CC BY
0MEDICAL SCIENCES
Bulak H.
Ph. D., Danylo Halytsky Lviv National Medical University Bobelyak M.
Doctor, Danylo Halytsky Lviv National Medical University Mychka M.
Doctor, Danylo Halytsky Lviv National Medical University
THE ATYPICAL COURSE OF KAWASAKI DISEASE IN A CHIL-DREN'S
HOSPITAL
ABSTRACT
Nearly 50 years has passed since the first described case of Kawasaki disease, but still etiology, pathogenesis, treatment and prevention remain unknown, while the incidence and prevalence of the disease are growing. There are many theories about the origin of Kawasaki disease, although currently there is no clear scientific evidence for any of them. This shows the relevance of the study and the need for new studies to answer these long-posed questions. In this article, we want to highlight the current understanding of Kawasaki disease and demonstrate the case report of atypical form of Kawasaki disease in 11-month-old baby.
Keywords: Kawasaki disease, intravenous immunoglobulin G.
Kawasaki disease was discovered by a Japanese pediatrician Tomisaku Kawasaki, who first dealt with this pathology in January 1961 and six years later published the first results in Japanese. He argued that it was a separate nosology that did not lead to complications. The debate ended in 1970, when 10 autopsies of sudden death cases after Kawasaki disease were performed. By the time of the first publication in English in 1974, the link between Kawasaki disease and vasculitis of the coronary arteries had been established. Kawasaki disease was independently recognized as a new and separate state by two pediatricians from the University of Hawaii in the early 1970s. 14 inspections nationwide in Japan showed that there are regional outbreaks of the disease, year there are about 5-6 thousand new cases annually, current estimates of 120 to 150 cases per 100 thousand population of children <5 years old, Kawasaki disease is 1.5 times more common in males and 85% of cases occur in children <5 years, repetition frequency is low (4%). Since then, Kawasaki disease has become the primary reason of acquired heart disease in children in Japan, North America, and South Korea, and it has been spreading in Europe. Kawasaki disease is characterized by acute systemic vasculitis that occurs mainly in children at the age from 6 months to 5 years. Clinical symptoms of Kawasaki disease are well described, but the causes of this disease are unrenowned [1,2].
Given this, Kawasaki disease is usually diagnosed by clinical symptoms such as: fever for 5 days or more, bilateral purulent conjunctivitis; changes on the lips or oral cavity, erythema or cracks on the lips, infection of oral cavity and pharynx, «strawberry» tongue; palmar erythema or erythema of feet; polymorphic rash on the trunk, changes in peripheral extremities followed by desquamation of the fingertips and not purulent lymphadenopathy in the neck more than 1.5 cm in diameter. In addition to these criteria, the new type-specific feature that may be screening for Kawasaki disease in children is erythema on Bacillus Calmette - Guerin (BCG), after the vaccination. In
Ukraine, BCG is included in the national immunization program in the neonatal period. The reaction to BCG is considered to be an important discovery for children under 2 years old. Besides, it is used as the screening method in South Korea [2,3,4].
Early diagnosis of Kawasaki disease is extremely important, as the disease can lead to devastating cardiovascular complications and sudden death in children. Kawasaki disease is of great clinical importance and requires special attention, because along with coronary artery disease it can lead to irreversible conditions, disability, or for a very long time it can manifest itself under the guise of various infectious diseases, which are difficult to differentiate from Kawasaki disease. Without proper timely treatment during the acute phase, coronary artery aneurysm may develop in about 20%-25% of patients. About 0,5 to 1% of patients may develop a giant aneurysm of more than 8 mm. After giant aneurysm is formed, recovery is almost impossible and it can lead to a variety of stenosis of coronary artery, ruptures or acute thrombosis. These complications can cause coronary heart disease or myocardial infarction, there are also cases of rare complications such as sudden death of a child. The occurrence of myocardial infarction in children with Kawasaki disease is a poor prognostic sign and literature data indicate that the death after the first myocardial infarction occurs in 22% of patients, and followed by the next episode of myocardial infarction mortality rate increases to 70-80% [2,5].
