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Biomedical subjects

F Wantke

Publications and source records attributed to F Wantke.

36 records · Page 2Linked to original sources
PubMed1996

Exposure to gaseous formaldehyde induces IgE-mediated sensitization to formaldehyde in school-children.

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.

Air Pollution, Indoor↗
PubMed1995

Anaphylaxis after dental treatment with a formaldehyde-containing tooth-filling material.

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.

Aged↗
PubMed1993

Histamine-free diet: treatment of choice for histamine-induced food intolerance and supporting treatment for chronic headaches.

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.

Adolescent↗
PubMed1993

Spontaneous histamine release in whole blood in patients before and after 4 months of specific immunotherapy.

Spontaneous histamine release (SHR) in whole blood was assessed before and after 4 months of specific immunotherapy (SIT) for allergic rhinoconjunctivitis in 32 patients. Spontaneous histamine release was significantly enhanced (P < 0.05) in patients prior to immunotherapy compared with 20 controls. Spontaneous histamine release decreased significantly in patients after 4 months of specific immunotherapy (P < 0.04) and almost reached the same values as spontaneous histamine release in controls. Clinical success of treatment after 4 months was seen in 15 patients (improvement > or =50%), 10 of whom showed a significant decrease in spontaneous histamine release. Decrease of spontaneous histamine release after 4 months indicates the efficacy of specific immunotherapy already at an early stage of treatment. Assessment of spontaneous histamine release appears to be a useful and easily performable method for monitoring success of treatment of patients during specific immunotherapy.

Adolescent↗
PubMed1993

Ethylmercuric chloride: the responsible agent in thimerosal hypersensitivity.

The causative agent of thimerosal allergy (sodium ethylmercury thiosalicylate) has not previously been thoroughly investigated. To evaluate whether the organic mercury component or the thiosalicylic acid molecule induces thimerosal sensitization, 23 patients positive to thimerosal were patch tested with ethylmercuric chloride, thiosalicylic acid and 8 different derivatives of mercury. To date, ethylmercuric chloride has not been tested in thimerosal allergy. 19/23 patients (82%) showed positive patch test reactions to ethylmercuric chloride. 4/23 patients negative to ethylmercuric chloride reacted positively to thimerosal 0.1% but not to thimerosal 0.05%. 8/23 patients (35%) also reacted to other mercurials. 20 controls negative to thimerosal showed negative patch test reactions to ethylmercuric chloride. Neither patients nor controls reacted to thiosalicylic acid. These results indicate that testing with thimerosal 0.1% leads to false-positive reactions and that the ethyl mercury component is the responsible agent in thimerosal allergy.

Adult↗
PubMed1993

[The histamine-free diet].

Food intolerance is not IgE-mediated but caused by histamine. A diminished histamine degradation based on a deficiency of diaminoxidase is suspected to be the reason. The therapeutic efficacy of a histamine-free diet was evaluated in 100 patients with food intolerance and allergic diseases, who were required to avoid fish, cheese, hardcured sausage, pickled cabbage, wine and beer for 4 weeks. Considerable improvement was observed in 57 patients, 15 of whom had total remission. The most striking treatment results were obtained in food or wine intolerance (80% P < 0.05; treatment of choice), bronchial asthma (80%), headache (64%) and urticaria (58%). After ingestion of food rich in histamine clearcut recurrence of atopic eczema was seen in 50% of the patients affected. Histamine plays a major part in food and wine intolerance. Histamine in food causes worsening of symptoms in atopics and patients suffering from headache. The results obtained indicate a deficiency of diaminoxidase in patients with intolerance to food or wine. Histamine levels in alcoholic beverages should be displayed on the labels.

Adolescent↗
PubMedDate not supplied

The red wine provocation test: intolerance to histamine as a model for food intolerance.

Sneezing, flush, headache, diarrhea, skin itch, and shortness of breath are symptoms occurring in patients intolerant to wine after drinking one glass of red wine. The role of histamine in wine intolerance was evaluated by a red wine provocation test in 28 patients with a history of wine intolerance and in 10 controls with good tolerance of wine. Patients were challenged with 125 ml red wine (equivalent to 50 micrograms histamine); blood samples were drawn before and after 15 and 30 minutes. Plasma histamine was assessed by a radioimmunoassay. Lung function tests were performed before and after the wine test. Twenty-two of twenty-eight patients had symptoms showing significantly higher plasma histamine levels 30 minutes after wine challenge (p < .01) compared with asymptomatic controls. Basal histamine levels of patients were higher (p < .05) than in controls. A slight asthmatic attack as well as a 30% decrease of FEF 25 was seen in 2/22 patients. Terfenadine premedication significantly eliminated symptoms in 10/12 patients (p < .05) in a subsequent wine test. Histamine assessment was done in 52 wines (red, white, and champagne) and in 17 beers by radioimmunoassay. Histamine levels ranged from 3-120 micrograms/l in white wines; 15-670 micrograms/l in champagnes; 60-3800 micrograms/l in red wines; and 21-305 micrograms/l in beers. Histamine is causing wine intolerance. Patients intolerant to wine seem to have diminished histamine degradation probably based on a deficiency of diamine oxidase.

Adult↗