Felix Wantke
Johns Hopkins University
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Contact Dermatitis | 1996
Felix Wantke; Wolfgang Hemmer; R. Jahisch; Manfred Götz
The age‐ and sex‐related distribution of positive patch lest 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 (≥70 years) with suspected allergic contact dermatitis using a European standard series. In girls Prom 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.
Allergy and Asthma Proceedings | 1994
Felix Wantke; Manfred Götz; Reinhart Jarisch
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.
International Archives of Allergy and Immunology | 1996
Reinhart Jarisch; Felix Wantke
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.
International Archives of Allergy and Immunology | 1996
Felix Wantke; Wolfgang Hemmer; Thomas Haglmüller; Manfred Götz; Reinhart Jarisch
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 id
The Journal of Allergy and Clinical Immunology | 1999
Felix Wantke; Donald W. MacGlashan; Jacqueline M. Langdon; Susan M. MacDonald
BACKGROUND We have previously shown that the human recombinant histamine releasing factor (HrHRF) caused histamine release from a subset of basophils from donors with allergy, and this release seemed to be dependent on the presence of a certain type of IgE, termed IgE+. IgE molecules that did not support HrHRF-induced histamine release were termed IgE-. However, subsequently we demonstrated that HrHRF primes anti-IgE-antibody-induced histamine release from all basophils, irrespective of the type of IgE on the cell surface. OBJECTIVE Because these data suggested that HrHRF does not exert its biologic effects by binding to IgE, but rather that it interacted with a surface receptor on the basophil, we wanted to obtain functional evidence that HrHRF did or did not bind to the IgE molecule. METHODS The rat basophilic leukemia cell line (RBL-SX38), which has been transfected to express a functional human FcepsilonRI (alpha-, beta-, and gamma-chains of the receptor) in addition to the normal rat FcepsilonRI, was used. The presence of the human FcepsilonRI receptor enables these cells to be sensitized with human IgE. Cells were passively sensitized with 1000 ng/mL human IgE+ or 1000 ng/mL human IgE- for 60 minutes at 37 degrees C. Unsensitized cells served as a control. After the cells were washed, 1 x l0(5) cells were stimulated in the presence of 1 mmol/L Ca2+ with 0.1 microg/mL anti-IgE, 40 microg/mL HrHRF, or 40 microg/mL mouse recombinant HRF (MrHRF), which has 96% homology to HrHRF. RESULTS Mean anti-IgE-induced histamine release was 33% +/- 15%, and there was no difference between IgE+ sensitization (32% +/- 12%) and IgE- sensitization (34% +/- 18%). However, in contrast to human basophil experiments, neither HrHRF (0% +/- 0%) nor MrHRF (3% +/- 5%) caused histamine release in RBL cells sensitized with IgE+. In addition, priming the transfected RBL-SX38 cells or the parental cell line, RBL-2H3 cells, with HrHRF or MrHRF did not increase anti-IgE-induced histamine release. CONCLUSION The results indicate that HrHRF does not bind to IgE, either IgE+ or IgE-. Therefore it appears likely that rHRF signals through its own specific receptor, which is not expressed or functional on RBL-SX38 or RBL-2H3 cells, but which seems to be expressed on basophils of atopic and nonatopic donors.
