Late Cutaneous Reactions Research Articles

Evidence from a breast cancer hypofractionated schedule: late skin toxicity assessed by ultrasound

BackgroundFeasibility of whole breast hypofractionated radiotherapy schedules in breast conserving therapy is recognized however concerns remain about the role of the boost dose on the overall treatment’s potential toxicity. In this study we report on the possibility to quantitatively evaluate radiation induced toxicity in patients treated with an abbreviated course with major concern in the irradiated boost region.MethodsEighty-nine patients who underwent conservative surgery for early-stage breast cancer followed by adjuvant accelerated hypofractionated whole breast radiotherapy were included in this study to assess skin and subcutaneous tissue late toxicity by means of ultrasonographic quantitative examination. For each patient the skin thickness was measured at four positions: on the irradiated breast, in the boost region and in the corresponding positions in the contra-lateral not treated breast. All patients were scanned by the same radiologist to reduce potential inter-operator variability, the operator was blind to the scoring of the patient CTCv3 late toxicity as well as patient treatment characteristics. Ultrasound assessment and clinical evaluation were compared.ResultsThe median time between the end of adjuvant radiotherapy and ultrasound examination was 20.5 months. The measured mean skin thickness in the irradiated breast was 2.13 ± 0.72 mm while in the mirror region of the contra-lateral healthy breast was 1.61 ± 0.29 mm. The measured mean skin thickness in the irradiated boost region was 2.25 ± 0.79 mm versus 1.63 ± 0.33 mm in the corresponding region of contra-lateral healthy breast. The mean increment in skin thickness respect to the counterpart in the healthy breast was 0.52 ± 0.67 mm and 0.62 ± 0.74 mm for the breast and the boost region respectively. A significant direct correlation was found between the increment in skin thickness in the irradiated breast and in the boost region with fibrosis (G ≥ 1).ConclusionsIn this study results from a breast cancer hypofractionated schedule in terms of late skin toxicity are reported. In particular our study confirms that late cutaneous reactions can be reliably assed by ultrasonographic examination, also discriminating between regions irradiated at different doses, and that this instrumental evaluation is in agreement with clinical stated toxicity.

The Influence of Schizophyllum commune on Asthma Severity

The sensitization and exposure to fungal allergens have been reported to be associated with asthma. The aim of this study was to clarify the impact of sensitization to Schizophyllum commune (S. commune) on the severity and exacerbations of asthma. Ninety-two patients with asthma of various levels of severity [mild (n=18), moderate (28), and severe (46)] and exacerbation severity [moderate (n=43) and severe (6)] were retrospectively examined with regard to fungal sensitization such as specific IgE or intradermal skin reactions against S. commune and other common allergens. We also classified the patients into three groups: (1) three or more asthma attacks during the past year (F-BA) (n=29),(2) one or two asthma attacks (NF-BA) (n=20), and (3) no asthma attack (C-BA) (n=43). The positive rate of late cutaneous reactions to S. commune was higher in patients with severe asthma (41.2%) than with moderate (26.1%) or mild asthma (6.7%), and was significantly different among the three groups (P<0.05). Although the ratio did not show a significant difference between the patients with severe (83.3%) or moderate (36.1%) exacerbation, it was higher in F-BA (60.9%) than in NF-BA (21.1%) and C-BA patients (10.0%), and it was significantly different among the three groups (P=0.0002). Multivariate analysis identified positive results for late-phase skin reactions to S. commune and the age of the patients as an independent determinant of asthma severity, and the skin results and %FVC an independent determinant of exacerbation frequency. This study demonstrated that S. commune is an environmental fungus that appears to enhance both the severity of asthma and the exacerbation frequency.

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Nonsteroidal anti-inflammatory drugs (NSAIDs) are responsible for 21-25% of reported adverse drug events which include immunological and nonimmunological hypersensitivity reactions. This study presents up-to-date information on pathomechanisms, clinical spectrum, diagnostic tools and management of hypersensitivity reactions to NSAIDs. Clinically, NSAID hypersensitivity is particularly manifested by bronchial asthma, rhinosinusitis, anaphylaxis or urticaria and variety of late cutaneous and organ-specific reactions. Diagnosis of hypersensitivity to a NSAID includes understanding of the underlying mechanism and is necessary for prevention and management. A stepwise approach to the diagnosis of hypersensitivity to NSAIDs is proposed, including clinical history, in vitro testing and/or provocation test with a culprit or alternative drug depending on the type of the reaction. The diagnostic process should result in providing the patient with written information both on forbidden and on alternative drugs.

