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Biomedical subjects

A G Carlos

Publications and source records attributed to A G Carlos.

15 recordsLinked to original sources

[Latex: a complex allergy].

The authors review several of the most important aspects of latex allergy, an increasing problem in Public Health, which should be understood by all health professionals. After briefly presenting the history of the origin latex, from Hevea brasiliensis the authors describe the antigens of latex: Hev b1 to Hev b8, major allergens. They also note the crossed reactivity not only with foods, exotic fruits, but also with pneumoallergens and in particular the pollens. The groups at risk are essentially workers in the latex industry, health professionals and finally infants with spina bifida or other severe urological anomaly. The clinical signs are reactions of type 1 hypersensitivity, to urticaria and/or angio-oedema and anaphylactic shock. Diagnosis is based on a search for specific serum IgE, skin tests and provocation tests. Prophylaxis depends on removal of all substances that are based on latex, especially replacement of gloves with vinyl, but also on a food diet that excludes all foods that have a cross-reactivity with latex.

Allergens

Influence of nasal provocation on FEV1/PEF of asthmatic patients with or without rhinitis.

BACKGROUND/AIMS: Rhinitis is a potential aggravating factor for asthma. Our objective was to evaluate if HDM nasal challenges would induce lung function changes, assessing any differences between asthmatics with and without rhinitis. MATERIAL AND METHODS POPULATION: 40 stable moderate persistent HDM allergic asthmatics, on inhaled steroids; 20 also had mild-moderate perennial HDM allergic rhinitis, treated only with oral cetirizine when needed. 10 non-allergic, non-asthmatic patients served as controls. Nasal provocation: standardised HDM extract, in powder-form, in sequentially increasing concentrations. Lung function: FEV1 before, 30 and 60' after the last nasal challenge. Peak-Expiratory-Flow (PEF) measurements were performed in the morning and evening, during the prior week and the 2 days following nasal provocation. MEDICATIONS ALLOWED: All patients maintained their inhaled steroids. Anti-histamines or b2-agonists in the preceding week constituted exclusion criteria. RESULTS: Nine asthmatic, rhinitis patients showed statistically significant lung function decreases versus only two of the asthmatic non-rhinitic and none of the controls. No patient had any clinically significant asthma exacerbation. CONCLUSIONS: Although not sufficient to induce asthma symptoms, nasal HDM provocation can induce slight lung function decrease, more frequently in patients who have both asthma and rhinitis than in patients with asthma without rhinitis.

Adult

Cells and cytokines in pollinosis.

Pollinosis is a spontaneous model of allergic disease self limited in time. In order to evaluate immune response during pollen exposition cellular populations CD2, CD4, CD8, CD19, CD22, CD23, CD28, CD29, CD45RA, CD45RO have been studied before, during and after pollen season by flux cytometry. Simultaneous assays of soluble CD23 and cytokines IL-2, IL-4 and IL-2 soluble receptor have been done by an ELISA method. A decrease of CD23 PBC was observed during pollen season maintained afterwards without significant changes in sol CD23. The level of CD45RO memory cells decreased during pollen season with an opposed pattern for CD45RA naive cells. PBC expressing integrin chain CD29 were also decreased during the peak of pollen season. These results show that allergen exposition triggers a turnover of CD45 PBC, a decrease of low affinity IgE receptor CD23 in PBC and a consumption or binding of cells presenting the CD29 integrin chain. Cellular mechanisms are deeply implied in the immune response to pollens and cellular changes can be used as allergic inflammation markers in pollinosis.

Allergens

Immunotherapy and mast cell activation.

Tryptase is the more specific markers for mast cell activation and mediators release and can be used as an index of mast cell activation after challenge. Nasal provocation tests have been done in patients allergic to the pollen of Parietaria (pellitory wall) before and after specific systemic immunotherapy and tryptase release evaluated in nasal lavage fluid. After specific immunotherapy the concentration of tryptase in nasal lavage was significantly decreased to all the concentrations used in challenge and the peack of tryptase release was delayed. These results confirm that assays of tryptase in nasal fluid after nasal provocation are a reliable markers of mast cell activation. Immunotherapy with specific allergen decreases mast cell reactivity to the same allergen.

Allergens

Anterior rhinomanometry in nasal allergen challenges.

Even simple and relatively safe provocation procedures like nasal allergen challenges, should aim to allow detection of positivity with the less possible discomfort to the patient. The objective of this work was to evaluate if the use of rhinomanometric measurements during nasal provocation procedures could allow a decrease in the total administered allergen dose, causing less symptoms to the patients but without increasing the number of false-negatives, comparatively to clinical scores or nasal peak-flow measurements. Our results showed that performing rhinomanometric measurements during nasal HDM challenge procedures can lead in many patients to a reduction in the total dose of allergen administered during the challenge, without loss of sensitivity or specificity. This allergen dose reduction translates in less time consumed during the provocation and less patients' discomfort.

Adult

Nasal allergen challenge and mediators release.

