Nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs most frequently involved in allergic reactions of which two main types exist: IgE-mediated and crossintolerance. The diagnosis of crossintolerance reactions is often based on the drug provocation test. The potential value of the basophil activation test (BAT) was evaluated using different basophil markers in the diagnosis of patients with crossintolerance to NSAIDs and cutaneous symptoms. We studied 46 patients with crossintolerance to NSAIDs and 45 tolerant controls. BAT was performed with acetyl salicylic acid, paracetamol, diclofenac, dipyrone, naproxen, and ibuprofen at four different concentrations using CD193 and CD203c as basophil markers and CD63 as activation marker. We compared BAT results using CD193 1 or CD193 1 CD203c 1 for basophil selection and found a significant increase in the stimulation index when using CD193 1 CD203c 1 in both patients and controls (P 5 0.004 and P 5 0.017, respectively). Selection of living cells only produced an increase in basophil stimulation in patients for both CD193 1 and CD193 1 CD203c 1 (P < 0.001 for both), whereas in controls there was no change with CD193 1 and a decrease with CD193 1 CD203c 1 (P 5 0.001). We found that CD193 1 CD203c 1 increased the percentage of positive cases in patients and controls when compared with CD193 1 . When excluding dead cells, there was an increase of 21.7% in patients and 10% in controls. These results indicate that using CD193 1 CD203 1 , excluding dead cells, is the best approach for BAT although this test is not recommended for the diagnosis of patients with crossintolerance to NSAIDs owing to its low sensitivity and specificity. V C 2014 International Society for Advancement of Cytometry Key terms hypersensitivity; nonsteroidal anti-inflammatory drugs; idiosyncratic reactions; basophils; CD63; CD193; CD203c NONSTEROIDAL anti-inflammatory drugs (NSAIDs) are the drugs most frequently involved in immediate or acute hypersensitivity reactions, accounting for 20-25% of patients evaluated in allergy units, with two main mechanisms involved (1-3). One is mediated by drug-specific-IgE antibodies and reactions occur with one NSAID but there is tolerance to other nonchemically related drugs (4,5). These reactions are known as single NSAID induced hypersensitivity reactions and involve NSAIDs such as paracetamol (6), acetyl salicylic acid (ASA) (7), diclofenac (8), ketorolac (9), dipyrone (10,11), and cyclooxygenase-2 selective inhibitors (COX-2) (12). The other type of reaction is mediated by a pharmacological mechanism in which the inhibition of cyclooxygenase-1 enzyme (COX-1) leads to a decrease in the synthesis of prostaglandin E 2, which in turn hampers the production of sulphidoleukotrienes