Acute coronary syndrome due to amoxicillin allergy.
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Biomedical subjects
Publications and source records attributed to A Moreno-Ancillo.
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Inhalation of dust from different enzymes can be the cause of occupational asthma in exposed workers. Enzymes from different sources are being increasingly used in food. Few cases of food allergy to alpha-amylase induced by eating bread have been reported. Those cases were reported in bakery-related patients and in a pharmaceutical-industry worker. A 25-year-old farmer suffered sneezing, rhinorrhea, oropharyngeal itching, hoarseness, cough, and non-wheezy dyspnea after eating white bread. Skin prick tests (SPT) with common aeroallergens and food allergens revealed only sensitization to Olea europaea pollen. SPT response was positive to Aspergillus oryzae alpha-amylase. Specific IgE against alpha-amylase was positive. A double-blind placebo-controlled challenge with 5 mg of uncooked -amylase induced sneezing, cough, oral angioedema within 10 minutes. The provocation test with 50 g of white bread gave similar findings. This case indicates that alpha-amylase contained in bread may provoke IgE-mediated food allergy. It is worth noting that in this case, the only source of alpha-amylases sensitization was bread.
BACKGROUND AND AIMS: Ingestion of Anisakidae larvae in raw seafood may cause anisakiasis. However, despite the high level of consumption of seafood in Spain, only a few cases of anisakiasis have been reported until now. Anisakis simplex can cause allergic reactions in sensitized patients as a result of its parasitism in the gastrointestinal tract. The purpose of this study was to analyse the clinical findings in 22 patients with gastroallergic anisakiasis. METHODS: Patients with allergic and/or gastric symptoms after seafood ingestion were evaluated in the emergency room of the La Paz General University Hospital. Skin testing for Anisakis simplex and tests on the implicated seafood were performed and amounts of serum-specific immunoglobulin E were assessed. A gastroscopy was performed in those patients with severe allergic or/and persistent gastric symptoms after ingestion of raw or undercooked seafood. RESULTS: Twenty-two patients were diagnosed with gastroallergic anisakiasis in 1 year. Most patients presented to the emergency room of our hospital with allergic symptoms. Gastric symptoms were usually moderate. Gastroscopy revealed local mucosal oedema and gastric erosion at the point of fixation. Two or more worms were detected in three patients. The mean time of latency of allergic symptoms was 5 h, while the mean time for gastric symptoms was 3 h. CONCLUSION: Anisakis simplex parasitism was the causative agent of allergic and gastric symptoms. Gastroallergic anisakiasis appears to be a relatively common disease, that may have been underdiagnosed.
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BACKGROUND: Anisakis simplex can cause allergic reactions in sensitized patients. Some of these reactions are related to acute parasitism, as is shown in gastroallergic anisakiasis (anisakiasis with digestive and predominantly allergic symptoms). At present, a nonseafood diet is recommended for all patients with any kind of A. simplex allergy. We wished to confirm the clinical suspicion that patients with allergic symptoms after ingestion of raw or undercooked seafood who are sensitized to A. simplex, and diagnosed with gastroallergic anisakiasis, can tolerate the ingestion of seafood when the parasites are dead and noninfective. METHODS: We included patients diagnosed with gastroallergic anisakiasis (positive skin prick test or/and serum specific IgE to A. simplex, with one or more parasites found by gastroscopy in the stomach). Patients included in the study gave written, informed consent. Specimens of A. simplex about 2 cm long were selected, placed in capsules, and frozen at -20 degrees C for more than 48 h to make them noninfective. We administered 11 specimens to every patient at the hospital. If they tolerated the larvae, they were told to eat well-frozen seafood (-20 degrees C at least 48 h). After 6 months, the patients were re-evaluated. RESULTS: Five patients accepted the challenge with noninfective A. simplex larvae. All tolerated the noninfective larvae. After eating deep-frozen seafood for 6 months, no patient suffered a reaction. CONCLUSIONS: In gastroallergic anisakiasis, the antigens of the live parasite probably cause the allergic symptoms. Patients with this disease can tolerate deep-frozen seafood, in which the parasites are dead.
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Case report of a 64-year-old woman with increasing dyspnea and cough. She cared at home for 8 parakeets (Melopsittacus undulatus). Subsequent studies revealed a restrictive pulmonary defect and transbronchial biopsy, a histological bronchiolitis obliterans (BO). No significant elevated anti-avian IgG could be detected, probably because of a transient hypogammaglobulinaemia. The implication of antigenic exposure to avian antigens in the pathogenesis of BO is discussed.