Contact Dermatitis | 1996
Felix Wantke; Margarete Focke; Wolfgang Hemmer; Manfred Götz; Reinhart Jarisch
Case Report A 4-year-old boy was stung by mosquitoes. Shortly afterwards, the insect repellent Anti-Muckenmilch was applied to his legs and forearms. Minutes later, generalized itch and urticaria developed and the boy wheezed and coughed for about 30 min. He was taken to a general practitioner who applied a topical antihistamine. The wheals had gone by the following morning. Anti-Muckenmilch, Gel tropic version® (Jaico, Belgium), was applied as an open patch test. In addition, the boy was prick-tested against Anti-Muckenmilch, mosquito (Culex pipiens), histamine 10 HEP and saline solution (negative control). Reading was done after 20 min. Total IgE, specific lgE against mosquito (Culex
Contact Dermatitis | 2006
Peter Jung; Gabriele Sesztak-Greinecker; Felix Wantke; Manfred Götz; Reinhart Jarisch; Wolfgang Hemmer
A 79-year-old lady presented with a 2-month history of soreness and swelling of her upper and lower lips, associated with dryness, cracking and ulceration. Prior to this, she had been intermittently applying Vaseline, her own lipsticks and Blistex (a brand of lip slave). Patch tests were performed to the departmental standard series (based on the European standard series with a few additional allergens), a hand and face series, several mint products and 3 of her own lip cosmetics including Blistex. Patch and photopatch tests were also performed to 2 sunscreens chemicals identified as constituents of the lip cosmetics (oxybenzone and ethylhexylmethoxycinnamate). The patch tests were entirely negative. The photopatch tests (UVA 5 J/cm) revealed photoallergy to oxybenzone (benzophenone-3) with no reaction at the non-irradiated site. The Blistex contained oxybenzone, which she was advised to stop using, as well as avoiding all other cosmetics containing this UV filter. At follow-up, 4 months later, the cheilitis had resolved. Discussion
Contact Dermatitis | 1996
Wolfgang Hemmer; Felix Wantke; Margarete Focke; Manfred Götz; Reinhart Jarisch
Case Report A 35-year-old man with oral candidiasis was treated with Daktarin® (miconazole) oral solution. 7 days later, he presented with a generalized, itchy, maculopapular eruption. After 3 weeks of treatment with oral corticosteroids, lesions resolved via desquamation. Patch tests were performed with the GEIDC standard series, Daktarin® solution and its constituents, and an azole battery. The results are shown in Table 1.
Contact Dermatitis | 1996
Wolfgang Hemmer; Margarete Focke; Felix Wantke; Manfred Götz; Reinhart Jarisch
Patients and Methods Over a period of 21/ 2 years, we patch tested 623 patients with suspected hypersensitivity to metals with a series of 21 metal compounds, including ferric chloride 2% aq. and ferrous sulfate 5% pet. Those positive to iron were further tested with the series in Table 1, substances being prepared on the basis of molarity, and applied in Finn Chambers on Scanpor tape. Readings were taken after 2 and 3-4 days and scored according to the recommendations of the ICDRG.
Contact Dermatitis | 1996
Felix Wantke; Wolfgang Hemmer; M. Görz; Reinhart Jarisch
Case Report A 44-year-old woman had applied a moisturizing cream (Clinique Advanced Cream®) daily to her face for at least 5 years. For the past 3 months, itching had occurred a few hours after application, and for the past 2 weeks there had been dermatitis on her face. She was patch tested with the European standard series, an ointment series, Clinique Advanced Cream®, and Clinique Dramatic Cream®. Subsequently, she was patch tested with the 23 individual ingredients of Clinique Advanced Cream® in pet., provided by Clinique USA; and finally with Clinique Advanced Cream®, jojoba oil 1.5% (Clinique), the mixture myristyllactate 0.5%/maleated soybean oil 1.5% (Clinique), myristyllactate 0.5% (Clinique), myristic acid 0.5% (CH3(CH2) 12 OOH, Fluka, Switzerland), myristoleic acid 0.5% (CHJCCH2) 3CH= CH(CH2) 7C02H, Sigma, Germany), maleated soybean oil, not deodorized, 1.5% (Clinique), maleated soybean oil, deodorized, 1.5% (Clinique), soybean oil 1.5%, the mixture glyceryl stearate 4.9%/polyoxyethylene 23-laurylether (Laureth 23) (Clinique), DL-alpha-stearin 4.9% (CH3(CH2)wCOOCH2CH(OH)H20H, Fluka, Switzerland) and stearic acid 4.9% (CH3(CH2)wCOOH). To exclude irritancy, we tested 20 controls (10 female, 10 male, mean age 36.0 years, range 14 to 71 years) with the substances used in the final patch tests. Results