Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
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Manifestations of fish allergy can include near-fatal anaphylactic reaction. In very sensitive patients, fish odors and cooking vapors may have some allergenic activity. We reported a case of life-threatening fish allergy in a girl of 39 months referred for three episodes of Quincke edema with wheezing, cyanosis and severe urticaria after fish consumption or inhalation. Reagins were found against codfish and direct skin prick test with fresh food (codfish) showed important local reaction. Strict avoidance of fish in the diet is usually the only recommended procedure. However, in this particular case, the life-threatening nature of the allergic reaction was the major consideration to perform a desensitization. The child was treated by RUSH immunotherapy using codfish extracts from BENCARD company, following the schedule for insect venom allergy described by Pharmacia. Immunotherapy was performed immediately after determination of the threshold of sensitivity by specific skin prick tests and intra-dermal injections. Desensitization was initiated with a 1/10 dilution of the cut-off solution and 5 subcutaneous injections were administered daily. When important local reactions were observed, additional doses were necessary to obtain tolerance. After the RUSH therapy, the child was submitted to uncooked codfish odors without any reaction. No reaction has been observed even when the child has accidentally eaten a little piece of codfish.
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PMID:Life-threatening fish allergy successfully treated with immunotherapy. 961 81

In the past 2 years, a 4 year-old boy has had an anaphylactic reaction whenever he contacted food prepared with fish. The symptoms included intense itching in the throat and eyes, which progressed to generalized urticaria and facial angioedema. This was accompanied by cough, wheezing and dyspnea. Many fish preparations caused these episodes including several different kinds of fish (cod, tuna, salmon, trout, eel...), fish soup, chopsticks contaminated with fish preparations and canned fish. Elevated levels of total serum IgE (224 IU/ml) and specific IgE for cod (93.1 IU/ml), tuna (> 100 IU/ml), salmon (> 100 IU/ml), trout (64.4 IU/ml), mackerel (41.2 IU/ml) and eel (28.1 IU/ml) were found by the Pharmacia CAP system RAST FEIA in our allergy clinic. A skin prick test for mixed fish extracts (contain flounder, cod and halibut) was positive. A fish challenge test for cod, tuna, salmon, trout and eel all showed anaphylactic reactions. His allergic symptoms stabilized gradually after strictly avoiding ingestion of fish and using drug treatment. He also had a similar anaphylactic reaction to frogs. The best treatment for fish allergy is avoidance. Avoidance of fish may need to include both ingestion and inhalation of cooking vapors.
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PMID:Fish induced anaphylactic reaction: report of one case. 968 28

One hundred and ninety one subjects showing histories of immediate hypersensitive response to egg white ingestion and/or positive IgE antibody titers specific for egg white were enrolled in double-blind placebo-controlled oral challenge with freeze and dried, heated or heated and ovomucoid-depleted egg white antigens. Seventy seven were male and 114 female, and their ages ranged from 11 month to 10 years 5 month; 118 of them had atopic dermatitis, seven had asthma and 33 had both atopic dermatitis and bronchial asthma and 33 had urticaria. One hundred four children developed 147 positive symptoms including 131 immediate reactions and 16 non-immediate reactions by oral challenge tests. Respiratory symptoms were observed in 25 cases (17%) including cough alone in 12 cases (8.2%), and both wheezing and cough in 13 cases (8.8%). These were all observed as immediate reactions and accompanied with dermal symptoms. Frequency of respiratory symptoms correlated with specific IgE antibody titers for egg white. Heated and ovomucoid-depleted egg white was more hypoallergenic that heated or freeze and dried egg white with respect to respiratory symptoms as well as other symptoms. We concluded that respiratory symptoms were provoked through oral challenges with egg white in a part of egg-allergic children.
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PMID:[Respiratory symptoms by oral challenge tests with egg white antigens in egg-allergic children]. 978 Apr 44

We hereby present a patient suffering several episodes of anaphylaxis (generalized urticaria, dyspnea, wheezing and intense cough) a few minutes after taking different drugs containing paracetamol. Intradermal test with pure paracetamol (100 mg/ml) was positive. It was negative in six controls. Serum specific IgE anti-paracetamol (by RIA) was negative. Anaphylaxis from paracetamol is rare but has been reported. Positive skin test with paracetamol have only been rarely described.
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PMID:Anaphylaxis to paracetamol. 981 9

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.
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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

