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Bei Patienten mit schwerem allergischen Asthma werden zum Reduzieren der Kortikosteroiddosis subkutan IgE-Antikörper verabreicht. Die Therapie mit IgE-Antikörpern bewirkt auch, dass akute Verschlimmerungen und Symptome geringer werden, weniger Akut-Medikation benötigt wird und sie zudem sicher zu sein scheint.
In patients with severe allergic asthma subcutaneously administered IgE antibodies are used to reduce corticosteroids. Therapy with anti-IgE also results in fewer exacerbations, symptoms and need of rescue medication and appears to be safe.
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Bei Patienten mit schwerem allergischen Asthma werden zum Reduzieren der Kortikosteroiddosis subkutan IgE-Antikörper verabreicht. Die Therapie mit IgE-Antikörpern bewirkt auch, dass akute Verschlimmerungen und Symptome geringer werden, weniger Akut-Medikation benötigt wird und sie zudem sicher zu sein scheint.
In patients with severe allergic asthma subcutaneously administered IgE antibodies are used to reduce corticosteroids. Therapy with anti-IgE also results in fewer exacerbations, symptoms and need of rescue medication and appears to be safe.
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An der Pathogenese von Asthma können mehrere Gene beteiligt sein, wobei bisher noch kein spezifisches Gen oder mehrere spezifische Gene mit Sicherheit identifiziert werden konnten. Der stärkste für Asthma prädisponierende Faktor ist eine Atopie, die bei etwa 30 bis 50 Prozent der Bevölkerung auftritt und durch die Bildung abnormer Mengen von IgE-Antikörpern gekennzeichnet ist.
Risk factors can be distinguished in hereditary and acquired factors and factors triggering acute exacerbation. Hereditary factors correspond to a genetic predisposition determining the development of asthma or allergic sensitization. Multiple genes may be involved in the pathogenesis of asthma but no particular gene or genes have been identified with certainty yet. Atopy, defined as the production of abnormal amounts of IgE antibodies, occurs in 30 to 50 percent of the population and is the strongest predisposing factor for asthma. Another factor with heritable component is airway hyperresponsiveness. It is associated with airway inflammation and remodelling indicating that it may precede the development of asthma.
Risk factors can be distinguished in hereditary and acquired factors and factors triggering acute exacerbation. Hereditary factors correspond to a genetic predisposition determining the development of asthma or allergic sensitization. Multiple genes may be involved in the pathogenesis of asthma but no particular gene or genes have been identified with certainty yet. Atopy, defined as the production of abnormal amounts of IgE antibodies, occurs in 30 to 50 percent of the population and is the strongest predisposing factor for asthma. Another factor with heritable component is airway hyperresponsiveness. It is associated with airway inflammation and remodelling indicating that it may precede the development of asthma.
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Die allergenspezifische, durch IgE-Antikörper vermittelte Reaktion ist wahrscheinlich nur einer von mehreren Mechanismen, die akute Asthmaanfälle auslösen oder für eine dauerhafte chronische Entzündung verantwortlich sind.
In predisposed individuals "acquired" environmental factors modify the development of asthma. The allergen-specific IgE-mediated reaction probably simply represents one of several mechanisms triggering acute asthma exacerbations or maintaining chronic inflammation. Other extrinsic factors include irritants from plants, organic or inorganic chemicals, often referred to as occupational sensitizers, and other irritants like tobacco smoke and air pollution defined as the atmospheric accumulation of irritants.
In predisposed individuals "acquired" environmental factors modify the development of asthma. The allergen-specific IgE-mediated reaction probably simply represents one of several mechanisms triggering acute asthma exacerbations or maintaining chronic inflammation. Other extrinsic factors include irritants from plants, organic or inorganic chemicals, often referred to as occupational sensitizers, and other irritants like tobacco smoke and air pollution defined as the atmospheric accumulation of irritants.