Evaluation of cutaneous hypersensitivity to aluminum by routine patch testing with A1C1(3).
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Biomedical subjects
Publications and source records attributed to R Jarisch.
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The age- and sex-related distribution of positive patch test reactions was investigated in 234 children (0-7 years, n = 72 and 8-14 years, n = 162), 1200 adults (20 to 50 years) and 295 elderly patients (> or = 70 years) with suspected allergic contact dermatitis using a European standard series. In girls from 0 to 7 years, the most frequent contact allergens were thimerosal (37.5%) and nickel (27.5%), in girls from 8 to 14 years, nickel (28.7%) and thimerosal (26.6%), in women, thimerosal (25.3%) and nickel (25.2%), and in elderly women, nickel (12.6%) and balsam of Peru (9.7%). The most frequent contact allergens in boys from 0 to 7 years were ethylmercuric chloride (28.1%) and thimerosal (25.0%), in boys from 8 to 14 years, thimerosal (30.9%) and ethylmercuric chloride (14.7%), in men, thimerosal (21.1%) and ethylmercuric chloride (13.7%) and in elderly men, nickel (11.2%) and balsam of Peru (6.7%). Females showed more positive reactions than males. Whilst 0 to 7 year-old girls and boys showed relatively more frequent reactions, the elderly of both sexes were clearly less affected. Nickel is the most frequent contact allergen in females of 8 years and more. In men, thimerosal is most frequent and reactions to balsam of Peru show a peak incidence in the elderly. Results indicate that patch testing should be considered in children and elderly patients with appropriate indications.
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Headache can be induced by histamine in wine in patients suffering from histamine intolerance, a disease characterized by impaired histamine degradation based on reduced diamine oxidase activity or a lack of the enzyme. Diamine oxidase is localized in the jejunal mucosa and is the most important enzyme metabolising histamine. It is competitively inhibited by alcohol and numerous drugs. In preliminary investigations, assessment of diamine oxidase levels gave decreased activity (0.03 nKat/l) in patients with histamine intolerance compared to healthy controls (0.07 nKat/l). In pregnancy, diamine oxidase levels are known to be about 500-fold elevated, giving mean levels of 25.0 nKat/l. Other biogenic amines such as phenylethylamine or serotonin may be causative for wine/food-induced headache. In experimental models, headache has been induced by histamine infusion as well as red wine provocation. Histamine-induced headache is a vascular headache likely to be caused by nitric oxide which probably represents a key molecule in vascular headaches. A histamine-free diet is the treatment of choice for patients with histamine intolerance and chronic headache. To start treatment, an antihistamine (H1 blocker) for 14 days as well as a histamine-free diet for at least 4 weeks are recommended. Clinical improvement to the diet as well as in vitro tests for plasma histamine and diamine oxidase in the serum as well as vitamin B6 levels have to confirm the diagnosis. As supportive treatment, a vitamin B6 (pyridoxal phosphate) substitution appears useful in histamine-intolerant patients as pyridoxal phosphate seems to be crucial for diamine oxidase activity. Histamine intolerance, based on reduced diamine oxidase activity or a lack in the enzyme is causative for wine/food-induced chronic headache. According to the localization of diamine oxidase in the jejunal mucosa, histamine intolerance is primarily a disease of intestinal origin. A histamine-free diet is the treatment of choice in histamine-intolerant patients suffering from chronic headache. In addition, it is also important to avoid diamine-oxidase-blocking drugs and alcohol which act as inhibitors of diamine oxidase. As avoidance of histamine-rich food is simple, inexpensive and harmless treatment, histamine-containing food such as cheese and alcoholic beverages should be labeled.
A 38-year-old woman with a history of seasonal rhinoconjunctivitis reported repeated attacks of wheezing after drinking various alcoholic beverages. Two consecutive histamine provocations using two identical samples of red wine containing 200 micrograms histamine/l and 3,700 micrograms/l, respectively, were performed in a double-blind placebo-controlled fashion to assess a possible histamine-induced bronchoconstriction. Lung function, plasma histamine, skin temperature, pulse rate and symptoms were assessed. In 3 male controls, four consecutive wine tests were performed in a randomised double-blind placebo-controlled fashion. Drinking wine with 3,700 micrograms histamine/l caused coughing and wheezing with a decrease in lung function. Plasma histamine showed an increase at 10 and 20 min and decreased at 30 min both after histamine-rich as well as histamine-poor wine, reaching the peak increase after histamine-rich wine. Controls did not react and plasma histamine levels did not increase. Bronchoconstriction after wine or food rich in histamine seems to be caused by diminished histamine degradation on the basis of reduced activity of diamine oxidase. Histamine in wine may induce bronchoconstriction in patients suffering from histamine intolerance.