Dose dependence and time course of the immunologic response to administration of standardized cat allergen extract

The immunologic response to allergen immunotherapy with 3 serial 5-fold doses of cat extract has been studied after approximately 5 weeks of immunotherapy. The highest dose containing 15 mug of Fel d 1 produced the most consistent and favorable response. It is unknown whether the comparative response on reaching a maintenance dose is maintained with long-term maintenance therapy. The purpose of this investigation was to evaluate the immunologic responses with these 3 serial doses of cat hair and dander extract at baseline, after reaching the maintenance dose (approximately 5 weeks), and after 1 year of maintenance immunotherapy. Twenty-eight patients with cat allergy randomized in a double-blind study were assigned to one of 4 treatment groups: placebo or cat hair and dander extract containing 0.6 mug of Fel d 1, 3 mug of Fel d 1, and 15 mug of Fel d 1 at maintenance. Studies included skin prick tests and late cutaneous reactions with cat hair and dander extract, titrated nasal challenges with the extract, serum cat allergen-specific IgG4 and IgE measurement, and flow cytometric and ELISA analysis of whole blood and intranasal cytokines (TGF-beta, IL-10, IFN-gamma, IL-4, and IL-5). Twenty-six subjects completed the study. After both 5 weeks and 1 year, significant and dose-dependent differences were seen with total symptom scores on nasal challenge ( P < .0001), with titrated skin prick testing with cat dander extract at 5 weeks ( P = .014) and 1 year ( P < .0001), and with cat-specific IgG4 measurement at 5 weeks ( P = .004) and 1 year ( P = .003). At 1 year, neither flow cytometry of whole blood nor ELISA evaluation of nasal cytokines demonstrated any significant differences among the treatment groups. The response to titrated nasal allergen challenge, titrated skin prick testing, and allergen-specific IgG4 measurement to cat immunotherapy at 5 weeks is predictive of the response at 1 year.

Efficacy and safety of desensitization to allopurinol following cutaneous reactions

To evaluate the long-term efficacy and safety of slow oral desensitization in the management of patients with hyperuricemia and allopurinol-induced maculopapular eruptions. A retrospective evaluation of an oral desensitization regimen using gradual dosage-escalation of allopurinol in 32 patients (30 with gout and 2 with chronic lymphocytic leukemia) whose therapy was interrupted because of a pruritic cutaneous reaction to the drug. Twenty-one men and 11 women with a mean age of 63 years (range 17-83 years), a mean serum urate level of 618 micromoles/liter (range 495-750) (or, mean 10.4 mg/dl [range 8.3-12.6]), and a mean serum creatinine level of 249 micromoles/liter (range 75-753) (or, mean 2.8 mg/dl [range 0.8-8.5]) were studied. Desensitization failed in 4 patients because of unmanageable recurrent rash. Twenty-eight patients completed the desensitization procedure to a target allopurinol dosage of 50-100 mg/day, 21 without deviation from the protocol for a mean of 30.5 days (range 21-56 days) and 7 requiring dosage adjustments because of a recurrent rash over 53.8 days (range 40-189 days). Seven of these 28 patients developed late cutaneous reactions 1-20 months postdesensitization, 4 responding to dosage modification and 3 discontinuing the drug. Twenty-five of the 32 patients (78%) continued to take allopurinol; their mean duration of followup was 32.6 months (range 3-92 months) and the mean postdesensitization serum urate level was 318 micromoles/liter (range 187-452) (or, mean 5.3 mg/dl [range 3.0-7.5]). The study confirms the long-term efficacy and safety of slow oral desensitization to allopurinol in patients with maculopapular eruptions, particularly in those with gout, who cannot be treated with uricosurics or other urate-lowering drugs. Although pruritic skin eruptions may recur both during and after desensitization, most of these cutaneous reactions can be managed by temporary withdrawal of allopurinol and dosage adjustment.

Isolated late cutaneous reactions to allergen skin testing in children.

