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

Anaphylaxis is a life-threatening allergic reaction, and food is one of the most common responsible allergens in the outpatient setting. The prevalence of food-induced anaphylaxis has been steadily rising. Education regarding food allergen avoidance is crucial as most of the fatal reactions occurred in those with known food allergies. The lack of a consensus definition for anaphylaxis has made its diagnosis difficult. Symptoms affect multiple organ systems and include pruritus, urticaria, angioedema, vomiting, diarrhoea, abdominal cramps, respiratory difficulty, wheezing, hypotension, and shock. Prompt recognition of anaphylaxis is essential as delayed treatment has been associated with fatalities. Although epinephrine is accepted as the treatment of choice, timely administration does not always occur, partly due to a lack of awareness of the diagnostic criteria. Several novel tools are currently being investigated, which will potentially aid in the diagnosis and treatment of food-induced anaphylaxis.
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PMID:Food anaphylaxis. 1745 12

To understand the antiallergic effect of Artemisia princeps (AP), which has been found to show inhibitory activity against degranulation and a passive cutaneous anaphylaxis (PCA) reaction, eupatilin and jaceosidin, as the active components, were isolated by degranulation-inhibitory activity-guided fractionation, with their antiallergic activity investigated. These isolated components potently inhibited the release of beta-hexosaminidase from RBL-2H3 cells induced by the IgE-antigen complex, with IC(50) values of 3.4 and 4.5muM, respectively. Eupatilin and jaceosidin potently inhibited the PCA reaction and scratching behaviors induced by IgE- antigen complex and compound 48/80, respectively. Orally administered jaceosidin more potently inhibited the PCA reaction than that of eupatilin, although the PCA reaction-inhibitory activity of intraperitoneally administered jaceosidin was nearly the same as that of eupatilin. Eupatilin and jaceosidin inhibited the gene expressions of TNF-alpha and IL-4 in RBL-2H3 cells stimulated by IgE-antigen complex. Eupatilin and jaceosidin inhibited the activation of NF-kB. Based on these findings, eupatilin and jaceosidin may be useful for protection from the PCA and itching reactions, which are IgE-mediated representative skin allergic diseases.
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PMID:Inhibitory effect of eupatilin and jaceosidin isolated from Artemisia princeps in IgE-induced hypersensitivity. 1799 77

Real allergy to local anesthetic (LA) is very rare. This study was performed to report a case of anaphylaxis to multiple "caine." A 25-years-old atopic nurse developed a very severe anaphylactic reaction on her third infiltration for low back pain with bupivacaine, lidocaine, and methylprednisolone: she developed a vagal reaction, followed during the next 30 minutes by a pruriginous skin rash, followed by a tongue edema and a severe bronchospasm. Adrenalin was injected with a poor response. She was intubated and transferred to the intensive care unit for a few days and, finally, she recuperated completely. Skin-prick tests were done on two occasions. In the first session, no reactions were observed with triamcinolone and methylprednisolone at 1 mg/cc, but a rapid extending maculopapular erythema developed with a final diameter of 50 mm with lidocaine 0.1% (group 2) and 25 mm with procaine 2% (group 1): control 0 mm, histamine, 3 mm. She also complained of itchiness in the neck and shoulder, which resolved in the next 90 minutes. In the second session, a test with bupivacaine 0.0005% (group 2) gave a papule with a diameter of >5 mm, and a test with mepivacaine 0.001% (group 2) was negative: control, histamine, 3 mm; no subsequent tests with mepivacaine were done because she developed a cough and throat pruritus, voice modification, and a sensation of throat narrowing, that resolved with treatment. We reported a case of anaphylaxis to multiple LA (groups 1 and 2), possibly via an IgE-mediated mechanism.
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PMID:Allergy to multiple local anesthetics. 1803 81

In order to compare the relative efficacy of topical antihistamines with balanced saline solution (BSS) and benzalkonium chloride (BC) in the early phase of allergic conjunctivitis in an animal model of ocular anaphylaxis, 96 male guinea pigs were sensitized with intraperitoneal egg albumin (EA) and aluminum hydroxide. Seventy-six animals were used for determination of Evans blue (EB) extravasation and 20 for clinical evaluation of the allergic response (redness, edema, discharge and itch-scratch response). Eighteen days after sensitization the animals were topically challenged by conjunctival instillation of EA and treated 15 min before and 15 min after challenge with commercially available drugs (ketotifen, ketotifen single dose units [SDU], olopatadine, azelastine, spaglumic acid and emedastine) and controls (BSS and BC). The animals used for EB quantification were anesthetized and received an intravenous injection of EB simultaneously to the topical challenge. The ocular extravasation of the colorant was determined by 620 nm absorbance spectrophotometry. The animals used for clinical evaluation were observed for clinical signs of the allergic reaction. EB ocular extravasation was significantly lower in the eyes treated by spaglumic acid and emedastine. The clinical scoring was consistent with EB extravasation, though the difference was not statistically significant. Spaglumic acid and emedastine seem to be the most useful drugs to reduce EB extravasation and allergic signs in an animal model of early phase allergic conjunctivitis.
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PMID:Comparative efficacy of topical antihistamines in an animal model of early phase allergic conjunctivitis. 1837 29

