Allergic diseases and other hypersensitivity reactions: causes, symptoms, diagnosis, treatment

Allergic diseases and other hypersensitivity reactions are the result of an inadequate, excessively expressed immune response that does not correspond to the severity of the disease or infectious process.

According to the classification of Gell and Koobs, there are 4 types of hypersensitivity reactions. Hypersensitivity reactions usually include several types.

Type I (immediate hypersensitivity) is mediated by IgE. Antigen binds to IgE (which attaches to tissue or blood basophils), triggering the release of preformed mediators (such as histamine, proteases, chemotactic factors) and the synthesis of other mediators (such as prostaglandins, leukotrienes, platelet-activating factor, IL). These mediators provide vasodilation; increase capillary permeability; lead to mucus hypersecretion, smooth muscle contraction, tissue infiltration by eosinophils, T-helper lymphocytes type 2 (Th2), and other cells involved in the inflammatory process. Type I reactions underlie atonic disorders (including allergic asthma, rhinitis, conjunctivitis), as well as allergies to latex and some foods.

Type II allergens occur when an antibody binds to cellular or tissue allergens or haptens associated with cells or tissues.

The antigen-antibody complex activates cytotoxic T lymphocytes or macrophages or the complement system, causing cellular or tissue damage (antibody-dependent cell-mediated cytotoxicity). Disorders related to type II reactions include acute rejection reactions in organ transplantation, Coombs-positive hemolytic anemia, Hashimoto's thyroiditis, Goodpasture's syndrome.

Type III are caused by inflammation in response to circulating antigen-antibody complexes that are deposited in tissues or vessel walls. These complexes can activate the complement system or bind to and activate certain immune cells, resulting in the release of inflammatory mediators. The degree of formation of immune complexes depends on the ratio of antibody to antigen in the immune complex. Initially, there is an excess of antigen in small antigen-antibody complexes that do not activate complement. Later, when the amount of antibodies and antigens is balanced, immune complexes become larger and tend to be deposited in various tissues (renal glomeruli, blood vessels), leading to systemic reactions. Type III reactions include serum sickness, SLE (systemic lupus erythematosus), RA (rheumatoid arthritis), leukocytoclastic vasculitis, cryoglobulinemia, hypersensitivity pneumonitis, bronchopulmonary aspergillosis, and some types of glomerulonephritis.

Type IV (delayed-type hypersensitivity) is mediated by T lymphocytes. There are four subtypes based on the T lymphocyte subsets involved: type 1 helper T lymphocytes (IVa), type 2 helper T lymphocytes (IVb), cytotoxic T lymphocytes (IVc), and IL-8-secreting T lymphocytes (IVd). These cells, sensitized after contact with a specific antigen, are activated after repeated exposure to the antigen; they have a direct toxic effect on tissues or through the cytokines released that activate eosinophils, monocytes and macrophages, neutrophils, or killer cells, depending on the type of reaction. Type IV reactions include contact dermatitis (eg, poison ivy), hypersensitivity pneumonitis, allograft rejection reactions, tuberculosis, and many forms of drug hypersensitivity.

Suspected autoimmune diseases

Probability	Violation	Mechanism or symptom
Highly probable	Autoimmune hemolytic anemia	Phagocytosis of antibody-sensitized erythrocytes
	Autoimmune thrombocytopenic purpura	Phagocytosis of antibody-sensitized platelets
	Goodpasture's syndrome	Anti-basement membrane antibodies
	Graves' disease	Antibodies (stimulating) to the TSH receptor
	Hashimoto's thyroiditis	Cell- or antibody-mediated thyroid cytotoxicity
	Insulin resistance	Insulin receptor antibodies
	Myasthenia gravis	Acetylcholine receptor antibodies
	Pemphigus	Epidermal acantholytic antibodies
	SKV	Circulating or locally generalized immune complexes
Probable	Andrenergic drug resistance (in some patients with asthma or cystic fibrosis)	Beta-adrenergic receptor antibodies
	Bullous pemphigoid	IgG and complement components to the basement membrane
	Diabetes mellitus (some cases)	Cell- or antibody-mediated islet cell antibodies
	Glomerulonephritis	Antibodies or immune complexes to the glomerular basement membrane
	Idiopathic Addison's disease	Antibodies or possibly cell-associated adrenal cytotoxicity
	Infertility (some cases)	Antisperm antibodies
	Mixed connective tissue diseases	Antibodies to extracted nuclear antigen (ribonucleoprotein)
	Pernicious anemia	Antibodies to parietal cells, microsomes, intrinsic factor
	Polymyositis	Non-histone antinuclear antibodies
	RA	Immune complexes in joints
	Systemic sclerosis with anticollagen antibodies	Antibodies to the nucleus and nucleolus
	Sjogren's syndrome	Multiple tissue antibodies, specific non-histone anti-bb-B antibodies
Possible	Chronic active hepatitis	Anti-smooth muscle cell antibodies
	Disorders of the endocrine glands	Tissue specific antibodies (in some cases)
	Post-infarction condition, cardiotomy syndrome	Myocardial antibodies
	Primary biliary cirrhosis	Mitochondrial antibodies
	Vasculitis	Lg and complement components in vessel walls, low serum component levels (in some cases)
	Vitiligo	Antibodies to melanocytes
	Many other inflammatory, granulomatous, degenerative and atopic disorders	No rational alternative explanations
	Urticaria, atopic dermatitis, asthma (some cases)	IgG and IgM to IgE

TSH - thyroid stimulating hormone, RA - rheumatoid arthritis, SLE - systemic lupus erythematosus.

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