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 diagnostic value for allergies of the low affinity IgE receptor and its soluble circulating fragment (sCD23) remains unclear. In particular, little is know about seasonal influences on serum sCD23 levels in subjects with pollen allergy. In the present study, to gain insight into pathophysiological role of sCD23, we have analyzed, in blood from patients allergic to Parietaria sCD23, IgE, and eosinophil cationic protein (ECP) serum levels. IgE were assessed as atopy markers and ECP as an inflammation marker. Patients were studied during and out of pollen season, and results were compared to those obtained in nonallergic subjects. The study population included 42 nonsmoking outpatients, living in Palermo (Sicily, Italy) or in other west Sicilian towns, with a clinical diagnosis of seasonal asthma or rhinitis and monopositive skin test to Parietaria pollen. The group of asthmatic subjects consisted of 25 patients who had one or more of the usual asthma symptoms (wheezing, dyspnea, and cough) only during the pollen season. The group of rhinitis patients consisted of 17 patients, who, during pollen season, had the nasal symptoms (nasal blockage, sneezing, nasal itching, and rhinorrhoea) but no signs of asthma. As a control group, we studied 10 nonatopic subjects from laboratory staff. They had no history of seasonal or perennial rhinitis, asthma, or urticaria and had negative skin tests to a panel of allergens. Soluble CD23, IgE, and ECP were assessed in blood during and out of pollen season. Total serum IgE levels were clearly higher in atopic patients, as classically established. Concerning sCD23 serum levels, a similar pattern of results was obtained. Accordingly, significant correlations were shown between the levels of sCD23 and IgE in all groups of patients. A completely different pattern was observed by analyzing serum ECP levels because ECP levels were significantly increased only in asthmatic patients during pollen season. Accordingly, no significant correlations were observed between the levels of sCD23 and those of ECP. Identifying immune factors associated with the development of atopy can enhance our understanding of the in vivo mechanisms involved and may have utility in paradigms designed to prevent diseases. As demonstrated by the close correlation with total serum IgE values and the lack of correlation with serum ECP values, serum levels of sCD23 appear to be an additional marker for the diagnosis of atopy but not for the follow-up of allergic diseases.
Allergy Asthma Proc
PMID:Serum levels of soluble CD23 in patients with asthma or rhinitis monosensitive to Parietaria. Its relation to total serum IgE levels and eosinophil cationic protein during and out of the pollen season. 1020 90

Between 8-20 percent of adult asthmatics experience bronchospasm following ingestion of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). Termed aspirin-induced asthma, this reaction is potentially fatal. Asthmatics with chronic rhinitis or a history of nasal polyps are at greater risk. The reaction rarely occurs in children. Patients initially present with an acute episode of vague malaise, sneezing, nasal obstruction, rhinorrhoea, and often a productive cough. Persistent rhinitis and nasal polyps may then develop. Asthma and aspirin sensitivity may appear in the following months. Within 20 minutes to 3 hours of taking a NSAID, aspirin-sensitive asthmatics can develop symptoms such as bronchospasm, rhinorrhoea, dyspnoea, cough, or urticaria-angiodema. NSAIDs (systemic or topical) should be used with caution in asthmatics and avoided in asthmatics with nasal polyps. Asthmatics should be told to seek medical help if symptoms worsen on initiation of a NSAID.
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PMID:NSAID-induced bronchospasm--a common and serious problem. A report from MEDSAFE, the New Zealand Medicines and Medical Devices Safety Authority. 1056 93

Allergic asthma and rhinitis, atopic dermatitis, urticaria and food allergy are genetic diseases present in infants and children. Several investigators have provided evidence for a genetic localization for atopy. Babies of atopic parents are at high risk of developing atopic diseases; however, the phenotypic expression of such diseases varies widely in that it can be very mild in some infants and children, severe and frustrating in many, even life-threatening in others, as well as also being common, disabling and chronic. A meta-analysis of all available studies on the age of onset of atopic march was carried out by selecting what appeared to be the most relevant articles in the literature rather than aiming for a comprehensive selection. It was found that in the first year of life, there is the onset of atopic dermatitis in 79.8% (60.2-100%) of babies, of cow's milk allergy in 72.7%, egg allergy in 71%, and fish allergy in 51.3%. Asthma starts in the first year of life in 41.8%, in the second in 49.3%, and within the eighth year in 92.5% of children. Allergic rhinitis begins in 35% of babies in the first year of life, and in 59% or 13-19% in those aged 2-5 years. It seems therefore that up until now the role of pediatric allergy and immunology has been somewhat obscured, as can be witnessed by atopic march. Instead, pediatric allergy and immunology have a substantial, unmatched role, focusing on the early and often very early onset of atopy, which requires strategic intervention in the very first months of life or even before birth. As the main goal of modern medicine is prevention of chronic and severe diseases, the possibility of preventing such disorders in predisposed children has stimulated the imagination of researchers since the beginning of the century, when atopic diseases were not as common as they are now.
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PMID:The growing genetic links and the early onset of atopic diseases in children stress the unique role of the atopic march: a meta-analysis. 1058

Intolerance or idiosyncrasy to acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs (NSAIDs) is a crucial problem because these drugs are frequently used in medical treatment. In this study, we tested whether nimesulide, a selective cyclooxygenase-2 (COX-2) inhibitor, might be a valid alternative for patients with histories of adverse reaction to ASA or NSAIDs. A single-blind, placebo-controlled oral challenge procedure was applied to 60 adult patients (19 male, 41 female; with a mean age of 40.31 +/- 10.44 years, range 20-68 years) with a reliable history of ASA/NSAIDs-intolerance. According to history, the clinical presentations of intolerance were urticaria/angioedema in 32 patients, anaphylactoid reaction in 2 patients, respiratory reaction in 19 patients, and respiratory and cutaneous reaction in 7 patients. Atopy was confirmed by means of skin prick test with inhalant allergens. Oral challenge protocol was started with 25 mg of nimesulide and the remaining 75 mg was given 1 hr later. During the challenge procedure, blood pressure, pulse, nasoocular, pulmonary, and cutaneous symptoms were monitored. Of the 60 patients tested, 55 (91.7%) tolerated the drug with no adverse reaction. Only five (8.3%) patients demonstrated a positive response to oral challenge. The clinical presentations of intolerance to nimesulide were urticaria/angioedema in three patients, mild rhinitis in one patient, and mild dyspnea in one patient. The atopy prevalence was higher, with a ratio of 41.7%, in patients with ASA/NSAIDs intolerance than that of the healthy adult population in Turkey (p < 0.05). We believe that nimesulide can be used as an alternative drug for patients with ASA/NSAIDs intolerance.
J Asthma 1999 Dec
PMID:The use of nimesulide in patients with acetylsalicylic acid and nonsteroidal anti-inflammatory drug intolerance. 1060 20

Pyrazolone drug hypersensitivity (PDH) may manifest as angioedema, urticaria, and/or life threatening anaphylactic shock. Although it has been suggested that PDH is an immunologic, probably IgE-mediated reaction, the diagnosis of PDH is still based on clinical history because there is no reliable in vitro diagnostic method currently used in clinical practice. The goal of this study was to evaluate the reliability of various methods to confirm a diagnosis of PDH. Twenty-eight patients with prior history of 71 reactions to pyrazolone drugs were studied. In all patients, pyrazolone drugs induced urticaria and angioedema. In addition, laryngeal edema occurred in 14 patients and anaphylactic shock with loss of consciousness in five patients. Skin prick test and intradermal tests using increasing concentrations of noraminophenazone were performed in 25 patients. Sera of all 28 patients were negative for pyrazolone-specific IgE as determined by an immunoenzymatic method. Peripheral blood mononuclear cells proliferative responses to pyrazolone were studied by a lymphocyte proliferation test with 3H-thymidine incorporation. Incubation of peripheral blood mononuclear cells with increasing concentrations of noraminophenazone did not induce any significant proliferation responses. Our study demonstrated that 1) intradermal skin tests correlate poorly with the clinical history of hypersensitivity reaction; and 2) in vitro tests are not useful in establishing a diagnosis of PDH.
Allergy Asthma Proc
PMID:Diagnosis of pyrazolone drug sensitivity: clinical history versus skin testing and in vitro testing. 1062 89

Health care workers (HCW) have been shown to be at significant risk for developing latex allergy. Natural rubber latex hypersensitivity has been reported in 2.9 to 17% of health care workers in previously published studies. This study describes the prevalence of latex hypersensitivity in a large cohort of medical center employees. A screening questionnaire was distributed to 1967 employees in six job categories exposed to latex, and 1331 questionnaires were returned (68%) between March and November 1995. Skin and serologic testing was performed on 156 volunteers. Of the 1331 HCWs who completed the screening questionnaire, 290 (21.8%) self-reported contact dermatitis to latex, 67 (5.0%) self-reported urticaria to latex, 163 (12.2%) self-reported rhinoconjunctivitis to latex, and 17 (1.3%) self-reported asthmatic symptoms to latex. Of the total population of 1967 employees, 38 (1.9%) were either skin test or blood test positive and 30 (1.5%) of these 38 were symptomatic around latex. This study suggests a minimum prevalence of IgE-mediated hypersensitivity to latex of 1.5% among medical center employees. Our reported prevalence figures are lower than previously reported, reflecting, in part, reporting methods using a denominator more consistent with the total population at risk. Our study also illustrates the pitfall of relying on self-reporting in making the diagnosis of latex allergy.
Allergy Asthma Proc
PMID:Minimum prevalence of latex hypersensitivity in health care workers. 1062 96

Histamine was the first allergic mediator identified in the early part of this century. It has three defined receptors, but most effects of histamine in allergic reactions are through the H1 receptor. The first H1 antagonists were introduced into clinical use in the late 1940s, and drugs of this class are still the preferred initial choice for management of allergic rhinitis and urticaria. The first-generation drugs were characterized by nonspecific binding to many receptors and penetration of the blood-brain barrier, resulting in multiple side effects. Within the central nervous system (CNS), interference with normal histamine binding to the H1 receptor is associated with drowsiness and psychomotor impairment. The second-generation drugs have a much improved benefit/adverse effect profile, largely based on greater potency, receptor specificity, and lower CNS penetration. The potency of antihistamines for blocking H1 receptors can be compared by their inhibition of the cutaneous wheal and flare response to histamine. These drugs seem to have additional antiallergic properties related to blockade of mediator release and interference with cellular recruitment and activation. Clinical trials comparing the efficacy of antihistamines in rhinitis and asthma are reviewed. Recent studies have explored the potential of antihistamines to prevent the progression of allergy and their enhanced efficacy when combined with leukotriene antagonists.
Allergy Asthma Proc
PMID:Molecular pharmacology of second-generation antihistamines. 1089 14

Idiopathic anaphylaxis presents a problem requiring rapid diagnosis and initiation of therapy. Some cases are complex and difficult to assess. We present four cases of unusual complexity to illustrate diagnostic and therapeutic problems. Two cases were found not to be idiopathic anaphylaxis, one being undifferentiated somatoform idiopathic anaphylaxis and the other very severe urticaria. Various conditions can be or mimic idiopathic anaphylaxis, and patience and observation can result in reasonable outcomes.
Allergy Asthma Proc
PMID:Idiopathic anaphylaxis: variants as diagnostic and therapeutic problems. 1089 15

Asthma is a common condition, affecting approximately 7% of people worldwide. However, the prevalence varies among countries, and in Australia, asthma affects 10% of adults and approximately 20% of children. For some of these patients, ingredients in some over-the-counter analgesics may pose problems. Aspirin sensitivity, defined as urticaria, angioedema, or rhinitis after aspirin ingestion, affects only 0.3% of the general population. However, certain patient groups, such as asthmatics, are at an increased risk, with reports of an incidence as high as 20% in this patient population. This phenomenon is not restricted to aspirin, as all nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit the enzyme cyclooxygenase display a high incidence of cross-sensitivity. In contrast, paracetamol (acetaminophen) is well tolerated by the majority of people with asthma and is seldom associated with cross-sensitivity. Determining who is likely to be affected is difficult because the sequence of symptoms is hard to predict, and patients often do not associate an asthma attack with the use of aspirin or an NSAID. The only definitive way to diagnose sensitivity is by provocation tests. In view of these difficulties, it is important for health care practitioners to take a pro-active stance by asking questions to determine whether aspirin sensitivity is a problem, counseling people about the risks, and helping them make an appropriate analgesic choice.
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PMID:Recommending analgesics for people with asthma. 1131 74

The efficacy of antihistamines in the treatment of allergic rhinitis and urticaria is compared. In treating allergic rhinitis, the new second- and third-generation antihistamines have multiple advantages including rapid onset of action, extended duration of action, and efficacy for nearly all the symptoms that are produced by allergen sensitization. These include non-nasal and nasal symptoms. These agents are generally nonsedating and can be administered either once or twice daily. There is minimal potentiation for QTC prolongation, and they are safe and effective as first-line therapies for seasonal allergic rhinitis. They are especially effective when combined with topical corticosteroids in reducing the whole constellation of symptomatology of allergic rhinitis. The treatment of chronic idiopathic urticaria should include second- and third-generation antihistamines as primary therapy. Additional therapy may include H2 antagonists, antihistamine-decongestant combinations, tricyclic antidepressants such as doxepin, and beta-adrenergic agonists including albuterol and epinephrine for acute angioedema. Corticosteroids may be required to treat significant exacerbations of chronic urticaria and/or to break a long-standing cycle of urticaria. Miscellaneous therapeutic agents include leukotriene antagonists combined with H1, H2 antagonists, calcium channel antagonists, plasmapheresis, cyclosporin and methotrexate.
Allergy Asthma Proc
PMID:The evolution of pharmacotherapy for rhinitis and urticaria. 1171 15


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