**4. Contact urticaria**

pre‐exercise propranolol 80 mg daily has been found effective in controlling the symptoms of CU [17]. These data have not been supported by further studies because of the fact that

The prognosis of CU is mostly pleasing. About 70% of the patients heal within 10 years of the diagnosis. Sibbald et al. estimated the duration of CU to be 3–16 years with an average of

Cholinergic urticaria must be distinguished from exercise‐induced anaphylaxis (EIA). The main symptoms of EIA include laryngospasm, bronchospasm, vascular collapse, fatique, vocal changes, gastrointestinal upset, flushing and hives [18]. In contrast to CU, the urticarial plaques are larger, up to 10–15 mm. All types of exercise including walking can be the trigger. In EIA, although the anaphylaxis symptoms are at the forefront, only a few cases of death

EIA is treated like any other forms of anaphylaxis. Epinephrine is the life‐saving treatment. Diphenhydramine 25–50 mg is helpful. Systemic steroids are used to prevent delayed bipha‐ sic reactions [20]. Any individual with the diagnosis of EIA should carry an epinephrine auto‐ injector [21]. Cetirizine and montelukast combination also has been reported to be useful in

CU can be differentiated from EIA with the size of the whealings. Also, in CU, the hives are in the front, whereas the edema and the anaphylaxis are in the front in case of EIA. In addition, passive warming test in a bath and methacholine injection tests are positive in CU [23].

Aquagenic urticaria (AU) is a rare form PU which is characterized by wheals following cuta‐ neous exposure to water, including tears and sweat. Mostly, 1–3 mm follicular wheals and 1–3 cm erythematous flares surrounding them are present. The lesions develop 20–30 min after exposure to water. Lesions usually resolve in 30–60 min after the cessation of contact to water [4]. Most of the patients are peri‐pubertal females. Trunk and proximal arms are the most commonly affected sites, sparing palms and soles [5]. Wheezing and dyspnea can accompany the lesions. When there is such a systemic symptom, large lesions rather than

Most of the AU cases are sporadic. However, there are some reports of familial cases. No spe‐ cific gene locus has been identified so far [5]. There are few cases showing the association of

The pathogenesis of AU is not clear yet. In 1981, Tkach hypothesized that sudden changes in osmotic pressure around hair follicles, leading to passive diffusion of water caused whealing [27]. A recent proposal involves existence of water‐soluble antigens in the epidermis which later migrate to dermis and cause histamine release [10]. The lack of a proper etiologic mecha‐

AU and HIV infection and papillary thyroid gland carcinoma [25, 26].

beta‐blockers, themselves, cause allergic reactions.

30 A Comprehensive Review of Urticaria and Angioedema

7.5 years [2].

have been reported [19].

preventing symptoms of EIA [22].

**3. Aquagenic urticaria (AU)**

1–3 mm punctate lesions are present [24].

nism makes AU difficult to treat.

Contact urticaria is the transient whealing and flare of the skin after contact with certain agents. The lesions appear within 60 min of contact and mostly resolve in 2–24 h [33]. Contact urticaria can be both immunological (IgE mediated) or non‐immunological. Mostly, non‐ immunological mechanisms are seen. It can be provoked in all persons without the need of prior sensitization [34].

The lesions in contact urticaria appear as a result of the release of vasoactive amines such as histamine, leukotrienes, substance P and prostaglandins, independent from immunological processes. The lesions are localized to the contact area causing no systemic symptoms. The causative contact agents can be insects, metals, alcohol, balsam of Peru, sodium benzoate, sorbic acid, fruits, vegetables, jellyfish, sea anemones and corals [33–35].

Contact urticaria is rarely due to immunological causes, that is, allergic. In this case, it is caused by antigen‐antibody type 1 IgE‐mediated hypersensitivity reaction. The contact antigen pen‐ etrates the skin and binds with specific IgE antibodies on dermal mast cells. Histamine and some other mediators such as kinin and prostaglandins are released. As a result, erythema and hives are observed [35]. Sometimes systemic symptoms (rhinitis, conjunctivitis and asthma) can accompany the cutaneous manifestations [36]. The triggering agent in contact urticaria can be rubber latex, antibiotics (cephalosporins and streptomycin), foods (potato, fish and apple), cosmetics (hair bleaching products and paraphenylenediamine) and chemi‐ cals (isocyanates, chlorhexidine and aluminum) [35].

The mainstay of the therapy is mainly avoidance in contact urticaria [7]. Barrier creams are being used recently with good results [37]. H1 antihistamines make the first line therapy. In case of failure, dose increment, leukotriene antagonists, cyclosporine, omalizumab can be used with variable success rates [34, 35, 37].