Recently published data show a steady increase in the prevalence of Kawasaki disease in South Korea by 100 thousand children less than 5 years:
From 2000 to 2002 - 84.4 cases Since 2003, up to 200 -105.0 cases From 2006 to 2008 - 113.1 cases
And in 2011 -134.4 cases per 100 thousand of children population <5 years.
The upward trend in the incidence of Kawasaki disease occurs in Europe. Instead, the United States and Canada show
stability without growth in the incidence of Kawasaki disease. Thus, it can be argued that Kawasaki disease is not a rare disease [2,5,6].
In 2005 the literature data showed that on the level of incidence per 100 thousand children at the age of 5 years are as follows: 134.2 for Japan; 104.6 for South Korea; 66 for Taiwan, compared with the data of 18.5 in the United States; 8.1 in the UK and 6.2 in Sweden. Besides, the family history's analysis which was carried out informed of the occurrence of Kawasaki disease in three among brothers of the same family for 6 years. Often, studies indicate occurrence of Kawasaki disease among brothers and sisters is much higher than for the general population. Studies to determine genetic predisposition are mainly focused on human leukocyte antigens (HLA), immunoglobulin allotypes, HLA-DRB1, HLA B5 testify about kinship with Kawasaki disease. Scientific research is aimed at searching the association of susceptibility to Kawasaki disease, severity and contraindications for immunoglobulin treatment, and the development of complications. Recently, literature data indicate that the main candidates for the association with Kawasaki disease are inositol-1,4,5-triphosphate 3-kinase (ITPKC) genes, the gene caspase-3 (CASP-3), B-lymphocyte kinase (BLK), CD40 gene, F fragment from Ig G 2a receptor (FCGR2A) shows low affinity and HLA. Data on these genes and their relationship with Kawasaki disease are presented by recent studies GWASes in Japan, Taiwan and South Korea [2,7]. The GWAS data also showed the most numerous association with Kawasaki disease in 12q24 and 19q13,2 chromosome regions [2,8]. ITPC is a secondary messenger that is involved in the molecular signaling Ca2+/NFAT and acts as a negative regulator of T-cell activation. By the activation of NFAT, it launches the mechanism of enhanced production of interleukin -2 (IL-2), also increases the activation of T cells with increased excretion of cytokines This relationship can lead to association with Kawasaki disease and correlate with disease severity. Also, the relationships of Kawasaki Disease with SNP in the gene CASP3 located on 4q34-35 are described, characteristic of European-American and Japanese populations, and gene polymorphisms ITPKC, rs4236089 C alleles in chloride intracellular channel 5 (CLIC5) located in 6p21,1 [2,8,9,11].
These polymorphisms could be results of diverse ethnic differences. CASP3 may be through apoptosis of immature cells. Replacement of G (guanine) with A (adenosine) within one exon CASP3 (rs113420705) reduces binding of NFAT with DNA, which can lead to relationship with Kawasaki disease. SNP in both ITPKC and CASP3 genes may be unfavorable for the introduction of IVIG, this can be explained by synergy effects of ITPKC and CASP3. Currently, for the treatment of patients with Kawasaki disease with resistance to IVIG, cyclosporine-A started to be used, which inhibits activation of NFAT. Also, literature data prompt an affinity of Kawasaki Disease with rs1801274 FCGR2A. FCGR2A is expressed by many immune cells such as dendritic cells, macrophages, neutrophils, monocytes and are able to interact with them. The evidence of immune activation can be CIC (Circulating Immune Complex) found in the blood of patients in the acute phase of Kawasaki disease, which obviously can be activated by using FCGR2A [10,11,12]. There is also an association of Kawasaki disease, which occurs in FAM167A-BLK region on chromosome 8p23-p22. The peak union at this locus accounts for intergenic region between BLK and FAM167A. BLK is a non-receptor tyrosine kinase of Src family, which plays a role in intracellular signal transduction and differentiation of B-lymphocytes. This may indicate the possible involvement of B cells in the development of Kawasaki disease.
