Environmental exposure plays a major role in the development of allergic diseases. The exposome can be classified into internal (e.g., aging, hormones, and metabolic processes), specific external (e.g., chemical pollutants or lifestyle factors), and general external (e.g., broader socioeconomic and psychological contexts) domains, all of which are interrelated. All the factors we are exposed to, from the moment of conception to death, are part of the external exposome. Several hundreds of thousands of new chemicals have been introduced in modern life without our having a full understanding of their toxic health effects and ways to mitigate these effects. Climate change, air pollution, microplastics, tobacco smoke, changes and loss of biodiversity, alterations in dietary habits, and the microbiome due to modernization, urbanization, and globalization constitute our surrounding environment and external exposome. Some of these factors disrupt the epithelial barriers of the skin and mucosal surfaces, and these disruptions have been linked in the last few decades to the increasing prevalence and severity of allergic and inflammatory diseases such as atopic dermatitis, food allergy, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis, and asthma. The epithelial barrier hypothesis provides a mechanistic explanation of how these factors can explain the rapid increase in allergic and autoimmune diseases. In this review, we discuss factors affecting the planet’s health in the context of the ‘epithelial barrier hypothesis,’ including climate change, pollution, changes and loss of biodiversity, and emphasize the changes in the external exposome in the last few decades and their effects on allergic diseases. In addition, the roles of increased dietary fatty acid consumption and environmental substances (detergents, airborne pollen, ozone, microplastics, nanoparticles, and tobacco) affecting epithelial barriers are discussed. Considering the emerging data from recent studies, we suggest stringent governmental regulations, global policy adjustments, patient education, and the establishment of individualized control measures to mitigate environmental threats and decrease allergic disease.

Background: Rapid drug desensitization (RDD) induces a temporary tolerance to chemotherapeutics that induce hypersensitivity reactions (HSRs). Purpose: Our objective is to report our experience with RDD to platins, taxanes, etoposide, doxorubicin, and irinotecan. Methods: The study was conducted as a retrospective chart review of patients with symptoms of HSRs to chemotherapeutics. HSRs were classified as grade I, II, or III, based on their severity. Skin prick/intradermal tests were performed with implicated chemotherapeutics. A 12-step RDD protocol was used. Results: The study consisted of 38 women and 3 men (mean age 53.3 ± 11.6 years). Patients had ovarian (n = 13, 31.8%), breast (n = 10, 24.4%), colon (n = 7, 17%), lung (n = 4, 9.8%), and other cancers (n = 7; endometrial sarcoma, testicular cancer, uterine cancer, ampulla of Vater tumor, choledochal tumor, peritonitis carcinomatosa, and Merkel cell carcinoma, n = 1, respectively). Twenty-two patients experienced HSRs to platins, 15 to taxanes, and 4 to other chemotherapeutics (doxorubicin, irinotecan, and etoposide). A total of 122 RDDs (47 to platins, 52 to taxanes, 23 to other chemotherapeutics) were performed. In 25 (61%) patients no reactions occurred during RDD, but breakthrough reactions developed in 16 patients (39%) with platins (n = 11), taxanes (n = 3), doxorubicin (n = 1), and irinotecan (n = 1). RDD procedures could not be completed in only 2 patients with grade II breakthrough reactions to carboplatin and oxaliplatin. Conclusion: In our experience, 98.3% of 122 RDDs were completed. We found that RDD was safe and effective in this the largest series of RDD with chemotherapeutics in our country.

