Local heat urticaria/angioedema: Evidence for histamine release without complement activation

Findlay, Steven R.; Thueson, David O.; Fine, Douglas P.; Krueger, Gerald G.

doi:10.1016/0091-6749(81)90049-x

Cited by 35 publications

(25 citation statements)

References 24 publications

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“…It is now more than 50 years since the first demonstration of histamine in the plasma of a patient with cold urticaria . This observation has been repeated for CSU and many types of inducible urticaria including cold urticaria, heat‐induced urticaria, solar urticaria, symptomatic dermographism, cholinergic urticaria, delayed pressure urticaria, and aspirin‐induced urticaria . Increased levels of histamine in the tissues have also been demonstrated.…”

Section: Evidence Of Increased Mast Cell Mediatorsmentioning

confidence: 90%

The role and relevance of mast cells in urticaria

Church

Kolkhir

Metz

et al. 2018

Immunological Reviews

223

198

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This review presents evidence that the skin mast cell, in particular the MC subtype, is the primary effector cell in urticaria. Mast cells are located in the upper dermis, the ideal situation for wheal formation and sensory nerve stimulation. Increased numbers of mast cells are found in both lesional and non-lesional skin in CSU and inducible urticaria. Mast cell degranulation in the area of wheals has been demonstrated repeatedly by light and electron microscopy. Histamine, PGD and tryptase are found in the venous blood draining wheal formation. The last 2 are specific for mast cells rather than basophils. Mast cell reactivity is increased in active urticaria by local inflammatory cytokines and neuropeptides. Mast cell cytokines and neuropeptides, particularly nerve growth factor, induce a Th2 type inflammation that is particularly obvious at the sites of whealing. In conclusion, autoimmunity, either of Type 1 viz. IgE antibodies to local autoallergens, or Type 2b, viz. IgG autoantibodies to IgE or its receptor, are considered to be the most frequent causes of CSU. In both cases, the mast cell is likely to be the axial cell in producing the wheals.

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Section: Evidence Of Increased Mast Cell Mediatorsmentioning

confidence: 90%

The role and relevance of mast cells in urticaria

Church

Kolkhir

Metz

et al. 2018

Immunological Reviews

223

198

View full text Add to dashboard Cite

show abstract

“…No randomized clinical trials were found. A total of 44 articles reporting information on 60 patients were analysed …”

Section: Methodsmentioning

confidence: 99%

“…Moreover, in 44% of cases of HU cutaneous lesions were induced from contact with warm objects (such as plates or coffee mugs, clothes, blankets and hot water bottles). Swelling, pruritus or irritation of the palate or lips could be induced by hot foods and drinks in about one‐third of patients with immediate‐onset HU, but never in the delayed type . Weals occurred at any skin area exposed to the heating stimulus.…”

Section: Clinical Characteristics Of Subtypes Of Heat Urticariamentioning

confidence: 99%

Heat urticaria: a revision of published cases with an update on classification and management

et al. 2016

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Heat urticaria (HU) is a rare type of physical inducible urticaria, characterized by itchy erythema and well-demarcated weals appearing soon after heat exposure. Most cases occur in female patients aged 20-45 years. Both localized and generalized forms exist, depending on the limitation of the reaction to the skin area directly exposed to the physical stimulus or the involvement of distant sites, respectively. In most cases, HU is an immediate reaction, but delayed forms (mostly familial) have been described. HU is a long-lasting disease with overall duration at diagnosis of approximately 2 years. In about half of cases it is associated with systemic symptoms such as weakness, wheezing, headache, flushing, nausea, vomiting, diarrhoea, tachycardia, even dyspnoea or syncope. The main differential diagnosis includes cholinergic urticaria, exercise-induced anaphylaxis and solar urticaria. The diagnosis of HU is established by provocation testing, which is also helpful to evaluate the critical temperature threshold. The mean threshold temperature is about 44 °C. A heat desensitization programme can be an effective treatment. Nonsedating H1 antihistamines administered at licensed doses are the mainstay of symptomatic therapy in nearly 60% of patients, but full symptom relief is achieved in only a minority of them. Omalizumab has proven effective in recent case reports.

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“…There are at least two subclasses of histamine receptors, HI and H 2 • Both classes appear to be present on human skin blood vessels and are involved in the production of erythema and wealing ) PHANUPHAK et al (1980) ROSE (1941 BEAVEN (1976) KAPLAN et al (1975), BENTLEY-PHILLIPS et al (1976) MISCH et al (1982), DAVIS et al (1981) GRANT et al (1981, ATKINS and ZWEI- MAN (1981) KAPLAN and BEAVEN (1976), TING et al (1983 (ROBERTSON and GREAVES 1978). There are at least two subclasses of histamine receptors, HI and H 2 • Both classes appear to be present on human skin blood vessels and are involved in the production of erythema and wealing ) PHANUPHAK et al (1980) ROSE (1941 BEAVEN (1976) KAPLAN et al (1975), BENTLEY-PHILLIPS et al (1976) MISCH et al (1982), DAVIS et al (1981) GRANT et al (1981, ATKINS and ZWEI- MAN (1981) KAPLAN and BEAVEN (1976), TING et al (1983 (ROBERTSON and GREAVES 1978).…”

Section: B Histaminementioning

confidence: 99%

Pharmacology of the Skin II

1989

Handbook of Experimental Pharmacology

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PrefaceThe recent interest in the pharmacology of the skin and the treatment of its diseases has come about for two reasons. The first is a realisation that many aspects of pharmacology can be studied as easily in human skin as in animal models, where they may be more relevant to human physiology and disease. Examples of this are the action of various vasoactive agents and the isolation of mediators of inflammation after UV irradiation and antigen-induced dermatitis. The second reason is the fortuitous realisation that a pharmacological approach to the treatment of skin disease need not always await the full elucidation of aetiology and mechanism. For example, whilst the argument continued unresolved as to whether the pilo-sebaceous infection which constitutes acne was due to a blocked duct or to a simple increase in sebum production, 13-cis retinoic acid, was found quite by chance totally to ablate the disease; again, whilst cyclosporin, fresh from its triumphs in organ transplantation, has been found able to suppress the rash of psoriasis, it has resuscitated the debate on aetiology.We are therefore entering a new era in which the pharmacology and clinical pharmacology of skin are being studied as a fascinating new way of exploring questions of human physiology and pharmacology as well as for the development and study of new drugs, use of which will improve disease control and at the same time help to define pathological mechanisms.It was because of this burgeoning interest in pharmacology of skin and its diseases, that this book came about. Indeed it is long overdue and was planned several years ago; we console ourselves with the thought that the delay may have served to help define certain principles which were then only just emerging.The book is divided into two volumes which are independent but complementary; the first being an account of the general pharmacology of skin, the second volume being more concerned with disease and drugs. The first volume is divided into two parts, the one dealing with the pharmacology of skin systems and their control and the other with autocoids in normal and inflamed skin. This second volume has three parts; the first part deals with the methods of measurement which are becoming of increasing importance both in studying the pharmacological effects of drugs and the clinical pharmacology of skin; the second deals with toxicology in its widest sense -including metabolism and percutaneous absorption; and the third is an account both of specific drugs and the drugs used for specific diseases.

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Local heat urticaria/angioedema: Evidence for histamine release without complement activation

Cited by 35 publications

References 24 publications

The role and relevance of mast cells in urticaria

The role and relevance of mast cells in urticaria

Heat urticaria: a revision of published cases with an update on classification and management

Pharmacology of the Skin II

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