Occasionally parents report a reaction developing at the site of an allergen skin test several hours after application of the test, despite there having been no immediate reaction. The medical literature contains little information regarding isolated late reactions (ILRs) to allergen skin testing. The goal of this project was to determine the incidence of ILRs in children undergoing allergen skin testing. Prick and intradermal (ID) skin testing was performed for routine clinical indications in an allergy clinic. Children with a positive histamine control, and at least one negative immediate reaction to allergen skin testing were enrolled in the study. The parents were given detailed instructions to examine the skin test sites 6 hours later, and to record the size of any erythematous indurated sites. Circles of various diameters were included on the report form to assist the parents' size estimates. Fifty-seven children enrolled in the study and 50 returned the forms. No patients reported ILRs to prick skin tests. Eighteen of the 50 respondents reported 40 ILRs to ID tests, of > or = 5 mm diameter; 7 of these were > or = 10 mm. The most common allergen causing ILR was cockroach, accounting for 20% of the ILRs. Each of the other allergens also caused ILRs. The clinical history did not show a definite correlation of symptoms with exposure to the allergens causing ILRs, although all 14 patients with ILRs to indoor allergens had year-round symptoms. There was no correlation between the incidence of ILRs and age, gender, or diagnosis of asthma. ILRs to allergen skin testing occurred in 36% of pediatric allergy clinic patients. The clinical significance of such reactions is unknown.

111 Attenuation of late cutaneous and asthmatic reactions following administration of short allergen-derived T cell peptide epitopes

111 Attenuation of late cutaneous and asthmatic reactions following administration of short allergen-derived T cell peptide epitopes

The effect of salmeterol and salbutamol on mediator release and skin responses in immediate and late phase allergic cutaneous reactions.

Salmeterol is a long-acting beta2-agonist which in animal studies has been shown to possess anti-inflammatory effects on early (EAR) and late (LPR) phase allergic responses. To evaluate the anti-inflammatory effects of intradermally injected salmeterol and salbutamol on clinical and biochemical EAR and LPR in human skin. Measurement of wheal and flare reactions to allergen, codeine, and histamine, and LPR (induration) to allergen. Assessment of histamine and prostaglandin D2 (PGD2) release by microdialysis technique in EAR, and measurement of mediators in LPR by suction blister technique. Both beta2-agonists inhibited allergen-induced histamine release and wheal and flare reactions with maximum inhibition of 40-50% at 10(-6) M, a concentration which reduced PGD2 synthesis by approximately 55%. Histamine release by codeine and skin reactions to codeine and histamine were not or only marginally reduced. Salmeterol and salbutamol (10(-6) M) inhibited clinical LPR at 6 h by 71% and 48%, Except for the clinical LPR, no statistical differences were found between the two drugs on any parameters. None of the drugs inhibited levels of histamine, tryptase, myeloperoxidase, or eosinophil cationic protein in LPR. Salmeterol and salbutamol inhibited allergen-induced skin responses, and reduced mediator release in EAR but not LPR. In general, the anti-inflammatory effects of salmeterol did not differ from those induced by salbutamol.

Effects of local treatment with salmeterol and terbutaline on anti-IgE-induced wheal, flare, and late induration in human skin

The capacity of terbutaline and the long-acting beta 2-agonist salmeterol to suppress wheal-and-flare reactions (WFRs) to intradermal antihuman IgE and to histamine was evaluated in 36 healthy volunteers. We also examined effects of the two drugs on the subsequent late cutaneous reaction (LCR) to anti-IgE. Salmeterol (10(-10)-10(-6) M) and terbutaline (10(-10)-10(-5) M), injected intradermally 2 or 15 min before anti-IgE challenge, produced a dose-dependent inhibition of the WFRs to anti-IgE (titer 1 : 10000) with a maximal effect of approximately 60% (wheal) and approximately 75% (flare) by both drugs. On a molar basis, salmeterol was approximately 10-100 times more potent than terbutaline in inhibiting the WFRs. Moreover, the wheal response to histamine (4 nmol) was antagonized by approximately 40% after pretreatment with either salmeterol (10(-5) M) or terbutaline (10(-4) M). We found that both salmeterol and terbutaline exhibited anti-WFR activity for up to 24 h, salmeterol being significantly more potent in this regard. When selecting a 15-min pretreatment interval with equieffective anti-WFR doses from the first dose-response experiments (i.e., a salmeterol: terbutaline ratio of 1 : 10), the WFRs to high-dose anti-IgE (titer 1 : 100) were inhibited by terbutaline (10(-5) M) by 25-30%, but not by salmeterol (10(-6)). On the other hand, salmeterol attenuated (by up to approximately 35%) the subsequent LCR more effectively than terbutaline. As compared to the pretreatment procedure, infiltration of the drugs (single doses) into the wheals 30 min after challenge with anti-IgE (titer 1 : 100) proved to be less effective on the development of LCRs. Taken together, salmeterol was found to express higher potency and have longer duration of action than terbutaline in inhibition of IgE-mediated inflammation in human skin.