Inborn errors of immunity (IEI) increase morbidity and mortality risks, particularly from respiratory tract infections. Hence, vaccination becomes pivotal for IEI patients. This study aims to examine the vaccination and respiratory tract infection rates in a diverse IEI patient cohort undergoing immunoglobulin replacement therapy (IGRT). We retrospectively evaluated IEI patients on IGRT at a tertiary care center. Data on vaccinations and respiratory infections were extracted from medical records. : The study included 33 patients (mean age= 37.7 ± 11.4 years; 17 male). The most common clinical phenotype in our cohort was primary antibody deficiencies (90.9%). Only two patients had a genetic diagnosis, both of whom were brothers diagnosed with Wiskott-Aldrich syndrome (WAS). Almost half (48.5%) of our patients had bronchiectasis and 81.8% were on prophylactic antibiotics. All patients with IEI included in the study were regularly receiving IGRT. The vaccination rate of patients against respiratory tract infections was 42.4%, 57.6%, and 78.8% for influenza, pneumococcus, and COVID-19, respectively. Only one patient (7.1%) who received the influenza vaccine developed an upper respiratory tract infection. However, viral panel analysis could not be performed for this patient as they did not present to the hospital. The COVID-19 vaccination rate was notably higher than that of other vaccines, likely due to increased awareness during the pandemic, aided by public advisories and media influence. We observed higher vaccination rates for the COVID-19 vaccine compared to other vaccines (influenza and pneumococcal vaccines). Although we observed the potential impact of social and governmental influence in increasing vaccination rates, it is crucial to acknowledge that vaccination decisions in IEI patients must be individualized.

Objective: Inborn errors of immunity (IEI), formerly known as primary immunodeficiencies, are a group of inherited diseases affecting different innate and adaptive immune system components. The most common finding in the heterogeneous group of patients with IEI is infections, which are associated with increased morbidity and mortality. This retrospective study aims to determine infections in a heterogeneous group of patients receiving immunoglobulin replacement therapy (IGRT). Methods: The medical records of the patients with IEI who received IGRT and were followed up in our clinic for the last five years were reviewed retrospectively. Results: In this study, including 45 patients diagnosed with IEI (55.6% male, average age 38.4±11.6 years), the most common subgroup was primary antibody deficiencies (40, 88.8%). The average age of diagnosis for patients was 26.8±14.8 years, with a median diagnostic delay of 6 years. Twenty (44.4%) of patients had bronchiectasis. All patients were receiving IGRT, with 82.2% using antimicrobial prophylaxis. Before diagnosis, the median annual number of infections was 4, which decreased to 1 post-treatment (p<0.001). Significant reductions in pneumonia and upper respiratory tract infection frequency were observed with IGRT compared to before the treatment (75.6% vs. 22.2%, p<0.001; 66.7% vs. 31.1%, p=0.003). Seventeen (37.8%) of patients were hospitalized due to infections during treatment. The rate of inactive influenza vaccination and the average body mass index (BMI) were significantly lower in patients with hospitalization than in those without hospitalization (20% vs 53.8%, p=0.034; 20.5 vs. 24.1 kg/m², p=0.019). Among those with bronchiectasis, the rate of pneumonia prior to diagnosis was significantly higher (95% vs. 60%, p=0.012). Lower BMI, the presence of bronchiectasis, and non-compliance with treatment were associated with more frequent infections under treatment. Conclusion: Many complications, especially infections, can be prevented by early diagnosis and treatment of IEI and increasing patient compliance with treatment. Therefore, increasing awareness of IEI both in society and among physicians from all specialties will enable patients to be diagnosed at an early stage and reduce hospitalization, mortality and morbidity.

Objectives: Lung injury is one of the most important risk factor for morbidity and mortality, especially in older people. There are several reasons causing acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) such as pneumonia, sepsis, viruses, oxidants, and trauma. Evidence has shown that carnosine has many properties, such as suppressing hydroxyl, superoxide, and peroxyl radicals, inhibiting peroxidation, membrane protection and wound healing. We aimed to analyze the effects of carnosine on lung injury in this systematic review. Content: A systematic research was performed in Pubmed, Web of Science, and Scopus databases for following keywords; “carnosine” AND “lungd” until October 31st, 2020. Bias analysis was done with RevMan 5.3 software. Summary: We screened totally 51 publications and only nine articles were used for the final analysis. Eight animal studies and one in vitro study were included in this study. All studies indicated that carnosine has beneficial effects on improving lung injury. Outlook: The study demonstrates that carnosine may be a promising new therapeutic agent and help to improve lung injury by reducing oxidative stress, proinflammatory cytokines, and apoptosis. Further investigations are needed to elucidate which mechanism is more effective to cure lung damage, especially in humans.