In addition, BLK is involved in the production of IL-17, which is manifested in the acute phase of Kawasaki disease. Increased levels of IL-17 in the acute phase may be due to polymorphism of BLK. However, the function of FAM167A is unclear. The involvement of B cells in the development of Kawasaki disease is also confirmed by other data such as GWAS report about the existence of association of Kawasaki Disease and SNP CD40 that is located on chromosome 20q12-q13,2. CD40 is expressed in B cells, monocytes / macrophages, endothelial cells, fibroblasts. Hence, it turns out that the signal path of CD40-CD40L may play a role in the onset and progression of Kawasaki disease. HLA associations with autoimmune diseases are well known [10,13,14].
There is a complex of immune disorders in the acute phase of Kawasaki disease, notably launching a cascade of cytokine stimulation with endothelial cells. An increase in cytokines and chemokines in the blood of patients with Kawasaki disease in the acute phase of the disease is the evidence of these disorders. Many processes still have to be found out, but it is known that the activation of endothelial cells and CD68+ monocytes/ macrophage system is actively involved in development of both Kawasaki disease and vascular complications. It is also known about the involvement of CD8+ T lymphocytes and oligoclonal IgA plasma cells in the development of coronary arteritis. Infiltration of these components in the respiratory tract in the conclusions of autopsies of fatal consequences of URTI (Upper respiratory tract infections) evokes the similarity with Kawasaki disease and may indicate that the airways can be used as a gateway for the penetration of the pathological agent, and that Kawasaki disease can masquerade as an infectious disease. Therefore, vigilance is required in the treatment of patients who do not respond to standard treatment of URTI. According to the literature data, the agent of Kawasaki disease most probably can come through the air and some scientists believe in its origin from the Pacific Ocean and fall with the movement of air in various beneficial organisms. This hypothesis can be plausible taking into account the fact that the agent can enter through the respiratory tract. There are many other hypotheses that stand for the possible involvement of enzymes such as matrix metalloproteinases (MMPs), which have capability to destroy all types of proteins of the cell wall, extracellular material and play a key role in the development of complications of Kawasaki disease, occurrence of vasculitis and aneurysms of the coronary arteries. MMP are also involved in cleavage of membrane receptors, the release of apoptotic ligand such as FAS (Free Alongside Ship), and activation of chemokines and cytokines. Therefore, the hypothesis about the involvement of CD40L, MMP-1 (intracellular collagenase) in the development of Kawasaki disease deserves special attention [2,15].
There is also heightened expression of toll-like receptor 2 (TLR-2) on monocytes of peripheral blood in patients with Kawasaki disease, which also may indicate their involvement in the pathogenesis of the disease. TLR2 provides functioning of innate immunity [16]. Also introduction innate immunity in the development of Kawasaki disease may be shown with found in mice with the ligand-induced coronary arteries - pathological Nod1, which enhances apoptosis, mediated by caspase-9. It induces the activity of NF-KB through the activation of RIPR2 and IKK-gamma. Here NF-kB releases from the inhibitory complex, translocates into the nucleus and activates the transcription of key genes. NF-KB is a universal transcription factor controlling the expression of genes of immune response, apoptosis and cell cycle. Dysregulation of NF-kB causes inflammation, and the development of autoimmune diseases,
viral infections and cancer pathology. It can be activated by cytokines (TNF and Il-1), T-, B-cell mitogens, bacterial and viral products (all ligands of toll-like receptors) and stress factors (reactive oxygen species or UV). With these data it can be summarized that innate immunity plays an important role in the development of Kawasaki disease. The literature data have reported that serum Kawasaki Disease, associated molecules have a common structure with Microbe-associated mo-lecular pattern (MAMP), Yersinia pseudotuberculosis, Staphylococcus aureus, Bacillus subtilis, Bacillus cereus, and the titers of these molecules reduce after the use of IVIG. It was suggested the version that heightened MAMPs and DAMPs (damage-associated molecular patterns) in serum in the acute phase of Kawasaki Disease can activate the immune system and vascular cells via PRR (pattern recognition receptor). PRR are proteins located on the surface of cells of the immune system and are able to learn standard molecular patterns (so-called patterns), specific for most groups of pathogens. They are also called pattern recognition receptors. In comparison with the system of adaptive immunity and associated immune mechanisms are evolutionary more ancient. Receptors connoisseurs of pattern in the course of evolution were selected for specificity against bacterial lipopolysaccharides and glycoproteins containing residues mannose [17].
