* A 56 year old man is referred to your allergy clinic with a 2 year history of daily urticaria and intermittent angioedema. He has not seen any benefit from standard dose antihistamines and has been placed on long term prednisolone to control his symptoms. In this document I will aim to cover the following issues pertaining to the Case history given above. 1. What is the mechanistic difference between allergic and non-allergic urticaria. 2. I will detail my approach to investigating the underlying cause of the daily urticaria and intermittent angioedema in this patient given the limited information. 3. I will provide a short discussion on why I have chosen to use an experimental treatment agent. 4. I will characterise the effectiveness of this agent and evidence to obtain continued funding of the treatment. Mechanistic difference between allergic and non-allergic urticaria. Urticaria is a dermal oedema resulting from vascular dilation and leakage of fluid into the skin in response to mediators released from skin mast cells namely histamine and proteases. The activation of mast cells is a complex process that can be initiated by various signals often through specific mast cell surface receptors (1). The mechanisms by which mast cells are activated and induce chronic urticaria is not fully understood, however they can separated into immunological and non-immunological (2). IgE mediated allergic urticaria is , also known as a Type 1 hypersensitivity and is initiated by antigen/allergen binding to mast cell surface bound IgE leading to cross linking on the surface of mast cells and basophilis thus causing degranulation with histamine release (3). Non allergic urticaria can be mediated by an auto immune response. Essentially auto-immune responses result from the binding of IgG autoantibodies to IgE and or to the IgE Fc receptors themselves on Mast Cells. These auto immune urticarias account for up to 50% of patients with Chronic Urticaria (2). Non immunological urticaria results from mast cell activation through membrane receptors involved in the innate immunity or direct toxicity. Immunological Urticaria results from activation of the mast cells through effectors of the adaptive immunity caused by antibodies or T Cells that are able to interact with membrane responses. Investigating the Underlying cause
Although rarely life threatening Chronic Urticaria causes both misery and embarrassment and has an impact on an individual’s Quality of Life comparable with that of severe coronary artery disease patients (4). Hence correct diagnosis and treatment is essential and life changing in many individuals. Many studies have shown that taking a detailed history is usually adequate to establish a diagnosis of chronic urticaria (5). This is further emphasised and supported in the EAACI and BSACI guidelines (4 & 6). The guidelines state that diagnosis is based primarily on the clinical history and further investigation may not be required (4&6). Hence a full history is essential, fully documenting the frequency of episodes, circumstances of the onset, timing, possible identified triggers, and patterns of reoccurrence and durations of attacks. These can be achieved from the patient by way of a symptom dairy, which is an important tool in the diagnosis. The history taking will also include site and duration of individual lesions and confirm if there is pain involved. Photographs can be particularly useful in confirming the nature of lesions (4). I would complete the history taking by using a comprehensive guide such as that displayed by Holgate et al p.250 (1) which details what should be included to confirm diagnosis and identify the relevance of common eliciting factors. Holgate et al (1) also suggest that Disease activity in spontaneous urticaria is measured using the daily score values for the number of wheals and intensity of puritis, this is known as the Urticaria Activity Score (UAS)....
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