Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The psychosomatic aspects of skin disease were studied both clinically and experimentally, from the standpoint of immunology. We found that emotional stress has a great influence on the immune system, as was manifested in skin disease. Skin test in allergic patients significantly improved with autogenic training and relaxation. For clarification of the effects of autogenic training and relaxation, various parameters were simultaneously assessed during the treatment. The serum levels of histamine and dopamine-beta-hydroxylase fluctuated, as determined by the microvibration test. The levels of IgE and findings on the PK test varied only slightly. Before the onset of urticaria, there were changes in the life-style and considerable stress in daily life as well as exposure to an allergen. Using mice subjected to stress, the functions of T cells and macrophages were evaluated. Stress appeared to have a definite influence on the functions of these cells, as related to the important role of the immune system and skin. Thus, the role of stress in clinical disease must always be given consideration.
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PMID:Psychosomatic aspects of skin diseases from the standpoint of immunology. 717 98

Neurogenic switching is proposed as a hypothesis for a mechanism by which a stimulus at one site can lead to inflammation at a distant site. Neurogenic inflammation occurs when substance P and other neuropeptides released from sensory neurons produce an inflammatory response, whereas immunogenic inflammation results from the binding of antigen to antibody or leukocyte receptors. There is a crossover mechanism between these two forms of inflammation. Neurogenic switching is proposed to result when a sensory impulse from a site of activation is rerouted via the central nervous system to a distant location to produce neurogenic inflammation at the second location. Neurogenic switching is a possible explanation for systemic anaphylaxis, in which inoculation of the skin or gut with antigen produces systemic symptoms involving the respiratory and circulatory systems, and an experimental model of anaphylaxis is consistent with this hypothesis. Food-allergy-iducing asthma, urticaria, arthritis, and fibromyalgia are other possible examples of neurogenic switching. Neurogenic switching provides a mechanism to explain how allergens, infectious agents, irritants, and possibly emotional stress can exacerbate conditions such as migraine, asthma, and arthritis. Because neurogenic inflammation is known to be triggered by chemical exposures, it may play a role in the sick building syndrome and the multiple chemical sensitivity syndrome. Thus neurogenic switching would explain how the respiratory irritants lead to symptoms at other sites in these disorders.
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PMID:Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity. 762 26

Cholinergic urticaria presents as wheals and erythroderma that develop in response to a variety of factors which stimulate muscarinic receptors, including exercise, heat, cold, sweat and emotional stress. We describe a 25-year-old man with ulcerative colitis who developed cholinergic urticaria diagnosed by a metacholine test. He had had seven previous attacks over 8 years, and the finding of elevated liver enzymes required admission to four different hospitals. The clinical picture was identical: urticaria, hepatosplenomegaly, lymphadenopathy and elevation of liver enzymes. The causative agent was never identified and recovery was complete, with or without antibiotic therapy. To the best of our knowledge, this is the first description of liver involvement in cholinergic urticaria noted in the English-language medical literature.
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PMID:Transient hepatocellular injury during attacks of cholinergic urticaria. 920 18

The possibility of a causal influence of emotional stress, especially of stressful life events, on the course of various skin diseases has long been postulated. Clinical wisdom and experience, as well as many anecdotal observations and uncontrolled case series, support this opinion. We reviewed the available evidence on the role of stressful life events in triggering or exacerbating skin diseases. The role of stressful events in vitiligo, lichen planus, acne, pemphigus and seborrhoeic dermatitis was either controversial or insufficiently explored. The role of stressful events in psoriasis, alopecia areata, atopic dermatitis and urticaria was apparently clearer. However, only a few studies met acceptable methodological standards for stress measurement. Also, few studies considered common potential confounding factors (e.g. age, duration of illness, familial factors), and no study controlled adequately for the influence of other crucial factors (e.g. discontinuation of treatment, seasonal effects). Adding that the large majority of studies were retrospective, it seems wise to conclude that only preliminary evidence has been published so far on the role of stressful life events in bringing on or worsening any dermatological disease. Further research is mandatory, either in the form of prospective studies or, more feasibly, of well-designed case-control studies with adequate statistical power. Future studies should also pay more attention to protective as well as vulnerability factors in stressful events. Further, it would be important to investigate other sources of psychological stress, such as chronic stress and everyday stress. Measuring stress appraisal, although difficult, would also be important.
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PMID:Stressful life events and skin diseases: disentangling evidence from myth. 1184 50

