Did you mean: (Urticaria camp; angioedema)?
- Genome-wide association study in NSAID-induced acute urticaria/angioedema in Spanish and Han Chinese populations. [Meta-Analysis]
- PPharmacogenomics 2013; 14(15):1857-69
- CONCLUSIONS: The associations described were different from those related to the metabolism of arachidonic acid and could provide new mechanisms underlying NSAID-induced AUA.
- Parameters of the classical complement pathway predict disease severity in hereditary angioedema. [Journal Article]
- CIClin Immunol 2011; 139(1):85-93
- Functional C1-inhibitor (C1-inh) and C4 are potential severity markers of hereditary angioedema due to deficiency of C1-inh (HAE-C1-inh), and the complexes generated through complement activation may...
Functional C1-inhibitor (C1-inh) and C4 are potential severity markers of hereditary angioedema due to deficiency of C1-inh (HAE-C1-inh), and the complexes generated through complement activation may be relevant. We studied the association between disease severity and complement parameters in 105 HAE-C1-inh patients. Disease severity was characterized by the number of angioedema attacks or alternatively, by the number of C1-inh concentrate ampoules (C1-inh-amp) used for the treatment of attacks. Median C1rC1sC1-inh level was higher (32.8 U/ml vs. 3.4 U/ml; p<0.0001) in patients, compared to controls. C1rC1sC1-inh and C1-inh strongly correlated with attack number and C1-inh-amp, both in the whole patient population and in the subgroup on danazol prophylaxis. Both C1rC1sC1-inh and C1-inh are suitable for predicting disease severity based on attack frequency and C1-inh-amp (OR=4.38[1.43-13.43], p=0.010 and 11.78[2.54-54.67], p=0.002, respectively). We presume that both C1rC1sC1-inh and C1-inh might prove sensitive predictors of the severity of HAE-C1-inh.
- Comparison of two basophil activation markers CD63 and CD203c in the diagnosis of amoxicillin allergy. [Controlled Clinical Trial]
- CEClin Exp Allergy 2008; 38(6):921-8
- CONCLUSIONS: CD203c seems to be a more sensitive activation marker of basophils than CD63 for the diagnosis of amoxicillin allergy.
- Immediate hypersensitivity to penicillins. Studies on Italian subjects. [Journal Article]
- AAllergy 1997; 52(1):89-93
- The IgE response, the involvement of the different penicillins available for therapeutic use, and the specificity of the IgE antibodies found in a group of penicillin-allergic subjects from Italy wer...
The IgE response, the involvement of the different penicillins available for therapeutic use, and the specificity of the IgE antibodies found in a group of penicillin-allergic subjects from Italy were studied. Thirty subjects with a history of allergic reactions to penicillins were studied. In vivo and in vitro specific IgE antibodies were determined to different penicillin determinants. Fifteen subjects developed anaphylactic responses and the remainder urticaria and angioedema. The drug most frequently involved in the patients' allergic reactions was ampicillin (AMP). The benzylpenicilloyl (BPO) skin test was positive in 16 (53.3%) patients, whereas 23 (76.6%) patients were positive to minor determinant mixture (MDM), benzylpenicillin (PG), AMP, or amoxicillin (AX). When classified according to initial reaction type, most anaphylactic patients (93.3%) were associated with minor determinant reactivity, whereas most urticaria patients (80%) reacted to BPO. RAST results for the anaphylactic and urticaria subgroups were similar. RAST inhibition showed that most sera contained highly cross-reactive IgE antibodies. There was evidence of a specific response to AX and PG (one patient each). These data show that in a population of penicillin-allergic patients from Italy, AMP was the main drug inducing the allergic reaction. In skin tests and RAST, patients exhibited heterogeneous IgE responses with little indication of specific reactivity to AMP.
- Immediate allergic reactions to amoxicillin. [Randomized Controlled Trial]
- AAllergy 1994; 49(5):317-22
- A large group of patients with suspected allergic reactions to beta-lactam antibiotics was evaluated. A detailed clinical history, together with skin tests, RAST (radioallergosorbent test), and contr...
