Journal of Investigational Allergology and Clinical Immunology最新文献

The terms refractory anaphylaxis and near-fatal anaphylaxis have gained prominence in the last 5-10 years. Refractory anaphylaxis has a clinical justification in that patients often do not respond to successive doses of adrenaline. Near-fatal anaphylaxis facilitates the study of fatal anaphylaxis, which is 10 times less frequent. In terms of epidemiology, refractory anaphylaxis and near-fatal anaphylaxis overlap, since refractory anaphylaxis can prove fatal, and the more severe the anaphylaxis (including cardiorespiratory arrest), the greater the need for adrenaline and fluid infusion. However, no specific pathogenesis or treatment has been described for either condition. Consequently, these are not distinct clinical entities, but different manifestations of severity. The risk factors for both types of anaphylaxis are the same as those described for severe anaphylaxis, namely, patient age, cardiac and respiratory comorbidities, and the (controversial) role of ß-blockers and angiotensin-converting enzyme inhibitors. If volume expansion and adrenaline infusion prove ineffective, treatment is based on intubation, ventilation, intravenous vasopressors, and glucagon. Patients should be transferred to the intensive care unit. This review provides a panoramic epidemiologic vision of both manifestations of severe anaphylaxis. We conclude that they share many risk factors and often occur together in severe anaphylaxis. Therefore, each should be considered a manifestation of severe anaphylaxis.

Background: To analyze causality between gut microbiota and chronic spontaneous urticaria (CSU) and to investigate the mediating effect of metabolic pathways.

Methods: We extracted genome-wide association study summary statistics for 211 microbiota taxa from the MiBioGen consortium (N=18 340), 205 microbiota metabolic pathways from the Dutch Microbiome Project (N=7738), and CSU from the FinnGen genomics initiative (N=450). Bidirectional Mendelian randomization (MR) was performed to detect genetic causality between gut microbiota, gut bacterial pathways, and CSU. Sensitivity analyses were performed to validate the robustness of the results. Mediation MR investigated mediators in the association between gut microbiota and CSU.

Results: MR analysis suggested that the family Peptococcaceae and its child taxon, the genus Peptococcus, were risk factors for CSU. In addition, the genera Collinsella, Lachnospiraceae UCG004, Ruminococcaceae UCG004, and Sellimonas were also risk factors for CSU, whereas Family XIII UCG001, Lachnospiraceae UCG010, and Methanobrevibacter had protective effects on CSU. As for metabolic pathways, NONMEVIPP-PWY, PWY-5022, and PWY-7221 were positively associated with CSU, although others, such as KDO-NAGLIPASYN-PWY, PWY- 6353, and PWY-7400 presented a suggestive association with CSU. Moreover, PWY-7400 was a mediator in causality between the family Peptococcaceae and CSU. These results were based on nominal significance (P<.05). None of the Bonferroni-corrected P values were <.05.

Conclusions: Our study confirmed a causal association between gut microbiota and CSU, with the the metabolic pathway being a potential mediator. Our findings provide new insights for further mechanistic and clinical studies in CSU.

Background and objectives: Background: Most patients with respiratory allergy are polyallergic. Combining different allergen extracts in the same allergen-specific immunotherapy is a common practice. However, it should be justified. Objective: To analyze the stability, safety, and immune response of allergen extract mixtures from nonhomologous groups.

Methods: We analyzed 2 depigmented-polymerized mixture extracts (DPmixEs): cat dander-grass pollen and Alternaria alternata-grass pollen. The stability of the mixtures was investigated by studying proteolysis and degradation effects. The allergenicity and humoral and cellular immune responses of DPmixEs were also evaluated using various technical approaches, including the Bradford assay, enzyme-linked immunosorbent assay, rabbit immunization, peripheral blood mononuclear cell culture, and flow cytometry. The results were compared with those of individual depigmented-polymerized extracts (DPEs) and native mixture extracts (NmixEs).

Results: The proteolytic activity of DPmixEs was lower than that of NmixEs. The protein content of DPmixEs remained stable for 18 months, whereas that of NmixEs decreased significantly during the first month. The allergenicity of DPmixEs was similar to that of DPEs and lower than that of NmixEs. Regarding the immune response, DPmixEs induced functional specific IgG antibodies in rabbits and blocked sIgEallergen binding. Moreover, DPmixEs induced IL-10 secretion in peripheral blood mononuclear cells from polyallergic patients, improving the Treg/TH2 cell balance.

Conclusions: These findings support the use of DPmixE as a promising formulation for allergen immunotherapy, combining stability, reduced enzymatic activity, and enhanced immunological stimulation, while preserving in vitro safety and efficacy comparable to separated depigmented-polymerized extracts.

Drug-induced enterocolitis syndrome (DIES), first described in 2014, is a poorly understood condition caused by a non-IgE-mediated hypersensitivity reaction to a drug. The pathophysiology of this condition remains to be fully elucidated. The symptoms are characterized by profuse vomiting, hypotension, pallor, lethargy, abdominal pain, and diarrhea, and the condition can progress to dehydration and hypovolemic shock. We aimed to review published cases to date and report a case recently diagnosed at our center. Additionally, we discuss and suggest recommendations for the current diagnostic criteria of this disease, the approach to drug provocation tests, and available therapeutic alternatives.