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

In this review I have described the pathophysiology of allergic disorders of the gastrointestinal tract. Situations where the intestine cannot be a complete barrier to foreign allergens and antigens were discussed and etiological factors of gastrointestinal allergy were detailed. Clinical features of gastrointestinal allergy include diarrhea, vomiting, abdominal pain and colic, intestinal hemorrhage and malabsorption as well as symptoms and signs outside the gastrointestinal tract such as chronic rhinitis and asthma in the respiratory system, urticaria, angioedema and eczema as dermatological signs, headache, insomnia, hyperkinesis as central nervous system manifestations, failure to thrive and anaphylaxis as constitutional reactions. Milk allergy was discussed as an example of food allergy. Immunology of the gastrointestinal tract was presented, with examples of four types of hypersensitivity reactions, and gastrointestinal disturbances of immunodeficiency disorders and syndromes were named. Lastly, the autoimmune mechanism and the gut were described, with particular discussion of ulcerative colitis as an example of an autoimmune disease.
 ...
PMID:The intestine in allergic diseases. 78 84

IgE levels in faecal extracts (Copro-IgE levels) were investigated in food allergy (FA) patients before and after the challenge test administration of food allergens. IgE levels were measured by time-resolved fluoroimmunometric assay. In addition, the effects of administration of oral sodium cromoglycate (SCG) on the Copro-IgE levels were studied. Copro-IgE levels in patients with FA, who were placed on an elimination diet, did not differ from those of healthy children. After a challenge test immediate symptoms of urticaria and wheezing were observed in all FA patients. Copro-IgE levels in each patient increased markedly within 24 h of the challenge test. Moreover, FA patients treated orally with SCG showed neither the increase in Copro-IgE levels nor any remarkable symptoms after the challenge. Our results suggest that the increased Copro-IgE levels may be a specific consequence of the local immune response to food allergen stimulation in the gut mucosa.
 ...
PMID:IgE levels in faecal extracts of patients with food allergy. 128 67

Study was made of immune responses in cow's milk allergy by a new immunoassay that measures total Ig-secreting cells and specific antibody-secreting cells during their maturation cycle in peripheral blood. These primed gut-associated lymphoid tissue-derived lymphocytes are assumed to reflect the intestinal immune responses. During diagnostic milk provocation, 15 patients had acute urticarial skin eruptions, eight patients had slow onset of eczema, and 15 showed symptoms from the gastrointestinal tract. A significant increase in IgM-secreting cells (means with 95% confidence intervals) from 382.2 (265, 552) to 621.4 (381, 1013)/10(6) cells, p less than 0.01, but not IgA- and IgG-secreting cells was associated with acute urticaria. In patients with eczematous skin eruptions and gastrointestinal symptoms, the response involved all these Ig isotypes. The magnitude of the postchallenge Ig-secreting cell responses in patients with gastrointestinal symptoms in the IgM class [from 657.9 (428, 1012) to 3544.0 (1696, 7406)/10(6) cells, p less than 0.001] and the IgA class [from 974.6 (590, 1610) to 2482.4 (1528, 4028)/10(6) cells, p = 0.001] significantly exceeded that of the patients with cutaneous symptoms. Notwithstanding the distinct increase in the total number of Ig-secreting cells, the specific antibody-secreting cell response specifically directed against beta-lactoglobulin and alpha-casein was small and inconsistent. These findings indicate that immune exclusion of milk antigens is defective in cow's milk allergy. The quality and extent of the response varied in the three reaction types, suggesting that different immunopathogenic mechanisms are operative in cow's milk allergy.
 ...
PMID:Local immune response measured in blood lymphocytes reflects the clinical reactivity of children with cow's milk allergy. 228 53

Allergic symptoms occur commonly in subjects working closely with locusts and are associated with specific IgE antibody. Extracts of intact locusts (Schistocerca gregaria and Locusta migratoria) were used to identify specific IgE antibody, to define the major allergens of the locust and their sources, and to estimate aeroallergen concentration in the working environment. With questionnaire, skin prick tests, and specific IgE measurements, 35 individuals, working in a research center, were surveyed. Of the 15 currently exposed individuals, contact with locusts provoked asthma, rhinitis, and contact urticaria in five, rhinitis and urticaria in three, and rhinitis alone in one individual. Symptoms provoked by locusts and skin test reactions to locust extracts were associated with specific IgE antibody in the serum. The "immunoblot" technique demonstrated the presence of multiple allergens in the locust extracts of approximately 68, 66, 54, 43, 37, 29, and 18 K daltons molecular weight. Locust antigen was identified in the atmosphere by means of an immunochemical method involving elution of high-volume air-sampler filters exposed in the locust breeding room and analysis of eluate allergen content by RAST-inhibition assays. Logit transformation of RAST-inhibition lines demonstrated that the filter extract shared a common slope with the locust extract and with an extract of locust gut. This gut extract also shared a common slope with extracts of locust feces and peritrophic membrane. The major source of allergen appears to be the peritrophic membrane that is present in the gut and is excreted surrounding the feces.
 ...
PMID:Occupational allergy to locusts: an investigation of the sources of the allergen. 334 82

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.
 ...
PMID:Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity. 762 26

