Lecture on urticaria and angioedema

2021-03-24 12:00 AM

Angioedema and urticaria classified as IgE mediated, complement-mediated, associated with cold, sunlight, pressure, or idiosyncrasies specific stimulation

The urticaria and angioedema include popular papules, usually itchy transient plaques and large oedematous areas of the skin and subcutaneous tissue (angioedema), or recurrent, acute or chronic.

The rate of 15 - 23% of the population has ever had this condition in their life.

Chronic urticaria accounts for 25% of all urticaria.

Leaven

Angioedema and urticaria were classified as IgE mediated, complement-mediated, by physical stimulation (cold, sunlight, pressure) or idiosyncrasies (Idiosyncrasies).

Specific types

Immunity:

IgE intermediates: there is a geo-allergenic background for food antigens (milk, eggs, salmon), medications: penicillin, parasites.

Complement-mediated, the activated complement complex induces Mast cell granulation.

Physical urticaria:

Dermographism: 4.2%, ordinary people have it.

Cold urticaria is often found in children and young people, diagnosed by a "rock" test.

Urticaria due to sunlight spectrum 290-500 nm, histamine is one of the chemical intermediates.

Cholinergic urticaria when exercising physical exercise increases sweating, small papules.

Angioedema: pressure, concussion, history of post-concussion swelling, ineffective antihistamines, and corticosteroids are helpful.

Urticaria due to mast cell-releasing drugs:

Intolerance reaction with salicylates, azo and benzoate dyes.

Urticaria associated with autoimmune connective tissue disease - blood vessels:

Urticaria is a form of cutaneous vasculitis with urticaria that lasts longer than 12 to 24 hours, may be associated with purpura or hemosiderin pigmentation may be seen, combined. decreased blood complement and kidney disease.

Hereditary angioedema:

Severe autosome disorder, facial angioedema, sometimes pharyngeal oedema, abdominal pain due to angioedema in the intestinal wall, complement system abnormality, decreased C1 esterase inhibitor (85%) or dysfunctional inhibitor ( 15%), low C 4 angioedema due to Bradykinin formation.

Urticaria - angioedema with severe angioedema:

There is urticaria pruritus on the face, neck, limbs, body lasting 7- 10 days. There is a fever (10-18%) due to fluid retention. Organs without damage, eosinophilia, leucocytosis 20 .000. - 70,000. Good prognosis.

Pathogenesis:

IgE-mediated urticaria injury caused by biologically active substances from the Mast cell and the alkaline cell released by the antigen, which are susceptible to an IgE type I antibody, increase the hypersensitivity type. .

In complement-mediated urticaria, the complement is activated by the immune complex to release Anaphylatoxins causing Mast cell granulation.

In chronic urticaria, histamine secreted from cutaneous Mast cells is the main mediator. Other mediators including eicosanoids and neuropeptides may also play a part in lesion formation, but direct measurement of these substances has not been reported.

Salicylate intolerance, food, food preservatives such as benzoic acid, sodium benzoate as well as some azo dyes including tartrazine and sunset gold are thought to mediate arachidonic abnormalities.
Urticaria produced by a non-cytokine mediator with a molecular weight greater than 1 million is identified as IgG. It releases histamine from both blood alkaline a-cells and cutaneous Mast cells (Hide M et al. N Engl J Med 1993 328. 1599). This is an autoantibody that acts on the IgE junction of the adjacent high gravity receptor. Thus, functional antibodies to functional anti-IgE or anti-FC G RE autoantibodies were identified in 48% of the serum samples of chronic urticaria and a positive correlation between disease activation was demonstrated. These autoantibodies may explain why treatment with pure plasma, intravenous immunoglobulin or cyclosporin helps. Some signs of chronic urticaria with signs of Mast cell autoimmune disease are considered to have an association with chronic urticaria with autoimmune thyroid disease.