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BACKGROUND: The ingestion of Anisakidae ssp larvae parasitized fish can cause anisakiasis. Allergic reactions after ingestion of safely cooked but parasitized fish have been reported. METHODS: Twenty-three patients who suffered allergic reactions after seafood ingestion, with negative skin tests were studied. Anisakis simplex sensitization was assessed by skin prick test and/or specific serum Immunoglobulin E (IgE). Total serum IgE and specific IgE against the implicated seafood and Ascaris lumbricoides were also determined. RESULTS: Manifestations of Anisakis simplex allergy were urticaria/angioedema (18/23) patients and anaphylaxis (5/23). Gastric symptoms were also observed (3/23). Sea fish and shellfish were implicated. Raw and cooked seafood ingestion caused reactions. Total serum IgE ranged from 13 to 7200 KU/L. Specific IgE to Anisakis simplex was positive (> 0.35 KU/L) in all patients, and skin tests were positive in 20. Serum-specific IgE and skin tests to the involved seafoods were negative in every patient. Serum-specific IgE to Ascaris lumbricoides was negative in 13 patients. No association between total IgE and the eosinophil count (r < 0.1) was observed, but there was some association between total IgE and specific IgE to Anisakis simplex (r = 0.58). CONCLUSION: Anisakis simplex sensitization is the cause of allergic reactions after seafood ingestion. It is important to pay attention to this new "food allergy" to diagnose correctly the etiology of adverse food reactions.
BACKGROUND: Dermatitis of and around the eye is common. Allergic contact reactions from phenylephrine are rare despite extensive use by ophthalmologists. Previous reports do not indicate crossreactivity between phenylephrine and other sympathomimetic drugs in patch testing. METHODS: We report three cases of allergic contact reactions (dermato-conjunctivitis) after eyedrops. Skin prick tests, epicutaneous testing with the implicated drugs, additives, and a complete patch test battery, TRUE test (Upjohn-Pharmacia, Sweden), were performed in each patient. RESULTS: All skin prick tests were negative. The three patients showed positive patch tests to phenylephrine and one of them also to ephedrine. Tolerance of the other eyedrops without phenylephrine was verified by challenge. CONCLUSION: Phenylephrine was the responsible agent for the reactions in our patients as confirmed by clinical findings and positive patch tests. Our findings suggest the central structure as the sensitizing part of drug in the second patient. Patch testing is essential for diagnosis of allergic contact reactions of and around the eye.
Hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis is a lung disease caused by a large group of inhaled antigens of various sources. The most common HP occurring in the farm environment is classically caused by exposure to various thermophilic actinomycetes and fungi that can grow in the farm environment. Pullularia species and thermophilic actinomycetes have been involved in HP related to humidifier water and saunas. Our case illustrates the value of a site visit in the diagnosis of HP. During a visit to the covered and heated swimming-pool where our patient used to swim we could see that favourable conditions to fungal growth existed. To determine the possible aetiological agents of a suspected HP, cultures from several parts of the swimming-pool were taken. These cultures showed an intense growth of thermophilic actinomycetes, Neurospora and Aspergillus species. Precipitating antibodies against Neurospora species and Mycropolyspora faeni were detected. A case of HP related to a covered and heated swimming-pool environment is reported. Thermophilic actinomycetes and Neurospora species may be the causing agents.
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Esparto grass (Stipa tenacissima), which is commonly found in the Mediterranean area, has a wide variety of uses. Five plaster workers from the same family developed cough, dyspnea, malaise, and fever after exposure to the esparto fiber used in their work for the previous few years. They showed a significant decrease in symptoms when away from work. Precipitating antibodies against an esparto extract were found in the sera of all patients. Specific IgG antibodies against Aspergillus fumigatus were detected. A. fumigatus was identified after microbiologic evaluation of esparto fiber samples. The dust derived from fungi-contaminated esparto fibers can cause hypersensitivity pneumonitis in exposed subjects. The causative antigen is A. fumigatus. When esparto fibers were strongly contaminated by fungi, all the workers developed a clinical picture compatible with hypersensitivity pneumonitis. The coincidental finding of an occupational and a familiar condition is unusual.
Carboplatin (CP) hypersensitivity reactions have been reported in nearly 12 % of patients treated with this drug. The pathophysiologic mechanisms of these reactions have not been entirely elucidated. Various hypotheses are under discussion. CP hypersensitivity reactions could be IgE-mediated, caused by low-molecular platinum compounds acting as haptens. Platinum salts are also able to release histamine from basophils and mast cells, and some events seem to be non-immune-mediated direct histamine release. We report a case of CP tolerance induction in a 65-year-old man. During the third course of CP he experienced an anaphylactic reaction. Skin testing was negative. Suspecting the possibility of an anaphylactoid reaction due to histamine release, we developed a protocol to induce tolerance. Pre-medication with corticosteroid and antihistaminic was performed before intravenous CP infusion. The bag with CP was first infused 60 ml/h for 30 minutes; the infusion was well tolerated and infusion was continued at 100 ml/h for the next 60 minutes and thereafter at 120 ml/h until the bag was finished. Following this "desensitization", monthly courses of CP using the same protocol have been well tolerated.