A comparison of the effects of oral cetirizine and inhaled beclomethasone on early and late asthmatic responses to allergen and the associated increase in airways hyperresponsiveness

Cetirizine is a non-sedating H1 antihistamine which is effective in the treatment of allergic rhinitis and urticaria. It inhibits eosinophil and basophil chemotaxis in late cutaneous allergic reactions in skin windows. Its effect on early (EAR) and late asthmatic reactions (LAR) is less certain. We examined the effect on EAR and LAR of 3 days treatment with oral cetirizine (15 mg twice daily) compared with a single dose of inhaled beclomethasone 10 min prior to allergen challenge in a placebo-controlled (oral and inhaled) double-blind cross-over design with three treatment arms separated by 14 days. Cetirizine did not significantly inhibit either the EAR or LAR documented by maximum percentage fall in FEV1 (0-3 and 6-9 h) or as area under the curve (AUC between 0 and 3 and 6-9 h). Beclomethasone inhibited the LAR compared with placebo (P = 0.02) when expressed as AUC (6-9 h). This did not quite reach statistical significance (P = 0.06) when expressed as maximal percentage late fall in FEV1 between 6 and 9 h. A greater than twofold increase in airways responsiveness to methacholine was observed 3 h after challenge which was significantly reduced by beclomethasone compared with placebo (P < 0.02) and cetirizine (P < 0.05). The data suggest that oral cetirizine does not significantly inhibit either the EAR or LAR. Beclomethasone inhibited both the early increase in airways responsiveness and the subsequent LAR. Our study also confirms the view that early increases in airway responsiveness precede the late response and suggests that these associated events are not dissociable by the pharmacological treatments employed in this study.

The skin as a model to study the pathogenesis of IgE-mediated acute and late-phase responses

101. Laroche D, Chrysanthou S, Lefran~ois C, et al. Evidence of a progressive degranulation of basophil in subjects operated on without adverse reaction. Agents Actions 1992;36(suppl C):C199-C200. 102. De Paulis A, Valentini G, Spadaro G, Lupoli S, Tirri G, Marone G. Human basophil releasability. VIII. Increased basophil releasability in patients with scleroderma. Arthritis Rheum 1991;34:1289-96. 103. Yunginger JW, Nelson DR, Squillace DL, et al. Laboratory investigation of deaths due to anaphylaxis. J Forensic Sci 1991;36:857-65. 104. Takeishi T, Martin TR, Katona IM, Finkelman FD, Galli SJ. Differences in the expression of the cardiopulmonary alterations associated with anti-immunoglobulin E-induced or active anaphylaxis in mast cell-deficient and normal mice: mast cells are not required for the cardiopulmonary changes associated with certain fatal anaphylactic responses. J Clin Invest 1991;88:598-608. 105. Sampson HA, Mendelson L, Rosen JP. Fatal and nearfatal anaphylactic reactions to food in children and adolescents [Comments]. N Engl J Med 1992;327:380-4. 106. Shalit M, Schwartz LB, yon Allmen C, Atkins PC, Lavker RM, Zweiman B. Release of histamine and tryptase during continuous and interrupted cutaneous challenge with allergen in humans. J ALLERCY CLIN IMVnJNOL 1990; 86:117-25. 107. Lavker RM, Schechter NM, Guzzo C, Lazarus GS. Aggressive topical corticosteroid therapy: a novel approach to mast-cell-dependent cutaneous disorders. Dermatologica 1987;175:213-6. 108. Lavker RM, Schechter NM, Lazarus GS. Effects of topical corticosteroids on human dermis. Br J Dermatol 1986;115:101-7. 109. Jarjour NN, Calhoun WJ, Schwartz LB, Busse WW. Elevated bronchoalveolar lavage fluid histamine levels in allergic asthmatics are associated with increased airway obstruction. Am Rev Resp Dis 1991;144:83-7. 110. Broide DH, Gleich GJ, Cuomo AJ, et al. Evidence of ongoing mast cell and eosinophil degranulation in symptomatic asthma airway. J A~LEROY CLlr~ IMMUNOL, 1991; 88:637-48. 111. Liu MC, Bleecker ER, Lichtenstein LM, et al. Evidence for elevated levels of histamine, prostaglandin D2, and other bronchoconstricting prostaglandins in the airways of subjects with mild asthma. Am Rev Respir Dis 1990; 142:126-32. 112. Sedgwick JB, Calhoun WJ, Gleich GJ, et al. Immediate and late airway response of allergic rhinitis patients to segmental antigen challenge: characterization of eosinophil and mast cell mediators. Am Rev Respir Dis 1991; 144:1274-81. 113. Liu MC, Hubbard WC, Proud D, et al. Immediate and late inflammatory responses to ragweed antigen challenge of the peripheral airways in allergic asthmatics: cellular, mediator, and permeability changes. Am Rev Respir Dis 1991;144:51-8. 114. Koshino T, Teshima S, Fukushima N, et al. Identification of basophils by immunohistochemistry in the airways of post-mortem cases of fatal asthma. Clin Exp Allergy 1993;23:919-25.

