The grounds for an etiologic classification of the phenomena of specific sensitiveness

Coca, Arthur F.

doi:10.1016/s0021-8707(29)90085-x

Cited by 28 publications

(24 citation statements)

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“…The term "atopy" was introduced in 1923 by COCA and COOKE [1] and refers to a hereditary predisposition to development of immunoglobulin E (IgE) antibodies to common environmental allergens, as expressed in atopic dermatitis (AD), allergic asthma (AA) and rhinitis. AD is a chronic inflammatory skin disease characterized by skin hyperreactivity, which is frequently (29-35%) associated with AA [2,3].…”

mentioning

confidence: 99%

Bronchial and skin reactivity in asthmatic patients with and without atopic dermatitis

Brinkman¹,

Raaijmakers²,

Bruijnzeel-Koomen³

et al. 1997

Eur Respir J

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It is unclear whether the presence and severity of atopic dermatitis (AD) is predictive for the occurrence and severity of early and late asthmatic responses to inhaled allergens. The aim of this study was to compare the bronchial effects of allergen inhalation challenge in allergic asthma (AA) and atopic dermatitis.We therefore studied these responses in: nine patients with mild-to-moderate AA without AD; eight patients with mild-to-moderate AA and mild AD; eight patients with severe AD and mild AA; and eight patients with severe AD without AA. Allergen challenge was performed by inhaling doubling doses until the dose provoking a 20% fall in forced expiratory volume in one second (PC20) was reached. The late asthmatic reaction (LAR) was defined as a fall of >20% in peak expiratory flow (PEF) between 3 and 8 h after the challenge.All but four of the patients with severe AD without AA developed an early asthmatic response (EAR). A LAR was seen in all patients with severe AD and mild AA, in four patients with mild AD and mild-to-moderate AA, and in three patients with mild-to-moderate AA without AD. The LAR was most pronounced in patients with a combination of mild AA and severe AD. This could be explained, in part, by a decreased skin sensitivity in these patients, which made the Cockcroft formula for prediction of PC20 allergen less accurate in such patients.We conclude that patients with severe atopic dermatitis and mild asthma are at risk for developing pronounced late asthmatic responses after allergen exposure. This suggests that eosinophils activated in atopic dermatitis also predispose to airway inflammation.

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confidence: 99%

Bronchial and skin reactivity in asthmatic patients with and without atopic dermatitis

Brinkman¹,

Raaijmakers²,

Bruijnzeel-Koomen³

et al. 1997

Eur Respir J

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“…Atopy was a term introduced by Coca & Cooke (1923) to describe the syndrome of common allergic diseases-hay fever, asthma, atopic eczema and urticaria-which had a genetic basis. The conundrum exists to this day as to why this complex immune system, involving B cells producing predominantly the IgE class of antibodies and a regulatory T cell system, basophils, mast cells and eosinophils, should be maintained when it apparently turns harmless environmental antigens into allergens detrimental to the health of the host.…”

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confidence: 99%

Atopy—A favourable prognostic factor for survival in Hodgkin's disease

Amlot¹,

Slaney²,

Brown³

1983

Br J Cancer

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“…Other types of mediators, such as immunoglobulin (Ig) E and atopia, have been investigated in IBS and linked to mast cells [27,28]. Degranulation of mast cells and, subsequently, the release of mast cell mediators can also be induced by IgE [28].…”

Section: Inflammation In Ibsmentioning

confidence: 99%

Inflammation as a Potential Therapeutic Target in IBS

Chira¹,

Chira²,

Dumitraşcu³

2016

Irritable Bowel Syndrome - Novel Concepts for Research and Treatment

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The pathogenesis of irritable bowel syndrome (IBS) has been intensively researched, and despite a long journey for unraveling all the structures and the pathways involved, it still remains partially obscure. Inflammation was the first to be hypothesized as a potential pathway for the pathogenesis of IBS. It remains a keystone in the complex machinery of the pathogenesis that is currently considered multifactorial. Elucidating the pathogenesis of IBS is crucial for a targeted therapy of the disease. In this chapter, we review information regarding gut inflammation in IBS, underlining some of the newest data or the cornerstones. Additionally, our aim was also to review treatment currently available and future perspectives regarding anti-inflammatory treatments for IBS. Newer techniques allow detection and research of mediators involved in inflammation, as well as their potential role to be targeted by pharmacological agents. Recent data supports not only further research of the newer agents that are currently being developed but also some of the available ones that do not have sufficient evidence. Emerging therapies that target inflammation are under evaluation, in trials. A multidrug or a multidisciplinary approach needs to be considered in some cases that fail to respond to current treatment.

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The grounds for an etiologic classification of the phenomena of specific sensitiveness

Cited by 28 publications

References 0 publications

Bronchial and skin reactivity in asthmatic patients with and without atopic dermatitis

Bronchial and skin reactivity in asthmatic patients with and without atopic dermatitis

Atopy—A favourable prognostic factor for survival in Hodgkin's disease

Inflammation as a Potential Therapeutic Target in IBS

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