Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)最新文献

Allergy is the result of genetic and environmental interactions, including time, route, and dose of food exposure in susceptible patients. Risk factors can be: 1) genetic and 2) environmental, and these, in turn, are divided into prenatal, perinatal and postnatal. Food allergy appears frequently and depends on multiple risk factors (genetic and environmental), which in turn are divided into: prenatal, natal and postnatal factors; They participate in the expression of the disease and clinical intervention is not possible in all cases.

The interaction between genetic potential and the environment, especially increased urbanization and inadequate waste management, contributes to the manifestation of allergic diseases. Pediatric patients are the most vulnerable, due to the immaturity of the respiratory and immune systems. Prenatal and postnatal exposure to air pollutants, both indoors and outdoors, accelerates or aggravates morbidity and mortality from allergic diseases. The "exposome," which encompasses all environmental exposures throughout life, influences health. Biological and chemical attacks alter the epithelial barrier, triggering inflammatory responses and favoring allergic diseases, such as food allergies. The uncontrolled use of toxic fuels, particulate matter, detergents and other factors contribute to the continuous deterioration of the intestinal epithelial barrier, increasing the risk of allergic diseases. It is important to take urgent action to address these issues and protect the health of the planet.

The pollen-food allergy syndrome, also known as oral allergy syndrome, is characterized by local reactions in the mouth and throat after consuming certain raw plant foods in individuals sensitized to pollen from grass, weeds, and trees. Birch-apple is the prototype of this syndrome, with apple, pear, and plum being the most commonly associated foods. Symptoms are usually limited to the oral cavity but can include systemic reactions, including anaphylaxis. Sensitization to pollen allergens, such as lipid transfer proteins, profilin, and PR-10 proteins, triggers this syndrome. Its prevalence varies by geographic region and the predominant pollen type, affecting between 30% and 60% of food allergies. Diagnosis involves a clinical history, skin tests, and, in ambiguous cases, double-blind, placebo-controlled oral food challenges. Treatment primarily involves avoiding trigger foods.

Food allergens are capable of producing adverse reactions through multiple mechanisms of an allergic or non-allergic nature, and through different routes of exposure; generally by ingestion or contact, as in protein contact dermatitis or contact urticaria, including inhalation. Food allergy reactions, in turn, can be mediated by immediate hypersensitivity mechanisms, delayed hypersensitivity or mixed immediate-delayed mechanisms. The reference diagnostic method in food allergy is the double-blind placebo-controlled food challenge test (DBPCFC), but skin and serological tests are important in the clinical context. The diagnosis of immediate food allergy depends on well-standardized allergological tests, such as the skin prick test (SPT) or specific IgE dosing, which are ideally tested by food challenge testing. However, the diagnosis of delayed mechanism food allergy and mixed allergies, which combine both immune mechanisms, is more complex. Delayed hypersensitivity reactions are evaluated with the epicutaneous patch test, or patch testing, for the diagnosis of contact dermatitis. The atopy patch test is initially used for the investigation of inflammatory reactions, which may be linked to food allergens in patients with atopic dermatitis. It was later applied in other diseases, whose pathogenesis is mainly mediated by a mechanism of delayed hypersensitivity to protein allergens: eosinophilic esophagitis, enterocolitis induced by food proteins, protein contact dermatitis, contact urticaria, among other disorders.

Oral provocation tests involve the supervised administration of suspected foods in increasing doses to evaluate a patient's allergic condition. Acknowledged as the superior method for diagnosing food allergies, it surpasses results from specific IgE serum or prick tests, which indicate sensitization but not necessarily allergy. The test is indicated in cases of diagnostic uncertainty, assessment of natural or induced tolerance, or cross-reactivity risks. Three types of tests exist: open, single-blind, and double-blind with a placebo. While the latter two reduce anxiety, open tests are more practical for children under three.

