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Troponin T elevation in lobar lung disease
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  1. O M P Jolobe
  1. Department of Adult Medicine, Tameside General Hospital, Fountain Street, Ashton under Lyne OL6 9RW, UK
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    http://dx.doi.org/10.1136/pmj.78.921.443-a

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      Troponin T blood concentrations are raised, not only in lobar pneumonia,1 but also in submassive pulmonary embolism.2 I hypothesise that this phenomenon is mediated by endothelial damage in the pulmonary vasculature, which has an abundance of angiotensin converting enzyme (ACE).3 Derangements in the renin/angiotensin/aldosterone system (RAAS), in which ACE plays a pivotal part, may, in turn, affect troponin blood concentrations, given the interdependence between the RAAS and troponin release.4 The latter was exemplified by a study documenting the inhibition of troponin release as a result of ACE blockade in patients with acute coronary syndromes characterised by non-ST segment elevation.4

      References

      1. ↵
        Weinberg I, Cukierman T, Chajek-Shaul T. Troponin T elevation in lobar lung disease. Postgrad Med J2002;78:244–5.
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      2. ↵
        Douketis JD, Crowther MA, Stanton EB, et al. Elevated cardiac troponin levels in patients with submassive pulmonary embolism. Arch Intern Med2002;162:79–81.
        OpenUrlCrossRefPubMedWeb of Science
      3. ↵
        Williams GH, Dluly RG. Diseases of the adrenal cortex. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s principles of internal medicine. 14th Ed. New York: McGraw-Hill Health Profession Division, 1998: 2035–57.
      4. ↵
        Kennon S, Barakat K, Hitman GA, et al. Angiotensin-converting enzyme inhibition is associated with reduced troponin release in non-ST-elevation acute coronary syndromes. J Am Coll Cardiol2001;38:724–8.
        OpenUrlCrossRefPubMedWeb of Science
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      Copyright 2002 The Fellowship of Postgraduate Medicine