To understand the etiopathogenesis of the disease animal models are required. In our opinion the most approximate mechanism of the development of Kawasaki disease is a summation of all results obtained from murine models, as well as data of the detected changes in the acute phase of Kawasaki disease. It follows that this hypothesis of evolution (development) vasculitis: a-mannan (polymer of sugars Mannose) binds to Dectin-2, SYK activates NF-kB. NF-kB activates cytokines genes, which in turn triggers a cascade of cytokines pro-IL-1p, IL-12 and IL-23. These cytokines stimulate the differentiation of Th17 cells, neutrophils and macrophages are recruited to inflammatory sites by stimulating the production of various proinflammatory cytokines, which stimulate the activation of endothelial cells and smooth muscle cells of blood vessels. Inflammatory cells stick to the activated endothelium and migrate into the vascular wall. Thus vasculitis is developing [2,18].
Given the urgency of the problem and the increased frequency of the disease, we want to present a clinical case of atypical course of Kawasaki disease in the girl at the age of 11 months and 27 days, who was hospitalized in the Department of pediatrics of City Children's Clinical Hospital (city of Lviv, Ukraine).
The child O. at the age of 11 months and 27 days in June 15, 2015 (on the 4th day of the disease) was hospitalized in the Department of pediatrics №1 of Lviv City Children's Clinical Hospital.
According to the anamnesis we know that the girl at the age of 11 months and 27 days was born from the first pregnancy at a gestational age of 39 weeks with body weight 3000 g, Apgar 8/8. Pregnancy course was uneventful. The girl was growing and developing according to age. She often suffers from URTI and bronchitis (4 times a year).
Clinically the child has signs of pharyngitis and conjunctivitis: oropharynx hyperemic clamps, lip with cracks, subfebrile body temperature, skin pale, moist, without lesions, perioral cyanosis; sharply reduced appetite, sleep disturbed. Nasal breathing is freely. Auscultation breathing is vesicular in the lungs. Heart sounds rhythmic, sonorous. The borders of relative heart dullness are within the age norm. Slightly
enlarged cervical lymph nodes (about 0.5 cm), undistempered, unconsolidated with surrounding tissues. Tongue is moist, clean. The abdomen is soft, undistempered, palpation are available in all departments. Peristalsis is active. The presence of the liver 2 cm below the costal margin. The spleen does not palpate. Physiological reflexes are age appropriate. Meningeal symptoms are negative. Physiological defecation is not broken.
Conducted additional primary research : General analysis of blood: erythrocytes —3,9 x1012 g/l, Nb — 129 g/l, leucocytes
— 13,1x109/l , eosinophils— 2%, stab — 2%, segmented -44%, monocytes — 2%, lymphocytes — 50% , platelets - 415* 109/l, ESR( erythrocyte sedimentation rate) — 19 mm/hour. Urinalysis: protein trace, epithelial cells —1-3 in sight, leucocytes — view all field, the bacteria is «+». Biochemical analysis of blood: total protein - 64,29 g/l, total bilirubin -7.80 mkmol /l , ALT -31,5 o/l , AST - 49,8/l , urea -3,93 mmol /l, creatinine-0,038 mmol/l, glucose 5.37 mmol/l, CRP (C-reactive protein) - 89,3 mg/ ml. Kawasaki disease is characterized by leukocytosis, thrombocytosis, increased erythrocyte sedimentation rate (ESR) and increased CRP. Conclusion of ultrasound of the abdomen: normal variant. Conclusion of ECG: sinus tachycardia (heart rate: 190 beats/min).
