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  • 1
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The protective effects of deflazacort against the inflammation that follows the conjunctival provocation test (CPT) by specific allergen were assessed in 24 patients with rhinoconjunctivitis caused by Parietaria judaica in a double-blind study. After a screening CPT, patients were randomized into four treatment groups, each being given deflazacort (oral tablets) at 6, 30, and 60 mg once daily, or matching placebo, for 3 d, outside the pollen season. Clinical evaluation (itching, hyperemia, lacrimation, and swelling of eyelids) and cytologic assessment (number of inflammatory cells in conjunctival scraping and evaluation of ICAM (intercellular adhesion molecule)-1/CD54 expression on epithelial cells) were performed at base line, 30 min (early-phase reaction (EPR), 6 h and 24 h (late-phase reaction (LPR)) after specific CPT, and before and after treatment. Neither the EPR clinical reactions nor the EPR total number of inflammatory cells was modified by deflazacort. However, the LPR clinical effects were significantly reduced by deflazacort at 30 or 60mg/d (P〈0.01), as compared with placebo. The total number of inflammatory cells during LPR was significantly reduced by deflazacort at 30 or 60 nig/d ((P〈0.01), as compared with placebo. Furthermore, CD54 expression was significantly reduced by deflazacort at 30 or 60 mg/d both in the EPR ((P〈0.01) and LPR ((P〈0.01), as compared with placebo. None of the studied indicators were modified at the 6 mg/d dose. This study shows that deflazacort has a highly protective action against clinical and cellular LPR effects induced by the specific CPT, In addition, deflazacort markedly reduces CD54 expression on the conjunctival epithelium during both EPR and LPR.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 47 (1992), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 49 (1994), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Canonica GW, Ciprandi G, Buscaglia S, Pesce G, Bagnasco M. Adhesion molecules of allergic inflammation: recent insights into their functional roles.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Lodoxamide is an antiallergic drug acting as a mast-cell stabilizer, which is effective in the treatment of allergic conjunctivitis. The study aimed to evaluate the effect of lodoxamide eye-drops on the inflammatory early-phase reaction (EPR) changes induced by allergen-specific conjunctival challenge (ASCC). This was a cross-over, double-blind, placebo-controlled, randomized study, including 10 outpatients suffering from allergic rhinoconjunctivitis due to Parietaria judaica. Patients received one drop of lodoxamide tromethamine 0.1% or placebo 30 min before each ASCC. Clinical evaluation and cytologic assessment were done at baseline and 30 min after each ASCC. Lodoxamide induced a reduction in total symptom score and hyperemia during the EPR (P 〈 0.05). Lacrimation, itching/ burning, and eyelid swelling were only slightly (nonsignificantly) reduced. Lodoxamide induced a reduction in the total number of inflammatory cells and neutrophils during the EPR (P 〈 0.02). Eosinophil and lymphocyte number and ICAM-1 expression showed only a slight, not statistically significant decrease. Placebo did not affect the studied parameters. Lodoxamide reduced early clinical events and cellular changes after ASCC consistently with its activity as mast-cell stabilizer. Moreover, lodoxamide was able to downregulate in vitro ICAM-1 expression on the continuously cultured, differentiated conjunctival cell line WK. This was shown both in basal conditions (P 〈 0.05) and upon interferon-gamma stimulation (P 〈 0.03), although at high concentration.