Vascular rings can give cough.
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Biomedical subjects
Publications and source records attributed to M C López-Serrano.
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BACKGROUND: Thiomucase is a mucopolysaccharidase obtained from ovine tissues mainly used to facilitate the diffusion of local anaesthetics and in the treatment of cellulitis. A patient with an anaphylaxis in relation to the intramuscular administration of Thiomucase is reported. OBJECTIVE: To investigate Thiomucase allergens and their possible relationship with dander allergens and animal albumins. MATERIAL AND METHODS: Skin prick tests (SPT) and serum-specific IgE were performed with Thiomucase and danders. Thiomucase SDS-PAGE immunoblotting was performed in order to study allergens. RAST/CAP inhibition and SDS-PAGE immunoblotting inhibition were carried out to study the cross-reactivity. RESULTS: Skin prick tests (SPT) were positive to Thiomucase, animal dander (cat, dog, sheep, other), bovine serum albumin (BSA), and echinococcus. Specific IgE was also positive to Thiomucase, animal dander (cat, dog, sheep, other), BSA and echinococcus. In the RAST-CAP inhibition assays BSA was nearly completely inhibited by Thiomucase, Thiomucase was partially inhibited by BSA and cat and Echinococcus granulosus was partially inhibited by sheep and Thiomucase. In the Thiomucase SDS-PAGE immunoblotting several proteins fixed IgE, ranging from 20 kDa to > 94 kDa, the strongest with 43 kDa. The IgE fixation to BSA, cat and sheep in the SDS-PAGE immunoblotting was completely inhibited by the preincubation of the serum with Thiomucase. CONCLUSIONS: An IgE-mediated anaphylaxis to Thiomucase is documented. Multiple allergens are recognized in Thiomucase by the patient serum, the main with 43 kDa. Partial cross-reactivity with BSA, cat dander and sheep dander is documented.
BACKGROUND: Human subjects can be parasitized by Anisakis simplex by eating raw or undercooked fish. Gastric anisakiasis is probably the most frequent clinical entity presenting with severe epigastric pain, vomiting, and diarrhea. In gastroallergic anisakiasis hypersensitivity symptoms predominate. OBJECTIVE: We sought to describe clinical features, laboratory data, and gastroscopic findings in gastroallergic anisakiasis. METHODS: We selected 40 patients presenting to the emergency department with an acute allergic reaction, and if we suspected acute parasitism by A simplex, a fiberoptic gastroscopy was performed. In 20 patients we could detect one or more nematodes; these patients are referred to as group A. Those in whom no worm could be found are referred to as group B (n = 20). A detailed history, clinical features, gastroscopic findings, laboratory data, and skin prick test responses were compared. RESULTS: Long-time intervals of up to 26 hours between fish intake and onset of hypersensitivity symptoms were found (group A, 5.4 +/- 6.3 hours; group B, 5.3 +/- 2.6 hours). Patients in groups A and B did not differ with respect to allergic symptoms (urticaria, angioedema, erythema, bronchospasm, and anaphylaxis) or the mainly light abdominal symptoms (upper abdominal pain, nausea, vomiting, and diarrhea). No significant differences were found with respect to age, time interval between fish intake and onset of symptoms, white cell and eosinophil counts, specific IgE levels against A simplex, or total IgE levels. CONCLUSIONS: The peculiar sometimes long-time interval between fish intake and onset of allergic symptoms render the diagnosis difficult. An early gastroscopy can confirm the diagnosis and prevent complications. We suggest that gastroallergic anisakiasis be considered a distinct clinical entity in which the predominant symptoms are hypersensitivity symptoms and in which the correct diagnosis is not only important in the management of the acute reaction but also in the prevention of further allergic episodes.
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.
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.
BACKGROUND: Sensitization to Anisakis simplex (A. simplex) has been documented to produce severe allergic reactions following ingestion of mainly raw or under-cooked parasitized fish. False positive skin prick tests (SPT) or specific IgE against this nematode and cross-reactivity restricts diagnosis. Gastric anisakiasis and gastro-allergic anisakiasis occur if fish is parasitized by live A. simplex OBJECTIVE: To investigate if serial serological analysis could be useful in the diagnosis of acute parasitation by this nematode. METHODS: We included 41 patients who experienced an allergic reaction and/or abdominal symptoms after ingestion of raw or undercooked fish and displayed specific IgE against A. simplex. Total and specific IgE were determined two times: in the 24-h period after onset of clinical symptoms and after 1 month. SPTs were performed against A. simplex and implicated fish. A fibre optic gastroscopy was performed in 22 patients. RESULTS: Median total IgE was 80.0 (Interquartile range [IQR] 41.5-186.5) kU/L in the first evaluation and 247.0 (IQR 96.5-649.5) kU/L after 1 month. Median specific IgE against A. simplex was 11.4 (IQR 7.1-33.5) kU/L in the first 24 h and 36.8 (IQR 19.5-79.5) kU/L after 1 month. A rise of total IgE was observed in 35 of 41 patients (P<0.00001) and a rise in specific IgE against A. simplex in 37 of 41 patients (P<0.00001). Mean percentage increment was 392% (215-571%; 95% confidence interval [CI]) for total IgE and 339% (177-502%; 95% CI) for specific IgE. In nine of 22 gastroscopic examinations at least one larva, identified as A. simplex, could be detected by our microbiology service. In this group (n = 9) a rise of total and specific IgE was detected in eight patients (89%) (P = 0.02). CONCLUSIONS: We consider a rise of total and specific IgE in the first month after an allergic reaction as a useful tool in the diagnosis of gastro-allergic anisakiasis (together with patient's history), even if the parasite cannot be seen with fibre optic gastroscopy. The important rise of total and specific IgE against A. simplex can be considered as a reaction induced by the live parasitizing larva in the context of a polyclonal immunological stimulation.