In genetic angioedema decreased or dysfunctional esterase inhibitors lead to increased kinin formation. Urticaria, eosinophilic angioedema may be an increase and decrease in eosinophils with angioedema and urticaria. There are morphological changes in the eosinophils including destruction and release of substances within it into the dermis, a number of large basal proteins distributed following the release of eosinophils in the collagen and cell membranes. Mast cells in the dermis are found to be dispersed.

Common types

Urticaria (<30 days):

Usually large, IgE-dependent urticaria, has an Atopic background, involves food, parasites, drugs, often in combination with angioedema.

Chronic urticaria (> 30 days):

Less dependent on IgE, unknown aetiology, 80 - 90% thought to be spontaneous, aggravating neurotransmitter, intolerance to salicylate benzoate, common urticaria in adults, more women than men.

Anamnesis

Time to appear lesions: many hours.

Skin symptoms: itching, pain when walking (in the affected leg) redness, burning and wheezing (in Cholinergic urticaria).

Systemic symptoms: fever in serum disease and urticaria - angioedema, increased eosinophil in angioedema, hoarseness, hissing breath, difficulty breathing. 
Organs: arthralgia (serum sickness, necrotizing capillaries, hepatitis).

Physical examination

Skin lesions

Transient urticaria - many small papules 1 - 2 mm are typical for Cholinergic urticaria, pruritus - urticaria small 1.0 cm to 8 cm plaques.

Angioedema a wide area of ​​colour such as the skin on part of the face (around the eyes, lips, lips) or on the extremities.

Colour: pink with extensive white markings surrounded by a red halo.

Oval shape, arc, ring shape, multi-shape, oval shape and strange shape.

Distribution: circular, arc, streaked.

Transient time, many hours.

Distributed locally or spread.

Common location: pressure position, open area (urticaria due to light) body, hands and feet, lips, ears.

Differential diagnosis

Urticaria: insect stings, drug reactions, urticaria contact dermatitis, urticaria capillary inflammation.

Special tests and examinations

Body examination excludes chronic urticaria (SLE, necrotic capillary inflammation, lymphoma).

Organization of skin pathology: oedema of the dermis and subcutaneous tissue, varicose veins but no evidence of damage to the capillaries and nucleus, and erythrocytes. Mast cells are dispersed. Perivascular inflammation is mainly lymphocytes, T helper, and HLA- DR is positive. In papules, there were secretions of Selectin E and ICAM I in vascular endothelial cells, and VCAMI in periarticular cells.

Serology:

Combined hepatitis antigen test.

Complement system evaluation.

IgE antibody evaluation by RAST technique.

Haematology:

Blood sedimentation increases in persistent urticaria (necrotizing capillary necrosis of Necrotizing vasculitis), decreased blood complement, transient eosinophilia in urticaria reacts to food, parasites and drugs. In urticaria syndrome - angioedema increased eosinophils.

Complement studies: functional inhibitors.

Ultrasound imaging for early diagnosis of intestinal damage, intestinal oedema.

Parasitology: stool test for parasites.

Diagnose

Ask carefully about the history of taking medications including aspirin, not - Steroids, if you suspect physical urticaria, you can do an appropriate test. The best diagnosed cholinergic urticaria is sweat exercise and injected into the skin with acetylcholine or methomyl will produce small oedema. Light-induced urticaria tests UVB, UVA and visible light. Urticaria caused by cold by pressure test of ice or tube containing ice cubes, ice. If urticaria does not disappear after 24 hours, urticaria capillary inflammation and skin biopsy should be performed. Urticaria-angioedema syndrome due to high fever eosinophilia, high white blood cells (mostly eosinophils) weight gain due to water retention.

Hereditary angioedema has a clear family history and features angioedema of the face and limbs as a result of seizures or abdominal pain and decreased levels of C4 and C 1 esterase inhibitors and dysfunctional inhibitors.

Pathogenesis

IgE-mediated urticaria injury caused by biologically active substances from the Mast cell and the alkaline cell released by the antigen, which is susceptible to an IgE type I antibody, increase the hypersensitivity type. .