Macrophage inflammatory protein-1 alpha and monocyte chemoattractant peptide-1 elicit immediate and late cutaneous reactions and activate murine mast cells in vivo.

We have previously reported that monocyte chemoattractant protein-1 (MCP-1) is the most potent histamine-releasing factor (HRF) for basophils. Macrophage inflammatory protein-1 alpha (MIP-1 alpha) has modest histamine-releasing activity. The objective of this study was to investigate whether MCP-1 and MIP-1 alpha would activate mast cells in vivo and induce a cutaneous inflammatory reaction in mice. To this goal, mouse hind footpads were separately injected with 20 microliters of human recombinant MCP-1 or MIP-1 alpha (10(-7) M). Diluent was used as a control in the second footpad. The footpad-swelling response was measured at 30 min, 1 h, and then hourly for 6 h. Both MCP-1 (2.72 +/- 0.2 vs 2.1 +/- 0.03 mm for diluent, n = 8, p < 0.02) and MIP-1 alpha (3.0 +/- 0.1 vs 2.1 +/- 0.03 mm for diluent, n = 8, p < 0.02) induced an immediate swelling reaction. The immediate reaction was followed by a sustained late reaction that peaked within 1 h and lasted for more than 6 h. Histologic examination of the footpads, obtained at hour 2, revealed that MCP-1 caused mild mononuclear cell infiltrates, moderate degranulation of mast cells, and soft tissue swelling. In contrast, MIP-1 alpha induced a severe inflammatory reaction that consisted of neutrophils, mononuclear cells, and degranulated mast cells. Electron microscope examination of the tissue revealed features of extensive mast cell degranulation by MIP-1 alpha and to a lesser extent by MCP-1. Thus, we conclude that mast cells are activated on injection of MCP-1, whereas degranulation of mast cells and recruitment of leukocytes contribute to the footpad reaction induced with MIP-1 alpha.

Eosinophils in late cutaneous reactions

Clinical & Experimental AllergyVolume 21, Issue 3 p. 378-378 Eosinophils in late cutaneous reactions J.-P. Rihoux, J.-P. RihouxSearch for more papers by this author J.-P. Rihoux, J.-P. RihouxSearch for more papers by this author First published: May 1991 https://doi.org/10.1111/j.1365-2222.1991.tb01673.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume21, Issue3May 1991Pages 378-378 RelatedInformation

Eosinophils in late cutaneous reactions

Eosinophils in late cutaneous reactions

Effect of H 1-receptor blockade on late cutaneous reactions to antigen: A double-blind, controlled study

This study is of the effect of the blockade of histamine H 1 receptors by a long-acting antihistamine on the immediate and late clinical response to antigen (Ag) and on the recruitment of eosinophils in the late-phase cutaneous reaction. Ten adult volunteers with late-phase reactions to the intradermal injection of either Dermatophagoides pteronyssinus or Phleum pratense (timothy) pollen performed a double-blind, crossover study. Each volunteer took astemizole, 10 mg, or identical placebo, daily for 2 weeks. Ag in the concentration that induced a late reaction in the screening visit was injected intradermally at the end of each drug period. The early reaction was measured serially for 30 minutes and the late reaction at 4 and 6 hours. Biopsies of the Ag and control sites were also performed at 6 hours. After a 6-week washout period, subjects then took the opposite medication for 2 weeks and returned for skin testing and biopsy. Skin testing demonstrated that astemizole inhibited the immediate response to both histamine and allergen but had no effect on the late response at 4 hours and at 6 hours. Biopsy specimens revealed no significant effect on eosinophil recruitment at 6 hours. We conclude that histamine H 1-receptor blockade has no effect on the late cutaneous reaction to Ag.