Nasal allergen challenges, despite not reproducing exactly natural allergen exposure, are a very useful method to understand the complex cellular kinetics and cellular interactions that occur in allergic rhinitis. Cell-specific soluble mediator measurements can give useful diagnostic information. In this paper we present data concerning eosinophil cationic protein (ECP) and tryptase measurements after nasal allergen challenge.

Allergens

[Systemic effects of inhaled corticosteroids. Various pending questions].

Inhaled steroids play a central and undisputed role in the management of Bronchial Asthma, since inflammation has been recognised as the main physiopathological mechanism in this disease. Indeed, the earlier introduction of inhaled steroids in the therapy of Bronchial Asthma is currently being recommended by several authors. However, accompanying the much broader use of these drugs, concerns about the possibility of induction of adverse systemic effects have appeared more and more frequently in the medical community and in medical literature. This article addresses the main concerns related to the systemic effects of inhaled corticotherapy, critically reviewing the clinical significance of some of the more relevant published studies.

Administration, Inhalation

[Latex anaphylaxis].

The authors present two case-reports of Latex Anaphylaxis--a rare but dangerous manifestation of latex allergy--, one in a patient belonging to a risk group and the other in a patient without previously identified risk factors. A review of latex allergy, and particularly of latex anaphylaxis, is made focusing on risk groups, aetiology, diagnosis, prevention and therapy. This paper also intends to draw attention to this health problem and stress the fact that it raises several medical and non-medical issues, requiring a multidisciplinary approach and discussion.

Adolescent

[Functional assessment of the autonomic nervous system in rheumatoid arthritis].

Sympathetic and parasympathetic nervous system evaluation was performed in 21 patients with rheumatoid arthritis. Every patient had autonomic nervous system (ANS) dysfunction, the parasympathetic involvement being the most frequent. ANS dysfunction may explain some manifestations and may well be the expression of a larger neuropathic involvement with pathogenic implications.

Adult

[State of the art in immuno-allergology: histamine-releasing factors (HRF)].

The present concepts on histamina releasing factors are discussed, their cellular origins, their effect on the target cells and its importance in asthma immunopathology. Personal results on the production of HRF by alveolar macrophages stimulated by allergen and its action on non atopic basophils are presented. Alveolar macrophages from atopic asthmatics release HRF in presence of allergen. Macrophage from non atopic do not. HRF has been tested in a Human Basophil Degranulation Test (HBDT) preparation, a significant degranulation induced by HRF from atopic patient being only observed when atopic basofils are used in HBDT. These results confirm that allergen could induce HRF production from alveolar macrophages and that this HRF could degranulate basophils in atopic and induce mediators release.

Basophil Degranulation Test

[The state of the art in immuno-allergology: histamine releasing factors (HRF)].

The present concepts on histamine releasing factors are discussed, their cellular origins, their effect on the target cells and its importance in asthma immunopathology. Personal results on the production of HRF by alveolar macrophages stimulated by allergen and its action on non atopic basophils are presented. Alveolar macrophages from atopic asthmatics release HRF in presence of allergen. Macrophage from non atopic do not. HRF has been tested in a Human Basophil Degranulation Test (HBDT) preparation, a significant degranulation induced by HRF from atopic patient being only observed when atopic basophils are used in HBDT. These results confirm that allergen could induce HRF production from alveolar macrophages and that this HRF could degranulate basophils in atopic and induce mediators release.

Basophil Degranulation Test

Platelet reactivity to "in vitro" allergen challenge in asthmatic patients.

Platelet involvement in inflammation and allergic states is now well documented. In fact, it has been suggested that platelets can be triggered by either activated cells as monocytes and macrophages or by allergen itself. This latter possibility is still a matter of controversy. In this study we analysed platelet "in vitro" response to allergen, by optical aggregation technique, in 25 asthmatic patients, being 20 atopic and 5 non atopic patients. Platelet aggregation response to epinephrine, ADP, collagen and arachidonic acid was studied in all patients. In addition, allergen was added to platelet rich plasma and platelet reactivity was recorded both before and after stimulations with collagen. Platelet aggregation studies confirmed and abnormality of ADP induced platelet aggregation, that exhibited great variability among patients. In most cases this defect was the only one found in asthmatic patients and it should be further analysed. Results also showed a nonspecific response to allergen when dissolved in glycerol. This was due to glycerol rather than to allergen, since lyophilized allergen did not affect platelets, and glycerol added to platelet rich plasma induced the same type of curve. So, allergen by itself does not imply platelet aggregation. Experiments with IgE did not provoke either platelet agglutination or platelet aggregation. Furthermore, previous incubation with allergen immediately before collagen induced aggregation did not significantly change platelet response. This study allows the conclusion that platelet reactivity to allergen contact must be an expression of multicellular cooperation rather than a direct effect on platelet IgE receptors stimulation.

Adenosine Diphosphate

Cytokines and asthma.

Some of the main cytokines involved in the pathophysiology of bronchial asthma, their pathogenic role, and evidence concerning the importance of their action in asthma exacerbations and in perpetuating airway inflammation are reviewed. Therapeutic approaches using cytokines which counteract the inflammatory process of asthma are also examined.

Animals