Biomedical subjects
B Przybilla
Publications and source records attributed to B Przybilla.
Molecular analysis of T-cell clonality with concomitant specific T-cell proliferation in vitro in nickel-allergic individuals.
BACKGROUND: The peripheral blood mononuclear cells (PBMC) of individuals with nickel contact allergy are reported to proliferate to a varying degree upon nickel stimulation in vitro. Different phenotypes of the T cells involved are described. With regard to preferential use of the T-cell receptor (TCR), analysis of the several families of the TCR-gamma gene allows rearrangement evaluation of all T cells regardless of predominant surface expression of TCR alpha/beta. METHODS: The PBMC of 10 nickel-allergic and five nonallergic individuals were cultured for 4 days in the presence of either medium, PHA, NiSO4, or tetanus toxoid (TT). Proliferation was measured by radioactive thymidine uptake and expressed as stimulation index (SI). T-cell clonality was assessed by analysis of the TCR-gamma chain gene, including the use of PCR with a primer combination covering the four main groups (Vgamma1-8, Vgamma9, Vgamma10, and Vgamma11) of the variable region of the TCR-beta chain gene. RESULTS: In the allergic individuals, proliferation to NiSO4 was significantly (P<0.05) higher than in nonallergics (mean SI: 18.05/17.87 vs 0.67/2.27). In unstimulated and PHA-stimulated cultures, there was a random TCR spectrum in both groups. In contrast, in nickel-allergic individuals or individuals with recent TT-booster, oligoclonality could be observed in the correspondingly stimulated cultures. CONCLUSION: In addition to proliferation assay, analysis of T-cell clonality may be a further means to characterize clinical hypersensitivity reactions on the basis of antigen-dependent oligoclonal T-cell expansion, as in the case of tissue-infiltrating lymphocytes.
'Deep impact' contact allergy after subcutaneous injection of local anesthetics.
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Ultrarush immunotherapy in patients with Hymenoptera venom allergy.
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Patients still reacting to a sting challenge while receiving conventional Hymenoptera venom immunotherapy are protected by increased venom doses.
BACKGROUND: Up to 20% of patients allergic to Hymenoptera venom are not protected by conventional venom immunotherapy (VIT) with 100 microg of any single venom. OBJECTIVE: We sought to evaluate the efficacy of an increased venom dose in patients allergic to Hymenoptera venom still reacting systemically to a sting challenge despite immunotherapy with 100 microg of venom every 4 weeks. METHODS: In this retrospective study patients were included who still had reacted systemically to a sting challenge with a living bee or wasp despite VIT with a maintenance dose of 100 microg every 4 weeks. The maintenance dose was increased to 150 or 200 microg every 4 weeks, and a second sting challenge was performed. If a patient reacted again, the dose was further increased. Baseline mast-cell tryptase levels were assessed by using a fluoroenzyme immunoassay in stored patient sera. RESULTS: While receiving a maintenance dose of 100 microg of venom every 4 weeks for 7 to 38 months, 18 patients reacted systemically to a bee sting and 22 reacted to a wasp sting. After an increase of the maintenance dose to 150 microg, 2 of 4 patients allergic to bee venom (BV) and 6 of 6 patients allergic to yellow jacket venom (YJV) no longer reacted systemically to the sting challenge. The respective rates of full protection were 13 of 14 and 15 of 16 in patients with an increase of the maintenance dose to 200 microg from the start. Of those 4 individuals not protected by the first dose increase, one patient allergic to BV (prior dose of 150 microg) and one patient allergic to YJV (prior dose of 200 microg) did not react systemically to a further sting challenge while receiving 200 microg of BV or 250 microg of YJV, respectively. One patient allergic to BV who had a systemic reaction to the sting challenge while receiving 150 microg was not protected after a dose increase to 200 microg; she later received a dose of 400 microg of BV, and no further sting challenge was performed. The patient allergic to BV who still reacted systemically after a first dose increase to 200 microg was a female patient with urticaria pigmentosa. She had repeated systemic adverse reactions to further BV immunotherapy, necessitating discontinuation of the treatment; however, she tolerated well VIT with 200 microg of YJV. In all other patients, no unusual adverse reactions to the increased venom doses were observed. Baseline serum tryptase levels were elevated above 13.5 microg/L (95th percentile in normal subjects) in 9 (28.1%) of 32 patients. CONCLUSIONS: The majority of patients allergic to Hymenoptera venom who still reacted systemically to a sting challenge despite VIT with a dose of 100 microg every 4 weeks can be fully protected by an increased maintenance dose. This dose increase is well tolerated by most patients. The rather high proportion of patients with elevated baseline serum tryptase levels necessitates further investigation of a possible association between mastocytosis and treatment failure of conventionally dosed VIT.