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Azelastine is a selective H1-receptor antagonist, which has previously been demonstrated to be effective in the treatment of allergic rhinitis. We have recently demonstrated that nasal azelastine inhibits the clinical and intlammatory events following nasal allergen challenge. Particularly, we focused our attention on ICAM-1 expression on epithelial cells, since it is the natural ligand of LFA-1, an adhesion molecule expressed by leucocytes, including eosinophils.Objective Since azelastine ocular drops are now available, the aim of the present study was the evaluation of the anti-allergic activity in the model of allergen specific conjunctival challenge (ASCC).Methods Twenty outpatients with allergic rhinoconjunctivitis due to Parietaria Judaica (Wall Parietary) were included outside the pollen season. The study was designed as randomized, placebo-controlled, double-blind and parallel group, developed in two parts. The fonner investigated the onset of effect of a single dose of azelastine eye drops administered 20min after clinical response due to ASCC. The latter evaluated the clinical and inflammatory parameters following ASCC after 7-days treatment with azelastine. Clinical parameters (hyperaemia, itching, lacrimation and eyelid swelling) were evaluated at baseline, 5, 10, 20 and 30 min (i.e. early phase reaction-EPR) and 6h (i.e. late phase reaction-LPR) after ASCC. Cytological assessment (number of neutrophils, eosinophils. monocytes and lymphocytes) and ICAM-1 expression on conjunctival epithelial cells were evaluated at baseline, 30 min (i.e. early phase reaction-EPR) and 6h (i.e. late phase reaction-LPR) after ASCC.Results When administered 30 min after ASCC, azetastine produced a clinical effect ranging between 10 and 20 min after eye drops administration (P 〈 0.01). After 7 days of treatment, 30 min after ASCC, azelastine induced a reduction of symptom scores during EPR and LPR (P〈0.01), a reduction of inflammatory cell infiltration during both EPR (P 0.01) and LPR (P 0.01), and a reduction of ICAM-1 expression during EPR and LPR (both P 0.01). Placebo did not modify any of the studied parameters.Conclusion Azelastine eye drops exert anti-allergic activity, inducing a rapid improvement of clinical events when administered after ASCC, and reducing both sytiiptoms and cellular infiltration when administered before ASCC. Finally, azelastine down-regulates ICAM-1 expression on epithelial conjunctival cells, confirming the results obtained at nasal level.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Levocabastine is a selective topical H1 antagonist, effective in the treatment of seasonal allergic rhinitis and conjunctivitis.Objective We evaluated the possible effects of levocabastine eye drops on early (EPR) and late phase (LPR) inflammatory changes induced by allergen-specific conjunctival challenge (ASCC). We focused our attention on the possible effect of levocubastine on expression of the intracellular adhesion molecule-1 (ICAM-1) on epithelial cells. Such a phenomenon is likely to play an important role in allergic inflammation.Methods The study was a double-blind, placebo-controlled, randomized trial, performed in cross-over, outside the pollen season. Ten out-patients suffcring from allergic rhinoconjunctivitis due to Parietaria Judaica (wall parietary) were enrolled. Patients randomly received levocabastine eye drops (0.5 mg/mL) or placebo eyedrops, one drop in the left eye (right eye as control), 30 min before ASCC. Clinical evaluation (hyperaemia, burning-itching, lacrimation and eyelid swelling) and cytological assessment (number of neutrophils, eosinophils and lymphocytes, and ICAM-1 expression on conjunctival epithelium) were evaluated at baseline, 30min and 6h after ASCC. In parallel, we evaluated the in vitro effect of levocabastine at concentrations ranging from 2 × 10−9 M to 2 × 10−5M on ICAM-l expression and shedding by a continuously cultured differentiated epithelial cell line (WK).Results Levocabastine reduced symptom scores during EPR (15min and 30min, P 〈 0.002), inflammatory cell infiltration duritig FPR (P 〈 0.002 for neutrophils, eosinophils and lymphocytes) and ICAM-1 expression on epithelium both during EPR (P 〈 0.002) and LPR (P 〈 0.02). LPR symptom scores and inflammatory cell infiltration were only slightly modified by levocabastine treatment. In vitro levocabastine at 2 ± 10−5 M concentration was able to down-regulate basal ICAM-1 expression, although it exerted no effect on ICAM-1 expression by interferon-γ (IFNγ)-stimulated WK cells and on soluble ICAM-1 release by epithelium.Conclusion Levocabastine exerts anti-allcrgJc activity, in that it reduces in vivo inflammatory cell infiltration due to ASCC, and also adhesion molecule expression on conjunctival epithelium. The latter phenomenon may be due, at least in part, to a direct effect of levocabastine on epithelial cells.