The patient was assigned to bed rest, antibiotic therapy is intravenous. In the first two days infusion therapy was conducted (5% glucose, 0.9% NaCl, rheo-sorbilact, 5% solution of ascorbic acid, cocarboxylase). Symptomatic treatment: Metamizole, Diphenhydramine age dosages.
The girl's condition deteriorated on the fifth day: increased weakness, continued fever, polymorphic rash in form of small flat red spots on the skin of the trunk appeared, proximal extremities, hyperemia of the conjunctiva became even more pronounced that was not accompanied with secretions, dryness and redness of the oral mucosa with cracked lips, cervical lymph nodes increased. Laboratory: leukocytosis with a shift leukocyte formula to the left was determined in the clinical analysis of blood, thrombocytosis, increased erythrocyte sedimentation rate; urine analysis - proteinuria and pyuria. Biochemical analysis of blood: Total protein -69,8 g/l, ALT-20,5 mm/l, AST-40,0 mmol/l, PSA-96,0, creatinine - 0.04 mkM/l, urea - 3.2 mM/l, glucose
- 4.5 mmol/L. Conclusion of ECG: sinus tachycardia (heart rate: 190 beats/min). Echocardiography: cardiac chamber size is normal. The course of the vessels is correct. Contractility is not impaired. Bacteriological examination of feces: Staphylococcus aureus KYO: * 104. The obtained data, as well as the symptoms gave us the idea of Kawasaki disease with atypical course.
The correction of therapy: 1) the use of IVIG (intravenous immunoglobulin G) at a dose of 250 ml v/v in the drip; 2) acetylsalicylic acid. After completion of the IVIG infusion in 12 hours after the girl's condition dramatically improved: body temperature was normal; heart rate is 121beats/min, the baby was active, had good appetite. Then there was a reverse development of the phenomena of conjunctivitis, rash; indicators of the General analysis of blood improved: erythrocytes -4,2x10i2/l, hemoglobin 130 g/l, white blood cells -5,6x109/l, e - 2%, -37%, l -52%, m -7%; except for the number of platelets (457,0x109/l). Response to therapeutic measures was proof of the thought of Kawasaki disease with atypical course.
The infant was discharged on the 11th day after admission in satisfactory condition with the following recommendations: 1) observation at place of residence; 2) to continue taking acetylsalicylic acid (2.5 mg/kg of body weight per day in 2 divided doses for 8 weeks. Also monitoring of the blood count is required (including platelet count) in two weeks, a month, three months. For the purpose of prevention of occurrence of
complications in the cardiovascular system it is necessary to conduct periodic ECG and Echocardiography study.
In two weeks after discharge the patient was undertaken an in-depth examination (in good health) in the conditions of city children's clinical hospital (city of Lviv, Ukraine).
