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Editor,—Ratjen et al suggest that differential cell counts in bronchoalveolar ravage (BAL) fluid can be of value in the differential diagnosis of pulmonary infiltrates in immuno-compromised children.1 Firstly I was confused by figure 1 whose legend states that the open bars represented children with bacterial or fungal infections. But this group, according to the figure, had the lowest, not highest, proportion of neutrophils. One or other part of the legend or the figure must be wrong. Secondly, inspection of the data in table 4 shows that the group with bacterial and fungal infection had a mean peripheral blood leucocyte count of 6.3, and neutrophil count of 4.1 × 109/1. It therefore remains possible that most were neither leukopenic nor had clinically important neutropenia. I could not find the median counts, although they state in the methods that medians were reported for all data. Were the counts skewed? It could be argued that their results do not support their claim to have found ‘marked cell proliferation on the bronchoalveolar surface despite systemic leukopenia’. Their results, as presented, suggest that differential counts of BAL fluid may be useful in immunocompromised children without systemic leukopenia/neutropenia, but it would have been interesting to see data from a substantial group of infected children all of whom were demonstrably leukopenic (or neutropenic). Such children usually cause us at least as much concern as those with adequate, normal, or raised counts. Furthermore, since we were not given the individual patient data, it is difficult to see how these results might help us make a diagnosis or institute appropriate therapy in an individual patient. The really important findings are the organisms isolated from the BAL fluid, whatever the cellular composition might be.
Dr Ratjen comments:
We regret the mistake in the legend of figure 1 where the first column (open bars) represents children without bronchopulmonary disease (who have the lowest percentage of neutrophils) while the second column represents immunocompromised children with bacterial or fungal infection (closed bars).
It is apparent from table 4 that a substantial number of children (16 of 28) were not neutropenic at the time of BAL. However, all children were neutropenic (most of them induced by chemotherapy) at the onset of their pulmonary illness. The timing of BAL was guided by the clinical course of the child’s pulmonary disease and varied between children. Of the 12 children with blood neutrophil counts below 1000/nl at the time of BAL, four had bacterial or fungal pathogens in their BAL. As the absolute number of patients in this subgroup is small, we have not described their results in greater detail. A standardised approach performing BAL early in the phase of neutropenia would be necessary to address the question how useful BAL differential cytology will be in this situation. The notion that we have found marked cell proliferation despite systemic neutropenia was included to reflect our observation that individual patients, who did not have any neutrophils in their bloodstream, still had raised neutrophil counts in BAL fluid. Our aim was to assess BAL cytology in all immunocompromised children who developed pulmonary infiltrates in the course of their illness and underwent BAL for clinical indications in a three year period. We agree with Dr Reid that the most important information is to be gained from cultures of BAL fluid. Nevertheless, our data suggest that BAL cytology provides useful additional information as it can show alterations in BAL cytology in response to pathogens that may be helpful in the differential diagnosis of pulmonary infiltrates in these immunocompromised children.
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