22 HOW TO TREAT : URTICARIA IN ADULTS ausdoc . com . au
3 NOVEMBER 2023
22 HOW TO TREAT : URTICARIA IN ADULTS ausdoc . com . au
Figure 2 . Pathomechanisms in chronic spontaneous urticaria .
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ACEIs may be a trigger , by directly impairing degradation of bradykinin and other vasoactive peptides , such as substance P . Other medications that can cause non-histaminergic angioedema via this mechanism include ARBs , dipeptidyl peptidase 4 inhibitors and neprilysin inhibitors . 31
In an allergic reaction , which accounts for a minority of acute urticaria , IgE-mediated hypersensitivity occurs in two phases . First , sensitisation takes place when an antigen ( for example , insect venom ) activates Th-2 cells and B-cells , which then differentiate into IgE-producing plasma cells . Circulating antigen-specific IgE from plasma cells binds to mast cells . In the second phase , upon re-exposure , the culprit antigen is recognised by IgE bound to mast cells , resulting in mast cell activation and degranulation .
Clinical assessment
History and skin examination are usually adequate to diagnose urticaria . History is typically of raised pruritic skin lesions , with each weal lasting less than 24 hours . As eruptions are transient , photographs of previous episodes ( see figure 3 ) can be useful to exclude an alternative cause .
Most subtypes of urticaria are indistinguishable on morphological examination . The exception is cholinergic urticaria , which presents with characteristic 1-3 mm pinpoint weals , sparing the palms of the hands and soles of the feet ( see figure 4 ). Most cases of chronic urticaria present with cutaneous weals alone ( about 60 %), with fewer patients having both weals and angioedema ( about 35 %) and an even smaller proportion presenting with angioedema alone ( about 6 %). 10
Transient intercurrent infection frequently causes acute urticaria ; therefore , infectious history should be elicited . 32 Assessment of recent food intake , medication exposure or insect venom sting at the time of onset is useful to exclude an allergic cause . Patients with chronic spontaneous urticaria ( see figure 5 ) will report relapsing episodes without any identifiable trigger . A medical history of autoimmune disorders , thyroid disorders and malignancy may be present . Up to 25 % of patients with chronic spontaneous urticaria have a family history of the same . 10
CIndU is readily identified on history , with patients describing a temporal relationship to eliciting triggers . Most episodes occur within a few minutes of exposure to the culprit trigger — except for delayed pressure urticaria , in which weals typically occur 4-6 hours later .
It is important to differentiate cholinergic urticaria from exercise-induced anaphylaxis ( EIA ). EIA is characterised by bronchospasm and / or vascular collapse within 45 minutes of exercise initiation . It can also be associated with an urticarial skin eruption . In contrast to pinpoint weals in cholinergic urticaria , the weal size in EIA is 10-15mm . 33 Systemic symptoms suggestive of respiratory or cardiovascular compromise should not typically be present in cholinergic urticaria .
Clues to rarer differential diagnoses , such as urticarial vasculitis , include painful weals lasting longer than 24 hours , with residual pigmentation on resolution . Prominent constitutional symptoms in older age groups raise suspicion of underlying malignancy . Systemic symptoms of arthralgia , mucosal ulceration or internal organ dysfunction may indicate evolving autoimmune disease .
Consider bradykinin-mediated causes when angioedema is present without urticaria . Recurrent attacks lasting days rather than hours , the presence of gastrointestinal symptoms , childhood onset and a family history of HAE may alert to this
Figure 3 . Raised pruritic skin lesions of urticaria .