Gronneberg R, Dahlen S-E: Interactions between histamine and prostanoids in IgE-dependent, late cutaneous reactions in man. J Allergy Clin Immunol 1990; 85:843–52, 1990.

Gronneberg R, Dahlen S-E: Interactions between histamine and prostanoids in IgE-dependent, late cutaneous reactions in man. J Allergy Clin Immunol 1990; 85:843–52, 1990.

Gronneberg R, Dahlen S-E: Interactions between histamine and prostanoids in IgE-dependent, late cutaneous reactions in man. J Allergy Clin Immunol 1990; 85:843–52, 1990.

Gronneberg R, Dahlen S-E: Interactions between histamine and prostanoids in IgE-dependent, late cutaneous reactions in man. J Allergy Clin Immunol 1990; 85:843–52, 1990.

Platelet-Activating Factor-Induced Immediate and Late Cutaneous Reactions

In atopic subjects, intradermal injection of platelet-activating factor (PAF), 40 and 400 ng, resulted in an immediate edema reaction markedly blocked by cetirizine, 10 mg twice a day. PAF challenge also induced a significant eosinophil accumulation evidenced by a skin window technique at 2, 4, 8 and 24 h. This inflammatory phenomenon was significantly inhibited by cetirizine. In patients with chronic urticaria, PAF, 100 micrograms intradermally, induced immediate and late cutaneous reactions (LCR) also blocked by cetirizine, 10 mg twice a day. These LCR were accompanied by an infiltration of the deep dermis by degranulated eosinophils. The pathophysiological mechanism of the PAF-induced skin reactions is discussed as well as the mechanism of action of cetirizine.

Interactions between histamine and prostanoids in IgE-dependent, late cutaneous reactions in man

The contribution of histamine and cyclooxygenase metabolites of arachidonic acid to the wheal-and-flare reaction (WFR) (0 to 30 minutes) and the late cutaneous reaction (LCR) (1 to 24 hours) evoked by intradermal injection of antihuman IgE was appreciated in a comprehensive study of human volunteers treated with H 1 and H 2 antihistamines, cyclooxy genase inhibitors, as well as the combination of both types of drugs. The findings reinforce the concept that histamine is the major, but not exclusive, mediator of the WFR. In contrast, histamine accounted for but a limited portion of the LCR, but 48 hours of pretreatment with three different cyclooxygenase inhibitors, acetylsalicylic acid, indomethacin, or diclofenac sodium, had but a minor influence on the WFR, whereas all drugs produced a distinct overall inhibition of the LCR. However, for indomethacin, the inhibition was preceded by a potentiation (at 1 to 2 hours), which was abolished by antihistamines, suggesting increased histamine release from skin mast cells after cyclooxygenase inhibition. Furthermore, there was synergism between indomethacin and antihistamines during the LCR, and the combination of diclofenac sodium with antihistamines produced additive inhibition. It is proposed that cyclooxygenase products, such as prostaglandins and thromboxanes, contribute to IgE-dependent skin reactions, both as modulators of mediator release and as vasoactive mediators.

Does reversed‐type anaphylaxis in healthy subjects mimic a real allergic reaction?

Immediate and late cutaneous reactions were induced in healthy and atopic subjects by anti-IgE challenge and a skin-window technique was used in order to verify if the pattern of cells observed at 24 hr was similar in both groups. The study was first performed under basal conditions, and in a second double-blind cross-over step, it was performed again during treatment with cetirizine 10 mg b.i.d. and terfenadine 60 mg b.i.d. Anti-IgE challenge was followed by a significant eosinophil accumulation in atopic subjects only. Cetirizine significantly inhibited this phenomenon while terfenadine showed a mild non-significant inhibitory effect.