet. This is why affected children frequently refuse to hold objects in their hands or to bear weight on their feet.^[5]^[18] 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.^[38] Around 11% of children affected by the disease may continue skin-peeling for many years.^[39] One to two months after the onset of fever, deep transverse grooves across the nails may develop (Beau’s lines),^[40] and occasionally nails are shed.^[40]

The most common cutaneous manifestation is a diffuse macular-papular erythematous rash, which is quite nonspecific.^[41] The rash varies over time and is characteristically located on the trunk; it may further spread to involve the face, extremities, and perineum.^[5] Many other forms of cutaneous lesions have been reported; they may include scarlatiniform, popular, urticariform, multiform-like erythema, and purpuric lesions; even micropustules were reported.^[42]^[43] It can be polymorphic, not itchy, and normally observed up to the fifth day of fever.^[44] However, it is never bullous or vesicular.^[5]

In the acute stage of Kawasaki disease, systemic inflammatory changes are evident in many organs.^[10] Joint pain (arthralgia) and swelling, frequently symmetrical, and arthritis can also occur.^[26] Myocarditis,^[45] diarrhea,^[13] pericarditis, valvulitis, aseptic meningitis, pneumonitis, lymphadenitis, and hepatitis may be present and are manifested by the presence of inflammatory cells in the affected tissues.^[10] 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.^[13] If treated quickly, this risk can be mostly avoided and the course of illness cut short.^[46]

Clinical manifestations and time course of Kawasaki disease^[18]^[47]

Other reported nonspecific symptoms include cough, rhinorrhea, sputum, vomiting, headache, and seizure.^[26]

The course of the disease can be divided into three clinical phases.^[13]

The acute febrile phase, which usually lasts for one to two 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.^[13] Myocarditis is common during this time, and a pericardial effusion may be present.^[18] 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 one to two 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 four weeks after the onset of fever. Coronary artery aneurysms usually develop during this time, and the risk for sudden death is highest.^[18]^[48]
The convalescent stage begins when all clinical signs of illness have disappeared, and continues until the sedimentation rate returns to normal, usually at six to eight weeks after the onset of illness.^[13]

The clinical presentation between adults and children differs, as adults' neck lymph nodes are more affected (93% of adults versus 15% of children), hepatitis (65% versus 10%), and arthralgia (61% versus 24-38%).^[13]^[49] Some patients have atypical presentations and may not have the classical symptoms. This occurs in particular in young infants;^[50] those patients are especially at higher risk for cardiac artery aneurysms.^[18]^[51]

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 Kawasaki disease. It is the main cause of heart disease acquired in childhood in the United States and Japan.^[13] In developed nations, it appears to have replaced acute rheumatic fever as the most common cause of acquired heart disease in children.^[18] 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 the peak frequency of coronary artery dilation or aneurysms occurs within four weeks of onset.^[48] Aneurysms are classified into small (internal diameter of vessel wall <5 mm), medium (diameter ranging from 5-8 mm), and giant (diameter > 8 mm).^[13] Saccular and fusiform aneurysms usually develop between 18 and 25 days after the onset of illness.^[18] Even when treated with high-dose IVIG regimens within the first 10 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 blood clot formation in a coronary artery aneurysm or to rupture of a large coronary artery aneurysm. Death is most common two to 12 weeks after the onset of illness.^[18]

Many risk factors predicting coronary artery aneurysms have been identified,^[24] including 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.^[5] Resolution one to two years after the onset of the disease has been observed in half of vessels with coronary aneurysms.^[59]^[60] Narrowing of the coronary artery, which occurs as a result of the healing process of the vessel wall, often leads to significant obstruction of the blood vessel and lead to the heart not receiving enough blood and oxygen.^[59] This can eventually lead to heart muscle tissue death (myocardial infarction).^[59]

MI caused by thrombotic occlusion in an aneurysmal, stenotic, or both aneurysmal and stenotic coronary artery is the main cause of death from Kawasaki disease.^[61] The highest risk of MI occurs in the first year after the onset of the disease.^[61] MI in children presents with different symptoms from those 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.^[18]

Valvular insufficiencies, particularly of mitral or tricuspid valves, are often observed in the acute phase of Kawasaki disease due to inflammation of the heart valve or inflammation of the heart muscle-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.^[5]^[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]

Eye 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 lesions are increasingly reported.^[86] The neurological complications found are meningoencephalitis,^[87] subdural effusion,^[88]^[89] cerebral hypoperfusion,^[90] cerebral ischemia and infarct,^[91] cerebellar 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 hearing 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

As the cause(s) of Kawasaki disease remain unknown, the illness is more accurately referred to as Kawasaki syndrome. Like all autoimmune diseases, its cause 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. Evidence increasingly points to an infectious etiology,^[101] but debate continues on whether the cause is a conventional antigenic substance or a superantigen.^[102] Researchers at Boston Children's Hospital reported, "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 show a clear correlation between Kawasaki disease and tropospheric wind patterns; winds blowing from central Asia correlate with Kawasaki disease cases in Japan, Hawaii, and San Diego.^[104] This association with tropospheric winds has been shown to be modulated at seasonal and interannual timescales by the El Niño–Southern Oscillation phenomenon,^[105] further indicating the agent responsible for the disease is a wind-borne pathogen. Efforts are underway to identify the suspected pathogen in air-filters flown at altitude above Japan.^[106]