"Allergy" is a term often used by patients to describe symptoms that arise after eating. The term "adverse reaction to food" is preferred unless the event has an immunologic basis. True food allergy, primarily mediated by immunoglobulin (Ig)E antibodies to food proteins, is present in 3% to 4% of US adults. Symptoms range from mild mouth itching ("oral allergy syndrome") to anaphylaxis. The diagnosis is established by history and appropriately performed skin testing or in vitro assays for specific IgE antibodies to the suspected food. Because food-allergic reactions can be fatal, it is important to identify and avoid the causative food. Food-allergic reactions are treated by prompt use of intramuscular epinephrine. Patients may be referred to an allergy/immunology specialist when the diagnosis is uncertain or if avoidance measures are not successful. Investigational therapies may ultimately be preventative or curative.
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PMID:Approach to patients with symptoms of food allergy. 1845 29

All chemotherapy agents can cause hypersensitivity reactions, which have limited the used of critical drugs in very sick patients for fear of inducing a more severe reaction and possibly death. The choice of an alternative chemotherapy regimen is often limited by tumor sensitivity and, because of the increasing number of cancer survivors, exposure to multiple courses of the same or similar chemotherapy agents. Increased exposures lead to sensitization and to hypersensitivity reactions in an increasing patient population. The need to offer first line therapy after cancer recurrence has spurred the clinical development of rapid desensitizations, which allow patients to be treated with medications to which they have presented hypersensitivity reactions. Desensitization protocols are available to treat hypersensitivity reactions to most chemotherapy agents including taxenes, platinums, doxorubicin, monoclonal antibodies and others, by gradual re-introduction of small amounts of drug antigens up to full therapeutic doses. Candidate patients include those who present mild to severe type I hypersensitivity, mast cell/IgE dependent, reactions during the chemotherapy infusion or shortly after. Symptoms include pruritus, flushing, urticaria, angioedema, respiratory and gastrointestinal distress, changes in blood pressure including hypotension, and shock with anaphylaxis. Associated musculoskeletal symptoms and pain can be present in patients reacting to taxenes as in anaphylactoid reactions, in which mast cell/IgE mechanisms cannot be demonstrated. There is now strong evidence that anaphylactoid reactions are amendable to treatment with the same rapid desensitization protocols as for type I hypersensitivity reactions. Initial rapid desensitizations should only be performed in settings with one on one nurse-patient care and where resuscitation personnel and resources are readily available. Temporary tolerization is achieved in a few hours. After the first desensitization, standard protocols are available for safe, repeated desensitizations in outpatient settings with similar conditions, which not only provides flexibility, but allows patients to remain in clinical studies. Breakthrough symptoms are less severe than the initial hypersensitivity reaction in all series reviewed, and deaths have not been reported. The aim of this review is to familiarize the medical community with the type of hypersensitivity reactions amendable to rapid desensitization and to review protocols for chemotherapy desensitization that can be used for most chemotherapy agents. Few studies have measured the cancer response to the chemotherapy agents delivered through rapid desensitizations. One patient population in which 26 patients were desensitized to carboplatin and 16 to paclitaxel had similar rates of remission as for non-desensitized patients. Education of nurses, pharmacists, oncology and allergy specialists will lead to the universal use of rapid desensitization protocols for all cancer patients with hypersensitivity reactions to chemotherapy agents. Basic research is needed to uncover the cellular and molecular mechanisms underlying the temporary tolerization induced by rapid desensitization, so that pharmacological interventions can improve its safety and efficacy.
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PMID:Rapid desensitization of hypersensitivity reactions to chemotherapy agents. 1869 Sep 34

Urticaria is a rash, that typically involves skin and mucosa, and is characterized by lesions known as hives or wheals. In some cases there is an involvement of deep dermis and subcutaneous tissue that causes a skin/mucosa manifestation called angioedema. Urticaria and angioedema are very often associated: urticaria-angioedema syndrome. The acute episodic form is the most prevalent in the pediatric population, and it is often a recurrent phenomenon (recurrent urticaria). Acute episodic urticaria it is usually triggered by viruses, allergic reactions to foods and drugs, contact with chemicals and irritants, or physical stimuli. In many instances it is not possible to identify a specific cause (idiopathic urticaria). Chronic urticaria is a condition that can be very disambling when severe. In children is caused by physical factors in 5-10% of cases. Other trigger factors are infections, foods, additives, aeroallergens and drugs. The causative factor for chronic urticaria is identified in about 20% of cases. About one-third of children with chronic urticaria have circulating functional autoantibodies against the high affinity IgE receptor or against IgE. (chronic urticaria with autoantibodies or "autoimmune" urticaria). It is not known why such antibodies are produced, or if the presence of these antibodies alter the course of the disease or influence the response to treatment. Urticaria and angioedema can be symptoms of systemic diseases (collagenopathies, endocrinopathies, tumors, hemolytic diseases, celiachia) or can be congenital (cold induced familiar urticaria, hereditary angioedema). The diagnosis is based on patient personal history and it is very important to spend time documenting this in detail. Different urticaria clinical features must guide the diagnostic work-up and there is no need to use the same blood tests for all cases of urticaria. The urticaria treatment includes identification of the triggering agent and its removal, reduction of aspecific factors that may contribute to the urticaria or can increase the itch, and use of anti-H1 antihistamines (and/or steroids for short periods if antihistamines are not effective). In some instances an anti-H2 antihistamine can be added to the anti-H1 antihistamines, even if the benefits of such practice are not clear. The antileucotriens can be beneficial in a small subgroup of patients with chronic urticaria. In case of chronic urticaria resistant to all the aforementioned treatments, cyclosporine and tacrolimus have been used with good success. When urticaria is associated to anaphylaxis, i.m epinephrine needs to be used, together with antihistamines and steroids (in addition to fluids and bronchodilatators if required).
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PMID:Urticaria and urticaria related skin condition/disease in children. 1870 Mar 29