The following results are obtained. General blood analysis: erythrocytes — 4,77x1012/l, hemoglobin 111 g/l, leucocytes — 4,7x109/l, ESR — 5 mm/h, platelets — 280x109/l, s — 9% p
— 3%, z— 40%, l — 39%, m — 10%. Biochemical analysis of blood: protein -70,6 g/l, albumins — 63%, 5 alpha 1% alpha 2— 7%,beta 10%, gamma — 15%, PSA —negative; bilirubin — 8.4 mkmol/l, ALT 95 OD/l, AST — 29 OD/l, cholesterol — 3,89 mmol/l, urea — 4,5 mmol/l, creatinine — 0,045 mmol/l, glucose
— 4.7 mmol/l, calcium — 2.58 mmol/l, phosphorus -1,74 mmol/l, alkaline phosphatase —85 OD/l; creatinphosphokinase
— 93,06 OD/l; troponin 1 — negative; a-TNF — 5,7 mkg/ml; the interleukin 10-1 mkg/ml; interleukin 6 — 0,73 mkg/ml; antinuclear antibody — negative; anti-DNA antibodies: strand
— 0,44; double strand — 0,89; antiphospholipid antibodies: anticardiolipin — 2 I/ml; an-tiphosphatidylethanolamine -7,1 I/ ml; antibodies to the endothelium of vessels are not specified. Immunological assays: IgG — 11.5 g/l, IgA -1.2 g/l, IgM 0.9 g/l, CEC -40 MO /ml; spontaneous NBT test — 28% (1), stimulated
— 40%, FR 9%. Lymphocyte subpopulations: lymphocytes — 57%; T- lymphocytes (SD3+) — 62,4%, T-helpers (SD4+) — 39,9%, T-cytotoxic (SD8+)—20,22%, Tx/Ts -2,0, b-lymphocytes (SD19+) — 26,04%, NK (SD56+) — 13,17%, activated NK -4,32%, NK (SD8+) — 80,1%. Coagulation: prothrombin index — 80%; recalcification time >120 sec, fibrinogen — 2.8 g/l, fibrinogen — B+. Blood clotting: the beginning 5 min. Urine test — no changes are installed. ECG results: heart rate is 121beats/min Echocardiography: pathological changes are not revealed. Given the good health of the child, the positive dynamics of clinical symptoms (disappearance of conjunctivitis, pharyngitis and complete disappearance of the rash ), and paraclinical results, it was decided to extend a nonsteroidal antiinflammatory therapy (acetylsalicylic acid 2.5 mg/kg/day twice a day two weeks later (at normal values of ESR, CRP, platelet count) — reduce dose to 2.5 mg/kg/ day for 15-20 months), desegregate therapy (Curantil) —two months; symptomatic therapy (remediation of the nasopharynx).
At the same time, there is a need to monitor blood count, platelet count, coagulation, CRP every two weeks. Repeated ECG and Echocardiography are in a month.
Conclusion:
1.The first symptoms of Kawasaki disease appear from 6 months to 5 years, and the peak of the disease accounts for 9 -11 months of life, as evidenced by this clinical case.
2.Typical clinical symptoms of the disease are: fever more than 5 days, polymorphous skin rash is characterized, bilateral conjunctivitis without discharge, dryness and redness of the mucous membranes of the mouth, increasing cervical lymph nodes, changes in blood count (leukocytosis with a shift formula to the left, thrombocytosis and increased erythrocyte sedimentation rate);
3. Targeted therapy of IVIG in combination with NAID therapy gives rapid clinical effect;
4. Presented clinical case draws attention of practitioners to the importance of early diagnosis of Kawasaki disease, given the risk of long-term effects and complications.
5. This disease can masquerade as various infectious diseases, as evidenced by the literature and our clinical case. Also it is important the timely recognition of the atypical course of the KD, thereby avoiding negative consequences and reversibility
of the process that we can observe in this case.
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Гудар'ян О.О.
ДЗ «Днтропетровська медична академiя МОЗ Укра'ши», д.мед.н., професор кафедри хiрургiчноi стоматологи, iмплантологii та паро-донтологи, декан стоматологiчного факультету
1дашкта Н.Г.
ДЗ «Днiпропетровська медична академiя МОЗ Укра'ши», к.мед.н., завiдувач кафедри хiрургiчноi стоматологи, iмплантологii та пародонтологи
Мадждi А.А.