[Anaphylactic reaction to Ficus benjamina (weeping fig)].
Ficus benjamina (weeping fig) is a widespread indoor ornamental plant. Allergens of Ficus benjamina are a well-known cause of IgE-mediated respiratory diseases. We treated a 32-year-old female who for 10 years had suffered from perennial rhinoconjunctivitis. When dusting her 2 meter high Ficus benjamina, she developed an anaphylactic reaction which resolved without sequelae. Skin prick testing revealed a strong immediate type reaction to a Ficus extract, the serum concentration of specific IgE-antibodies to Ficus was > 100 kU/I (CAP class 6). In view of these strong test reactions and the conclusive history, no challenge tests with Ficus allergens were performed. After removal of the Ficus plants which she had owned for 17 years and after thorough cleaning of her dwelling, the patient's symptoms of perennial rhinoconjunctivitis stopped. The patient also was sensitized to, but not allergic to natural rubber latex, which occurs frequently in Ficus allergy and probably is due to cross reactivity to allergens from both sources. As Ficus benjamina is an important source of indoor allergens, it should not be used in dwellings or work places.
Intolerance of osteosynthesis material: evidence of dichromate contact allergy with concomitant oligoclonal T-cell infiltrate and TH1-type cytokine expression in the peri-implantar tissue.
BACKGROUND: We report on a 37-year-old man without history of previous allergic disease who developed an aseptic intolerance reaction to a chromium-cobalt alloy, with local discomfort, loosening, and absence of fracture healing. Both in vivo and in vitro allergoimmunologic diagnostic tests were performed. METHODS: Patch testing was done with a European standard series. Specific serum IgE was measured by CAP-FEIA. In addition to immunohistology (APAAP method), peri-implantar tissue was further analyzed by PCR to determine T-cell-receptor-gamma rearrangement and thus the potential clonal (antigen-driven) T-cell repertoire. The actual tissue mRNA expression for IL-4, IL-6, and IFN-gamma was visualized by RT-PCR. RESULTS: Skin testing gave a delayed-type reaction to dichromate. Specific serum IgE to natural rubber latex and grass pollen was found--but without clinical symptoms. Immunohistology revealed a monocytic and dense T-cell infiltrate. The latter, instead of being random, showed an oligoclonal T-cell receptor rearrangement. In addition, there was TH1-type mediator expression (IL-6 and IFN-gamma, but not IL-4). CONCLUSIONS: Skin test, examination of peri-implantar tissue, and the prompt healing after replacement of the osteosynthesis material suggest an allergic reaction. PCR analysis of peri-implantar tissue can further help to identify and understand allergy-mediated implant intolerance reactions.
Systemic vitamin C and vitamin E do not prevent photoprovocation test reactions in polymorphous light eruption.
The possible influence of oxidative stress is discussed in the pathogenesis of polymorphous light eruption (PLE). A double-blind, placebo-controlled study of prophylactic treatment with systemic administration of vitamin C (3 g/d) and E (1500 IU/d) for 8 days was undertaken in 9 patients with PLE (verum, n=4; placebo, n=5). Evaluation of the maximal effects after photoprovocation before and after intake of the antioxidants revealed a reduction of most skin reactions (overall skin reaction, papules/vesicles) in both groups with marked differences in the placebo group. The antioxidants in the doses given and over the time period used did not influence the development of PLE, but might interfere with immunosuppressive effects of repeated photoprovocation tests.
Cheilitis due to nickel contact allergy in a trumpet player.
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Delayed prick test reaction identifies amoxicillin as elicitor of baboon syndrome.
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Association between actinic keratoses and potentially photosensitizing drugs.
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[Exertion-induced anaphylaxis after eating pork and beef].
HISTORY AND CLINICAL FINDINGS: A 72-year-old woman developed generalized urticaria. Quincke oedema, shortness of breath and hypotension two hours after eating a meal containing pork and after mild physical activity (ironing) in-between. She was treated by an emergency physician and then admitted to hospital for one day of monitoring her condition. During the past several years such episodes of generalized urticaria had recurred twice to four times a year. INVESTIGATIONS: Pin-prick tests gave an immediate-type reaction to beef but not to pork. Specific serum IgE antibodies were demonstrated to pork and beef, cat's epithelia, milk albumin and casein. Oral provocation tests were negative for pork and beef. But when pork and beef were eaten mild physical activity (bicycle ergometry at 20 W), generalized urticaria occurred after eating pork and beef, but not after drinking milk. TREATMENT AND COURSE: Exercise-induced anaphylaxis to pork and beef was diagnosed. No allergic reaction has occurred in more than 12 months of avoiding eating these meats. CONCLUSION: The picture of exercise-induced anaphylaxis caused by food allergy can be precipitated by even mild activity. This must be taken into account in the diagnosis of systemic rapid-reaction response and in the performance of provocation tests.
