Abstract 86: Pentraxin 3 Can Be A Candidate For Biomarker Of Kawasaki Disease

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Yasuhiro Katsube ◽  
Miharu Akao ◽  
Yoshiaki Hashimoto ◽  
Kouji Hashimoto ◽  
Makoto Watanabe ◽  
...  

Background: Kawasaki disease (KD) is a systemic vasculitis and the leading cause of acquired heart disease. There are some cases that show unresponsiveness to initial intravenous immunoglobulin (IVIG) and require addition treatment. High incidence of coronary artery lesions (CAL) is seen in unresponsive cases. Pentraxin 3 (PTX3) is produced at the site of vascular inflammation, and used as a new biomarker for vasculitis. The aim of this study is to explore the application of PTX3 to KD. Methods: 128 patients with KD are enrolled. Blood samples are collected at before IVIG and 1, 3, 6 month later from the onset of KD. PTX3 values are compared with IVIG unresponsive scoring system by Kobayashi et al. (Circulation, 2006). Results: Mean values of PTX3 before IVIG and 1, 3, 6 month were respectively 25.1*, 7.1*, 3.8, 3.6 ng/ml (asterisk shows statistical significance with age-matched control: 3.6). Mean values of PTX3 in unresponsiveness (n=20) and responsiveness (n=108) at before IVIG and 1, 3, 6 month were 46.8* vs. 20.9, 9.1* vs. 6.7, 4.2 vs. 3.7, 3.9 vs. 3.5 ng/ml (asterisk shows statistical significance between two groups). There is statistical positive correlation between PTX3 and score points by Kobayashi et al. (r=0.602, p=0.000). According to the statistical analysis, the area under the ROC curve (AUC) was 0.87 and sensitivity and specificity of PTX3 as IVIG unresponsiveness prediction were 90 and 81 %, if cut off value was set as 28 ng/ml. Conclusions: 1. vasculitis continues at least 1 month after onset of disease. 2. PTX3 can be a candidate biomarker for prediction of unresponsiveness in patients with KD.

2021 ◽  
Vol 12 ◽  
Author(s):  
Toshiyuki Kitoh ◽  
Tsuyoshi Ohara ◽  
Taichiro Muto ◽  
Akihisa Okumura ◽  
Reizo Baba ◽  
...  

Kawasaki disease (KD) is a febrile disease of childhood characterized by systemic vasculitis that can lead to coronary artery lesions (CAL). This was a prospective cohort study to determine the levels of the pentraxin 3 (PTX3), soluble CD24-Subtype (Presepsin) and N-terminal pro-brain natriuretic peptide (NT-pro BNP) in consecutive KD patients. From January 2013 to March 2015, all patients with KD admitted to Aichi Medical University Hospital who provided consent had their plasma saved before IVIG administration. In total, 97 cases were registered. 22 cases of incomplete KD were excluded from the outcome analysis. The total 75 cases were used for statistical analyses. A PTX3 threshold of >7.92 ng/ml provided a specificity of 88.5 %, a sensitivity of 94.4 %, and a likelihood ratio as high as 15.92 for the diagnosis of KD compared with febrile non-KD controls. Although an echocardiographic diagnosis of CAL in the early course of the disease was confirmed in 24 cases, it was not in the remaining 51 cases. Neither NT-proBNP nor Presepsin had statistical significance for the prediction of the echocardiographic CAL diagnosis. Only PTX3 was significantly predictive of the echocardiographic CAL diagnosis (p=0.01). The PTX3 level was significantly higher in the intravenous immunoglobulin (IVIG) non-responders (45.9±7.45) than in the IVIG responders (17.0 ± 1.46 ng/ml) (p< 0.001). The PTX3 level also correlated with the number of IVIG treatment courses needed to resolve fever (R² =0.64). Persistent CAL (pCAL) formation was observed in three cases; one of aneurysm only and two aneurysms with dilatations. The patients with pCAL had significantly higher PTX3 levels (85 ± 8.4 ng/ml) than patients without pCAL (22 ± 2.2 ng/ml) (p< 0.0001). In terms of pCAL prediction, the area under the curve (AUC) of receiver operating characteristic ROC curve of PTX3 was 0.99, and it was significantly greater than that of Presepsin (0.67) or NT-proBNP (0.75). PTX3 is a soluble pattern recognition molecule that acts as a main component of the innate immune system. These data suggest that PTX3 can be utilized as a definitive biomarker for the prediction of IVIG resistance and subsequent CAL formation in patients with KD.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Nathan Jamieson ◽  
Davinder Singh-Grewal