Acute urticaria and angio-oedema are common in primary care and in the emergency unit. Food allergy is one possible cause. We describe gastric anisakiasis, in which symptoms are often not obviously related to eating raw fish. A study was made of patients presenting at the emergency department who had allergic symptoms such as urticaria or angio-oedema and had recently eaten raw or undercooked fish. They were divided into two groups. Patients in group A (n = 13) also had abdominal symptoms and were diagnosed as having gastric anisakiasis by fibre-optic gastroscopy where third-stage larvae of Anisakis simplex were visualized and extracted. Skin prick tests and specific IgE to A. simplex were positive. Patients in group B (n = 13) had only allergic symptoms after eating raw fish. Eleven of 13 patients had positive skin prick tests and specific IgE to A. simplex. Three of 15 control subjects had positive skin prick tests and specific IgE to A. simplex. Allergic symptoms appeared from 2 to 20 h (mean 5.0) after ingestion in group A and from 20 min to 23 h (mean 4.3 h) in group B. Gastric symptoms in group A disappeared rapidly after extraction of the larvae. Allergic symptoms disappeared in most cases within the first 24 h. We suggest that the allergic symptoms in group A as well as in group B were mainly due to parasitization by A. simplex in sensitized patients. Gastric anisakiasis may be a widely underdiagnosed clinical entity.
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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.
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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Hypersensitivity pneumonitis or extrinsic allergic alveolitis can be defined as a lung disease caused by a wide group of antigens that reach the lung by inhalation of organic and/or inorganic dust of various sources. The esparto (Stipa Tenacissima and Ligeum Spartum) is an herbaceous of the grass family used in the production of ropes, canvas, sandals, mats, baskets, and so forth. It is also used in the construction industry for the production of paper paste. Inhalation of esparto dust has been reported as cause of hypersensitivity pneumonitis. The existence of precipitating antibodies against esparto extract has been proved. During the esparto fiber manufacturing process, esparto grass can be contaminated by moulds and thermophilic actinomycetes, which have been described as the causing antigens of hypersensitivity pneumonitis in plaster workers. We present a case of occupational hypersensitivity pneumonitis in a plaster worker. Clinical findings, precipitating antibodies, and evolution, after having removed him from his work, confirmed the diagnosis. In our case, Aspergillus species contaminating esparto are probably the antigens that caused the disease.
A 65-year-old woman experienced immediate itchy erythematous patches at the subcutaneous injection sites of sodium enoxaparin. An erythematous and infiltrated 40 x 20 mm lesion on the abdominal wall could be observed at the site of enoxaparin injection when she was referred to our clinic 48 h after injection. Lesions subsided spontaneously within 1 week. She had been on this treatment 1 and 3 years before without any adverse reaction. To clarify the nature of the reaction, epicutaneous tests with sodium enoxaparin, calcium nadroparin and calcium heparin were performed, all with negative results. Skin prick test with sodium enoxaparin was also negative. Biopsy of the cutaneous lesion showed spongiotic dermatitis, strongly suggesting a delayed hypersensitivity mechanism. We report here on a new case of delayed hypersensitivity to enoxaparin. Being female, overweight and having prolonged application of the drug were suggested risk factors present in our patient. Biopsy was essential for diagnosis. Although type IV hypersensitivity reactions to enoxaparin are rare, we should start to suspect this condition in order not to underdiagnose it.
We report the case of a woman who after taking ampicillin and amoxicillin developed two severe cutaneous reactions with generalized erythema and maculopapular rash, which later turned into blisters with subsequent desquamation. She was clinically diagnosed with erythema multiforme syndrome after positive delayed cutaneous tests with benzylpenicillin, amoxicillin and ampicillin allowed for a more specific diagnosis. There are very few references to patients with drug reactions to betalactams who have positive skin prick or intradermal test but show delayed hypersensitivity, as was the case in our patient.
Different allergenic proteins have been involved in cross-reactivity among animals. Albumins seem to be cross-sensitizing allergenic components. The aim of this study was to assess the importance of albumin as a cross-reactive allergen in patients sensitized to cat, dog and horse. One hundred and seventeen patients sensitized to cat were tested for IgE reactivity using skin prick tests and RAST assays with cat, dog and horse hair/dander extracts and their purified albumin extracts. RAST-inhibition studies were carried out to assess cross-reactivity among cat, dog and horse and among their purified albumins. It was found that 22% of patients exhibited specific IgE to cat albumin; 41% of patients sensitized to cat were also sensitized to dog and horse. Out of these patients, 21% had IgE to three albumins and 17% to two. Reciprocal inhibitions were observed among cat, dog and horse albumins and also among cat, dog and horse hair/dander extracts, using in the latter experiment sera from patients not sensitized to albumins. IgE binding to horse extract was inhibited 30% by its homologous albumin and IgE binding to cat and dog extracts in almost 15% by their respective albumins. It was concluded that albumins from these three animals share some epitopes that account for the cross-reactivity observed in around one-third of patients sensitized to cat, dog and horse. Nevertheless, more than 50% of specific IgE that cross-reacts among these three animals is directed to allergens other than albumin.