Allergen-specific immunotherapy is highly effective in the treatment of IgE-mediated allergy diseases such as rhinitis, conjunctivitis, asthma, and venom allergy hypersensitivity. It is the only treatment that leads to lifelong tolerance against previously disease-causing allergens due to restoration of the normal immunity. (more…)

A variety of proinflammatory cells, mediators, and cytokines orchestrate the development of airway hyperresponsiveness, which results in the episodic airflow obstruction characteristic of asthma. As a consequence, modulation of the underlying disease process with antii-nflammatory agents is firmly established as being the cornerstone of successful management. Inhaled corticosteroids are the most potent antiinflammatory agents available and satisfactorily suppress underlying airway inflammation in most individuals. (more…)

Some of the immediate sequelae of injury are uncomfortably familiar: Soon after an injury occurs, the affected site and its surrounding tissues become reddened, warm, swollen, and painful. These four signs which are probably the most useful and ubiquitous diagnostic clues in all of clinical medicine are hallmarks of acute inflammation, the body’s initial physiologic reaction to tissue distress. In its simplest form, inflammation is a response carried out by blood vessels and by the endothelial cells that line them. (more…)

Normally present at very low levels in plasma, antibodies of the immunoglobulin E (IgE) isotype were first discovered in 1967, decades after the description of IgA, IgG, and IM. IgE antibodies are produced primarily by plasma cells in mucosal-associated lymphoid tissue and their levels are uniformly elevated in patients suffering from atopic conditions like allergic rhinitis, asthma and atopic dermatitis. Production of allergen-specific IgE in atopic individuals is driven both by a genetic predisposition to the synthesis of this isotype as well as by environmental factors, including chronic allergen exposure. (more…)

The mediators released by mast cells and basophils can be grouped into two categories:
(1) preformed substances contained within granules and
(2) newly generated chemicals synthesized following cellular activation.

These mediators comprise the effector function of the mast cell. Together they are able to increase vascular permeability, dilate vessels, cause bronchospasm, contract smooth muscle, and summon inflammatory cells. Few cells in the body produce compounds with such a large and varied spectrum of activity. (more…)

Systemic allergic reactions are a relatively common clinical emergency. In their mildest form, they may just manifest as systemic cutaneous reactions with pruritis, allergy urticaria and angioedema. In more severe cases there are cardiorespiratory symptoms such as stridor, wheeze, difficulty in breathing or hypotension. Anaphylaxis has been defined as a ‘severe, life-threatening generalized or systemic hypersensitivity reaction’. The prevalence of systemic allergic reactions is unclear because of the lack of a clear, consistent definition and large prospective population studies. (more…)

The symptoms of asthma occur together with variations in the diameter of medium- size airways such that it is increasingly difficult to exhale. Narrowing of the airways can occur because of smooth muscle contraction, edema or swelling of the wall, or increased mucus in the airways. However, it is increasingly clear that the pathologic event underlying most cases of asthma is acute inflammation of the airway walls. (more…)

Antihistamines have been shown to be effective in seasonal allergic rhinitis and chronic idiopathic urticaria. They improve quality of life scores, acute inflammatory response markers in atopic dermatitis asthma and symptom scores. Newer histamine H1-receptor antagonists may also have an antiplatelet-activating factor effect and are equally effective in seasonal allergic rhinitis. The antileukotrienes were developed in the 1980s. The first compounds of this novel class of anti-asthma drugs were registered in the second half of the 1990s. The mechanism of action of the cysteinyl leukotriene receptor antagonists (LTRAs) is based on counteracting the effects of cysteinyl leukotrienes at their receptor site (CysLT1 receptor) within the airways. (more…)

By definition, allergy is a condition where a person has hypersensitivity to an environmental, drug, or food antigen (allergen) caused by an altered or unusual immune system reaction to the antigen.

Allergenic foods can impact the lungs when an allergic reaction individual inhales food particles that may have been released when the food was cooked or that were dispersed in aerosol form. Allergy to the allergens in cooked food has been reported by highly allergic patients who were exposed to their allergenic foods (say, fish, shellfish, or eggs) in an enclosed area (for example, a restaurant dining room) or during meal preparation. Most cases of asthma triggered by aerosolized food allergens involve adults engaged in specific occupations that regularly expose them to the allergens. In contrast, most cases of asthma in children are triggered when the allergen is eaten, not inhaled.

Many experts believe that if a baby can be protected from becoming sensitized to the most highly allergenic foods when their healthy immune system and the digestive tract are in the most vulnerable stage for allergy to develop, the incidence of lifelong food allergy and potentially life-threatening anaphylactic reactions to foods will be reduced and hopefully entirely prevented. When a baby has been identified to be at risk for developing allergy, measures to reduce allergic sensitization might be implemented at birth and the problems associated with future food allergy may be significantly reduced. However, as we shall see in later discussions, experts disagree on the best way to avoid this early allergic sensitization.

The reaction of asthmatics to these chemical compounds is not an allergy, but is more correctly described as allergy intolerance because the initial response is not a triggering of the immune system. The process involves an increase in the level of the inflammatory mediators that are responsible for the bronchospasm of asthma. These mediators include histamine and leukotrienes. They are released during the reaction to an allergen, and cause the muscular contractions that result in the difficulty in breathing and wheezing that are typical of asthma. By inhibiting (or turning off) other types of mediators, the chemicals in the food additives cause an increase in the level of antihistamine and leukotrienes. This results in increased bronchospasm, and a definite worsening of the asthma symptoms.

Oral allergy syndrome is an allergic reaction to food that is confined to the oral cavity (i.e., to the lips, and around the lips, roof of the mouth, tongue, hard and soft palate, and uvula) and adjacent structures. It differs from other food allergy in that its symptoms do not appear in any other location in the body, and always accompany respiratory allergy to inhaled allergens of plants, particularly plant pollens. Of course, symptoms in the mouth, throat, and upper respiratory tract can be part of a generalized reaction to foods, but in this case they are more accurately described as oral allergy symptoms. The term oral allergy syndrome applies specifically to pollen allergy (pollinosis) accompanied by reactions to certain raw foods when they are in direct contact with oral tissues. Individuals with Oral allergy syndrome typically have hay fever symptoms caused by allergies to trees, grasses, and weeds. They experience irritation in the mouth (lips, tongue, roof of the mouth) and sometimes the throat after eating specific types of raw fruits, vegetables, and sometimes nuts.

Leukotrienes are present in increased amounts in exhaled breath condensate (EBC) in patients with asthma. So far, no data have been reported about leukotriene levels in non-asthmatic patients with Seasonal Allergic Rhinitis. The aim of the study was to find out whether the leukotriene levels in exhaled breath condensate were increased in the non-asthmatic adult patients with Seasonal Allergic Rhinitis both during and after the pollen season in comparison with healthy controls, and to assess changes in leukotriene levels after the pollen season. Twentynine non-asthmatic adult patients with Seasonal Allergic Rhinitis and 50 healthy non-smoking controls underwent measurement of exhaled leukotrienes in the exhaled breath condensate during and after the pollen season. Spirometry, skin-prick tests and total IgE were also evaluated. (more…)