Allergies

Background: Dermatitis affecting the earlobe is a highly frequent clinical presentation, predominantly attributed to Allergic Contact Dermatitis (ACD) caused by metallic ions like nickel from earrings. However, a significant subset of patients presents with recurrent eczematous lesions highly suggestive of ACD but with inconclusive or negative patch test results, posing a profound diagnostic and therapeutic dilemma. Objective: This comprehensive review critically evaluates the differential diagnosis of earlobe eczema in the context of negative patch tests. Drawing from a representative case of a 30-year-old female with recurrent earlobe eczema and a strong family history of psoriasis, we explore alternative non-immunological and endogenous mechanisms, specifically Irritant Contact Dermatitis (ICD) and the Koebner Phenomenon on a background of Psoriatic Diathesis. Methods: We performed an extensive review of the current literature focusing on the epidemiology and pathogenesis of metal ACD, non-allergic mechanisms of jewelry-induced dermatitis (ICD), the molecular basis of the Koebner phenomenon, and the clinical overlap between eczema and psoriasis (Eczematous Psoriasis). Results: The localized nature of the inflammation, coupled with the absence of generalized nickel sensitivity, strongly suggests that the mechanical and occlusive trauma from earrings can induce a purely irritant reaction. Crucially, the presence of a familial psoriatic diathesis supports the hypothesis that this local irritation acts as a Koebner phenomenon trigger, leading to an eczematous manifestation of an underlying psoriatic tendency. Conclusions: Not all recurrent eczematous lesions at common contact sites are caused by ACD. Clinicians must adopt an integrated diagnostic approach, factoring in personal and family history alongside patch test results, to differentiate true allergy from ICD and the Koebner phenomenon. This nuanced perspective is vital for providing appropriate counseling (strict jewelry avoidance) and targeted, often steroid-sparing, management (e.g., topical calcineurin inhibitors) for a durable therapeutic outcome.

Food allergy diagnosis remains challenging due to the difficulty of distinguishing true clinical allergy from asymptomatic sensitization. Inaccurate diagnosis may result in unnecessary dietary restrictions, reduced quality of life, or, conversely, failure to identify individuals at risk of severe allergic reactions. This review critically analyzes the efficacy, limitations, and clinical utility of currently available diagnostic tests for food allergy, with particular emphasis on their ability to predict true clinical reactivity. A comprehensive literature review was conducted to evaluate the sensitivity, specificity, and predictive values of both traditional and emerging diagnostic modalities. English-language guidelines, systematic reviews, and key clinical studies published primarily within the past 15 years (up to 2025) were identified through PubMed and Google Scholar. Classic diagnostic tools, including skin prick testing (SPT) and serum-specific IgE (sIgE), were assessed alongside novel approaches such as component-resolved diagnostics (CRD), basophil activation test (BAT), mast cell activation test (MAT), atopy patch testing (APT), cytokine profiling, and omics-based diagnostics. Particular attention was given to how these tests compare with the oral food challenge (OFC), which remains the diagnostic gold standard. The findings demonstrate that while conventional tests offer high sensitivity and are valuable for initial risk assessment, their limited specificity often leads to overdiagnosis. Emerging molecular and cellular assays show improved specificity and functional relevance, especially in complex cases involving polysensitization or unclear clinical histories and may reduce reliance on OFCs in the future. However, accessibility, cost, and lack of standardization currently limit their widespread clinical application. Advances in artificial intelligence and data integration hold promise for improving diagnostic accuracy through enhanced interpretation of complex immunological data. Based on the synthesized evidence, this review proposes an evidence-based, stepwise, and individualized diagnostic algorithm for food allergy. Integrating clinical history, targeted testing, and selective use of OFCs can improve diagnostic certainty, enhance food safety, minimize unnecessary dietary avoidance, and optimize patient outcomes. The review underscores the need for continued research, standardization, and validation of novel diagnostic tools to support personalized and precise food allergy management.

Background: Presence of milk, fruits, eggs, fish, nuts and wheat antigens in the amniotic fluid is described in the literature. Studies show a contradictory relationship between maternal exposure to allergens and early sensitization of the fetus to allergens. Hemochorionic type of the human placenta allows for easier transfer of nutrients and antibodies from the mother’s blood to the fetal circulation through the direct contact of maternal blood with the fetal chorion. During the third trimester of pregnancy, immunoglobulin G (IgG) is actively transferred through the placenta into the fetal via neonatal FcRN receptor (FcRN). In addition, monomeric immunoglobulin E (IgE) cannot cross the placenta Aim: The objective of our study is to track intrauterine sensitization to essential food proteins at birth in umbilical cord blood in mothers with established peripheral blood eosinophilia and in their infants using allergen-specific IgE and IgG. Methods: An observational study was carried out in a cohort of 22 mothers with eosinophilia and their babies. Differences in expression between groups were assessed. Blood samples were collected to determine serum IgE and IgG specific to a set of inhalant and food allergens. Results: We did not find a significant correlation between specific IgE to cow’s milk (p = 0.857), egg white (p = 0.926) and egg yolk (p = 0.096) in umbilical cord blood and maternal blood samples taken immediately before birth. Spearman’s correlation of the specific IgE and IgG in umbilical cord blood showed no dependence between the two variables. In contrast, statistical analysis showed that maternal eosinophilia in peripheral blood could be a risk factor for the development of allergy in the offspring (χ², p = 0.0347). However, given the small number of patients, this claim needs to be confirmed with further studies. Conclusions: Due to the functional immaturity of the developing immune system of the fetus, the generation and maintenance of an independent immune response to allergens are incomplete. Maternal IgG (specific) passes to the baby and high maternal IG to a specific allergen reduces babies IgE production. In addition, low maternal specific IgG may promote IgE production in the baby under the influence of microenvironmental factors (cytokine background). The main limitation of our study is the small number of patients. Further research is needed in this direction to clarify the mechanisms and risk factors for early sensitization in newborns.