Investigators set out to determine whether plasma levels of follistatin-like protein 1 (FSTL-1), which is produced by cardiac myocytes, correlate with Kawasaki disease (KD) and acquired coronary artery aneurysms (CAA), of which KD is a major cause.
Investigators set out to determine whether plasma levels of follistatin-like protein 1 (FSTL-1), which is produced by cardiac myocytes, correlate with Kawasaki disease (KD) and acquired coronary artery aneurysms (CAA), of which KD is a major cause.
Frozen plasma samples drawn from 48 children were analyzed at acute presentation of typical KD and at
2 weeks, 6 weeks, and 6 months later; 1 of these children developed CAA. Researchers also analyzed 6 additional acute samples from patients with KD in whom CAA were known to have developed subsequently, as well as plasma samples from 23 healthy children who served as controls.
Enzyme-linked immunosorbent assays showed that plasma FSTL-1 levels in children with acute KD were elevated compared with levels in control patients. Levels remained elevated at 2 weeks after disease onset, but by 6 weeks, levels in patients with KD and controls were not significantly different, and KD samples returned to control levels by 6 months.
Investigators also observed a positive correlation between FSTL-1 levels and height of fever in patients with KD and no aneurysms. They concluded that high levels of FSTL-1 might be a biomarker for development of CAA in KD (Gorelik M, et al. J Pediatr. 2012;161[1]:116-119).
Commentary
This observation may lead to increased understanding of the pathophysiology of coronary aneurysms after KD. Or, even better, maybe researchers will find a role for FSTL-1 in making the diagnosis, predicting prognosis, and even in preventive treatment in KD. -Michael Burke, MD
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