BACKGROUND: Beta (β)-lactam antibiotics (BLAs) are the first-line therapy for non-nosocomial and nosocomial bacterial infections and are
most commonly reported to cause allergic reactions. Approximately 50% of all allergic patients in Europe and the USA suffer from drug
allergies and BLA allergies. The AIM of the study was to assess cross-reactivity reactions between 2nd and 3rd generation cephalosporins in patients with a medical history of BLA reactions and the risk of adverse reactions to BLAs based on the results of the basophil activation test.
MATERIALS AND METHODS: we examined 48 females and 8 males (in all 56 patients) aged 26 to 61 with primary reactions to BLAs and
24 healthy volunteers (control group). 19 (34%) patients were treated with amoxicillin, 18 (32,1%) patients were receiving amoxicillin+clavulanic acid, 6 (10,7%) patients were treated with cefuroxime, and 13 (23,2%) patients with ceftriaxone. Quantitative determination of the CD63 marker of basophil degranulation upon antigen stimulation in whole blood was performed with the use of Flow CAST (FK-CCR) (Bühlmann Laboratories AG, Switzerland). Based on the obtained ВАТresults, the patients were divided into two subgroups: the first group included 33 patients with positive stimulation index but lower CD63 expression (<10%), and the second group included 15 patients with a significantly higher level of CD63 expression (>10 %).
THE RESULT: We showed that patients from the second subgroup had the highest level of CD63 expression and stimulation index when
amoxicillin, whereas the level of CD63 expression and stimulation index were lower whith ceftriaxone; at the same time, the level of CD63 expression and stimulation index were the lowest with cefuroxime. The patients who treated with and reacted to amoxicillin, as shown by high
BAT, also had high CD63 expresiion after ceftriaxone and cefuroxime stimulation. In the first subgroup, urticarial and bronchospasm disappeared within 3 hours of the onset of symptoms in 51.5% of patients, the symptoms persisted for 2-3 days in 42.4% of patients with urticaria and angioedema, whereas maculopapular exanthema persisted for more than a week in 6.1% of the patients. Patients from the first subgroup (with low CD63 expression) had a weak reaction to the culprit antibiotic. Patients from the second subgroup had the strongest reaction to culprit antibiotics: anaphylaxis – 60.0%; Stevens-Johnson syndrome – 6.7%. We established that in patients with hypersensitivity to antibiotics the higher the baseline test scores after in vitro stimulation, the more severe clinical symptoms.
CONCLUSION: for patients with clinical manifestations of BLA in case of conflicting anamnesis data, it is recommended to establish true sensitization to antibiotics and to predict the occurrence of cross-reactions

Advanced glycation end products (AGEs) are formed in a nonenzymatic reaction of the reducing sugars with amino groups of proteins, lipids, and nucleic acids of different tissues and body fluids. A relatively small number of studies have been conducted on the role of AGEs in allergic inflammation. In this study, patients with allergic rhinitis (AR) were examined for the presence of Epstein-Barr virus and the content of fluorescent and nonfluorescent AGEs. We have also determined the level of a unique epitope (AGE10) which was recently identified in human serum using monoclonal antibodies against synthetic melibiose-derived AGE (MAGE). The levels of AGE10 determined with an immunoenzymatic method revealed no significant difference in the patients' blood with intermittent AR and chronic EBV persistence in the active and latent phases. It has been shown that there is a statistically significantly smaller amount of AGEs and pentosidine in groups of patients, both with and without viremia, than in healthy subjects. In turn, higher levels of immune complexes than of AGE10 were detected in the groups of patients, in contrast to the control group, which had lower levels of complexes than AGE10 concentration. In patients with active infection, there is even more complexes than of noncomplexed AGE10 antigen. The lower level of AGE in allergic rhinitis patient sera may also be due, besides complexes, to allergic inflammation continuously activating the cells, which effectively remove glycation products from the body.