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(Chest. 2004;125:354.)
© 2004 American College of Chest Physicians

Mycobacteria in Pathogenesis of Sarcoidosis

Robert M. Rutherford, MB and John J. Gilmartin, MD

Department of Respiratory Medicine, Merlin Park Regional Hospital, Galway, Ireland

Correspondence to: Robert Rutherford, MB, Consultant Respiratory Physician, North Tyneside General Hospital, Tyne and Wear, UK; e-mail robert.rutherford{at}northumbria-healthcare nhs.uk

To the Editor:

We read with great interest the study by Brown et al (February 2003)1 investigating the role of bloodstream cell wall-deficient forms (CWDFs) of mycobacteria in the pathogenesis of sarcoidosis. CWDFs have been implicated in the pathogenesis of sarcoidosis for some considerable time2 ; however, this is the first study investigating bloodstream CWDFs since the provocative study of Almenoff et al3 in 1996, who cultured CWDFs of likely Mycobacterium tuberculosis origin from a high proportion of sarcoid patients but from none of a control group. In the present study, a much greater number of patients and control subjects were recruited, and all patients had blood cultures within 6 months of diagnosis. CWDFs were not identified more frequently in patients compared to control subjects (38% vs 41%, although in a further one fourth of cases there was observer disagreement), prompting the authors to suggest that investigating bloodstream CWDFs is unlikely to be a fruitful etiologic approach in sarcoidosis.

In contrast, we feel that this conclusion is suspect. Human leukocyte antigen association studies4 suggest that susceptibility or resistance to the development of sarcoidosis may relate to carriage of particular class II alleles, and therefore the presence of CWDFs in an equal proportion of healthy control subjects does not necessarily exclude an etiologic role in sarcoidosis. Moreover, the timing of blood culture may have had a critical bearing on the number of positive yields. Sarcoidosis is characterized by granulomatous inflammation whose function is a presumed "walling-off" of offending antigens. It is possible, therefore, that bacteremia only occurs very early in the disease course before granulomatous structures are fully developed. Mycobacteremia may also not occur in all patients and, perhaps, is confined to only those with multisystem involvement. An important aspect of interpretation of the data from this study should therefore include a correlation of the number of positive blood culture findings with time from disease onset, not necessarily diagnosis, and the presence of extrapulmonary manifestations. If no such correlation exists, we would concur that an etiologic role for these organisms could not be supported and that tissue-based approaches are likely to the most productive way forward.

References

  1. Brown, ST, Brett, I, Almenoff, PL, et al (2003) Recovery of cell wall-deficient organisms from blood does not distinguish between patients with sarcoidosis and control subjects. Chest 123,413-417[Abstract/Free Full Text]
  2. Judge, MS Evidence implicating a mycobacterium as the causative agent of sarcoidosis, and comparison of this organism with the blood-borne mycobacterium of tuberculosis [PhD dissertation]. 1979 Wayne State University. Detroit, MI:
  3. Almenoff, PL, Johnson, A, Lesser, M, et al Growth of acid-fast L forms from the blood of patients with sarcoidosis. Thorax 1996;51,530-533[Abstract/Free Full Text]
  4. Foley, PJ, McGrath, DS, Puscinska, E, et al Human leukocyte antigen-DRB1 position 11 residues are a common protective marker for sarcoidosis. Am J Respir Cell Mol Biol 2001;25,272-277[Abstract/Free Full Text]




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