Hypersensitivity reactions to antineoplastic agents are defined as unexpected reactions with signs and symptoms inconsistent with known toxicity of antineoplastic drugs. These reactions are uncommon and usually associated with certain antineoplastic categories, such as taxanes, platinum-containing compounds, epipodofyllotoxins, asparaginase, procarbazine and, more rarely, with doxorubicin and 6-mercaptopurine. The mechanisms that are responsible for hypersensitivity reactions are unclear and vary between agents. Symptoms of these reactions range from mild skin rashes to more severe reactions, such as arthralgia, respiratory arrest or even death in some cases. Once hypersensitivity reactions are observed, basic principles that allow their management and possible continuance and completion of the regimen should be followed.

Background: The impact of chronic spontaneous urticaria (CSU) on health-related quality of life (HRQoL) is widely held to be mainly influenced by disease activity and comorbidities. Objective: To assess the correlation between disease activity and HRQoL impairment by using validated disease-specific instruments. Methods: The Chronic Urticaria Quality of Life Questionnaire (CU-Q₂oL) was translated into Greek and subsequently applied to 110 CSU patients along with the Dermatology Life Quality Index and the Urticaria Activity Score. After the validity and reliability of the Greek CU-Q₂oL had been determined, we assessed the relation between disease activity and HRQoL impairment by computing correlations as well as by performing multiple regression analysis. Results: Exploratory factor analysis revealed a six-scale structure of the Greek CU-Q₂oL that explained 67.9% of its total variance. The internal consistency was satisfactory with Cronbach's α >0.7. Disease activity was the only predictor of quality of life impairment, but it only moderately correlated with the CU-Q₂oL total score (r = 0.40, p < 0.0001). Conclusion: Our results suggest that there are additional factors to disease activity that are responsible for the pronounced reduction of HRQoL in CSU, and this supports the recommendation to assess and monitor both disease activity and quality of life in CSU patients.

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Based on these findings, we speculate that vascular remodelling and MC hyperplasia in patients with CSU occurs independently and via different mechanisms. Targeting of the mechanisms that drive neoangiogenesis in CSU may result in novel therapeutic strategies for the management of patients with angio-oedema.

Internet surveys can be a useful tool for screening the general population for common allergic disorders, such as urticaria.

The unique environmental conditions and the aerobiology of each area clearly affect the clinical features of respiratory allergy.

Chronic spontaneous urticaria (CSU) is a common and disabling skin disease which is often associated with psychiatric comorbidities such as anxiety and depression. These conditions are widely thought to cause, drive and/or maintain CSU, and have been reported as making an important contribution to the low quality of life in patients with CSU. Almost half of all patients with CSU have autoreactive CSU which can be readily diagnosed by the autologous serum skin test. The prevalence and effects of psychiatric comorbidities in this important subgroup are largely unknown. We carried out a study on two groups of patients with CSU, and found that the anxiety and depression scores were lower in patients with autoreactive CSU than in those with nonautoreactive CSU, the first such finding, to our knowledge. In addition, we found that patients with autoreactive CSU were less likely to have Hospital Anxiety and Depression Scale scores indicative for anxiety or depression compared with patients with nonautoreactive CSU. Our results support the view that autoreactive CSU represents a distinct CSU subgroup with a different disease pattern and a lower rate of psychiatric comorbidities.

We propose a simple "rush" VIT protocol in an outpatient setting as an easy-to-perform alternative option for VIT induction phase.