ДЗ «Днтропетровська медична академiя МОЗ Укра'ши» асистент кафедри хiрургiчноi стоматологи, iмплантологii та паро-донтологП
ОСОБЛИВОСТ1 Л1КУВАННЯ ПЕРЕЛОМ1В НИЖНЬО1 ЩЕЛЕПИ З ВИКОРИСТАННЯМ БРЕКЕТ-ТЕХН1КИ
THE FEATURES OF TREATMENT OF MANDIBULAR FRACTURES WITH USING OF BRACKET-TECHNIQUE
Gudaryan A.A., Professor of Oral surgery, implantology and periodontology department, Dean of Faculty of Stomatology, SE «Dnipropetrovsk medical academy Ministry of Health of Ukraine», DMedS
Idashkina N.G., Head of Oral surgery, implantology and periodontology department, SE «Dnipropetrovsk medical academy Ministry of Health of Ukraine», PhD
Majdi A.A. Assistant of Oral surgery, implantology and periodontology department, SE «Dnipropetrovsk medical academy Ministry of Health of Ukraine»,
АНОТАЦ1Я
Клiнiко-рентгенологiчнi до^дження у 32 хворих з переломами ниж-ньо'1' щелепи в межах зубного ряду, яких левами за методом двощелепного шинування i3 застосуванням стандартно'1' методики з використанням брекет-техтки довели ii ефективнiсть лише за умов первинно'1' вiдсутностi зсуву вiдламкiв та порушень прикусу. У хворих iз змщенням вiдламкiв збтьшуеться ризик повторного змщення вiдламкiв, що погiршуe умови для загоення перелому (остеогенез вiдбуваeться переважно шляхом вторинного зрощення) та призводить до сповшьнення консолiдацii вiдламкiв.
ABSTRACT
Clinico-roentgenological researches at 32 patients with the mandibular fractures in the area of dentition, in which treatments carried out the intermaxillary splintage with application of standard method with the use of bracket-technique, proved that such method was effective only at the terms of primary absence of displacement of bone fragments and malocclusion. The risk of the repeated displacement of mandibular fragments which worsens terms for cicatrization of break (osteogenesis takes place mainly by the way of secondary union) and led to the delayed consolidation offractures as results, is higher for the patients with primary displacement.
Ключовi слова: переломи нижньо'1' щелепи, репозицiя, шини, брекети, ускладнення.
Keywords: fractures of the mandible, reposition, splints, brackets, complication.
Рш ввд року юнуе невпшна динамта до зростання травматизму щелепно-лицево! дшянки. Це пов'язано зi збшь-шенням побутового травматизму, дорожньо-транспортних пригод, поширенням зон вшськових конфлжпв та терорис-тичних напащв. Незважаючи на зростаючий попит щодо нових хiрургiчних метсдав лшування травматичних пошко-джень исток лицевого черепу, до 90 % переломiв нижньо! щелепи в межах зубного ряду л^ють методом двощелепного шинування [1,2,3]. Загальновщомо, що тсля здшснення ручно! репозицп ввдламшв нижньо! щелепи та подальшого накладення назубних шинуючих пристро!в будь-яко! кон-струкци неможливо зберегти вiрне зютавлення вщламшв, через те, що тд час шинування ввдламки знов зсуваються [4,5,6]. Закршлеш шини стабшзують невiрне положення ввдламшв з утворенням сходинки по нижньому краю щеле-
пи. Як наслщок, ми спостерпаемо недостатню репозицш вщламшв та порушення прикусу, яке неможливо виправити нешвазивними методиками.
Останшм часом все бшьшо! популярносп набувають ме-тоди л^вання переломiв нижньо! щелепи з використанням адгезивно! брекет-техшки для фшсацп ввдламшв [7,9]. Не визивають сумнiвiв певш переваги, що пов'язаш зi змен-шенням травматичносп, кращою ппешчшстю [10,11], од-нак вiдсутнiсть всебiчного та ретельного аналiзу результатiв застосування ще! методики лiкування у хворих з переломами нижньо! щелепи, невизначешсть показань та протипоказань до використання адгезивно! брекет-технiки шд час фшсацп вiдламкiв, значно обмежують можливiсть !! практичного впровадження [8]. Нажаль, даш, що стосуються якостi репозицп вiдламкiв пвд час використання саме брекет-техшки, в