An association has been identified with an SNP in the ITPKC gene, which codes an enzyme that negatively regulates T-cell activation.^[107] Regardless of where they are living, Japanese children are more likely than other children to manifest the disease, which suggests genetic susceptibility.^[103] The HLA-B51 serotype has been found to be associated with endemic instances of the disease.^[108]

Diagnosis

Criteria for Diagnosis of Kawasaki Disease
Fever of ≥5 days' duration associated with at least four† of these five changes
Bilateral nonsuppurative conjunctivitis
One or more changes of the mucous membranes of the upper respiratory tract, including throat redness, dry cracked lips, red lips, and "strawberry" tongue
One or more changes of the arms and legs, including redness, swelling, skin peeling around the nails, and generalized peeling
Polymorphous rash, primarily truncal
Large lymph nodes in the neck (>1.5 cm in size)
Disease cannot be explained by some other known disease process
†A diagnosis of Kawasaki disease can be made if fever and only three changes are present if coronary artery disease is documented by two-dimensional echocardiography or coronary angiography.
Source: Nelson's essentials of pediatrics,^[109] Review^[15]

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). No specific laboratory test exists 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^[110] plus four of five diagnostic criteria must be met to establish the diagnosis. The criteria are:

erythema of the lips or oral cavity or cracking of the lips;
rash on the trunk;
swelling or erythema of the hands or feet;
red eyes (conjunctival injection);
swollen lymph node in the neck of at least 15 mm.

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 may reveal normocytic anemia and eventually thrombocytosis
Erythrocyte sedimentation rate will be elevated
C-reactive protein will be elevated
Liver function tests may show evidence of hepatic inflammation and low serum albumin

Other optional tests include:

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).^[103] Treatment should 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^[111] 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)^[112] 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.^[113]

Corticosteroids have also been used,^[114] 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.^[115] Additionally, corticosteroid use in the setting of Kawasaki disease is associated with increased risk of coronary artery aneurysm, 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.

IL-1 Receptor antagonist (anakinra) can prevent coronary lesion in the mouse KD model. This prevention shows even with three-days-delay in treatment in mice.^[116]

Treatments exist for iritis and other eye symptoms. Another treatment may include the use of infliximab. Infliximab works by binding tumour necrosis factor alpha.^[117]

Prognosis

With early treatment, rapid recovery from the acute symptoms can be expected, and the risk of coronary artery aneurysms is 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]^[118] The likelihood that an aneurysm will resolve appears to be determined in large measure by its initial size, in which the smaller aneurysms have a greater likelihood of regression.^[119]^[120] Other factors are positively associated with the regression of aneurysms, including 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.^[5] The worst prognosis occurs in children with giant aneurysms.^[121] This severe outcome may require further treatment such as percutaneous transluminal angioplasty,^[122] coronary artery stenting,^[123] bypass grafting,^[124] and even cardiac transplantation.^[125]

A relapse of symptoms may occur soon after initial treatment with IVIG. This usually requires rehospitalization and retreatment. Treatment with IVIG can cause allergic and nonallergic 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 nontreatment. Also, evidence indicates 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, 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 (about one in 450 children). At this present attack rate, more than one in 150 children in Japan will develop Kawasaki disease during their lifetimes.

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. About 2,000-4,000 cases are identified in the U.S. each year (9 to 19 per 100,000 children younger than 5 years of age).^[103]^[126]^[127]

In the United Kingdom, estimates of incidence rate vary because of the rarity of Kawasaki disease. However, it is believed to affect fewer than one in every 25,000 people.^[128] Incidence of the disease doubled from 1991 to 2000, however, with four cases per 100,000 children in 1991 compared with a rise of eight cases per 100,000 in 2000.^[129]

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 in January 1961, and he later published a report on 50 similar cases.^[130] Later, Kawasaki and colleagues were persuaded of definite cardiac involvement when they studied and reported 23 cases, of which 11 (48%) patients had abnormalities detected by an electrocardiogram.^[131] In 1974, the first description of this disorder was published in the English-language literature.^[132] In 1976, Melish et al. described the same illness in 16 children in Hawaii.^[133] Melish and Kawasaki had independently developed the same diagnostic criteria for the disorder, which are still used today to make the diagnosis of classic Kawasaki disease.