Tako-Tsubo's syndrome (apical ballooning or broken heart syndrome) is a reversible left ventricular dysfunction due to apical asynergy that occurs typically after sudden emotional stress in a subject without coronary disease. It is characterized by acute onset of chest pain or dyspnoea or both and is associated with electrocardiographic changes such as ST segment elevation and/or T wave inversion. Myocardial biomarkers may be normal or slightly elevated. Anaphylaxis is a severe, life-threatening, generalized hypersensitivity reaction, most often starting with urticaria and/or angioedema, that may involve cardiovascular and respiratory systems. Cardiovascular symptoms, including hypotension, cardiac arrhythmia and chest pain, are presumably linked to cardiac mast cell mediator release. We describe the case of a young woman who experienced a profound reversible cardiomyopathy with typical features of Tako-Tsubo's syndrome during an anaphylactic reaction.
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PMID:Tako-Tsubo-like syndrome during anaphylactic reaction. 1682 94

Emotional stress can affect, reveal or even exacerbate a number of skin disorders including psoriasis, atopic dermatitis, pruritus, alopecia areata, lichen planus, seborrheic dermatitis, rosacea or urticaria, although the direct pathophysiologic link between stress factors and cutaneous disease manifestation remains unclear. However, there is an increasing evidence that stress influences disease processes and contributes to the inflammation through modulating hypothalamic-pituitary-adrenal axis and releasing neuropeptides, neurotrophins, lymphokines and other chemical mediators from nerve endings and dermal cells. The central role in cellular skin reactivity to various stressors might be attributed to dermal mast cells, as they show close connections with sensory nerve endings and may release a huge number of proinflammatory mediators. However, many other cells also actively take part in skin response to stress. Although our knowledge is still not complete, one of the most distinct aspect is that the skin, endocrine, nervous and immune systems cannot longer be treated autonomously, but have to be considered as a large multidirectional complex of which interacting nature is still poorly understood.
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PMID:Stress and the skin. 2046 95

We report a rare case of exercise-induced anaphylaxis (EIA), occurring exclusively with exercise, without any other associated trigger, detected in the prodromal phase, and prevented from additional anaphylaxis episodes by treatment with cetirizine and 10 mg daily of antileukotriene montelukast to date. EIA is a syndrome in which patients experience a spectrum of the symptoms of anaphylaxis ranging from mild cutaneous signs to severe systemic manifestations such as hypotension, syncope, and even death after increased physical activity. Many people have triggers, such as, a variety of foods, various medications, alcohol, cold weather, humidity, and seasonal and hormonal changes along with exercise that cause the symptoms. Typically, either exercise or the specific trigger alone will rarely cause symptoms. It is differentiated from cholinergic urticaria by the absence of response to passive body warming and emotional stress.
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PMID:Exercise-induced anaphylaxis and antileukotriene montelukast. 2631 2

Chronic spontaneous urticaria (CSU) is often associated with organ specific autoimmunity but is rarely caused by food allergy. Colourings and preservatives in pre-packaged foods, so called pseudoallergens, have also been implicated. Factors that promote inflammation or reduce anti-inflammatory mechanisms may however, predispose susceptible individuals to CSU. Chronic underlying infection and mental and emotional stress can sometimes precede the onset of CSU and once established can exacerbate the symptoms. There is early evidence of dysbiosis within the gastrointestinal tract in people with CSU and reduced levels of vitamin D are also evident. The latter may be related to the importance of vitamin D3 in increasing T regulatory function which can control a tendency to autoimmunity. It is quite possible that a state of on-going chronic inflammation with reduced anti-oxidant mechanisms may underlie the not infrequent association between CSU and metabolic syndrome. Effective treatment of CSU should involve the use of anti-histamines, intermittent steroids and anti-IgE therapy. For recalcitrant disease immune modulatory therapy has a place. However, talking therapies that reduce stress and anxiety, vitamin D3 supplementation, correction of intestinal dysbiosis and treatment of any chronic infection should also be considered.
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PMID:Stress, pseudoallergens, autoimmunity, infection and inflammation in chronic spontaneous urticaria. 3152 63