Urticaria and angioedema

Published on 05/03/2015 by admin

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Last modified 05/03/2015

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Urticaria and angioedema

Urticaria (hives) is a common eruption characterized by transient, usually pruritic, wheals due to acute dermal oedema from extravascular leakage of plasma. Angioedema signifies a larger area of oedema involving the dermis and subcutis. A classification is shown in Table 1.

Table 1 Classification of urticaria and angioedema

Allergic (IgE mediated) mast cell degranulation SystemicSkin contact Food, drugs, latex (aerosols)Animal saliva, pollen, latex
Non-allergic (non-IgE mediated) mast cell degranulation Chronic ordinaryPhysicalPharmacological No cause identifiable (commonest subtype)Dermographism, cholinergic, cold, solar, heat, delayed pressureAspirin, opiates, non-steroidal drugs, food additives, ACE inhibitors (p. 87)
  Autoimmune disease Systemic lupus erythematosus (p. 80), thyroid antibodies, anti-IgE receptor antibodies, urticarial vasculitis (p. 77)
  Genetic C1 esterase inhibitor deficiency (p. 77), mastocytosis (p. 116)
  Other Infection, paraneoplastic, skin contact (nettle sting)

Aetiopathogenesis

Urticaria is mediated through immune (allergic) or non-immune mechanisms. Lesions result from the release from mast cells of biologically active substances, particularly histamine, which produce vasodilatation and increased vascular permeability. Several pathways are recognized:

image IgE-mediated (type I) hypersensitivity (p. 11) is the best understood mechanism; antigen cross-links immunoglobulin (Ig) E molecules on the surface of mast cells, resulting in degranulation with release of vasoactive agents.

image Complement activation can produce dermal oedema, as in hereditary angioedema or urticaria associated with circulating immune complexes.

image Direct release of histamine from mast cells, in a non-immune manner, is caused by some drugs, e.g. opiates and contrast media.

image Blocking of the prostaglandin pathway from arachidonic acid, by some drugs such as aspirin and non-steroidal anti-inflammatory agents, promotes urticaria by accumulating vasoactive leukotrienes.

image Anti-IgE receptor (anti-FcεR1) antibodies have been shown to be present in 40% of cases of ‘chronic’ urticaria, which is capable of inducing autoimmune mast cell degranulation.

Pathology

The dermis is oedematous with dilatation of vessels and mast cell degranulation. Vessel damage and a lymphocytic infiltrate may be seen with urticarial vasculitis.

Clinical presentation

Three-quarters of cases of urticaria fall into the ‘chronic idiopathic’ or acute categories. Another 20% are due to dermographism, cholinergic urticaria or physical factors. Other causes are rare.

Chronic idiopathic urticaria

Itchy pink wheals appear as papules or plaques anywhere on the skin surface (Fig. 1

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