Herbex-kid (HK), a polyherbal formulation was evaluated in various experimental allergic models of Type I hypersensitivity reactions. Compound 48/80 (C 48/80) has been shown to induce rat mesentery mast cell degranulation and HK (1.07, 10.75 and 107.5 mg ml(-1)) inhibited the mast cell degranulation in a dose dependent manner. HK (1.07, 10.75 and 107.5 mg kg(-1); p.o.) showed dose-dependent protection against C 48/80 induced systemic anaphylaxis in male Balb/C mice. In active anaphylaxis model, male Wistar rats orally administered with 10.75 and 107.5 mg kg(-1) of HK showed significant (P < 0.01) protection against mast cell degranulation, while in passive anaphylaxis model, only at 107.5 mg kg(-1) showed significant (P < 0.01) reduction in mast cell degranulation. HK at all dose levels was able to significantly decrease the time spent in nasal rubbing in Wistar rats sensitized to ovalbumin, while only at 107.5 mg kg(-1) it showed significant (P < 0.01) reduction in number of sneezes. In C 48/80-induced skin itch model, all dose levels of HK significantly (P < 0.001) decreased the time spent in itching and the number of itches. HK did not produce any significant inhibition in histamine induced contraction in guinea pig ileum. From the above findings we conclude that the HK possesses antiallergic activity mediated by reducing of the release mediators from mast cells and also by 5-HT antagonism without the involvement of histamine (H1) receptors.
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PMID:Herbex-kid Inhibits Immediate Hypersensitivity Reactions in Mice and Rats. 1883 Apr 58

Adverse Drug Reactions (ADRs) and drug allergies- as a subset of ADRs- make a significant public health concern, complicating 5 to 15% of therapeutic drug courses. They may result in diminished quality of life, increased physician visits, health care costs, hospitalizations, and even death. The incidence of serious ADRs in hospitalized patients was estimated to be 6.7% and for fatal ADRs to be 0.32%, so recognizing and taking action on ADRs is an important aspect of medication management. Allergic reactions to drugs refer to those ADRs that involve immune mechanisms which account up to 15% of ADRs and can be identified as being a type I through IV immune reaction that the most common immunologic mechanism is IgE-mediated- type I reaction. Clinical manifestations of allergic reactions range from pruritus and rash to serious reactions such as systemic anaphylaxis and cardiovascular emergencies and they are responsible for 2-3% of hospitalized patients. Health professionals should be aware of the ADRs presenting clinical features and the risk factors and should be able to differentiate between allergic and non-allergic adverse drug reactions. This will lead to increased opportunities to review drug selection and prescribing practices affecting patients' outcome. This article will review the definition and estimated incidence, the features, classification and types of ADRs and drug allergies and related patents. It will highlight the role of detecting, reporting, and assessing suspected ADRs and drug allergies in the most clinically relevant drugs group. Priorities in the evaluation and management of the conditions of patients who have experienced allergic and non-allergic drug reactions also will be discussed.
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PMID:Understanding adverse drug reactions and drug allergies: principles, diagnosis and treatment aspects. 1907 90

We report the case of a 17-year-old boy who experienced 4 episodes of exercise-induced anaphylactic reaction after ingestion of lentil and 2 episodes of anaphylaxis following ingestion of chickpea. His medical history revealed that he had allergic rhinitis with positive results after skin prick tests (SPT) with mites. His SPTs and specific immunoglobulin E antibody testing with lentil and chickpea were positive. Oral challenge with chickpea was not performed due to patient refusal. Treadmill exercise challenge tests in the fasting state and 1 hour after a meal not containing lentil were negative. However, an exercise challenge test 1 hour after intake of lentil soup resulted in pruritus of the hands, forearms, shoulders, and back, urticarial lesions on the face and shoulders, mild angioedema of the lips, and mild hoarseness and cough. To our knowledge, this is the first case of food-dependent exercise-induced anaphylaxis due to lentil.
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PMID:Food-dependent exercise-induced anaphylaxis to lentil and anaphylaxis to chickpea in a 17-year-old boy. 1912 39


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