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At least 307 records · Page 17Linked to original sources
PubMed1998

Inhibition of immediate type allergic reactions by the aqueous extract of Kum-Hwang-San.

We studied the effect of aqueous extract of Kum-Hwang-San (KHS) on mast cell-mediated immediate type allergic reactions. KHS (1-100 microg/site) inhibited concentration-dependently mast cell-dependent ear swelling response induced by compound 48/80 (200 microg/site) in mice by both topical and intradermal application. KHS (0.1-100 microg/site) inhibited concentration-dependently passive cutaneous anaphylaxis induced by anti-dinitrophenyl (DNP) IgE in rats by both topical and intradermal application. KHS also inhibited concentration-dependently the histamine release from the rat peritoneal mast cells (RPMC) by compound 48/80 and anti-DNP IgE. Moreover, KHS had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha (TNF-alpha) secretion from RPMC. These results indicate that KHS inhibits immediate type allergic reactions by inhibition of histamine release and TNF-alpha secretion from mast cells in vivo and in vitro.

Animals↗
PubMedDate not supplied

Allergic reaction to latex: a risk factor for unsuspected anaphylaxis.

Allergic reactions to latex, including anaphylaxis may be a problem in certain individuals exposed to latex. Four atopic patients with symptoms of rhinitis, asthma, anaphylaxis, and/or urticaria upon contact with latex products were studied. The patients showed IgE binding to latex RAST disks ranging from 1.0 to 27.3 times the negative control. Latex products (gloves, balloons, and condoms) directly bound IgE from all four patients. Eluted proteins from the latex products inhibited IgE binding to commercial latex RAST disks. SDS-PAGE demonstrated multiple latex protein bands by Coomassie Blue staining between 14 and 66 kD. Immunoblotting showed specific IgE binding to latex proteins at 30 and 66 kD. These results indicate that latex-allergic patients have IgE directed against specific latex proteins. Allergy to latex can pose a substantial health risk to susceptible individuals.

Adult↗
PubMed1996

[Allergic reactions to local anesthetics].

In this article type I and type IV allergic reactions evoked by local anaesthetics are discussed. Contact dermatitis (type IV) reactions are mainly caused by local anaesthetics of the ester-type like procaine. Both contact dermatitis and anaphylactic reactions (type I) can be caused by anaesthetics of the amide-type (e.g. lidocaine), but these reactions are rare. Intra- and epicutaneous tests can be useful to prove allergy, but sometimes provocation tests are necessary. Many reactions are not caused by an allergic mechanism.

Anaphylaxis↗
PubMed1981

Effect in man of anti-allergic drugs on the immediate and late phase cutaneous allergic reactions induced by anti-IgE.

Wheal and flare reactions as well as a late cutaneous allergic reaction (LCAR) were induced by anti-human IgE in healthy subjects. The effect of the beta 2-adrenoceptor stimulant terbutaline, the histamine-1 (H1) receptor blocking agent mepyramine and the synthetic glucocorticoid betamethasone on these reactions was studied. All administrations were given intradermally (i.d.). The immediate reaction to anti-IgE was inhibited by 3 micrograms terbutaline and 30 micrograms mepyramine (P less than 0.01) whereas 50 micrograms betamethasone had no effects. Terbutaline had no effect on the flare response induced by i.d. injected histamine but a slight effect on whealing. Terbutaline and mepyramine weakly reduced the LCAR throughout the observation period of 24 h (P less than 0.01). In contrast, betamethasone almost completely abolished the LCAR. It is concluded that the two phases of the skin reaction to anti-IgE are interrelated since an inhibition of the early phase was followed by an attenuation of the LCAR. The mechanism of action of steroids seems to differ fundamentally from that of other anti-allergic drugs since inhibition of the early step in the reaction is not essential to the action on the late step. It is further suggested that terbutaline inhibits anti-IgE-mediated cutaneous reactions by inhibition of the mast cell release reaction.

Adolescent↗
PubMed2006

Allergic reactions due to mizolastine.

