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Query: UMLS:C0033774 (pruritus)
14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report two cases of anaphylactic reactions to peach with negative result of ImmunoCAP to peach. Case 1 is a 35-year-old man, who felt an itch in his oral cavity immediately after ingesting a whole fresh peach. He rapidly developed generalized urticaria, dyspnea, vomiting, and loss of consciousness. He recovered after treatment at a local hospital, thereafter he was referred to our hospital because ImmunoCAP conducted for screening allergens revealed a negative test result to peach and the cause of anaphylaxis remained unclear. He had a history of pollinosis. He reported that he previously felt an itch on his oral cavity after ingesting melon, watermelon, apple, and strawberry. Serum total IgE was 436 IU/ml. CAP-RAST revealed negative results to peach, strawberry and kiwi. Skin prick tests (SPTs) with raw peach pulp, canned peach pulp, strawberry and kiwi were positive. Case 2 is a 30-year-old woman who felt an itch on her oral cavity accompanied by blepharedema, rhinorrhea, generalized urticaria, nausea, abdominal pain and diarrhea after eating peach. She had a history of pollinosis. She reported that she previously developed urticaria after ingesting an apple. Serum total IgE was 85 IU/ml. ImmunoCAP revealed negative results to peach and apple. SPTs with canned yellow peach, strawberry and apple were positive. Consequently, the two patients were diagnosed with anaphylaxis due to peach, and allergic symptoms have never recurred since they avoided ingesting peach. Furthermore, in two patients ImmunoCAP to rPru p 1, rPru p 3, and rPru p 4 were negative. However, in IgE-immunoblotting of peach, serum IgE antibodies of two patients were bound to approximately 10 kDa proteins. Meanwhile, the cross-reactivity between Rosaceae fruits, such as peach, apple, apricot, and plum, has been reported. These results suggest that in patients, who are suspected of having peach anaphylaxis and show a negative ImmunoCAP result to peach, the additional testing, such as SPT with peach, should be performed for diagnosis.
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PMID:[Anaphylaxis due to peach with negative ImmunoCAP result to peach allergens, including rPru p 1, rPru p 3, AND rPru p 4: a report of two cases]. 1932 77

Anaphylaxis is currently classified as an immunologically triggered response with reactions that are IgE-mediated and reactions that are not IgE-mediated. This immunologically mediated phenomenon can result in various clinical manifestations, including decreased blood pressure, generalized skin inflammation, such as hives and pruritus, and respiratory symptoms, such as wheezing or bronchospasm. The severity of anaphylaxis can range from a mild allergic reaction to a potentially fatal anaphylactic shock. Numerous causative agents trigger anaphylactic reactions, and some of the best described include food and bee sting allergens. Monoclonal antibodies, which are increasingly used in the treatment of various malignancies, also can cause anaphylaxis. In this review, the mechanisms governing anaphylaxis along with treatment strategies are reviewed. Diagnostic aids for anaphylaxis are also discussed. Increased awareness of the mechanisms, symptoms, and treatment of anaphylaxis can aid caregivers to make informed decisions when new agents, such as monoclonal antibodies, are introduced into the clinic.
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PMID:Anaphylaxis: implications of monoclonal antibody use in oncology. 1938 61

Mast cell tryptase can be an indicator of type I hypersensitivity reaction and thus may serve as a surrogate marker of anaphylaxis. A 34-year-old white male patient presented with a history of systemic lupus erythematosus. Shortly after administration of cefazolin for dialysis, he developed pruritus and shortness of breath. He expired an hour later. Autopsy excluded anatomic causes of death. There was an elevated postmortem mast cell tryptase level, 29.2 ng/mL. For mast cell tryptase level to be useful, the patient must survive long enough after exposure to an allergen for mast cells to release this enzyme. A credible allergen must be identified. In this case such, mast cell tryptase could establish anaphylaxis as the cause of death. The case suggests that in a patient with autoimmune disease, it may be prudent to test for immune reaction to a drug before administering it a second time via pinprick or other method.
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PMID:Mast cell tryptase in a case of anaphylaxis due to repeat antibiotic exposure. 1951 97