BACKGROUND: Children attending a primary school showed symptoms such as headache, cough, rhinitis and epistaxis. Assessment of specific IgE to formaldehyde gave positive results in some children. OBJECTIVE: Was IgE-mediated sensitization as well as symptoms in children associated with formaldehyde exposure at school? METHODS: Sixty-two 8-year-old children attending three forms at a primary school were investigated. Indoor formaldehyde concentrations were measured in classrooms of both schools (one frame construction with particleboard used extensively as panelling vs a brick building) which were consecutively attended. Assessment of specific IgE to formaldehyde was done in all children. Children were transferred to a brick building and 3 months later specific IgE to formaldehyde in pupils showing initially elevated radioallergosorbent test (RAST) values reassessed. In all children symptoms were evaluated by questionnaire before and 3 months after changing school. RESULTS: In the school panelled with particleboard the World Health Organization (WHO) threshold for formaldehyde of 0.050 ppm was crossed in two classrooms (0.075 ppm and 0.069 ppm) whereas in one classroom 0.043 ppm was found. RAST classes of > or = 2 were found in three children, two of them attending the classroom with 0.075 ppm formaldehyde. Elevated RAST classes of > or = 1.3 were found in another 21 pupils. Thirty-eight pupils as well as 19 control children showed RAST classes in the normal range of < or = 1.2. Headache, nose bleeding, rhinitis, fatigue, cough, dry nasal mucosa and burning eyes were found in the affected children. There was a good correlation between symptoms and the formaldehyde concentrations in the classrooms. However, elevated IgE levels to formaldehyde did not correlate with symptoms. Formaldehyde concentrations in the classrooms of the brick built school were 0.029 ppm, 0.023 ppm and 0.026 ppm. After transferral specific IgE to formaldehyde decreased significantly from 1.7 +/- 0.5 to 1.2 +/- 0.2 (P < 0.002) as did the incidence of symptoms. CONCLUSION: Gaseous formaldehyde, besides its irritant action, leads to IgE-mediated sensitization. As children are more sensitive to toxic substances than adults, threshold levels for indoor formaldehyde should be reduced for children.
Specific immunotherapy is the treatment of choice in the therapy of inhalant allergies. Application route and dose regimen, selection and quality of allergens, as well as the individual patient represent different variables of immunotherapy to be considered. Premedication by oral antihistamines is mandatory for the reduction of side effects. Histamine-intolerance represents a contraindication for immunotherapy. Specific immunotherapy is highly efficacious leading to a 50-100% reduction of symptoms in nearly 90% of patients.
A 67-year-old patient developed systemic reactions after application of a formaldehyde-containing tooth filling. She had a clearly positive RAST result for formaldehyde, whereas skin prick testing and patch tests were negative. Sensitization to formaldehyde appears to have occurred 1 year previously. Induction of formaldehyde allergy may represent a major complication during dental treatment, and assessment of specific IgE should be considered in patients at risk.
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Histamine-induced food intolerance is not IgE-mediated. Skin-prick testing and specific IgE to food allergens are typically negative. Food rich in histamine or red wine may cause allergy-like symptoms such as sneezing, flush, skin itching, diarrhoea and even shortness of breath. The suspected reason is a diminished histamine degradation based on a deficiency of diamine oxidase. As diamine oxidase cannot be supplemented, a histamine-free diet was implemented to reduce histamine intake. Forty-five patients with a history of suffering from intolerance to food or wine (n = 17) and chronic headache (n = 28) were put on the diet over months to years. Fish, cheese, hard cured sausages, pickled cabbage and alcoholic beverages had to be avoided. Complaint intensity and drug-use per week prior to and 4 weeks after a histamine-free diet were compared. After 4 weeks on the diet 33/45 patients improved considerably (P < 0.01), eight of them had total remission. In 12/45 patients, however, no changes in symptoms were observed. Symptoms of food or wine intolerance significantly decreased (P < 0.02; treatment of choice), headaches decreased in frequency (P < 0.001), duration and intensity. After eating histamine-rich food symptoms were reproducible and could be eliminated by anti-histamines in most patients. These data indicate the role of histamine in food and wine intolerance and that histamine-rich food causes a worsening of symptoms in patients suffering from chronic headaches. Results obtained support the hypothesis of a deficiency of diamine oxidase in patients with intolerance to food or wine.