NK Cells in Sarcoidosis

The question of whether the initial eosinophilia in case 2 of our report could have been due to Aspergillus infection, perhaps allergic bronchopulmonary Aspergillus (ABPA), can be answered with reasonable certainty. In our opinion the patient did not have specific evidence for the diagnosis of an Aspergillus infection. Cultures for clinically significant Aspergillus are identified in two to six days.’ Aspergillus is a ubiquitous organism,2 and identification over three weeks following set up of cultures is, in our opinion, most likely a contaminant. This interpretation is corroborated by other data including: 1) negative specific serum immunoprecipitins for Aspergillus, 2) no evidence of Aspergillus or ABPA on lung biopsy, 3) repeated negative sputum cultures for Aspergillus, and 4) no evidence of Aspergillus at autopsy. In a patient with the widespread disease that our case 2 presented, repeated negative sputum cultures for Aspergillus should make one wary of the diagnosis of ABPA. On the other hand, the evidence for coccidiomycosis is, in our opinion, quite convincing. Negative skin tests and serologies performed during the first week of illness do not exclude the diagnosis of coccidioidomycosis. Seventeen percent of skin tests are negative during the first week of clinical illness and complement fixation and immunodiffusion tests are known to be delayed in their conversion as compared to other serologic tests.4 Conversion of serologic titers at a little over one month following onset of clinical symptoms supports the diagnosis of coccidioidomycosis. While skin tests and serologies are frequently helpful in diagnosing coccidioidomycosis, they must be used properly and occasionally (as in this case) become positive too late in the clinical course to be of use. We disagree with the philosophy of blindly increasing doses of steroids and cytotoxic drugs in the absence of a well established diagnosis. A complete evaluation, even to the extent of repeat lung biopsy (when the diagnosis is obtainable by less invasive means) is necessary to ensure proper care when faced with the clinical problem of a patient who is deteriorating on immunosuppressive therapy with no known diagnosis. Most patients who develop eosinophilic types of pulmonary hypersensitivity reactions have histories of atopy and may have elevated IgE levels for a variety of reasons.2 In this case, no specific immunoprecipitins were identified and we are unable to comment any further on the significance of this patient’s elevated IgE level. As with all patients transferred to Stanford University for medical care, this patient’s medical records were reviewed. Unfortunately, they were incomplete, as noted by Dr. Douglas. Nevertheless, the additional information she provides is interesting and helps further support our conclusions. We thank her fur drawing it to our attention.