The antiallergic effect of mangiferin isolated from the rhizome of Anemarrhena asphodeloides Bunge (family Liliaceae) was measured in vitro and in vivo. Orally and intraperitoneally administered mangiferin potently inhibited passive cutaneous anaphylaxis (PCA) reaction induced by IgE-antigen complex as well as pruritus induced by compound 48/80 in mice. Mangiferin also inhibited the expression of the proinflammatory cytokine TNF-alpha and the IgE-switching cytokine IL-4 as well as transcription factor NF-kappaB activation in RBL-2H3 cells stimulated by IgE-antigen complex. These findings suggest that mangiferin may improve PCA reaction and pruritus.
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PMID:Mangiferin inhibits passive cutaneous anaphylaxis reaction and pruritus in mice. 1953 81

Proteinase-activated receptor-2 (PAR2) may be an important regulator of skin mast cell function during cutaneous inflammation and hypersensitivity. However, little is known of the role of PAR2 in allergic pruritus, because mast cells, which are thought to be responsible for this symptom, can release a number of different pruritogens. In the present study, we investigated the effects of several agents on passive cutaneous anaphylaxis-induced scratching behavior in ICR mice. As a result, cetirizine and ketanserin produced dose-dependent inhibition of scratching behavior induced by passive cutaneous anaphylaxis. Combined cetirizine with ketanserin exhibited significant inhibitory effects for the number of passive cutaneous anaphylaxis-induced scratching behavior. Pretreatment of the experimental animals with PAR2-neutralizing antibody and protease inhibitor leupeptin significantly inhibited passive cutaneous anaphylaxis-induced scratching behavior. Furthermore, we found that topical application of tacrolimus significantly reduced the number of scratching behavior induced by passive cutaneous anaphylaxis in a dose-dependent manner. Combined cetirizine with tacrolimus also exhibited significant inhibitory effects for the number of passive cutaneous anaphylaxis-induced scratching behavior. Tacrolimus in doses of 3% and 10% significantly inhibited tryptase-induced scratching behavior. These results suggest that PAR2 may be involved in passive cutaneous anaphylaxis-induced scratching behavior and tacrolimus produces an anti-allergic pruritus effect in ICR mice.
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PMID:Participation of proteinase-activated receptor-2 in passive cutaneous anaphylaxis-induced scratching behavior and the inhibitory effect of tacrolimus. 1957 80

We are reporting a case of one patient who have experienced itching of palms and soles, thorax erythema, conjunctive injection immediately after oral administration of amoxicillin, and hypotension after 3 hours. In E.D. hypotension was monitored because he was a cardiopatic but it wasn't treated even if it was protracted. A positive result of immediate-reading intradermal test with amoxicillin at 2 mg/ml concentration was found confirming the diagnosis of allergic biphasic anaphylaxis to amoxicillin.
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PMID:A case of protracted hypotension as unique symptom of a biphasic anaphylaxis to amoxicillin. 1958 62

Mastocytosis denotes a wide range of disorders characterized by having abnormal growth and accumulation of mast cells. Mast cells contain histamine and other inflammatory mediators, which have diverse actions within the body, and play crucial roles in acquired and innate immunity. The diverse actions of these inflammatory mediators can lead to puzzling symptoms in individuals with mastocytosis. These symptoms can include flushing, pruritus, nausea, vomiting, abdominal pain, diarrhea, vascular instability, and headache. These clinical features generally divide into cutaneous and systemic manifestations, giving rise to the two divisions of mastocytosis: cutaneous mastocytosis (CM) and systemic mastocytosis. CM has a highly favorable clinical prognosis. Systemic mastocytosis has a range of severity, with the milder forms often remaining chronic conditions, while the severe forms have rapid complex courses with poor prognoses. Generally, treatment is aimed at avoiding mast cell degranulation, inhibiting the actions of the constitutive mediators released by mast cells and, in severe cases, cytoreductive and polychemotherapeutic agents. Behavioral intervention includes avoidance of triggers, such as heat, cold, pressure, exercise, sunlight, and strong emotions. Treatment for released histamine and other inflammatory mediators includes H1 antihistamines, H2 antihistamines, proton pump inhibitors, anti-leukotriene agents, and injectible epinephrine (for possible anaphylaxis). For severe cases, treatment includes cytoreductive agents (interferon alpha, glucocorticoids, and cladribine) and polychemotherapeutic agents (daunomycin, etoposide, and 6-mercaptopurine). For very specific and severe cases, tyrosine kinase inhibitors, imatinib and midostaurine, have shown promise.
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PMID:Contemporary challenges in mastocytosis. 1963 28

