Sir,
I congratulate the authors Dattagupta A and Sathyamurthy I for the lucid presentation about the very important topic, sST2 current status in the article titled ‘ST2: Current status’.1 In this article, they have mentioned that ‘while ST2 is associated with allergic and immunologic diseases such as asthma, among normal subjects, sST2 was not found to be higher in them’.
We wish to add some additional information regarding the non-cardiac conditions which can elevate the serum levels of sST2. These conditions are rheumatoid arthritis, systemic lupus erythematosus (SLE), macrophage activation syndrome, juvenile idiopathic arthritis and bronchial asthma.2, 3, 4, 5
Serum sST2 levels were found to be higher in patients of rheumatoid arthritis than in the healthy subjects. The levels of IL-33, sST2 and C-reactive proteins decreased after the conventional DMARD treatment.2 In the cases of SLE, serum sST2 levels were higher than healthy controls and showed the positive correlation with the disease activity (by using the SLEDAI index and serum anti-DNA antibody).3 Similarly, in the patients with macrophage activation syndrome and in juvenile idiopathic arthritis, the levels of sST2 were higher than those in healthy persons. In these cases, levels of sST2 correlated well with the activity and reduced during the phase of remission.4
Serum sST2 levels serve as a biomarker for the severity in bronchial asthma such as pneumonia and sepsis. It also can predict the exacerbation within 3 months. High serum sST2 levels are strongly related to the neutrophilic and not the eosinophilic inflammation in asthma. Neutrophilic asthma is the most severe phenotype of bronchial asthma.5
Despite the effect of these immunological and inflammatory diseases on serum sST2 levels, it stands as the best prognostic biomarker in the cases of heart failure to predict risk stratification and is even better than galectin-3. In comparison with sST2, natriuretic peptides are better cardiac biomarkers for the diagnosis of heart failure, but they get affected by age, body mass index and serum creatinine.6
Conflict of Interest
None declared.
Footnotes
Response to the Editor,
Appendix A. Supplementary data
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References
- 1.Dattagupta A., Sathyamurthy I. ST2:Current status. Indian Heart J. 2018;70:96–101. doi: 10.1016/j.ihj.2018.03.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Hong Y.S., Moon S.J., Joo Y.B. Measurement of interleukin-33[IL-33] and IL-33 receptors [sST2 and STL] in patients with rheumatoid arthritis. J Kor Med Sci. 2011;26:1132–1139. doi: 10.3346/jkms.2011.26.9.1132. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Mok M.Y., Huang F.P., IP W.K. Serum levels of IL-33 and soluble ST2 and their association with disease activity in systemic lupus erythematosus. Rheumatology [Oxf] 2010;49:520–527. doi: 10.1093/rheumatology/kep402. [DOI] [PubMed] [Google Scholar]
- 4.Ishikawa S., Shimizu M., Ueno K., Sugimoto N., Yachie A. Soluble ST2 as a marker of disease activity is systemic juvenile idiopathic arthritis. Cytokine. 2013;62:272–277. doi: 10.1016/j.cyto.2013.03.007. [DOI] [PubMed] [Google Scholar]
- 5.Watanabe M., Nakamoto K., Sada M. Serum sST2 levels predict severe exacerbation of asthma a potential implication for neutrophilic asthma. Am J Respir Crit Care Med. 2017;195:A7571. doi: 10.1186/s12931-018-0872-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Binas D., Daniel H., Richter A. The prognostic value of sST2 and galactin-3 considering different aetiologies in non-ischemic heart failure. Eur Heart J. 2016;37:599–983. doi: 10.1136/openhrt-2017-000750. [DOI] [PMC free article] [PubMed] [Google Scholar]
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