To the Editor:
Dettmeyer et al. acknowledge that our results did not confirm those of their studies and suggest they may be a result of different methods. They used MAb to CD45RO to identify T lymphocytes in the myocardium in their study (1); however, this antibody may identify macrophages and Langerhans cells (2); other studies have also shown a lack of specificity for T lymphocytes (3). CD45RO lymphocytes, the memory T lymphocytes, are a subset of the total T-lymphocyte population that includes CD45RA (or naïve) T lymphocytes. In contrast, we used MAb against CD3, which identify all T lymphocytes. Dettmeyer et al. searched for viral genome in myocardial samples fixed for <48 h in neutral-buffered formalin; these samples could be expected to potentially yield more viruses than ours, which had been embedded in paraffin for months to years after buffered formalin fixation (4). They also searched for a larger number of viruses than we did. Both of these factors may help explain the different rates of viral detection in the two studies.
Whether the criteria for myocarditis used by Dettmeyer et al. are more rigorous than those used for adults is perhaps moot given the sudden infant death syndrome (SIDS) and control cases in both their and our studies were infants. More importantly, however, the minimal level of myocardial inflammation necessary to cause sudden infant death has yet to be established in humans and in animal models. That is why we chose to simply semiquantitatively assess the number of myocardial T lymphocytes and macrophages per unit area rather than use another's or our own arbitrary baseline cell number to define myocarditis, thereby speculating that it is sufficient to cause sudden infant death. Nevertheless, this will remain a very complicated and complex issue because less inflammation located directly in the conduction system is presumably required to cause a lethal arrhythmia than the amount of inflammation located elsewhere in the myocardium. In this regard, we certainly agree with Dettmeyer et al. that multiple sections of myocardium should be examined in all cases of sudden infant death in which a cause of death is not apparent from the death scene or the gross autopsy examination.
Given differing results from our studies, we agree that further research into the role of myocardial inflammation and viral agents, possibly interacting with underlying cardiac genetic disorders, in causing sudden infant death is warranted.
References
Dettmeyer R, Baasner A, Schlamann M, Padosch SA, Haag C, Kandolf R, Madea B 2004 Role of virus-induced myocardial affections in sudden infant death syndrome: a prospective postmortem study. Pediatr Res 55: 947–952
Berti E, Aversa GG, Soligo D, Cattoretti G, Delia D, Aiello A, Parravicini C, Hall BM, Caputo R 1991 A6—a new 45RO monoclonal antibody for immunostaining of paraffin-embedded tissues. Am J Clin Pathol 95: 188–193
Cabecadas JM, Isaacson PG 1991 Phenotyping of T-cell lymphomas in paraffin sections—which antibodies?. Histopathology 19: 419–424
Rogers BB, Alpert LC, Hine EA, Buffone GJ 1990 Analysis of DNA in fresh and fixed tissue by the polymerase chain reaction. Am J Pathol 136: 541–548
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Krous, H., Grossfeld, P. & Arnold, J. Response. Pediatr Res 66, 714–715 (2009). https://doi.org/10.1203/PDR.0b013e3181c1b786
Issue Date:
DOI: https://doi.org/10.1203/PDR.0b013e3181c1b786