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The intercellular adhesion molecule ICAM-1 has been detected by immunohistochemical methods on epithelial cells of the conjunctiva and nose during allergic inflammation.Objective The aim of the present study was to evaluate whether ICAM-1 expression on conjunctival epithelium derives from endogenous synthesis or is merely due to passive uptake of soluble ICAM-1 released from inflammatory cells.Methods In situ hybridization was performed using a 3’end dygoxygenin-labelled specific DNA oligonucleotide probe on fixed conjunctival smears from allergic subjects challenged with, or naturally exposed to the allergen, and from healthy subjects. Immunocytochemistry for ICAM-1 was performed by alkaline phosphatase antialkaline phosphatase.Results Results In allergic patients, both naturally exposed to the allergen and after specific challenge, a clear hybridization pattern on epithelial cells was apparent. Out of allergen exposure, some symptomfree pollinosic subjects, as well as a few healthy volunteers showed mild ICAM-1 mRNA cytoplasmic staining in the absence of immunohistochemically detectable ICAM-1. This finding may explain the very early appearance of ICAM-1 on conjunctival epithelium following specific challenge in allergic individuals.Conclusions These results indicate that the presence of ICAM-1 on conjunctival epithelium during allergic inflammation derives from endogenous synthesis and not from uptake of soluble ICAM-l.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 50 (1995), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Buscaglia S, Palma-Carlos AG, Canonica GW. European Academy of Allergology and Clinical Immunology ‘EAACI’ guidelines for continuing medical education. Essentials for accreditation, standards for commercial support, and system of credits.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 45 (1993), S. S35 
    ISSN: 1432-1041
    Keywords: CD54 (intercellular adhesion molecule-1 [ICAM-1]) ; Conjunctival provocation test ; Deflazacort ; early phase reaction ; inflammatory response ; late phase reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The protective effects of deflazacort, (a new heterocyclic glucocorticoid and derivative of prednisolone, with calcium and glucose-sparing effects) on the inflammatory reaction following an allergen-specific conjunctival provocation test (CPT) were assessed in a doubleblind study, in 24 patients suffering from rhinoconjunctivitis due toParietaria judaica. After an initial screening CPT, patients were randomized to four treatment groups, to receive deflazacort, 6, 30 or 60 mg, once daily or placebo, for 3 days, during the low-pollen season. Clinical evaluations (itching, hyperaemia, lacrimation and eyelid swelling), cytological assessment (number of inflammatory cells, i. e. neutrophils, eosinophils and lymphocytes, sampled by conjunctival scraping) and immunocytochemical evaluation of CD54 (intercellular adhesion molecule-1 [ICAM-1]) expression on epithelial cells were performed after CPT, at baseline, after 30 minutes (early-phase reaction [EPR]) and after 6 and 24 hours (late-phase reaction [LPR]), before and after treatment. Neither the nature or severity of clinical events nor the total number of inflammatory cells during the EPR changed during treatment with deflazacort. The severity of the clinical events during the LPR were significantly reduced by deflazacort, 30 and 60 mg/dayP 〈 0.01) compared to the placebo-treated group. The total number of inflammatory cells during the LPR was also significantly reduced by deflazacort, 30 and 60 mg/ day (P 〈 0.01) compared to the placebo-treated group. CD54 expression was significantly reduced by deflazacort, 30 and 60 mg/day both during the EPR (P 〈 0.01) and LPR (P 〈 0.01) compared to the placebo-treated group. Deflazacort, 6 mg/day did not significantly alter clinical, cellular or immunocytochemical variables compared to the placebo-treated group. This study shows that deflazacort has a highly protective effect on clinical and cellular LPR events induced by specific CPT. In addition, deflazacort markedly reduces CD54 expression on conjunctival epithelium during both the EPR and LPR.
    Type of Medium: Electronic Resource
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