Chronic urticaria is a disease of unknown etiology. One type of the disease is accompanied by gastrointestinal complaints. The aim of the present study was to determine the prevalence of Helicobacter pylori (H. pylori) infection in patients with chronic urticaria, and measure the effectiveness of eradication of HP on the skin disease. Patients with chronic urticaria of other origin were excluded from the study. Forty patients out of 95 studied fulfilled the criteria of gastrointestinal urticaria. H. pylori was measured both by measuring H. pylori-specific IgG in the serum and by direct staining of biopsy specimen taken upon endoscopy prior to and after the treatment. Seventeen patients out of 40 with gastrointestinal urticaria were H. pylori positive which incidence (43%) is not higher than that of the age matched healthy population in Hungary. H. pylori positive patients were treated with amoxycillin (4 x 500 mg/die), bismuth subsalicilate (3 x 512 mg/die) and metronidazole (2 x 500 mg/die) for two weeks, respectively, and those remaining positive were treated by omeprazole (2 x 20 mg/die) and amoxycillin for additional two weeks. Eradication of HP infection was successful in all patients. Follow-up was conducted from 6-18 months for urticaria (frequency, duration) and antihistamine drug requirement. Chronic urticaria did not disappeared after the eradication of H. pylori, but there was a significant reduction both in frequency, duration of urticaria and the need for antihistamine therapy after eradication of H. pylori. It was concluded that H. pylorilinfection has no effect on the course of chronic urticaria. Reduction in frequency of urticaria symptoms and reduction of antihistamine requirement is partly due to the natural course of the disease and likely due to the altered bacterial flora of the gut following the combined antibiotic treatment.
 ...
PMID:[Connection between Helicobacter pylori infection and chronic gastrointestinal urticaria]. 892 50

Numerous undesirable reactions to alcoholic beverages, foods, drugs and other substances are characterized by allergy-like signs and symptoms and yet show unambiguously negative allergy test results. Such persons should be assessed for evidence of histamine intolerance caused by histamine overload and/or diamine oxidase deficiency. Diamine oxidase is the main histamine degrading enzyme with a predominantly gut activity. This would explain why nutritional allergies are often primarily suspected. The clinical evidence for histamine intolerance is based on chronic headache, diarrhoea, vomiting, flush, urticaria, asthma-like symptoms, rhinitis and others. Histamine restricted food, supported if necessary by H1 antihistamine blockade are simple but highly efficacious measures as shown by us in large patient groups. Intolerance to red wine probably is the most outstanding clinical characteristic and a directed question must be included into any allergy history in order to avoid missing a very major diagnostic spectrum with good therapeutic maneuverability.
 ...
PMID:[Pseudo-allergies are due to histamine intolerance]. 901 5

The myriad of systemic manifestations induced by food hypersensitivity responses is testament to the ability of localized exposure to foods in the gastrointestinal tract to result in symptoms in distal target organs. Cow's milk protein, for example, may induce hives (urticaria), atopic dermatitis, isolated gastrointestinal symptoms, or severe generalized anaphylaxis in different individuals or in the same person at different times. These diverse manifestations are the result of complex interactions among the causal food protein, gut, immune system, and target organs. The dynamic state of these interactions is demonstrated by the development of food tolerance in most subjects and by the ability to experience the development of new allergies in some subjects. This review explores the variety of clinical manifestations of food hypersensitivity disorders in the context of the question: What determines the local or systemic expression of food allergy in a given individual at a particular time? Evidence is provided for both systemic and local immune activation. The role of food-protein chemistry, absorption and processing of ingested allergen, immune responses (type, degree, and specificity), and target organ hyperreactivity are considered as determinants in the expression of food allergic disorders.
 ...
PMID:Determinants of systemic manifestations of food allergy. 1108 Jul 40

We report a case of a patient who suffered generalized urticaria, chest tightness, wheezing, nausea, vomiting, hypotension, and loss of consciousness. Two hours earlier she had taken Eulitop Retard following lunch. She had tolerated all the implicated food after the reaction. Allergy evaluation revealed intense positive responses to intradermal tests with bezafibrate active component and Eulitop Retard (skin tests in control subjects were negative). Specific IgE tests (RAST) to Eulitop Retard were negative. An IgE mechanism is suggested to be responsible for this adverse reaction on the basis of the positive skin tets. The delayed onset (two hours) of this anaphylactic shock is unusual. Although infrequent, it may be caused by the specific pharmacokinetic characteristics of this drug, which is a slow releasing agent, mainly absorbed in the gut. The drug was taken just after lunch, and this concomitant food ingestion could also have produced a delay in gastric drainage and a retarded drug absorption. An IgE-mediated accelerated type reaction could also explain this delay. Apparently the patient reacted after the first contact to the drug, and the absence of a sensitization period is not usual in this type of immune reponse. Finally, we recommend the performance of prick and intradermal skin tests prior to any systemic challenge when allergic reactions to fibric acid derivatives are suspected.
 ...
PMID:Bezafibrate-induced anaphylactic shock: unusual clinical presentation. 1143 73

Anisakis pathology is due mainly to two mechanisms: allergic reactions (from isolated urticaria and angioedema to life-threatening anaphylactic shock associated with gastrointestinal symptoms or 'gastroallergic anisakiasis'), and direct tissue damage, due to invasion of the gut wall, development of eosinophilic granuloma, or perforation (gastric or intestinal anisakiasis). Anisakiasis is a misdiagnosed and underestimated cause of acute abdomen: most patients undergo laparotomy, and virtually no cases are diagnosed before surgery. In some cases, diagnosis is obtained accidentally during other pathologic investigations. We report a case of acute abdomen due to terminal ileum involvement. Microscopic examination of the resected segment showed the presence of helminthic sections consistent with larvae of Anisakis spp. A history of raw fish ingestion was recorded. Histopathologic features are illustrated. A short but up-to-date review of the literature on diagnostic devices (particularly imaging and serology), clinical aspects and therapy is presented.
 ...
PMID:Intestinal localization of anisakiasis manifested as acute abdomen. 1292 20


1 2 3 4 Next >>