Clinical Experience
IgE-mediated reactions
In sensitised individuals, Asparagus can induce symptoms of food allergy through ingestion, respiratory symptoms through inhalation, or cutaneous allergy through skin contact (1). Occupational contact dermatitis, contact urticaria, rhinoconjunctivitis and asthma have been reported (13-15).
Both delayed cell-mediated reactions and IgE-mediated reactions secondary to Asparagus have been described. IgE-mediated reactions can occur as food allergy or can be due to cutaneous or respiratory exposure, which is often occupational. Most reports of allergic reactions to Asparagus are from occupational settings. Anaphylaxis is the most common clinical picture of food allergy, while contact urticaria, rhinitis and asthma, appearing either isolated or associated, are typical clinical pictures of occupational allergy. Sensitisation to different allergens is the likely cause of the different reactions to Asparagus (4,16).
Significantly, there appears to be no single typical clinical pattern for the expression of Asparagus allergy. In a Spanish study of 27 patients who had been diagnosed in the previous 5 years with hypersensitivity to Asparagus, 10 were diagnosed with urticaria or allergic contact dermatitis. All of these 27 cases seemed to result from occupational exposure (80% packing employees and 20% housewives). IgE antibodies for Asparagus were detected in 19 patients. Five had associated symptoms of respiratory allergy. Ten patients were diagnosed with rhinoconjunctivitis, of whom 8 had coexisting occupational asthma, confirmed by means of bronchial provocation. With the exception of 1 patient with asthma who had experienced an episode of severe anaphylaxis, all the others consumed Asparagus without symptoms. The authors attribute this to the fact that the LTPs are located preferentially in the external layers of the plant, which were removed before its consumption. In a group of 3 subjects who were diagnosed with allergy from ingestion of Asparagus, in 2 the symptoms were those of anaphylaxis, and 1 experienced only oral allergy syndrome. None of these were occupationally exposed to Asparagus. The authors concluded that the Asparagus LTPs appeared to be associated with more severe symptoms, e.g., anaphylaxis (12).
These findings were further elaborated upon in a second report evaluating these 27 subjects: 8 had allergic contact dermatitis alone, 17 had IgE-mediated allergy, and 2 had both allergic contact dermatitis and IgE-mediated allergy. Positive patch tests with crude Asparagus extract but not with lipid transfer protein were observed in subjects with allergic contact dermatitis (n=10). Of 19 patients with IgE-mediated disease, 10 had contact urticaria after Asparagus handling. Of these, 5 subjects and 5 others without skin allergy showed respiratory symptoms. Eight were diagnosed with occupational asthma, and this was confirmed by positive Asparagus inhalation challenge, whereas the remaining 2 had isolated rhinitis. Four patients experienced immediate food-allergic reactions following ingestion of Asparagus; 3 reported anaphylaxis, and 1 experienced oral allergic syndrome. IgE antibody-binding proteins of 15 and 45-70 kDa were detected in 10 subjects. Of 10 subjects with skin reactivity to lipid transfer proteins, 6 showed bands at 15 kDa. The presence of IgE antibodies or skin reactivity for lipid transfer proteins was demonstrated in those with asthma (62%) and anaphylaxis (67%). The study concluded that Asparagus may result in occupational allergy, inducing allergic contact dermatitis as well as IgE-mediated reactions, that severe disease (anaphylaxis or asthma) is common, and that lipid transfer proteins appeared to play a major role (5).
In a study assessing the role of lipid transfer proteins in asparagus allergy, 18 patients with allergy to asparagus were enrolled. Asparagus allergy resulted in symptoms of asthma in 7, anaphylaxis in 1, rhinoconjunctivis in 1, oral allergy syndrome in 1, contact urticaria in 6, and contact dermatitis in 2. Three patients had a combination of two symptoms. IgE antibody testing was positive in all, varying from 0.43 to 12.7 kUA/l. The majority were exposed to Asparagus in an occupational setting (4).
Conjunctivitis, rhinitis, tightness of the throat and coughing during preparation of fresh Asparagus have been reported in 2 individuals. No symptoms occurred while the individuals were eating the cooked food. The authors suggest that the allergen was inhaled. Skin-prick tests with native green and white Asparagus were strongly positive, but negative with cooked Asparagus. Both patients had measurable levels of IgE antibodies against Asparagus (3.0 and 6.2 kU/l respectively). The Asparagus-specific IgE antibodies of the 2 patients were inhibited only by Asparagus, indicating that the patients were specifically sensitised by Asparagus and were not affected by cross-reactivity. No immunological cross-reactions could be detected (17).
Allergy to Asparagus may not always be obvious. In a 4-year-old child with multi-food allergy, significant skin reactivity was found to be directed at a number of foods, including Asparagus. However, IgE antibody testing was not able to detect Asparagus IgE above 0.35 kUA/l (18).
Acute urticaria after ingestion of Asparagus has been reported (19). Two patients were reported with IgE-mediated contact urticaria to canned Asparagus (2).
Occupational asthma and rhinoconjuctivitis within 10 minutes were reported to occur in a 28-year-old man due to inhalation of Asparagus allergens during cutting of the spears while harvesting Asparagus (1).
Other reactions
Allergic contact dermatitis and contact urticaria have been caused by Asparagus (9,20). A 53-year-old farm worker presented with a 3-year history of occupational allergic contact dermatitis to Asparagus (8).
Fixed food eruptions caused by Asparagus in a 50-year-old white woman were reported. She presented with 2 sharply marginated, round, slightly elevated erythemas on her right forearm and left chest wall that appeared a few hours after ingestion of tinned Asparagus and persisted for more than 4 weeks, then faded slowly without treatment, leaving circumscribed areas of hyperpigmentation. She later experienced another 2 episodes at exactly the same locations after eating either fresh or tinned Asparagus. These areas of erythema never developed independently of Asparagus intake (21).
A 55-year-old cook presented with seasonal (always in May) recurrent eczema on both hands, which prevented him from working. He also reported several episodes of dysphagia and dyspnoea after ingestion of asparagus. IgE antibody level to Asparagus was 15.1 kUA/l whereas IgE antibodies directed against other Liliaceae vegetables including Garlic and Onion could not be detected. Skin reactivity detected using prick-to-prick tests with native material of fresh, raw Asparagus and Asparagus cooked at 100 °C were positive, whereas Onion, Garlic, and Leek were negative. Epicutaneous patch testing with Asparagus resulted in a strong delayed-type skin reaction with a peak response on day 2 (22).
Asparagus is associated with the production of malodorous urine. This occurs in approximately 43% of people, and the propensity has been shown to remain with individuals for virtually a lifetime. Genetic studies suggest an autosomal dominant trait. Those who produce this odour assume that everyone does, and those who do not produce it have no idea of its potential olfactory consequences (23-24).
