Kawasaki disease is a severe type of vasculitis in infants and young children that is identified through a range of clinical signs that can imitate other benign conditions in childhood (Ling et al. 2011; Huang et al. 2010; Cho et al. 2011). Aetiology of the disease is unknown (Huang et al. 2010). Moreover, there are no precise laboratory-identified tests and procedures to diagnose cases of Kawasaki condition in patients. Consequently, physicians rely on certain characteristic clinic symptoms rather than defined diagnostic tests to determine the disease (Huang et al. 2010). Given such challenges in understanding the molecular basis of Kawasaki disease, researchers and physicians have developed various techniques to understand and diagnose it.
Ling et al. (2011) proposed certain models based on blood leukocyte gene expression and plasma or urine protein excretion because they believed that these elements were linked with Kawasaki disease. It is noted that such biomarkers could offer significant perspectives to the pathophysiology of the disease and provide further insights into its aetiology.
Consequently, researchers have focused on proteomic and genomic techniques with regard to biomarkers in order to understand and diagnose this condition (Ling et al. 2011). According to some studies, transcriptional analyses of white blood cells have shown disease-specific expression outcomes, while protein biomarkers examinations have established significantly higher levels of cytokines, chemokines and acute phase reactants. Nevertheless, none of these outcomes is exceptionally prominent in Kawasaki disease (Ling et al. 2011).
Most researchers strive to develop a specific diagnostic algorithm that could assist physicians in discovering Kawasaki disease from other febrile conditions (Ling et al. 2011). On this note, Ling et al. (2011) concluded that hybrid technique with a multi-step diagnostic algorithm combining both clinical and molecular findings could be useful in differentiating causes of acute Kawasaki disease from febrile controls in patients.
Huang et al. (2010) noted that the serum haptoglobin/apolipoprotein A-I ratio could act as an effective biomarker for categorising cases of acute Kawasaki disease.
Other researchers say that the disease is difficult to discover because its understanding and diagnosis rely on clinical data and non-pathognomonic symptoms (Cho et al. 2011; Popper et al. 2009). In addition, it also lacks specific diagnostic tests. On this note, Cho et al. (2011) mention that the evaluation of serum BNP or NT-pro-BNP could be relevant in recognising Kawasaki disease. They concluded that NT-pro-BNP was more reliable in diagnosis than hs-CRP, particularly in patients with cases of incomplete clinical features of the disease.
It is imperative to note that acute cases of Kawasaki disease could be difficult to distinguish from other conditions that show rash or fever because of poor characterisation of aetiological agents and pathophysiology (Popper et al. 2009). Popper et al. (2009) showed that analyses of genes revealed that platelet and neutrophil B cell activations were more expressed in patients with Kawasaki disease than in others with acute adenovirus infections except for cases of scarlet fever. The study findings provided critical insights into molecular algorithm techniques that could be applied to classify Kawasaki disease among other febrile illnesses, as well as offer a model for developing diagnostic reagents for the disease with regard to the response of the host (Popper et al..2009).
Ling et al. (2010) showed that urine-based proteomic technique could provide a novel way of developing non-invasive biomarkers for Kawasaki disease diagnosis.
Overall, many researchers have developed various techniques to understand and diagnose the molecular basis of Kawasaki disease because it lacks specific diagnostic tests. Thus, physicians must decide on patients’ care provision.
Reference List
Cho, S, Kim, Y, Cha, H, Suh, T, Han, Y, & Lee, J 2011, ‘Adjuvant laboratory marker of Kawasaki disease; NT-pro-BNP or hs-CRP?’, Annals of Clinical & Laboratory Science, vol. 41, no. 4, pp. 360-3.
Huang, Y, Gupta-Malhotra, M, Huang, J, Syu, K, & Huang, Y 2010, ‘Acute-phase reactants and a supplemental diagnostic aid for Kawasaki disease’, Pediatric Cardiology, vol. 31, no. 8, pp. 1209-13. Web.
Ling, B, Mellins, D, Sylvester, G, & Cohen, J 2010, ‘Urine peptidomics for clinical biomarker discovery’, Advances in Clinical Chemistry, vol. 51, pp. 181-213.
Ling, X, Lau, K, Kanegaye, J, Pan, Z, Peng, S, Ji, J, Liu, G, Sato, Y, Yu, T, Whitin, J, Schilling, J, Burns, J, & Cohen, H 2011, ‘A diagnostic algorithm combining clinical and molecular data distinguishes Kawasaki disease from other febrile illnesses’, BMC Medicine, vol. 9, p. 130. Web.
Popper, J, Watson, E, Shimizu, C, Kanegaye, T, Burns, C, & Relman, A 2009, ‘Gene transcript abundance profiles distinguish Kawasaki disease from adenovirus infection’, The Journal of Infectious Diseases, vol. 200, no. 4, pp. 657-66. Web.