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M. Nurkić

Društvene mreže:

M. Al‐Ahmad, T. Rodriguez-Bouza, M. Nurkić

Background: A history of nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity with cross-intolerance to several drugs is common in some patients with coronary artery disease. We present a series of patients with acute coronary syndrome undergoing ASA desensitization prior to a possible stent to evaluate the short- and long-term efficacy and safety. The aim was to evaluate the outcomes of an ASA desensitization protocol developed by our center based on the guidelines proposed by the EAACI drug allergy expert recommendations. Methods: We developed a desensitization protocol that was based on both the patient characteristics and onset of reaction after NSAIDs, including premedication with a leukotriene antagonist and the H1-antagonist antihistamine. The clinical entities were NSAID-induced urticaria and/or angioedema in the absence of chronic spontaneous urticaria (NIUA) and NSAID-exacerbated respiratory disease (NERD). Results: A total of 23 patients were challenged or desensitized with ASA: 19 NIUA and 4 NERD. All patients tolerated the protocol at the different times of 30, 45, 90, and 120 min. The dosages of oral ASA that were given included 10, 21, 41, 81, and 162 mg (cumulative dose 315 mg). One patient reacted during the procedure and 1 during follow-up. Symptoms were limited to the skin without manifestations in other organs. All patients tolerated the required dose of ASA within 30–120 min. Those requiring urgent catheterization were desensitized within 90 min. Conclusions: Our protocol addresses challenge or desensitization with the contribution of a specialist allergist. It provides an effective, dynamic, safe, and short administration of 81 mg or higher of ASA in patients with a history of NSAID hypersensitivity with skin involvement.

ABSTRACT Aim of the work: Examine clinical characteristics of aerobic vaginitis and mixed infection for the purpose of better diagnostic accuracy and treatment efficiency. Materials and methods: Prospective research has been conducted at Clinic for Gynecology and Obstetrics, Department for Microbiology and Pathology at Polyclinic for laboratory diagnostic and Gynecology and Obstetrics Department at Health Center Sapna. Examination included 100 examinees with the signs of vaginitis. Examination consisted of: anamnesis, clinical, gynecological and microbiological examination of vaginal smear. Results: The average age of the examinees was 32,62±2,6. Examining vaginal smears of the examinees with signs of vaginitis in 96% (N-96) different microorganisms have been isolated, while in 4% (N-4) findings were normal. AV has been found in 51% (N-51) of the examinees, Candida albicans in 17% (N-17), BV in 15% (N-15), Trichomonas vaginalis in 13% (N-13). In 21% (N-21) AV was diagnosed alone while associated with other agents in 30% (N-30). Most common causes of AV are E. coli (N-55) and E. faecalis (N-52). AV and Candida albicanis have been found in (13/30, 43%), Trichomonas vaginalis in (9/30, 30%) and BV (8/30, 26%). Vaginal secretion is in 70,05% (N-36) yellow coloured, red vagina wall is recorded in 31,13% (N-16) and pruritus in 72,54% (N-37). Increased pH value of vagina found in 94,10% (N-48). The average pH value of vaginal environment was 5,15±0,54 and in associated presence of AV and VVC, TV and BV was 5,29±0,56 which is higher value considering presence of AV alone but that is not statistically significant difference (p>0,05). Amino-odor test was positive in 29,94% (N-15) of associated infections. Lactobacilli are absent, while leukocytes are increased in 100% (N-51) of the examinees with AV. Conclusion: AV is vaginal infection similar to other vaginal infections. It is important to be careful while diagnosing because the treatment of AV differentiates from treatment of other vaginitis.

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