Skin tests, also known as prick tests, in food allergies are restricted to IgE-mediated food allergies, with results that barely indicate sensitization to a certain food and do not necessarily suggest food allergy. The clinical context of the patient is the decisive point before performing any type of food allergy skin test; Contextualizing and relating the patient's clinical picture with the immunological mechanism of IgE-mediated allergies will allow a better selection of the allergy test for each case. Positive tests should be interpreted more carefully, and consider that during early childhood it is common that several patients may have negative specific serum IgE tests in the blood for food allergens compared to those performed on the skin, which are positive. Skin testing can be carried out with standardized strata of foods, but they are not always available for all foods and some are very unstable. Skin tests can even be performed with raw foods, using the prick to prick technique to perform the puncture with fresh foods (especially fruits or vegetables) or other products that are not commercially available. The skin prick test is a test where, after having placed the allergenic extract in drops or with fresh food itself, the puncture must be carried out with a standardized lancet.

Anaphylaxis, a potentially life-threatening reaction, is characterized by acute symptoms affecting various systems and requires immediate medical intervention. While the overall mortality rate is low, anaphylaxis induced by foods and drugs has seen an increase. Common triggers include foods, drugs, and Hymenoptera venom. Epidemiology varies by region and age, with a global incidence of 50-112 episodes per 100,000 people annually. Implicated foods vary by age and region, with peanuts and nuts being common triggers. Two mechanisms of anaphylaxis are recognized: IgE-mediated and non-IgE-mediated. Diagnosis is based on clinical criteria and serum tryptase levels. Treatment includes epinephrine, oxygen, and intravenous fluids. Exercise-induced food-dependent anaphylaxis is addressed, where exercise, combined with certain foods, triggers anaphylactic reactions. Proper understanding and management are crucial to mitigate risks.

Objective: To compare whether adolescents who are exposed to truck smoke have a higher prevalence of asthma symptomatology versus those who are not exposed.

Methods: A cross-sectional, descriptive, and comparative study. Adolescents aged 13 and 14 years were included and completed a self-report questionnaire. Subjects were selected following the same methodology as in ISAAC phase III. They underwent an epidemiological survey for the presence of symptoms. Ex- posure to truck smoke was defined as passing trucks most of the day as perceived by the patient. The distribution was assessed with the Kolmogorov-Smirnov test. Comparisons with Chi-square or Student's t-test, as appropriate. A value of p³0.05 was considered statistically significant.

Results: A total of 492 patients were included. The demographic variables can be seen in Table 1. When performing the association between the groups of ad- olescents with asthma exposed to truck smoke, a significant difference was found in the prevalence of respiratory symptomatology and asthma (26.0% vs 9.6%, p=0.000) (Table 1).

Conclusions: Adolescent patients with asthma who are exposed to truck smoke demonstrated a significant difference in the presence of respiratory symptom- atology and asthma compared to patients without exposure.

Background: Hereditary angioedema type 1 (HAE1) is an autosomal dominant disorder, characterized by quantitative and qualitative deficiency of C1 inhibitor, excessive production of bradykinin and causing recurrent angioedema in varying degrees of severity that affects quality of life and life itself. from the patients. Lanadelumab is a human monoclonal antibody, a specific inhibitor of plasma kallikrein, approved for long-term prophylaxis of HAE1.

Case report: A 59-year-old female patient, diagnosed with HAE 1 since November 1987, without therapeutic response to danazol, fresh frozen plasma, or C1 inhibitor derived from intravenous plasma, requiring 3 to 9 monthly vials of icatibant acetate due to angioedema. laryngeal, cutaneous and visceral with highly altered quality of life indices. Lanadelumab 300 mg subcutaneously every 14 days was started. At the start of treatment, the AECT1 score was 1 point; AE-Qol2: 57 points, AAS3: 32 points, being followed up at 5, 10 and 12 months. After one year of treatment, the records showed an AECT1 of 19 points; AE-Qol2: 36 points and AAS3: 5 points. The requirement for icatibant acetate has been no more than 3 vials per month.

Conclusion: In accordance with the literature, lanadelumab offered a significant decrease in angioedema activity and a significantly positive impact on the pa- tient's quality of life, confirming that lanadelumab is an effective option for long-term HAE prophylaxis. .