BACKGROUND: An IgE-mediated allergic reaction to an antihistamine sounds like a paradox and is rare. OBJECTIVE: To describe 2 patients with anaphylaxis caused by mizolastine. In one patient, differential diagnosis from food allergy was necessary, whereas in the other patient, the history was clear. METHODS: History and in vivo skin testing were used for diagnosis. A challenge test to mizolastine was also proposed, but both patients refused to give consent. RESULTS: Skin test results were positive to mizolastine, whereas tests to the inert ingredients of the mizolastine tablets and to other H1 and H2 blockers had negative results. CONCLUSIONS: In vivo tests are highly sensitive, and they confirmed the diagnosis of the uncommon antihistamine allergy.

Adult↗
PubMed2001

Characterization of Ascaris-induced biphasic skin allergic reaction model in mice: possible roles of mast cells in early-phase and CD4-positive T cells in late-phase reactions.

We established an Ascaris-induced biphasic skin allergic reaction in mice. In the early-phase reaction (EPR), mast cell degranulation was observed, and tranilast inhibited ear edema. In mast-cell-deficient mice (WBB6F(1)-W/W(V) mice), ear edema in the EPR disappeared, whereas that in the late-phase reaction (LPR) remained. Eosinophils increased, and CD4-positive T cells tended to increase in the LPR. Anti-CD4 antibody, anti-IL-4 antibody and anti-IL-5 antibody all inhibited ear edema and had a tendency to inhibit eosinophil infiltration in the LPR. These data suggest that the EPR is induced by histamine released from mast cells, whereas the LPR is induced by IL-4 and IL-5 produced from CD4-positive T cells.

Animals↗
PubMed1987

Allergen-induced nasal hyperreactivity appears unrelated to the size of the nasal and dermal immediate allergic reaction.

It has been previously demonstrated in nasal challenge studies that there is an increased sensitivity to allergen following an initial allergen challenge. A similar feature has been demonstrated following natural allergen exposure in patients with seasonal allergic rhinitis. To further explore the characteristics of this "priming" phenomenon and its relationship to other expressions of their allergic airway disease, 28 hay fever patients with strictly seasonal disease were studied. Skin tests with the relevant pollen allergen and histamine were performed and the size of the immediate and late phase allergic reaction was determined. An initial nasal allergen challenge was followed by a rechallenge of the nose with allergen 24 h later using a lavage technique. Determinations of TAME-esterase activity, as a biochemical marker of the allergic reaction, were made in the returned lavage fluid. The number of sneezes was counted and nasal symptoms were also assessed using a scoring technique. 19 of 28 patients (67%), displayed an increased responsiveness at rechallenge with similar findings in terms of symptom scores and TAME-esterase measurements. The increase was statistically significant for the symptoms of nasal blockage, which increased from 0.7 +/- 0.1 (mean +/- SEM) to 1.1 +/- 0.2 (P less than 0.05), and nasal secretion which rose from 1.1 +/- 0.2 to 1.7 +/- 0.2 (P less than 0.01). A composite nasal symptom score which also took account of the number of sneezes, increased from 2.9 +/- 0.4 to 4.0 +/- 0.3 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Mechanisms and management of allergic reactions in the surgical patient.

The use of anesthetic agents, drugs and chemicals during anesthesia induces a certain number of anaphylactoic or anaphylactoid reactions. The incidence of anaphylaxis during general anesthesia, according to a recent study, is 1:4500. Despite appropriate treatment, mortality is about 6%. Different mechanisms are involved in mortality. Multiple risk factors have been identified in at-risk patients. With adequate understanding of the pathophysiological events that occur during anaphylaxis, anesthetists may avoid the occurrence of allergic reaction or be better prepared to manage these serious situations that may become fatal. This article covers different areas associated with anaphylactic and anaphylactoid reactions. Focus is placed on the different mechanisms of allergic reaction, and special attention is given to the clinical aspects of this complication. Treatment of these reactions as well as steps in prevention perioperatively are highlighted.

