Physical urticaria/angioedema as an experimental model of acute and chronic inflammation in human skin

Soter, Nicholas A.

doi:10.1007/bf01891887

Cited by 8 publications

(6 citation statements)

References 37 publications

(29 reference statements)

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“…64 Overall, ColdU is an excellent experimental model disease for in vivo drug evaluations that can provide valuable mechanistic insights into wheal formation. 60,95,96 Antihistamine treatment with cyproheptadine resulted in a reduction of clinical symptoms without affecting HR in five of six patients; however, in one patient there was a significant HR reduction. 97 Prednisolone at an oral dose of 20-25 mg for 1-5 days was shown to suppress cold-induced HR in all but one ColdU patient, whereas the clinical response following prednisolone was unchanged suggesting that histamine cannot solely explain all vascular phenomena in ColdU.…”

Section: Ta B L Ementioning

confidence: 97%

“…Overall, ColdU is an excellent experimental model disease for in vivo drug evaluations that can provide valuable mechanistic insights into wheal formation 60,95,96 . Antihistamine treatment with cyproheptadine resulted in a reduction of clinical symptoms without affecting HR in five of six patients; however, in one patient there was a significant HR reduction 97 .…”

Section: Aetiopathogenesismentioning

confidence: 99%

“…[92][93][94] Cryoglobulins are thought to activate complement components C3a and C5a and generate permeability, thereby mediating vessel damage in cryoglobulinemic vasculitis (CryoVas). 95 In ColdU, according to the study by Kaplan and colleagues, purified plasma IgE is functional as a monomer, does not polymerize in the cold, thus refuting the hypothesis of IgE cryoprotein. 64 Overall, ColdU is an excellent experimental model disease for in vivo drug evaluations that can provide valuable mechanistic insights into wheal formation.…”

Section: Ta B L Ementioning

confidence: 99%

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Cold urticaria – What we know and what we do not know

Maltseva

Borzova

Fomina

et al. 2020

Allergy

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Cold urticaria (ColdU) is a common form of chronic inducible urticaria characterized by the development of wheals, angioedema or both in response to cold exposure. Recent research and guideline updates have advanced our understanding and management of ColdU. Today, its pathophysiology is thought to involve the cold‐induced formation of autoallergens and IgE to these autoallergens, which provoke a release of proinflammatory mediators from skin mast cells. The classification of ColdU includes typical and atypical subtypes. We know that cold‐induced wheals usually develop on rewarming and resolve within an hour and that anaphylaxis can occur. The diagnosis relies on the patient's history and cold stimulation testing. Additional diagnostic work‐up, including a search for underlying infections, should only be done if indicated by the patient's history. The management of ColdU includes cold avoidance, the regular use of nonsedating antihistamines and the off‐label use of omalizumab. However, many questions regarding ColdU remain unanswered. Here, we review what is known about ColdU, and we present important unanswered questions on the epidemiology, underlying pathomechanisms, clinical heterogeneity and treatment outcomes. Our aim is to guide future efforts that will close these knowledge gaps and advance the management of ColdU.

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Section: Ta B L Ementioning

confidence: 97%

Section: Aetiopathogenesismentioning

confidence: 99%

Section: Ta B L Ementioning

confidence: 99%

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Cold urticaria – What we know and what we do not know

Maltseva

Borzova

Fomina

et al. 2020

Allergy

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“…All models rely on the use of some chemical or physical method of inducing in¯ammation in the skin, followed by various methods of quantifying the in¯ammatory response. Examples of in¯ammatory stimuli include topical application of irritants such as capsaicin, 1,2 anthralin, 3 or arachidonic acid; 4 intradermal injection of in¯ammatory mediators such as histamine or C5a; 4± 10 injection of mast cell secretagogues such as compound 48/80, substance P, opioids, or allergens to which the subjects are sensitive; 4±7,11±13 inducing in¯ammation with injected bacterial lipopolysaccharide; 12 and mild physical injury with heat 14 or UV light. 15 The in¯ammatory responses are then measured using simple visual scoring, planimetry, skin thickness measurement, laser Doppler velocimetry for microcirculatory blood¯ow, or histological analysis.…”

Section: Introductionmentioning

confidence: 99%

Use of induced cutaneous immediate‐type hypersensitivity reactions to evaluate anti‐inflammatory effects of triamcinolone topical solution in three dogs

DeBoer¹,

Cooley

2000

Veterinary Dermatology

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The anti‐inflammatory effect of a triamcinolone topical solution (TTS) was evaluated by use of induced cutaneous immediate‐type hypersensitivity reactions in dogs. Healthy dogs (n = 3) were treated on one side of the lateral thorax with TTS, and on the contralateral side with vehicle solution. After 7 days of treatment, serial dilutions of inflammatory stimuli (histamine, compound 48/80, anticanine IgE, substance P, and morphine sulphate) were injected intradermally on both sides. Resulting immediate reactions were subjectively scored, their diameters were measured in millimetres, and microcirculatory blood flow at each site was measured using laser Doppler velocimetry. The magnitude of the differences between TTS and vehicle‐treated sides varied with the type of measurement and the stimulus used. With compound 48/80, anti‐IgE, substance P, and morphine sulphate‐injected sites, for at least one concentration, the reaction scores and sizes were notably less on the TTS‐treated sides. Punch skin biopsy specimens were obtained from selected sites 24 h after injection. A pathologist examined stained tissue sections and scored each section as to degree of late‐phase dermal cellular infiltrate. Dermal infiltrate scores were generally lower at the TTS‐treated sites; the composite score from all TTS‐treated sites was 30% lower than that from the vehicle‐treated sites. Observations suggest that TTS may be effective in decreasing some aspects of the inflammatory response in canine skin.

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“…There are two distinct forms of heat urticaria. The more common is the generalized form in which pruritic weals develop after a rise in body temperature due to overheating (Hopkins, Kesten & Hazel, 1938;Jorizzo & Smith, 1982;Soter, 1981). The other form is localized heat urticaria which is very rare.…”

mentioning

confidence: 99%

Localized heat urticaria associated with a decrease in serum complement factor B (C3 proactivator)

et al. 1984

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A case of localized heat urticaria is reported in a 51-year-old woman who within a few minutes of contact with warm water developed erythema and swelling sharply localized to the heated area. After a hot bath urticarial lesions appeared over large areas of her body, accompanied by a feeling of weakness, but no other systemic symptoms. After challenge with heat by immersing her left arm in water heated to 42 degrees C, a rapid decrease of her serum complement level of factor B was demonstrated, suggesting that activation of an alternative complement pathway plays a role in this form of urticaria. Biopsies for immunofluorescent study of complement and immunoglobulins were negative at 30 and 180 min after heat challenge. The dermal fibres and endothelial cells of dermal vessels were capable, in vitro, of complement binding before and after exposure to heat.

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Physical urticaria/angioedema as an experimental model of acute and chronic inflammation in human skin

Cited by 8 publications

References 37 publications

Cold urticaria – What we know and what we do not know

Cold urticaria – What we know and what we do not know

Use of induced cutaneous immediate‐type hypersensitivity reactions to evaluate anti‐inflammatory effects of triamcinolone topical solution in three dogs

Localized heat urticaria associated with a decrease in serum complement factor B (C3 proactivator)

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