Zur Pathogenese der cholinergischen Urticaria

Illig, L; Heinicke, A.

doi:10.1007/bf00509213

Cited by 32 publications

(5 citation statements)

References 8 publications

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“…During both situations tem perature values remained practically unchanged. In these two special cases, therefore, we sug gest a non-thermal stimulation of the neuroglan dular junction of the eccrine sweat glands which, according to lllig & Heinicke (10). is a real "con ditio sine qua non" for the provocation of any cholinergic rash.…”

Section: Discussionmentioning

confidence: 71%

“…Nothing can be stated, however, about the boundary between the physical and chemical components ofthe trigger mechanism. In cold contact urticaria (localized type) an immune mechanism with a positive Prausnitz-Kustner reac tion has already been proved but unfortunately in these experiments the two different types of cold urticaria were not exactly differentiated (9,10). A similar immune mechanism in the generalized type of cold urticaria must therefore still be shown.…”

Section: Acta Dnmlltovener (Stocklrolm) 60mentioning

confidence: 83%

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Experimental investigations on the trigger mechanism of the generalized type of heat and cold urticaria by means of a climatic chamber

Illig¹,

Paul²,

Brück³

et al. 1980

Acta Derm Venereol

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The physical conditions of challenge were investigated in a climatic chamber on 8 patients with cholinergic urticaria and 10 patients with generalized cold urticaria. The cholinergic urticaria was induced by passive or active (physical exercise) heating and psychological stimulation; the generalized cold urticaria was induced by general cooling at rest and during physical effort. The ambient temperature was varied, and the mean body temperature was recorded continuously at different measuring points. The experiments revealed that in both types of urticaria the physical trigger mechanism seems to be strictly related to thermoregulatory processes; the crucial point is neither the actual temperature of the skin surface, the average skin temperature, nor even the "core" temperature, but a rise or fall in the weighted average body temperature. In cholinergic urticaria it was not relevant whether skin lesions were provoked by passive heating of the body at rest (sauna-like conditions) or by active heating at low ambient temperature. A basically different challenge mechanism must be assumed therefore in the generalized type of heat and cold urticaria, in contrast to their localized contact types.

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Section: Discussionmentioning

confidence: 71%

Section: Acta Dnmlltovener (Stocklrolm) 60mentioning

confidence: 83%

Experimental investigations on the trigger mechanism of the generalized type of heat and cold urticaria by means of a climatic chamber

Illig¹,

Paul²,

Brück³

et al. 1980

Acta Derm Venereol

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“…An increase of specific muscarinic receptors in a lesion of cholinergic urticaria has been demonstrated in one patient (SHELLEY et al 1983). This may occur in cholinergic urticaria, either by a direct effect or mediated by an immune mechanism, possibly IgE, as passive transfer has been demonstrated in cholinergic urticaria (ILLIG and HEINICKE 1967). Cholinergic impulses can cause mast cell degranulation (CHO and OGLE 1979).…”

Section: K Acetylcholinementioning

confidence: 98%

“…Though most of the attention has focused on IgE-mediated mast cell histamine release, there is little evidence of an immunological process in most cases of idiopathic urticaria (CHAMPION et al 1969). In some physical urticarias there is evidence of a passive transfer factor in the serum, which when characterised appears to be IgE-like: in dermographism (AOYOMA 1971;NEWCOMB and NELSON 1973); in cold urticaria (HOUSER et al 1970;KAPLAN et al 1975;AKIYAMA et al 1981); in cholinergic urticaria (ILLIG and HEINICKE 1967). In some physical urticarias there is evidence of a passive transfer factor in the serum, which when characterised appears to be IgE-like: in dermographism (AOYOMA 1971;NEWCOMB and NELSON 1973); in cold urticaria (HOUSER et al 1970;KAPLAN et al 1975;AKIYAMA et al 1981); in cholinergic urticaria (ILLIG and HEINICKE 1967).…”

Section: Mast Cell Releasementioning

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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“…The effects of treatment with antibiotics 11 , such as doxycycline 29 , can be beneficial for patients with CU even with complete remission of symptoms, as shown by several case reports [30][31][32][33][34] . A retrospective analysis using 200 mg/day of doxycycline for 7 to 28 days showed complete remission in 19% of patients and partial remission in 15% after treatment.Response assessment before and after antibiotic therapy was conducted after the discontinuation of antihistamines for at least 48 h. This response was not associated with disease duration or severity, patient age, or treatment period 29 .…”

Section: Treatmentmentioning

confidence: 99%

Cold urticaria and your risk of anaphylaxis

Belluco¹,

Sifuentes²,

Ferreira³

2021

Rev Cienc Saude

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Cold urticaria (CU) is characterized by the appearance of wheals or angioedema after exposure to cold. It presents with mild to severe symptoms and can even lead to anaphylaxis. The risk of systemic reactions is high. We discuss this important pathology and show its strong relationship with anaphylaxis. Cold weather is one of the most common triggers for the onset of symptoms, with variables including humidity and thermal sensation. It is divided into acquired or familial forms. The diagnosis is made in patients with a medical history suggestive of the disease and should be confirmed with a stimulation test. The central aspect of treatment is to avoid cold stimuli. The prescription of self-injectable epinephrine for groups that are at high risk of systemic reactions is ideal. In conclusion, health professionals should be aware of CU in order to recognize the risk of anaphylaxis in these patients.

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Zur Pathogenese der cholinergischen Urticaria

Cited by 32 publications

References 8 publications

Experimental investigations on the trigger mechanism of the generalized type of heat and cold urticaria by means of a climatic chamber

Experimental investigations on the trigger mechanism of the generalized type of heat and cold urticaria by means of a climatic chamber

Pharmacology of the Skin II

Cold urticaria and your risk of anaphylaxis

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