[Latex-free explantations?].
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["Acute generalized exanthematic pustulosis induced by nystatin"].
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[Induction of penicillin tolerance in therapy of neurosyphilis in penicillin allergy].
Pharmacologically or immunologically induced hypersensitivity to penicillin is frequent. Immunological, i.e., allergic, hypersensitivity reactions are among the most important side effects and can lead to severe and life-threatening reactions. All types of allergic reactions have been described secondary to penicillin therapy. Immediate type hypersensitivity reactions, the symptoms of which range from urticaria and angioedema to respiratory and cardiovascular symptoms, and finally to life threatening full anaphylactic shock are particularly dangerous. This case-report demonstrates that in a patient allergic to penicillin, in whom there is a vital indication to administer this compound, the drug can be given safely after tolerance induction.
[Tryptase, a marker for the activation and localization of mast cells].
The serine protease tryptase (ECNr. 3.4. 21.59), which is almost exclusively expressed in mast cells, is released by mast cell degranulation in an enzymatically active form together with other mediators, e.g. histamine, into the extracellular space and the circulation. The capability of the enzyme to directly stimulate several cell types as well as to cleave polypeptide hormones and to activate pro-enzymes suggests a role for tryptase in inflammatory and tissue-remodeling processes. Therefore, in the skin, a role of tryptase is suggested not only in mastocytosis and immediate type hypersensitivity reactions, but also in other inflammatory diseases, degenerative or neoplastic conditions as well as in wound healing, where an accumulation and/or activation of mast cells is found. Extracellular tryptase may be superior to histamine as a parameter for the onset and course of immediate type reactions and as an indicator for the activation of mast cells in other conditions. Its absence during histamine-liberating reactions may suggest basophil activation. In addition, tryptase has been shown to be a sensitive and specific marker for the localization of mast cells in tissues.
Mastocytosis associated with severe wasp sting anaphylaxis detected by elevated serum mast cell tryptase levels.
A markedly elevated serum level of mast cell tryptase (77.6 microg/L; 95th percentile in normals 13.5 microg/L) was detected in a patient treated for 5 years with wasp venom immunotherapy because of severe anaphylaxis following a wasp sting. Retrospective analysis of stored serum samples taken during the course of immunotherapy revealed that the tryptase level had been elevated for at least 3 years. Despite several dermatological examinations, skin changes of mastocytosis had been missed. Re-examination of the patient revealed sparse macules on the thorax and thighs; Darier's sign was negative. Histologically, mast cell accumulation in these lesions was demonstrable. No signs of systemic mastocytosis were detected. The most appropriate diagnosis was telangiectasia macularis eruptiva perstans. Even in patients with highly elevated tryptase levels, mastocytosis may go undiagnosed. As mastocytosis predisposes to severe anaphylaxis, the condition should be looked for in patients with such reactions by clinical examination and measurement of serum tryptase levels.
Delayed contact hypersensitivity to non-steroidal anti-inflammatory drugs.
Several non-steroidal anti-inflammatory drugs (NSAIDs) are available for topical treatment of acute soft tissue trauma or degenerative musculoskeletal disorders; the NSAID bufexamac is mainly used for therapy of chronic inflammatory skin diseases. In order to assess the occurrence of contact allergy to NSAIDs in 371 consecutive patients presenting for diagnosis of presumed contact allergy, patch tests were performed with a standard series and additionally with a series of NSAIDs, comprising acetylsalicylic acid, bufexamac, diclofenac, etofenamate, felbinac, flufenamic acid, ibuprofen, indomethacin, and piroxicam. 17 individuals (4.6%) exhibited delayed hypersensitivity to one of the NSAID preparations: 12 patients (3.2%) had patch test reactions to bufexamac, 2 (0.5%) to etofenamate, 2 (0.5%) to indomethacin, and 1 patient (0.3%) to flufenamic acid. These patch test results corresponded well to the individual history in 11 individuals (including 10 patients with reactions to bufexamac), and in 2 patients the clinical relevance of the reactions was probable. In view of the high frequency of allergic contact reactions to bufexamac, we propose to test this drug particularly in patients with atopic eczema or other chronic eczematous diseases.