Anaphylaxis↗
PubMedDate not supplied

Acute myocardial infarction in a patient with normal coronary arteries after an allergic reaction.

The case is described of a man aged 51 years who, one hour after a coronary angiographic examination that showed coronary arteries without lesions, suffered an acute inferior myocardial infarction as the result of an acute allergic reaction, probably to the iodinated contrast agent that was used. Acute myocardial infarction following an allergy is an extremely rare clinical entity that, according to existing data, is due to the local release of vasoconstrictive substances as a result of the allergic reaction.

Angina Pectoris↗
PubMed1989

Allergic reaction to antipyrine, a marker of hepatic enzyme activity.

Antipyrine is a pyrazole derivative used extensively as a marker for hepatic drug metabolizing enzyme activity. A subject participating in a clinical trial employing antipyrine experienced an acute allergic reaction to the drug which was characterized by diaphoresis, flushing, swelling of the throat, difficulty in breathing, vomiting, swelling of the upper lip, and a diffuse urticarial rash. Intravenous administration of diphenhydramine markedly improved the symptomatology. Clinical investigators as well as study participants should be alerted to the potential for antipyrine to cause an acute allergic reaction.

Acute Disease↗
PubMed1998

Specific inhibition of immunoglobulin E-mediated allergic reaction using antisense Fc epsilon RI alpha oligodeoxynucleotides.

We have investigated the ability of an antisense immunoglobulin E (IgE) receptor alpha-subunit oligodeoxynucleotide (Fc epsilon RI alpha ODN) specifically to inhibit IgE-mediated allergic reactions in the mouse. Synthetic antisense Fc epsilon RI alpha ODN dose-dependently inhibited passive cutaneous anaphylaxis and histamine release from the mouse peritoneal mast cells (MPMC) activated by anti-dinitrophenyl (DNP) IgE. Northern blot analysis showed that the mast cells treated with antisense Fc epsilon RI alpha ODN exhibited no detectable levels of L-histidine decarboxylase mRNA after anti-DNP IgE stimulation, whereas the cells treated with sense Fc epsilon RI alpha ODN possessed significant amounts of this mRNA. Examination of the elevation of cAMP levels in MPMC following the activation with anti-DNP IgE demonstrated a significant rise in activated cells, but not in the antisense Fc epsilon RI alpha ODN-treated cells. Moreover, antisense Fc epsilon RI alpha ODN had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-alpha production. Our results demonstrated that antisense Fc epsilon RI alpha ODN inhibited the IgE-mediated allergic reaction in vivo and in vitro.

Animals↗
PubMed2005

[Anaphylactic shock due to French galette. Type I allergic reaction to buckwheat].

A 37-year-old woman twice developed a life-threatening anaphylactic reaction after eating galettes, a special French pancake from Brittany. She had tolerated ordinary pancakes and crepes for many years. The allergological work-up revealed a Type I allergic reaction to buckwheat contained in the galettes. A prick test to buckwheat was positive and specific IgE antibodies to buckwheat were found in her serum. In contrast to wheat, buckwheat is not a cereal but a gluten-free knot-grass, initially from Asia. Whenever a patient suffers from allergic reactions due to pastries, a buckwheat allergy should be considered.

Adult↗
PubMed2000

Exposure to diesel exhaust aggravates nasal allergic reaction in guinea pigs.

Diesel exhaust particulates (DEP) () and exposure to diesel exhaust (DE) induce nasal mucosal hyperresponsiveness to histamine. Therefore, in the present study, we investigated whether or not exposing guinea pigs to DE aggravates the nasal allergic reaction induced by repeated nasal administration of ovalbumin (OVA). Guinea pigs were exposed to filtered air or to DE (DE containing 0.3 or 1.0 mg/m(3) of DEP) for 5 wk. During exposure to filtered air or to DE, guinea pigs were administered 1% of OVA in saline into the nasal cavities once a week. Sneezes were counted and nasal secretions were measured as indices of sneezing responses and rhinorrhea for 20 min after OVA administration. Titers of specific anti-OVA-IgG and anti-OVA-IgE and the number of eosinophils infiltrated into both nasal epithelium and subepithelium were measured at the end of the exposure to DE. Exposure to DE enhanced the number of sneezes and the amount of nasal secretions induced by OVA. Titers of specific anti-OVA-IgG and anti-OVA-IgE also significantly increased in DE-exposed animals. Exposure to DE also augmented the number of eosinophils that infiltrated both the nasal epithelium and the subepithelium induced by OVA. These results suggest that exposure to DE enhances the nasal allergic reaction induced by repeated antigen administration in guinea pigs.

