Principles of classification of antiallergic agents
Modern pharmacology classifies drugs that affect immune and allergic processes according to their specific site of action within the pathological cascade. An allergic reaction is a complex chain of biochemical events, and it can be interrupted at various stages. To achieve this, H₁-histamine receptor blockers, mast cell membrane stabilizers, leukotriene pathway inhibitors, drugs binding free immunoglobulin E (IgE), and glucocorticoids are used.
H₁-histamine receptor blockers
To understand the mechanism of action of classical antihistamines, it is necessary to examine the pharmacodynamics of the receptors themselves. Histamine receptors in the body are closely coupled with G proteins.
When a histamine molecule excites an H₁ receptor, the following cascade is triggered inside the cell:
- A specific enzyme—phospholipase C—is activated.
- There is a sharp increase in the concentration of calcium ions (Ca²⁺) inside the cell.
- The calcium surge leads to smooth muscle contraction and a pathological increase in blood vessel permeability, which clinically manifests as edema and spasm.
The mechanism of action of this group of drugs consists in the competitive blockade of H₁ receptors. The medicinal substances occupy the site of histamine, preventing the initiation of the calcium cascade. It is important to emphasize that these agents act selectively: during an allergy, they primarily block specific H₁ receptors rather than all existing types of histamine receptors simultaneously. Typical representatives of this group are diphenhydramine and loratadine.
Alternative targets: mast cells, leukotrienes, and IgE
In addition to the direct blockade of histamine receptors, other pharmacological strategies exist:
- Mast cell membrane stabilizers. These drugs directly block the degranulation process, preventing allergy mediators from entering the extracellular space. They include cromoglicic acid and nedocromil sodium.
- Leukotriene pathway blockers. Leukotrienes act as potent inflammatory mediators. Drugs of this group (montelukast, zafirlukast, zileuton) are capable of inhibiting either the synthesis of leukotrienes itself or their ultimate effects in tissues.
- Anti-IgE therapy. The drug omalizumab works at the stage of binding free IgE. It interrupts the bond between immunoglobulin E and the specific receptor on the surface of the mast cell, thereby preventing the sensitization process.
Glucocorticoids in allergy treatment
Glucocorticoids (GCs, GCS) are a broad group of steroid hormones of the adrenal cortex and their synthetic analogs. In the human body, natural glucocorticoids are synthesized in the zona fasciculata and zona reticularis of the adrenal cortex. Their basic physiological effect is directed at the regulation of carbohydrate and protein metabolism. This fundamentally distinguishes them from mineralocorticoids, which are produced in the zona glomerulosa and regulate primarily mineral metabolism.
In clinical practice, glucocorticoids are valued for their pronounced anti-inflammatory, immunosuppressive, anti-shock, and potent antiallergic effects.
Mechanism of the antiallergic action of glucocorticoids:
- Blockade of the activity of the enzyme phospholipase A₂.
- Subsequent reduction in the production of arachidonic acid.
- Creation of an obstacle to mast cell degranulation.
- Complete blocking of the release of allergy mediators into surrounding tissues.
To memorize the sites of drug action, imagine a fortress siege: omalizumab intercepts the enemy on distant approaches (binds free IgE), cromoglicic acid reinforces the gates (stabilizes the mast cell membrane), glucocorticoids deprive the opponent of weapons (block phospholipase A₂), and loratadine locks the keyholes in the houses (competitively blocks H₁ receptors from already released histamine).
Class and exam questions
How exactly does histamine affect body cells during an allergy?
Histamine excites H₁ receptors coupled with G proteins. This activates the enzyme phospholipase C, which leads to a sharp increase in the concentration of calcium ions inside the cell, causing smooth muscle contraction and increased vascular permeability.
Do antihistamine drugs block absolutely all histamine receptors?
No, they act selectively. The drugs competitively block specific types of receptors—primarily H₁ receptors, which play a major role in the development of the allergic reaction, without affecting other types simultaneously.
What is the fundamental difference between glucocorticoids and mineralocorticoids?
Glucocorticoids are synthesized in the zona fasciculata and zona reticularis of the adrenal cortex, regulate protein and carbohydrate metabolism, and possess a powerful antiallergic and anti-inflammatory effect. Mineralocorticoids are produced in the zona glomerulosa and are responsible for mineral metabolism.
What else to study on this topic
- Pharmacokinetics and potential side effects of diphenhydramine and loratadine.
- Indications for the use of synthetic glucocorticoid analogs (prednisolone, dexamethasone).
- The role of arachidonic acid and leukotrienes in the development of inflammatory reactions.
- Mechanisms of the immunosuppressive and anti-shock action of glucocorticoids.
- Drugs of choice for treating an immediate-type allergic reaction (anaphylaxis).
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