Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypersensitivity to natural rubber latex (NRL) in health care personnel exposed to powdered latex gloves appears as conjunctivitis, rhinitis, nasal congestion, cough, dyspnea, or bronchial asthma in approximately 30% of all cases with latex allergy while most of the patients have contact urticaria. The purpose of the present study was to determine the prevalence of latex-induced allergic rhinitis in health care workers using NRL gloves on a daily basis. Clinical examination accompanied by skin prick test (SPT) with latex glove extracts and common aeroallergens, measurements of specific IgE to NRL, and lung function tests were performed in 25 symptomatic workers and 11 latex-exposed asymptomatic controls. Sensitization to NRL was detected using SPT in one (4%) of 25 symptomatic workers but not in any of the asymptomatic controls. Positive SPT to aeroallergens was demonstrated in 8/25 symptomatic workers and 6/11 controls. Measurements of forced vital capacity, forced expiratory volume in I sec, and bronchial methacholine challenge did not show any significant differences between the study groups. In conclusion, NRL-aeroallergen-induced occupational rhinitis may occur among physicians and nurses who have a frequent use of latex gloves on a daily basis at hospital work. However, a relatively low prevalence of NRL-induced occupational rhinitis is associated with profuse consumption of no-powder sterile gloves.
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PMID:Glove-related rhinopathy among hospital personnel. 884 46

Urticarial vasculitis (UV) is a primary syndrome or a cutaneous vasculitic lesion occurring in the course of a collagen disease, as the systemic lupus erythematosus (LE). UV is a recently recognized disorder which affects most exclusively the female sex and may be differentiated from common (nonvasculitic) urticaria because it is characterized by inflammation and necrosis of blood vessels (vasculitis). UV and common urticaria may be induced by a variety of factors and pathogenetic mechanisms. It seems that a continuum exists, ranging from benign cutaneous lesions of urticaria to vasculitis with strong immunological involvement. On the basis of the clinical evaluation, two major groups of UV have been classified, the normocomplementemic, with a less severe clinical course, and the hypocomplementemic UV, a rare immune complex-mediated disorder related to LE as for as the similar pathogenesis and systemic involvement are concerned. A case of a young female patient with a unique syndrome characterized by crises of urticarial recurrent painful lesions of unknown origin, associated with angioedema of the tongue and soft palate, severe malaise, arthralgias and abdominal pain is reported. Dyspnea and cough were sometimes present, but fever was absent. Symptoms were caused by physical stress, heat or pressure and were little responsive to corticosteroids. Although skin biopsy did not prove with certainty the occurrence of vasculitis, clinical data and laboratory findings (normal levels of complement fractions, raised erythrocyte sedimentation rate, presence of cryoglobulins and ASMA, nDNA and AMA autoantibodies and absence of ANA autoantibodies and LE cells) suggest a normocomplementemic UV, excluding a classic LE. The family doctors and the internist must become familiar with the "lupus-like" syndromes, which include UV. In fact, a correct diagnosis of this syndrome is important because, although prognosis of UV may not be severe, the possibility exists of a systemic involvement (mainly renal) with progression to LE.
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PMID:[Urticarial vasculitis syndrome. A case report and review of the literature]. 945 98

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

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

A forty-four-year-old Japanese female, who had persistant rhinorrhea, was administered Benza block tablets orally along with two other medicines. Immediately after ingestion, the patient displayed itching of the right upper eyelid, followed by coughing, sneezing, nasal discharge, nasal obstruction, nausea, vomiting, swelling of the face, and dyspnea. She had edema, a wheal extending from the face to the neck, and swelling of the eyelids and lips. Her symptoms subsided after treatment. Her reaction to ibuprofen, which was contained in the Benza Block tablets, was confirmed by a positive reaction to prick testing. From the results of these examinations, our patient was diagnosed as having anaphylaxis due to the ibuprofen in the Benza Block tablets. A review of the literature revealed no previous reports of anaphylaxis due to ibuprofen, although a few cases of ibuprofen urticaria have been reported.
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PMID:A case of anaphylaxis due to ibuprofen. 1087 2

Food intolerance is a reproducible adverse reaction to a specific food ingredient that is not psychologically based. Food allergy is a form of food intolerance in which there is evidence that the response is caused by an immunological reaction to food. Other mechanisms of food intolerance include enzyme defects (e.g. lactase deficiency), pharmacological effects (e.g. histamine), toxic properties (e.g. haemagglutinating lectins) and irritants (e.g. spices). Food allergy in children is a highly contentious subject and there is often a striking lack of published evidence from which to base clinical decisions. The true prevalence of food allergy in children is unknown, although there is evidence of an increasing incidence of allergic reactions to some foods, especially peanuts. Our understanding of why some children are unable to tolerate certain foods (e.g. cow's milk, egg), or how they grow out of this intolerance, is very poor. Symptoms of food allergy in children are diverse and include vomiting, poor weight gain, abdominal pain, malabsorption, cough, wheeze, rhinitis, atopic eczema, urticaria and angioedema. Despite the lack of objective data to support the notion that food intolerance contributes to behaviour in children, this is a belief firmly held by many parents and some professionals. The gold standard for diagnosing food intolerance is the double-blind placebo-controlled food challenge (DBPCFC). There is often a poor correlation between the results of food provocation tests and those of skin prick tests of radioallergosorbent tests for specific food antibodies. For proven food allergy, elimination diets are the mainstay of management. In children these must be closely supervised to avoid nutritional deficiency and compromise of growth. Some children who have had severe (anaphylactic) reactions after food need to have a supply of self-injectable adrenaline made available to their parents and teachers and must also practice strict avoidance of the offending food.
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PMID:Food allergy and food intolerance in childhood. 1113 67

Corticosteroids intended for inhalation into the lungs or into the nose have been used since the 1970s. Only 2 attempts to assess contact allergy attributable to inhaled corticosteroids in patients with asthma and/or rhinitis have been made, and only 1 single case of contact allergy attributable to budesonide and tixocortol pivalate was found. However, several case reports of allergic mucosal and skin symptoms caused by corticosteroids applied locally to the mucosa have been published. Local adverse effects from nasal corticosteroids have ranged from nasal congestion, pruritus, burning, and soreness to perforation of the nasal septum. Inhalation of corticosteroids into the lungs has been reported to cause pruritus, dryness, erythema and oedema of the mouth, a dry cough and odynophagia. Systemic signs reported from the use of nasal corticosteroids and inhalation of corticosteroids into the lungs have been eczematous lesions, particularly on the face, sometimes with spreading to the trunk and flexures. Urticaria has also been noted.
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PMID:Skin reactions to inhaled corticosteroids. 1141 63


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