Aims. Kawasaki disease is an acute systemic vasculitis and is the most common cause of acquired heart disease in children in the developed world. This review aims to synthesise recent insights into the disease and provide an update for clinicians on diagnostic and treatment practices.Methods. We conducted a review of the literature exploring epidemiology, aetiology, diagnosis, and management of Kawasaki disease. We searched MEDLINE, Medline In-Process, Embase, Google Scholar, and reference lists of relevant articles.Conclusions. Kawasaki disease is a febrile vasculitis which progresses to coronary artery abnormalities in 25% of untreated patients. The disease is believed to result from a genetically susceptible individual’s exposure to an environmental trigger. Incidence is rising worldwide, and varies widely across countries and within different ethnic groups. Diagnosis is based on the presence of fever in addition to four out of five other clinical criteria, but it is complicated by the quarter of the Kawasaki disease patients with “incomplete” presentation. Treatment with intravenous immunoglobulin within ten days of fever onset improves clinical outcomes and reduces the incidence of coronary artery dilation to less than 5%. Given its severe morbidity and potential mortality, Kawasaki disease should be considered as a potential diagnosis in cases of prolonged paediatric fever.


2020 ◽  
Vol 60 (5) ◽  
pp. 283-6
Author(s):  
Yudha Fadhol Arafah ◽  
Sasmito Nugroho ◽  
Noormanto Noormanto ◽  
Nadya Arafuri ◽  
Indah Kartika Murni

Kawasaki disease (KD), or mucocutaneous syndrome, is an acute, systemic vasculitis of small- and medium-sized arteries that predominantly affects patients younger than five years.1  KD is the leading cause of childhood acquired heart disease in the developed world.2 The incidence in those aged under 5 years varies widely throughout the world, accounting for 8.4 per 100,000 in the UK, 17.5 to 20.8 per 100,000 in the USA, and 239.6 per 100,000 in Japan.2 The diagnosis of classic KD is based on the simultaneous presence of high fever for 5 or more days with at least four of five other symptoms (bilateral conjunctival hyperemia, ulcerations of the lips and inflammation of the oral cavity, polymorphous rash, edema and desquamation of the extremities, and cervical lymphadenopathy), or fever associated with less than 4 of the diagnostic criteria and echocardiographic abnormalities of the coronary arteries.3


2018 ◽  
Vol 2017 (3) ◽  
Author(s):  
Hala M Agha ◽  
Hala S Hamza

[first paragraph of article]Kawasaki disease (KD) is a hybrid condition at the junction of infectious diseases, immunology, rheumatology, and cardiology.1 KD is a systemic vasculitis of unknown etiology predominately affecting medium-sized vessels such as the coronary arteries, which mainly affects infants and children2. The disease itself may be the characteristic manifestation of a common pathway of immune-mediated vascular inflammation in genetically susceptible hosts3. Untreated KD may lead to the formation of coronary artery aneurysms and sudden cardiac death in children. The diagnosis of KD is based on the clinical features of fever of at least 5 days together with at least 4 or 5 other features including rash, bilateral conjunctival injection, changes in peripheral extremities, lymphadenopathy and oropharyngeal changes4. The diseases that must be differentiated from KD because of similar clinical findings include viral infections (measles, adenovirus, enterovirus, and Epstein-Barr virus), scarlet fever, staphylococcal scaled skin syndrome, toxic shock syndrome, polyarteritis nodosa, bacterial cervical lymphadenitis, and juvenile rheumatoid arthritis5,6. Because each of the symptoms commonly occurs in other childhood illnesses, the disease can be difficult to diagnose, especially in children who present with an incomplete form of the disease. KD has not been previously reported from Egypt and there are special challenges in recognizing complete KD in a country where physicians have limited experience with the disease. The diagnosis of incomplete KD is thus even more challenging in this setting. 


2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Samin Alavi ◽  
Alireza Fahimzad ◽  
Farzaneh Jadali ◽  
Farid Ghazizadeh ◽  
Armin Rashidi

Kawasaki disease (KD) is a systemic vasculitis of unknown etiology and a leading cause of acquired heart disease. It is assumed that there is an activation of the immune system by an infectious trigger in a genetically susceptible host. Neuroblastoma is the most common extracranial solid tumor in young children. It mainly originates from primordial neural crest cells that generate the adrenal medulla and sympathetic ganglia. A diagnosis of concurrent KD and neuroblastoma in a living child has been made in only one previous report. We report the second case and review the literature.


2021 ◽  
Vol 9 ◽  
Author(s):  
Daisuke Maruyama ◽  
Begüm Kocatürk ◽  
Youngho Lee ◽  
Masanori Abe ◽  
Malcolm Lane ◽  
...  