A large group of patients with suspected allergic reactions to beta-lactam antibiotics was evaluated. A detailed clinical history, together with skin tests, RAST (radioallergosorbent test), and controlled challenge tests, was used to establish whether patients allergic to beta-lactam antibiotics had selective immediate allergic responses to amoxicillin (AX) or were cross-reacting with other penicillin derivatives. Skin tests were performed with benzylpenicilloyl-poly-L-lysine (BPO-PLL), benzylpenicilloate, benzylpenicillin (PG), ampicillin (AMP), and AX. RAST for BPO-PLL and AX-PLL was done. When both skin test and RAST for BPO were negative, single-blind, placebo-controlled challenge tests were done to ensure tolerance of PG or sensitivity to AX. A total of 177 patients were diagnosed as allergic to beta-lactam antibiotics. We selected the 54 (30.5%) cases of immediate AX allergy with good tolerance of PG. Anaphylaxis was seen in 37 patients (69%), the other 17 (31%) having urticaria and/or angioedema. All the patients were skin test negative to BPO; 49 of 51 (96%) were also negative to MDM, and 44 of 46 (96%) to PG. Skin tests with AX were positive in 34 (63%) patients. RAST was positive for AX in 22 patients (41%) and to BPO in just 5 (9%). None of the sera with negative RAST for AX were positive to BPO. Challenge tests with AX were performed in 23 subjects (43%) to establish the diagnosis of immediate allergic reaction to AX, and in 15 cases (28%) both skin test and RAST for AX were negative. PG was well tolerated by all 54 patients. We describe the largest group of AX-allergic patients who have tolerated PG reported so far. Diagnosis of these patients can be achieved only if specific AX-related reagents are employed. Further studies are necessary to determine the exact extent of this problem and to improve the efficacy of diagnostic methods.
- Eczematous and immunologic diseases. [Review]
- JAJ Am Acad Dermatol 1984; 11(5 Pt 2):948-56
- Mast cells in allergic diseases and mastocytosis. [Review]
- WJWest J Med 1982; 137(3):195-212
- Mast cells with their stores of vasoactive and chemotactic mediators are central to the pathogenesis of allergic diseases. The cross-linking of receptorbound IgE molecules on the surface of mast cell...
Mast cells with their stores of vasoactive and chemotactic mediators are central to the pathogenesis of allergic diseases. The cross-linking of receptorbound IgE molecules on the surface of mast cells initiates a complex chain of events, including calcium ion influx, phospholipid methylation and turnover and cyclic nucleotide metabolism, ultimately resulting in the release of mediators of immediate hypersensitivity. These mast cell mediators are important in smooth muscle reactivity, in the recruitment of eosinophilic and neutrophilic leukocytes and in the generation of secondary chemical mediators. Histologic evidence of mast cell degranulation, biochemical evidence of mast cell mediators in blood and tissues and clinical evidence of signs and symptoms reproducible by these mediators have strongly supported the crucial role of mast cells in asthma, urticaria, anaphylaxis, rhinitis and mastocytosis. Because of their unique location at host environment interfaces, mast cells may both participate in allergic diseases and promote homeostasis.
- The regulation of complement activity by pharmacologic agents. [Review]
- JIJ Immunopharmacol 1980; 2(1):1-47
- The immunological basis of immediate hypersensitivity. [Journal Article]
- AFAust Fam Physician 1979; 8(1):38-9, 41-3, 45-6
- IgE is a homocytotropic antibody which binds to the surface of the mast cell. Antigen with affinity for IgE triggers conformational change at the cell surface, resulting in the release of chemical me...
IgE is a homocytotropic antibody which binds to the surface of the mast cell. Antigen with affinity for IgE triggers conformational change at the cell surface, resulting in the release of chemical mediators from the mast cell granules. The mediators histamine, slow reacting substance of anaphylaxis and eosinophil chemotactic factor cause smooth muscle contraction, increased capillary permeability, eosinophil attraction and increased glandular secretions. The release of mediators from the mast cell granules is controlled by intracellular levels of cyclic nucleotides. In particular, elevated cyclic AMP inhibits mediator release. Adrenergic, cholinergic and prostaglandin receptors all influence mediator release. The characteristic immunopathology of immediate hypersensitivity reactions is a result of local or systemic mediator release. Such reactions include anaphylaxis, asthma, allergic rhinitis, urticaria and angioedema. Similar immunopathology may sometimes result from mechanisms not involving IgE or histamine mediators. Routine investigation of patients with immediate hypersensitivity should include eosinophil counts and IgE levels in blood and secretions, and immediate hypersensitivity skin tests. RAST testing is not routine. Therapeutic principles of these reactions include restoration of inhibitory levels of cyclic nucleotides, antagonism of mediator effects and immunological manipulation of the IgE mediated allergic reaction.
- The human plasma kallikrein-kinin system. [Review]
- PHProg Hematol 1971; 7(0):255-98