Animals↗
PubMed2006

Gene-gene interactions of IL13 and IL4RA variants in immediate allergic reactions to betalactam antibiotics.

OBJECTIVES: Immediate reactions - particularly anaphylactic ones - to betalactams are the most common adverse reactions to antibiotics mediated by a specific immunologic mechanism. The genetic risk factors influencing these mechanisms are poorly known. We aimed to evaluate the association between immediate allergic reactions to betalactams and the polymorphisms of IL13 (R130Q and -1055C>T variants) and IL4RA (I50V, S478P, and Q551R variants). METHODS: We determined these gene variants in 210 patients and 265 age-paired and gender-paired control subjects from Italy. RESULTS: The combination of the less frequent allele of the IL13 R130Q polymorphism with any of the predominant homozygous genotypes of the three polymorphisms of IL4RA was more significantly associated with the risk of betalactam allergy (P=0.0006, 0.0077, and 0.0041, respectively) than any polymorphism considered alone (P=0.1745, 0.0268, 0.1812, 0.0152, respectively). The same associations were observed with serum IgE levels (IL13/IL4RA variant combinations: P=0.0009, 0.0007, 0.0020, respectively and each variant: P=0.0201, 0.0021, 0.0531, and 0.0417, respectively). The combination of IL4RA variants with -1055 C>T polymorphism produced similar associations. CONCLUSION: Our data suggest that these combinations of IL13 and IL4RA variants are predictors of immediate allergic reactions to betalactams through a mechanism related to IgE production.

Adult↗
PubMed2004

The diagnostic interpretation of basophil activation test in immediate allergic reactions to betalactams.

BACKGROUND: Basophil activation by allergens, including drugs, has been used to determine sensitivity and to study IgE recognition and cross-reactivity. OBJECTIVE: We sought to determine the sensitivity and specificity of a basophil activation test (Basotest) in patients with immediate allergic reactions to betalactams, with a later comparison between patients who were selective (those recognizing the culprit drug excluding benzylpenicillin (BP)) and cross-reactors (those recognizing several penicillin determinants including BP). METHODS: Basotest to different haptens was performed in 70 patients with immediate allergic reactions to betalactams, classified into three groups: (A) skin test positive independently of CAP/RAST immunoassay value, (B) skin test negative and CAP/RAST positive, and (C) skin test and CAP/RAST negative but drug provocation test positive. Basotest was carried out by flow cytometry following the manufacturer's instructions using different betalactam determinants and results expressed as a stimulation index. RESULTS: Of the 70 patients, 34 (48.6%) were positive to Basotest (sensitivity: 48.6%), 31 (44.3%) to CAP/RAST and 46 (65.7%) to either one or the other. Considering the different groups, Basotest was positive in 50.9% of patients in Group A, 60% in Group B and 14.3% in Group C. The specificity was 91.3%. Positivity to the haptens was 28.6% to amoxicillin (AX), 21.7% to BP, 20% to benzylpenicilloyl-poly-l-lysine, 12.5% to ampicillin and 2.2% to minor determinant mixture. In patients with cephalosporin reactions, Basotest to the culprit cephalosporin was positive in 77.7%. There were differences between the two reactor groups in the sensitivity of Basotest (selective to AX=50%, cross-reactors=28.6%; chi(2)=10.809, P=0.004) and in the CAP/RAST (selective to AX=28.6%, cross-reactors=61.9%; chi(2)=8.944, P=0.011). CONCLUSIONS: The sensitivity of Basotest is similar to immunoassays (CAP/RAST). Sensitivity is improved when used in combination. Although further studies are required, Basotest results for cephalosporin allergy seem very promising. This technique does not help differentiate between selective reactors and cross-reactors.

