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To the Editor: The incidence of constrictive pericarditis in HIV uninfected patients with pericardial tuberculosis is very high (31.65 cases per 1000 person-years) despite modern rifampicin-based antituberculosis treatment.1 The cellular mediators and molecular mechanisms of post-tuberculous pericardial fibrosis are unknown. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous tetrapeptide with important antifibrotic properties and galectin-3 is an activator of myofibroblasts, promoter of collagen and extracellular matrix deposition and is associated with organ fibrosis.2 ,3 Ac-SDKP, which is inactivated by ACE, exerts part of its antifibrotic effect by inhibiting galectin-3 (figure 1).4 Currently, it is not known whether endogenous Ac-SDKP and galectin-3 are present in normal pericardial effusion, and whether there are any changes in the context of pericarditis.