In many situations, the diagnosis of food allergy rests simply upon a history of an acute onset of typical symptoms, such as hives and wheezing, following the isolated ingestion of a suspected food, with confirmatory laboratory studies of positive prick skin tests or Radioallergosorbent tests. However, the diagnosis is more complicated when multiple foods are implicated or when chronic diseases, such as asthma or atopic dermatitis, are evaluated. The diagnosis of food allergy and identification of the particular foods responsible is also more difficult when reactions are not mediated by IgE antibody, as is the case with a number of gastrointestinal food allergies. In these latter circumstances, well-devised elimination diets followed by physician-supervised oral food challenges are critical in the identification and proper treatment of these disorders. Because childhood food allergies to common allergenic foods such as milk, egg, wheat and soy are usually outgrown, oral food challenges are also an integral part of the long-term management of these children.
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PMID:Food allergy: when and how to perform oral food challenges. 1067 17

Anaphylactic shock is a life-threatening allergic reaction with cardiovascular collapse. The cardiovascular collapse may occur suddenly without warning signs or may be preceded by symptoms such as pruritus, wheezing, dyspnea, urticaria, pallor, digestive symptoms, and weakness. Food allergens, injected drugs and hymenoptera stings are the main etiologies. Anaphylactic shock requires an emergency treatment with immediate intramuscular or subcutaneous epinephrine injection. Subsequent avoidance of the inciting allergens is mandatory together with the availability of a first aid kit including ready-to-use epinephrine syringes. Besides its absolute necessity in any doctor's office, such first aid kits should be available in any children's group.
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PMID:[Anaphylactic shock in the infant]. 1114 73

The cause of allergy is multi-factorial, and the development of an allergic disease seems to be the result of an interaction between genetic and environmental factors. The goal for preventing the development of allergic diseases is to avoid sensitization to allergens. The aim of this work was to study whether or not exposure to environmental allergens early in infancy would influence the occurence of various allergic diseases in later life. On an annual basis, a total of 931 healthy newborns were followed-up until they reached 3 years of age. The occurence of allergic diseases was recorded by trained medical students during visits. Measurement of Dermatophagoides pteronyssinus (Der p 1) concentration in house dust was performed when each baby was 18 and 36 months old. Total and specific immunoglobulin E (IgE) antibodies against Der p 1, cow's milk, and egg white were evaluated at birth and at 18 months of age. The following results were obtained: at 3 years of age, 10.4% had bronchial asthma (BA), 21.4% atopic dermatitis (AD), 7.0% urticaria, and 46.8% had experienced wheezing; higher family allergy scores led to a higher incidence of AD (p=0.0012); exposure to a mite allergen concentration of 1 microg/g of dust may be associated with a higher incidence of AD (p=0.0156); the presence of Der p 1 IgE antibody at 18 months of age was associated with a higher incidence of BA (p=0.0001); and children sensitized to egg whites at 18 months of age had an increased risk of developing AD at 3 years of age (p=0.0187). Hence, early exposure to mite allergen is a risk factor for the development of atopic dermatitis, but seems not to be related to the development of bronchial asthma. Early sensitization to egg whites increases the risk of developing AD. The early detection of serum Der p 1 IgE antibody is associated with a higher incidence of bronchial asthma.
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PMID:Exposure to a high concentration of mite allergen in early infancy is a risk factor for developing atopic dermatitis: a 3-year follow-up study. 1125 59

We report a case of a patient who suffered generalized urticaria, chest tightness, wheezing, nausea, vomiting, hypotension, and loss of consciousness. Two hours earlier she had taken Eulitop Retard following lunch. She had tolerated all the implicated food after the reaction. Allergy evaluation revealed intense positive responses to intradermal tests with bezafibrate active component and Eulitop Retard (skin tests in control subjects were negative). Specific IgE tests (RAST) to Eulitop Retard were negative. An IgE mechanism is suggested to be responsible for this adverse reaction on the basis of the positive skin tets. The delayed onset (two hours) of this anaphylactic shock is unusual. Although infrequent, it may be caused by the specific pharmacokinetic characteristics of this drug, which is a slow releasing agent, mainly absorbed in the gut. The drug was taken just after lunch, and this concomitant food ingestion could also have produced a delay in gastric drainage and a retarded drug absorption. An IgE-mediated accelerated type reaction could also explain this delay. Apparently the patient reacted after the first contact to the drug, and the absence of a sensitization period is not usual in this type of immune reponse. Finally, we recommend the performance of prick and intradermal skin tests prior to any systemic challenge when allergic reactions to fibric acid derivatives are suspected.
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PMID:Bezafibrate-induced anaphylactic shock: unusual clinical presentation. 1143 73

This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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PMID:Breathless. 1196 14


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