Kawasaki disease (KD), an acute febrile childhood illness and systemic vasculitis of unknown etiology, is the leading cause of acquired heart disease among children. Experimental data from murine models of KD vasculitis and transcriptomics data generated from whole blood of KD patients indicate the involvement of the NLRP3 inflammasome and interleukin-1 (IL-1) signaling in KD pathogenesis. MicroRNA-223 (miR-223) is a negative regulator of NLRP3 activity and IL-1β production, and its expression has been reported to be upregulated during acute human KD; however, the specific role of miR-223 during KD vasculitis remains unknown. Here, using the Lactobacillus casei cell wall extract (LCWE) murine model of KD vasculitis, we demonstrate increased miR-223 expression in LCWE-induced cardiovascular lesions. Compared with control WT mice, LCWE-injected miR-223-deficient mice (miR223−/y) developed more severe coronary arteritis and aortitis, as well as more pronounced abdominal aorta aneurysms and dilations. The enhanced cardiovascular lesions and KD vasculitis observed in LCWE-injected miR223−/y mice correlated with increased NLRP3 inflammasome activity and elevated IL-1β production, indicating that miR-223 limits cardiovascular lesion development by downmodulating NLRP3 inflammasome activity. Collectively, our data reveal a previously unappreciated role of miR-223 in regulating innate immune responses and in limiting KD vasculitis and its cardiovascular lesions by constraining the NLRP3 inflammasome and the IL-1β pathway. These data also suggest that miR-223 expression may be used as a marker for KD vasculitis pathogenesis and provide a novel therapeutic target.


2003 ◽  
Vol 42 (148) ◽  
Author(s):  
S Shrestha ◽  
N Adhikari

Kawasaki disease, first described by Tomisaku Kawasaki in1967, is an acute systemic vasculitis of infancy and childhood.It is now the leading cause of acquired heart disease indeveloped countries. The most common age group affected isbetween 6 months to 5 years and the peak incidence is inchildren aged 9 to 11 months. The disease has malepreponderance with the male female ratio of 1.5:1. Thoughthe exact etiology is not known the disease is known to beassociated with unusual degree of immune activation andimmunoregulatory abnormality.


2012 ◽  
Vol 1 (8) ◽  
pp. 226-228
Author(s):  
Dayana Nicholas ◽  
Kenneth Nelson ◽  
Azmi Sarriff

disease (KD) is an acute systemic vasculitis that predominantly affects pre-school aged children. It is characterized by fever, bilateral nonexudative conjunctivitis, erythema of the lips and oral mucosa, changes in the extremities, rash, and cervical lymphadenopathy, and irritation and inflammation of the mouth, lips, and throat. Serious complications of KS include coronary artery dilatations and aneurysms, and KS is a leading cause of acquired heart disease. It has a predilection to coronary arteries, and its precise etiology is still unknown. Many infectious agents, including viruses and bacteria, have been suggested as potential causes of the disease.DOI: http://dx.doi.org/10.3329/icpj.v1i8.11256 International Current Pharmaceutical Journal 2012, 1(8): 226-228 


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Chee Fu Yung ◽  
Xiangmei Ma ◽  
Yin Bun Cheung ◽  
Bee Khiam Oh ◽  
Sally Soh ◽  
...  

Abstract Kawasaki disease (KD) is a systemic vasculitis mainly affecting young children and the leading cause of acquired heart disease in developed countries. We performed a self-controlled case series analysis to investigate the association between PCV13 and KD. All hospitalized KD cases <2 y old from our hospital in Singapore from 2010 to 2014 were included. Complete KD cases were classified based on the definitions of the American Heart Association. During the study period, 288 KD cases were identified. A total of 21 KD cases (12 were classified as Complete KD) had date of onset within the risk interval of day 1 to day 28 post PCV13. The age-adjusted Relative Incidence (RI) for KD following PCV13 dose 1, dose 2 and dose 3 were 1.40 (95%CI, 0.72 to 2.71), 1.23 (95% CI, 0.62 to 2.44) and 0.34 (95% CI, 0.08 to 1.40) respectively. There were seven Complete KD cases with onset during the risk interval after dose 1 of PCV13 (age-adjusted RI 2.59, 95%confidence interval (CI), 1.16 to 5.81). We did not detect a significant increased risk for overall KD among PCV13 recipients. However, a significant association between PCV13 and Complete KD was noted following receipt of the first dose of PCV13.


Author(s):  
K. Rokde ◽  
S. Kumar ◽  
A. Bhardwaz ◽  
S. S. Mahour ◽  
S. P. Nema ◽  
...  

This study was carried out on clinical cases of retained fetal membranes in crossbred cows presented at College Clinics and College dairy farm and from Villages in and around Mhow. The blood samples were collected from jugular vein just before 12 hr. postpartum and on 7th day postpartum. Haematological profile revealed that the mean values of haemoglobin, neutrophil and monocyte count after 12 hrs and 7th day postpartum were significantly lower and lymphocyte count was significantly higher in RFM cows (n=18) than normally calved cows (n=6). The differences in mean TLC, eosinophil and basophil counts were non-significant at 12 hrs postpartum, however on 7th day postpartum the TLC and eosinophil count were significantly higher and basophil count was non-significantly different in RFM cows than the normally calved cows.


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