Effect Of Topical Corticosteroids Research Articles

The effects of topical corticosteroids and pimecrolimus skin barrier function, gene expression, and topical drug penetration in atopic eczema and unaffected controls

The effects of topical corticosteroids and pimecrolimus skin barrier function, gene expression, and topical drug penetration in atopic eczema and unaffected controls

The effect of topical corticosteroids in combination with alefacept on circulating T‐cell subsets in psoriasis

Background: Novel therapies against psoriasis are emerging. Alefacept is such a treatment. It selectively targets the memory effector population of T cells and thereby diminishes the psoriatic plaques. In some cases, however, the use of alefacept as a monotherapy is not sufficient. Objective: In the present study we investigate the safety and efficacy of adding topical steroids to alefacept treatment during the initial 4 weeks. Methods: Peripheral blood was obtained from all patients and the presence of specific T‐cell subsets was assessed by flow cytometry. Fourteen patients were included and treated with 15 mg alefacept intramuscularly for a period of 12 weeks. Each of them was randomized to use either betamethasone‐dipropionate cream or a vehicle cream during the first 4 weeks of the alefacept course. Results: Additional topical corticosteroid treatment during the first 4 weeks of alefacept treatment does not have a beneficial effect on the clinical efficacy. Marked changes were seen in the absolute cell counts of various of the analysed T‐cell subsets in peripheral blood after 12 weeks of alefacept, either with or without additional local steroid application. The CD45RO+, CD8+CD45RO+, CD8+CD161+, CD4+CD25+, CD4+CLA+ and CD8+CLA+ populations showed a statistically significant decrease immediately after the treatment period. Further analysis revealed that the addition of local steroid therapy to alefacept results in marked decreases of all T‐cell subsets analysed in this study, in contrast to the addition of the vehiculum only. Conclusion: Alefacept selectively targets the CD45RO+ lymphocyte population, as well as some other subpopulations of lymphocytes. This effect is independent of the use of additional topical therapy during the first 4 weeks. The extent of the decrease, on the contrary, is dependent on the use of corticosteroids.

The Effect of Topical Corticosteroid on Basic Fibroblast Growth Factor in Nasal Polyp Tissue

The etiology of nasal polyposis and pathophysiological mechanisms of polyp formation is still poorly understood. Experimental models have suggested that nasal polyp growth requires extracellular matrix formation and is associated with fibroblast proliferation. Intranasal corticosteroids appear to be useful in reducing nasal polypoid lesions and the likelihood of polyp recurrence after surgery. Basic fibroblast growth factor (bFGF) is a potent angiogenesis factor and is mitogenic for a wide range of cell types. We investigated the alteration of bFGF levels in nasal polyp tissue after administration of topical corticosteroid. Nasal polyp tissues were obtained from 36 patients with diffuse nasal polyposis before and after topical nasal steroid treatment. As a topical nasal steroid mometasone furoate was given for 4 weeks in a dosage of 200 microg/day. The bFGF levels were measured by competitive enzyme immunoassay method. The mean levels of tissue bFGF, before and after topical nasal steroid treatment, were 1485 +/- 826 ng/mg protein (range, 416-3434 ng/mg) and 1340 +/- 749 ng/mg protein (range, 330-3288 ng/mg), respectively. The levels of bFGF in nasal polyps were significantly lower than those before treatment after administration of topical nasal steroid (p = 0.011). Administration of topical nasal steroid decreases bFGF levels of nasal polyp. It may be suggested that one of the effects in diminishing the size of nasal polyps is by decreasing the bFGF.

FS14.5 No suppression of nickel patch reactions by local betamethasone

Background: Topical corticosteroids are usually banned on test areas prior to patch testing. The previous literature on the effect of topical corticosteroids is conflicting.Methods: Patients allergic to nickel sulphate were patch tested on 4 sites with nickel on Day 0. Intracutaneous betamethasone was injected to test sites on Day −1, Day 0 and Day 1. NaCl injection on Day −1 was control. The patch test reactions were evaluated clinically and with laser doppler.Observations: There were no differences in patch test reaction intensities on sites treated with intracutaneous betamethasone as compared to control.Conclusions: A single local dose of potent corticosteroid does not suppress allergic patch reactions to nickel. The current practice of avoiding topical corticosteroid use prior to patch testing should be re‐evaluated.