THE CHIEF POINTS PRESENTED IN THIS PAPER ARE: 1. Following the ingestion of buckwheat (plant or seed) varicolored guinea pigs, white swine and goats exhibited symptoms of photosensitization, the degree of sensitization being in the order given. 2. Rabbits, dogs, white mice and rats did not manifest symptoms of photosensitization. 3. The symptoms and reactions were: agitation, itching, scratching of the ears, weakness, urticaria with sloughing and symptoms similar to those in anaphylaxis. 4. Microscopic examinations showed the lack of marked pathologic change. The lesions, such as petechial hemorrhage of the lungs, brain, liver, stomach and kidneys, suggest that profound toxemia has been present. 5. Lesions were not found which appeared to be suggestive of malignant neoplasms. 6. Irradiation by a quartz mercury vapor lamp apparently develops a resistance to photosensitization, probably because of increased pigmentation induced by ultra-violet light. 7. From the nature of the physiologic and pathologic reactions produced under various filters and from a consideration of the percentages of transmission of solar energy in the visible spectrum, it would seem that the region of photosensitization lies between 580 millimicrons (yellow) and the red end of the spectrum. This conclusion, moreover, is substantiated by the fact that irradiation by a quartz mercury vapor lamp (which radiates no energy in the visible spectrum at a wave-length greater than 579 millimicrons) produces no symptoms or reactions. 8. Spectrophotometric determinations of alcoholic extracts of grass (non-toxic) and of buckwheat (toxic) show the presence of two additional bands in the absorption spectrum of buckwheat with maxima at about 540 and 600 millimicrons, respectively, together with the common absorption zones at 430 to 490 millimicrons and 630 to 690 millimicrons. 9. Spectrophotometric determinations of blood serums of sensitized animals show, besides the usual absorption bands peculiar to oxyhemoglobin (with maxima at 540 and 580 millimicrons respectively), two zones with maxima at 600 and 660 millimicrons respectively. 10. The fluorescence of chlorophyll per se, as suggested by previous investigators, is not, in all probability, the cause of the sensitization induced by buckwheat. 11. Hematoporphyrine is not the photodynamic substance in all probability. 12. Phylloporphyrine may be the photodynamic substance. In this regard, also, the possibility of cholehematin is not to be ruled out.
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PMID:PHOTOSENSITIZATION OF ANIMALS AFTER THE INGESTION OF BUCKWHEAT. 1986 46

The cause of pruritus can be as benign as dry skin or as serious as liver disease. A variety of other conditions may trigger itching in active people, including eczema, heat rash, Grover's disease, sunburn, cholinergic urticaria, exercise-induced anaphylaxis, contact and systemic allergic reactions, infections, parasites, and several systemic diseases. Most of these conditions can be effectively managed with treatments that range from avoidance of environmental irritants to the use of topical agents, antihistamines, systemic corticosteroids, or antibiotics.
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PMID:Itching in active patients: causes and cures. 2008 59

Most arthropod bites and stings cause limited swelling, itching, pain, and redness and can be managed by ice application and tetanus prophylaxis as necessary. Stings by bees, wasps, and stinging ants can cause anaphylaxis that may require treatment with epinephrine and antihistamines and respiratory and cardiac maintenance measures. Widow spider bite management is controversial, but interventions for systemic reactions include calcium gluconate, methocarbamol, diazepam, narcotics, and antivenom. Victims of brown spider bites may need hospitalization if lesions enlarge rapidly or there are signs of systemic poisoning. Those stung by a bark scorpion may require oxygen, an intravenous line, pulse oximetry, and cardiac monitoring.
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PMID:Managing arthropod bites and stings. 2008 33


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