Heart 98:1326-1328 doi:10.1136/heartjnl-2012-302196
  • PostScript
  • Correspondence

Scientific letter: Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) and Galectin-3 levels in tuberculous pericardial effusion: implications for pathogenesis and prevention of pericardial constriction

Open Access
  1. Bongani M Mayosi1
  1. 1The Cardiac Clinic, Department of Medicine, Groote Schuur Hospital and University of Cape Town, Cape Town, South Africa
  2. 2Clinical Infectious Diseases Research Initiative, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Observatory, South Africa
  3. 3Department of Medicine, Imperial College, London, UK
  4. 4MRC National Institute for Medical Research, London, UK
  5. 5Division of Medical Biochemistry, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Observatory, South Africa
  1. Correspondence to Dr Bongani M Mayosi, Department of Medicine, J Floor Old Groote Schuur Hospital, Anzio Road, Observatory, 7925, Cape Town, South Africa; bongani.mayosi{at}
  1. Contributors The idea of the study was conceived by BMM and EDS. BMM, EDS, MN, KAW and RJW were involved in the design of the experiment. The experimental work was carried out by MN, KM and JW. MB conducted the statistical analysis of the data. MN wrote the first draft of the manuscript, and all authors participated in the finalisation of the manuscript.

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.

Figure 1

Hypothesised mechanism by which the tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits fibrosis Ac-SDKP is generated from the G-actin binding peptide, thymosin β4, by …