A question was raised whether the disease only started during the period between 1960 and 1970, but later a preserved heart of a seven-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 Kawasaki disease.^[134] Kawasaki disease 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.^[135]

References

Notes

^ or mucocutaneous node disease

Citations

^ 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.
^ Wang CL, Wu YT, Liu CA, Kuo HC, Yang KD (November 2005). "Kawasaki disease: infection, immunity and genetics". The Pediatric Infectious Disease Journal 24 (11): 998–1004. doi:10.1097/01.inf.0000183786.70519.fa. PMID 16282937.
^ "Merck Manual, Online edition: Kawasaki Disease". Retrieved May 9, 2010.
^ 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.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j ^k ^l 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.
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^ Lee Y, Schulte DJ, Shimada K, et al. (March 2012). "Interleukin-1β is crucial for the induction of coronary artery inflammation in a mouse model of Kawasaki disease". Circulation 125 (12): 1542–50. doi:10.1161/CIRCULATIONAHA.111.072769. PMC 3337219. PMID 22361326.
^ 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. 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. 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 43 (5): 558–62. doi:10.1046/j.1442-200X.2001.01464.x. PMID 11737728.
^ 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.
^ 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.
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^ 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 - Stanford Children's Health
Kawasaki Disease Research Program
Kawasaki Disease Foundation
Kawasaki Disease information from Seattle Children's Hospital Heart Center

UpToDate Contents

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1. 川崎病：臨床的特徴および診断 kawasaki disease clinical features and diagnosis
2. 川崎病：初期治療および予後 kawasaki disease initial treatment and prognosis
3. 不完全（非定型）川崎病 incomplete atypical kawasaki disease
4. 川崎病：疫学および病因 kawasaki disease epidemiology and etiology
5. 川崎病：合併症 kawasaki disease complications

English Journal

Point-of-care differentiation of Kawasaki disease from other febrile illnesses.

Ling XB, Kanegaye JT, Ji J, Peng S, Sato Y, Tremoulet A, Burns JC, Cohen HJ.SourceDepartment of Surgery, Stanford University, Stanford, CA 94305-5178, USA.
The Journal of pediatrics.J Pediatr.2013 Jan;162(1):183-188.e3. doi: 10.1016/j.jpeds.2012.06.012. Epub 2012 Jul 20.
OBJECTIVE: To test whether statistical learning on clinical and laboratory test patterns would lead to an algorithm for Kawasaki disease (KD) diagnosis that could aid clinicians.STUDY DESIGN: Demographic, clinical, and laboratory data were prospectively collected for subjects with KD and febrile con
PMID 22819274

Interleukin-21 receptor gene polymorphisms in kawasaki disease.

Kim MH, Bae YJ, Lee HK, Lee YR, Lee DH, Bae K, Koh SB, Namgoong MK, Cha BH, Lee HY.SourceDepartment of Pediatrics, Yonsei University Wonju College of Medicine, Wonju, Korea.
Korean circulation journal.Korean Circ J.2013 Jan;43(1):38-43. doi: 10.4070/kcj.2013.43.1.38. Epub 2013 Jan 31.
BACKGROUND AND OBJECTIVES: Interleukin-21 receptor (IL-21R) gene polymorphism is related with the development of systemic vasculitis. In this study, we investigated the polymorphisms of IL-21R gene in patients with Kawasaki disease (KD).SUBJECTS AND METHODS: We genotyped the promoter region of IL-21
PMID 23407404

A child with severe relapsing Kawasaki disease rescued by IL-1 receptor blockade and extracorporeal membrane oxygenation.

Cohen S, Tacke CE, Straver B, Meijer N, Kuipers IM, Kuijpers TW.
Annals of the rheumatic diseases.Ann Rheum Dis.2012 Dec;71(12):2059-61. doi: 10.1136/annrheumdis-2012-201658. Epub 2012 Jun 11.
PMID 22689319

Japanese Journal

(転載・ひと言)川崎病(MCLS)の眼症状

堀貞夫
東京女子医科大学雑誌 82(E1), E288-E294, 2012-01-31
NAID 110008767993

川崎病の既往を有する親の疫学特性

上原里程,YASHIRO Mayumi,NAKAMURA Yosikazu,YANAGAWA Hiroshi
Pediatrics international : official journal of the Japan Pediatric Society 53(4), 511-514, 2011-08-01
NAID 10029558978

Related Pictures

★リンクテーブル★

リンク元	「川崎病」「MLNS」「急性皮膚粘膜リンパ節症候群」
関連記事	「node」「syndrome」「mucocutaneous」「nod」

「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	article/965367
Patient UK	Kawasaki disease
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

「MLNS」

　　[★] 川崎病。mucocutaneous lymph node syndrome, 急性皮膚粘膜リンパ節症候群

「急性皮膚粘膜リンパ節症候群」

　　[★] 川崎病。mucocutaneous lymph node syndrome, MLNS, MCLS

「node」

　　[★]

n.

結節、リンパ節、節、ノード

関: clause、ganglia、ganglion、ganglionic、knot、lymph node、nodal、nodose、nodulate、section、tubercle、tubercular、tuberosity

「syndrome」

　　[★]

n.

症候群

「mucocutaneous」

　　[★]

adj.

粘膜皮膚の

「nod」

　　[★] 　　　　　　　　

[1] r mucocutaneous node disease

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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	article/965367
Patient UK	Kawasaki disease
MeSH	D009080

匿名

検索

案内

mucocutaneous lymph node syndrome