In complement-mediated urticaria, the complement is activated by the immune complex to release Anaphylatoxins causing Mast cell granulation.

In chronic urticaria, histamine secreted from cutaneous Mast cells is the main mediator. Other mediators including eicosanoids and neuropeptides may also play a part in lesion formation, but direct measurement of these substances has not been reported.

Salicylate intolerance, food, food preservatives such as benzoic acid, sodium benzoate as well as some azo dyes including tartrazine and sunset gold are thought to mediate arachidonic abnormalities.
Urticaria produced by a non-cytokine mediator with a molecular weight greater than 1 million is identified as IgG. It releases histamine from both blood alkaline cells and cutaneous Mast cells (Hide M et al. N Engl J Med 1993 328. 1599). This is an autoantibody that acts on the IgE junction of the adjacent high gravity receptor. Thus, functional antibodies to functional anti-IgE or anti-FC G RE autoantibodies were identified in 48% of the serum samples of chronic urticaria and a positive correlation between disease activation was demonstrated. These autoantibodies may explain why treatment with pure plasma, intravenous immunoglobulin or cyclosporin helps. Some chronic urticaria signs of Mast cell autoimmune disease are considered to have a combination of chronic urticaria with autoimmune thyroid disease.

In genetic angioedema decreased or dysfunctional esterase inhibitors lead to increased kinin formation. Urticaria, eosinophilic angioedema may be an increase and decrease in eosinophils with angioedema and urticaria. There are morphological changes in the eosinophils including destruction and release of substances within it into the dermis, a number of large basal proteins distributed following the release of eosinophils in the collagen and cell membranes. Mast cells in the dermis are found to be dispersed.

Progress and burners First
Half of the patients with urticaria lesions lasted a year, 20% of 20-year lesions.
The prognosis is mostly good except for hereditary angioedema that can be fatal if left untreated.

Treatment

Prevention of urticaria attacks by eliminating the aetiology of drugs and chemicals, aspirin, and food, especially in chronic recurrent urticaria, with few results.

Antihistamines: H1 blockers such as hydroxyzine, terfenadine and if fail to use H1 and H2 blockers (cimetidine) and the drug stabilizes Mast cells (Ketotifen). Tricyclic doxepin, an antidepressant with a distinct H1 antihistamine effect in the presence of severe urticaria with discomfort and depression.

Prednisolone indicated for urticaria-angioedema syndrome blood eosinophilia.

Danozol long-term therapy for complete hereditary angioedema or C1 esterase inhibitor during exacerbations.

Features of all kinds of chronic urticaria

Locket type

age of the patient

Main clinical features

combined angioedema

Diagnostic test

Spontaneous chronic urticaria

20-50

less or more disseminated popular or urticaria, pink or pale, usually ring-shaped with itchy papules.


Have

 

Dermographism
Stock dermatographia urticaria

20- 50

Itching, urticaria streaks, lines, bright red around, in the position of scratching.

Is not

Light streaking on the skin causes an immediate, itchy urticaria

Other physical urticaria: cold

10- 40

Itching, redness, or pale coloration where exposed to cold or water.

Have

10 minutes of applying an ice cube causing a papule to appear within 5 minutes of removing the ice cube.

Urticaria due to pressure

20- 50

Itchy red or painful swelling in the place where pressure is applied (feet, palms, or hips)

Is not

Apply pressure perpendicular to the skin resulting in persistent red swelling after a latent period of 1-4 hours.

Urticaria caused by sunlight

20- 50

Itchy red swelling at the location of UV or visible light

Have

Illuminate artificial light of 2.5 KW (290- 690 nm) for 30- 120 seconds causing papules within 30 minutes.

Cholinergic urticaria

10- 50

Itching, <5 mm. Pink or pale, monolithic papules of the torso, neck, and extremities

Have

Physical exercise or a hot bath can give rise to a rash