The medical term leukotriene already indicates the white blood cells. In the Greek language "leukós" means "white". Leukotrienes were first discovered in the white blood cells.
The chemical derivation is based on arachidonic acid and other polyunsaturated C20 fatty acids. Leukotrienes are highly active biological substances. The biosynthesis is dependent on the enzyme 5'-lipoxygenase. Arachidonic acid reacts in two steps with 15'-lipoxygenase and 5'-lipoxygenase.
Leukotrienes are derived from arachidonic acid. They are active tissue hormones. They act as mediators that respond to inflammatory and allergic reactions by attracting neutrophilic leukocytes.
They increase vascular permeability and trigger asthma attacks by bronchoconstriction. Leukotrienes have three conjugated triene compounds (double compound). They belong to the substance group of the Eikosanoide. Leukotrienes and prostaglandins go back to the arachidonic acid that forms the parent substance. This acid is derived from phospholipids in cell membranes. Inflammatory cells such as mast cells, monocytes, endothelial cells and neutrophils, eosinophils and basophils are able to produce leukotrienes. The synthesis of the prostaglandins takes place via the cyclooxygenase. Leukotrienes arise via lipoxygenase. Inhibition of prostaglandins releases more arachidonic acid to form leukotrienes.
Through this process arises ASA-induced asthma. Leukotrienes play an important role in inflammatory and allergic reactions in the human body. They are also referred to as inflammatory mediators and are important for the course of lung disease. The leukotriene "D4" narrows the airway musculature and increases the mucus production of the upper airway organs. The bronchi are also affected by this process. There are several leukotrienes with names such as B, C and D. The cysteinyl leukotrienes "LTC4-LTE4 have a bronchoconstrictive and secretory effect. They are capable of inducing anaphylactic or allergic reactions within the lungs. These events lead to narrowed airways and thus to asthma attacks.
A chemical stimulus (chemotaxis) causes the adhesion (adhesion) of the leukocytes to the blood vessel wall. Inflammation is promoted and tissue can be destroyed during this process by superoxide radicals. Leukotrienes interact with interferons and interleukins. At this stage of the disease course, leukotriene antagonists, for example montelukast, become active in order to eliminate the undesirable effects on the lung, respiratory tract and bronchi. They block the receptors of the original messenger. These unwanted messengers occur in the form of stimulants such as house dust, pollen or cold air, which affects especially asthma patients.
The leukotriene antagonists dilate the bronchi, fight the inflammation in the lungs and counteract the narrowing of the airway muscles. Symptoms such as coughing, a constant feeling of tightness and a reduced oxygen supply due to respiratory problems are reduced and the function of the lungs is improved. Leukotriene receptors acting as antagonists are used against the suppression of asthmatic, allergic and inflammatory processes in the human body. The first drug of choice is Montelukast Singulair®.
This medication dissolves the cramped bronchial muscles and reduces the formation of mucus in hay fever (allergic rhinitis) and bronchial asthma (bronchial asthma). Infants with intermittent asthma are treated with montelukast at the beginning of an episode of asthma during short periods of therapy. Most asthma patients can live well with their condition by taking this medicine. The side effects are usually lower than the treatment success.
Leukotriene antagonists are used to treat asthma and allergic rhinitis. In the treatment of asthma they belong in the field of controllers. Controllers are long-term medications, they are taken permanently. Leukotriene antagonists are in competition with glucocorticoid therapy, which is more effective but has more side effects and a greater risk of treatment.
Montelukast may be used in children up to fourteen years of age as an alternative to glucocorticoid therapy, if appropriate treatment is indicated. As monotherapy Montelukast is not approved in Germany in people over the age of 15 years. According to the international guidelines, it may only be used if the attending physician advocates glucocorticoid therapy, for example if the patients show side effects in which the damage is to be classified as higher than the expected treatment success. Even patients who are unable to inhale glucocorticoids are entitled to alternative treatment with montelukast.
Leukotriene antagonists may also be used in combination with glucocorticoids and beta-2-sympathomimetics (eg, ambroxol, clenbuterol, bambuterol) to achieve a decreased dosage. However, the patients must be grown up. Montelukast acts as a so-called "add on" in this therapy. It is not suitable to treat an acute asthma attack. However, the prevention of stress asthma is possible. Here, the drug is in addition to the basic medication of inhaled glucocorticoids and beta-adrenergic substances (adrenoceptors). These are phylogenetic coupled receptors (GPCRs), which are related to the G protein. They are triggered by the hormone adrenaline.
Leukotriene antagonists are administered orally in tablet form. They are also available as chewable tablets or as granules. Their maximum effect is about two hours after ingestion.
Despite the potential side effects, montelukast is generally well tolerated. The side effects depend on the individual situation of the patient. These include mental disorders, skin rash, upper respiratory tract infections, gastrointestinal symptoms, muscle and joint pain, Churg-Strauss syndrome (lung and asthma) and increased bleeding.Tags: