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)

Plasma samples from 20 patients with acquired cold urticaria were studied. The C1-esterase inhibitor activity was found to be low, but the total C1-esterase inhibitor concentration was normal. Prekallikrein, plasmin-alpha 2-antiplasmin complex, and kallikrein-like activity were also found to be within normal limits. Cold-promoted activation of coagulation factor VII occurred in 45% of the patient plasmas and resulted in a considerable drop in C1-esterase inhibitor activity.
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PMID:On the role of the C1-esterase inhibitor in cold urticaria. 620 79

Anaphylaxis is a life-threatening disease that characteristically presents with multiple arrays of dermatologic, respiratory, cardiovascular, and gastrointestinal derangements, in general, suddenly after exposure to an allergen. It can, however, occur without an identifiable precipitant or event, and this well-defined entity has been called idiopathic anaphylaxis. The diagnosis of idiopathic anaphylaxis is made after an appropriate allergic evaluation and exclusion of a provocative trigger. We report an unusual case of manifesting with gastroenteritis, urticaria, hypotension, and syncope. Measurement of serum tryptase, a mast cell enzyme, was used to substantiate the diagnosis. Tryptase level is a useful test that can be used to help diagnose this potentially fatal disease.
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PMID:Serum tryptase in idiopathic anaphylaxis: a case report and review of the literature. 801 May 39

Adverse reactions to antibacterial agents are not uncommon in children. They are classified as 'immediate' or 'nonimmediate' according to the time interval between drug administration and onset. Immediate reactions occur within 1 hour and are manifested by urticaria and/or angioedema, bronchospasm and anaphylactic shock; immunological reactions are mediated by IgE antibodies. The main nonimmediate reactions (occuring after more than 1 hour) are maculopapular rash, urticaria and serum sickness; T lymphocytes may participate in maculopapular rash. Clinical assessment of such reactions is complex. The patient's history is fundamental; the allergological examination includes in vivo and in vitro tests selected on the basis of the clinical features and the phase of reaction. In the late phase, prick and intradermal tests are sensitive in evaluating beta-lactam allergy. Together with delayed-reading intradermal testing, patch testing seems to be useful in diagnosing maculopapular reactions to systemically administered aminopenicillins. Determination of specific IgE levels is the most common in vitro method for diagnosing immediate reactions. In the acute phase, serum tryptase and urinary N-methylhistamine assays are reliable in diagnosing type I pathogenic mechanisms in immediate reactions. Unfortunately, there are few in vitro tests for evaluating other reactions, and most are not fully validated. In selected cases, provocation tests should be performed.
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PMID:Recognising antibacterial hypersensitivity in children. 1093 62

Proton pump inhibitors (PPI) are widely used for the treatment of peptic ulcer, but cases of anaphylactic reactions have rarely been described. We present a patient who experienced an episode of urticaria 30 minutes after oral intake of an omeprazole capsule. Skin prick tests to omeprazole, pantoprazole and lansoprazole were positive. Challenge test with lansoprazole was carried out and within 45 minutes the patient developed urticaria, facial edema, vomiting, and hypotension. Oral challenge with other imidazole derivatives (ketoconazole, cimetidine, metronidazole) were carried out with good tolerance. Serum tryptase levels determined 3 hours after the adverse reaction to lansoprazole were elevated. Specific IgE to PPI were not detected by an enzyme-linked immunosorbent assay technique. The clinical findings, positive skin prick test to PPI and elevated serum tryptase levels suggest that an IgE-mediated mechanism was implicated in the reactions to both omeprazole and lansoprazole. Skin prick tests may be a useful tool for detecting patients sensitized to PPI. An experimental protocol was used to detect specific IgE antibodies against PPI, which may explain RAST negativity. The previous findings suggest that cross-reactivity between PPI exists, but not with other imidazoles.
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PMID:Anaphylaxis to proton pump inhibitors. 1246 68

Systemic mastocytosis (SM), as opposed to cutaneous-only mastocytosis, implies the presence of neoplastic mast cell infiltration in extracutaneous tissue. Mast cell disease in adults is often systemic and often involves the bone marrow. Typical clinical and laboratory features of SM include urticaria pigmentosa, mast cell mediator symptoms (eg, headache, flushing, lightheadedness, urticaria and pruritus, nausea, diarrhea, abdominal pain, and vasodilatory shock), bone pain (eg, osteoporosis, lytic bone lesions, and fractures), hepatosplenomegaly, cytopenia, eosinophilia, elevated serum tryptase and histamine, and bone marrow fibrosis and angiogenesis. SM may be indolent (no evidence of organ dysfunction), aggressive (presence of organ dysfunction), associated with another often chronic myeloid hematologic disease (SM-AHD), or present as mast cell leukemia or sarcoma. Mast cell-mediator symptoms are treated with histamine antagonists and cromolyn sodium. Indolent SM does not require cytoreductive therapy. Aggressive SM and SM-AHD are managed based on their molecular profile. Recent information suggests that FIP1-like-1-platelet-derived growth factor receptor-alpha(+) SM responds well to imatinib mesylate, whereas interferon-alpha should be considered as a first-line treatment in all of the other cases, including patients with Asp816Val(+) SM. Cladribine has been shown to be effective in patients who develop resistance to interferon treatment.
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PMID:Systemic mastocytosis: current concepts and treatment advances. 1508 68

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with activation of interacting inflammatory cells including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. It is caused via inflammatory mediators released during inflammatory cell activation. A variety of conditions, drugs, and environmental exposures can induce Kounis syndrome. A patient suffering from coronary artery disease and taking metoprolol and aspirin was stung by wasps and developed cutaneous allergic signs including rash, urticaria and orbital oedema. This was followed by retrosternal pain, chest discomfort and electrocardiographic changes compatible with acute myocardial ischemia. Cardiac enzymes, troponins and blood pressure remained normal but serum tryptase was raised. The clinical implications and pathophysiology of this rare association are discussed.
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PMID:Hymenoptera sting-induced Kounis syndrome: effects of aspirin and beta-blocker administration. 1709 68

We describe the case of a 30-year-old woman who reported several episodes of anaphylaxis with angioedema and relapsing urticaria. Some events were related to nonsteroidal anti-inflammatory drug intake and one episode followed alcohol ingestion, but in most cases no triggers could be identified. Specific immunoglobulin E determination was negative for food and drug allergens, C3 and C4 were in the normal range, C1 inhibitor was slightly reduced and serum tryptase was undetectable. In vivo autologous serum skin test and in vitro basophil histamine release assay were positive indicating the presence of circulating histamine-releasing factors. When oral tolerance tests were performed, only doxycycline was tolerated whereas levofloxacin, clarithromycin, nimesulide and tramadol caused mild urticaria. Premedication with cetirizine allowed the patient to tolerate levofloxacin, clarithromycin and nimesulide. The demonstration of circulating histamine-releasing factors in a patient with idiopathic anaphylaxis and multiple drug allergy syndrome provides a new mechanistic insight and might open the way to new therapeutic approaches.
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PMID:Detection of serum histamine-releasing factors in a patient with idiopathic anaphylaxis and multiple drug allergy syndrome. 1746 Sep 52

Exercise-induced anaphylaxis (EIA) was defined for the first time in 1980. EIA is associated with different kind of exercise, although jogging is the most frequently reported. The clinical manifestations progress from itching, erythema and urticaria to some combination of cutaneous angioedema, gastrointestinal and laryngeal symptoms and signs of angioedema and vascular collapse. Mast cell participation in the pathogenesis of this syndrome has been proved by the finding of an elevated serum histamine level during experimentally-induced attacks and by cutaneous degranulation of mast cells with elevated serum tryptase after attacks. As predisposing factors of EIA, a specific or even aspecific sensitivity to food has been reported and such cases are called "food-dependent EIA". Many foods are implicated but particularly wheat, vegetables, crustacean. Another precipitating factor includes drugs intake (non steroidal anti-inflammatory drugs), climate variations and menstrual cycle factors. Treatment of an attack should include all the manoeuvres efficacious in the management of conventional anaphylactic syndrome, including the administration of epinephrine and antihistamines. Prevention of the attacks may be achieved with the interruption of the exercise at the appearance of the first premonitory symptoms. To prevent the onset of EIA it is also suitable to delay the exercise practice after at least 4-6 hours from the swallowing of food.
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PMID:[Exercise-induced anaphylaxis]. 1875 20

Antihistamines are widely used drugs. Hypersensitivity reactions with these drugs are rare and a challenge for the physician. We describe 5 outpatients who experienced urticaria after taking antihistamines. All 5 were treated at our outpatient clinic over a period of 15 years. The allergy workup included a clinical history, skin prick testing, patch testing with antihistamines, and single-blind placebo-controlled oral challenge tests. Biopsy samples were taken and serum tryptase levels were determined in 1 patient. The results of the skin prick tests and patch tests were negative in all patients but 1, in whom the prick test result was positive to some antihistamines. We confirmed all diagnoses using a single-blind challenge test. The biopsy obtained from 1 patient strongly supported urticaria. We present 5 cases of antihistamine-induced urticaria where the immunologic mechanism remains unclear. Hypersensitivity reactions should be taken into account in patients receiving antihistamines, especially in those who experience urticaria.
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PMID:Urticaria caused by antihistamines: report of 5 cases. 1963 29

A healthy 29-year-old woman received epidural block for severe lumbago in an outpatient clinic. Fifteen minutes after injection of mepivacaine 0.5% with dexamethasone into the epidural space, the patient complained of itching of eyelids followed by generalized pruritus. Hypotension, erythema and generalized urticaria were observed. Initial treatment was with 100% oxygen through face mask, and additional intravenous fluids, followed by administration of adrenaline, chlorpheniramine and dopamine. Cardiac ultrasound examination showed mildly impaired movement of inferior to septal wall. Her plasma histamine level was transiently elevated during the anaphylactic event; however the serum tryptase level was not. Biological assays for confirming the causative agent and cutaneous test were all negative, but clinical symptoms positivity showed nonimmunological anaphylactic reaction to mepivacaine or dexamethasone. This case report confirms the need for systematic allergological investigation in a case of immediate hypersensitivity reaction occurring during nerve block in patients who had even received similar nerve blocks repeatedly. Pain clinician should be aware of the possibility of anaphylactic reactions involving any drug or substance used for an outpatient.
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PMID:[Anaphylactic reaction to epidural block in an outpatient]. 2096 Sep 5


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