Adult↗
PubMedDate not supplied

Exercise-induced asthma/other allergic reactions in the athlete.

Many US athletes with exercise-induced asthma (EIA) and allergies won medals in the 1984 Olympics, proving that EIA need not sideline an athlete. This article reviews EIA and the pathophysiology of the condition as well as other allergic reactions. The development of EIA is influenced by the type and duration of exercise and by air contaminants. Air temperature and humidity have been recognized recently as more important factors. Exercising in a warm, humid environment and breathing slowly through the nose help to control EIA. Four groups of drugs that are safe and effective against EIA are discussed. Other allergic reactions include the upper respiratory tract, i.e., nose and sinuses as well as skin reaction to environmental exercises.

Asthma↗
PubMed1998

Hyposensitization to allergic reaction in rDer f 2-sensitized mice by the intranasal administration of a mutant of rDer f 2, C8/119S.

C8/119S is a mutant of recombinant Der f 2 (rDer f 2), and lacks a disulphide bond possessed by wild-type rDer f 2. In humans and mice, C8/119S has a very weak IgE-binding capacity compared with the wild-type, but possesses a T cell reactivity comparable to that of the wild-type. C8/119S may thus be a safe immunotherapeutic agent for house dust mite allergy. The aim of the present study was to evaluate whether the intranasal administration of C8/119S could suppress an immediate allergic reaction in mice sensitized with wild-type rDer f 2, possessing an allergic activity comparable to native counterparts purified from mite extract. Seven-week-old male A/J mice were immunized with wild-type rDer f 2 four times, and then intranasally administered 0.2-2 microg of wild-type, 0.2-20 microg of C8/119S, or PBS alone, three times a week for 4 weeks. Seven days after the last administration, the mice were examined for an immediate allergic reaction. The animals administered 2 microg of C8/119S (C2.0 group) showed significantly reduced immediate bronchoconstriction provoked by the i.v. injection of 1 and 10 microg of wild-type rDer f 2, compared with the PBS-treated mice. Similar results were obtained when we examined mice 10 weeks after the last administration. The reactions in the other groups given wild-type or C8/119S also tended to decrease in severity in comparison with the animals of the PBS group. The allergic phenotypes of the T cells, B cells, and basophils in the C2.0 group were shifted to that of naive mice without immunization. We conclude that C8/119S has hyposensitizing activities in mice sensitized with wild-type rDer f 2. C8/119S may be useful for immunotherapy of house dust mite allergy.

Administration, Intranasal↗
PubMed2001

Inhibitory effects of mast cell-mediated allergic reactions by cell cultured Siberian Ginseng.

The crude drug "Siberian Ginseng (SG)" has long been used in empirical Oriental medicine for the nonspecific enhancement of resistance in humans and animals. In this study, we investigated the effect of cell cultured SG by oral administration in mast cell-mediated allergic reactions. SG dose-dependently inhibited compound 48/80-induced systemic allergy with doses of 10(-2) to 1 g/kg 1 h before oral administration. Of special note, SG inhibited systemic allergy with the dose of 1 g/kg by 25%. SG (1 g/kg) also inhibited passive cutaneous allergic reaction by 51%. SG dose-dependently inhibited histamine release from rat peritoneal mast cells. When SG (0.01 mg/ml) was added, the secretion of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 in antidinitrophenyl (DNP) IgE antibody-stimulated mast cells was inhibited 39.5% and 23.3%, respectively. In addition, SG inhibited anti-DNP IgE antibody-stimulated TNF-alpha protein expression in mast cells. Our studies provide evidence that SG may be beneficial in the treatment of various types of allergic diseases.

Anaphylaxis↗