The Effects of Topical Corticosteroids and a Coal Tar Preparation on Dithranol-Induced Irritation in Patients with Psoriasis

Dithranol has been a mainstay in the treatment of psoriasis for more than 80 years. Although a safe approach, the irritation of the clinically uninvolved perilesional skin remains a major limitation of this treatment. Corticosteroids and coal tar solution have an anti-inflammatory potential. The aim of the present study was to investigate the clinical and cell-biological effects of two topical corticosteroids and a coal tar preparation on dithranol-irritated skin. During 4 consecutive days, 2% dithranol cream was applied to six uninvolved skin sites (3 cm in diameter) on the lower back of 9 patients with psoriasis. Dithranol was left on the skin for 1 h, subsequently removed with water and soap and the skin was dried with a towel. Subsequently, Site 1 was treated with 0.05% clobetasol-17-propionate ointment (CP), Site 2 with unguentum cetomacrogolis (vehicle 1), Site 3 with 0.005% fluticasonpropionate ointment (FP), Site 4 with 10% coal tar solution in lanettewax cream (CTS), Site 5 was left untreated (control) and Site 6 was treated with lanettewax cream (vehicle 2). Erythema, oedema and vesicle formation was scored every day. On day 5, punch biopsies were taken from the six sites. The expression of epidermal proliferation, differentiation and inflammation markers and the clinical irritation scores indicate that the application of a high potency corticosteroid (CP) is the best approach to minimise dithranol irritation, whereas CTS had virtually no effect on dithranol irritation during this 4-day experimental model.

Effects of Topical Corticosteroids and Nonsteroidal Anti-Inflammatory Drugs on Prostaglandin E2-Induced Aqueous Flare Elevation in Pigmented Rabbits

We evaluated the effects of anti-inflammatory potency of corticosteroids and nonsteroidal anti-inflammatory drugs on prostaglandin E₂ (PGE₂)-induced aqueous flare elevation in pigmented rabbits. Transcorneal diffusion of PGE₂, 25 µg/ml (7.09 × 10^–2 mmol/l), with the use of a glass cylinder was achieved to produce aqueous flare elevation. Anti-inflammatory drugs were topically administered once before PGE₂ application. Aqueous flare was measured with a laser flare-cell meter. Topical single instillation of dexamethasone sodium metasulfobenzoate 0.1%, dexamethasone sodium phosphate 0.1%, and fluorometholone 0.1% 6 h before PGE₂ application inhibited 56, 59, and 43% of flare elevation, respectively. Topical single instillation of bromfenac sodium 0.1% and pranoprofen 0.1% 1 h before PGE₂ application inhibited 33 and 15% of flare elevation, respectively. Indomethacin 0.5% did not inhibit flare elevation. Corticosteroid eyedrops needed several hours from topical instillation to exhibit inhibition of flare elevation. Most nonsteroidal anti-inflammatory drug eyedrops inhibited aqueous flare elevation when instilled 1 h before PGE₂ application.

The effect of topical corticosteroids on Ki67 and p53 expression in vulval lichen sclerosus.

Topical corticosteroids have become the treatment of choice for genital lichen sclerosus (LS) and are believed to be required for long-term relief of symptoms. To compare vulval LS that had been treated with topical corticosteroids, vulval LS that had not received topical corticosteroids, and histologically normal vulval skin. We used immunohistochemistry to look for Ki67 expression and abnormal p53 expression. We found a statistically significant difference for p53 overexpression, with increased levels seen when comparing corticosteroid-treated LS with normal genital skin (P = 0.011). Ki67 expression was also significantly higher in the corticosteroid-treated group compared with normal genital skin (P = 0.001), and increased levels were also found in the treated group compared with untreated LS (P = 0.05). Our data suggest that topical corticosteroids have an effect on cell cycle proteins in genital skin and, in particular, genital skin with LS changes.

Outpatient management of traumatic microhyphema

ObjectiveThis study was performed to evaluate the clinical course of patients treated for traumatic microhyphema and the occurrence of elevated intraocular pressure (IOP) and secondary hemorrhage in these patients. DesignRetrospective noncomparative case series. ParticipantsRecords of all patients treated for traumatic microhyphema through the Wills Eye Hospital Emergency Department from January 1997 through September 1999 were analyzed retrospectively. Patients examined for 3 consecutive days after presentation and 2 weeks after initial presentation were included. Patients with open-globe injury were excluded. A total of 162 patients met the study criteria. InterventionAll patients were treated initially as outpatients according to the standard Wills Eye Hospital protocol for traumatic microhyphema (atropinization, bedrest, shield, restriction of antiplatelet medications). Three patients were subsequently hospitalized. Main outcome measuresThe occurrence of IOP elevation (greater than 21 mmHg) and rebleeding was recorded. The effect of topical corticosteroids was evaluated. ResultsIOP was elevated in 14 patients. Six patients had IOP less than 26 mmHg and required no treatment. Six patients had IOP greater than 26 mmHg and received medical treatment. In two patients, IOP increased after initial presentation. Of 150 patients with normal IOP at presentation, only one (0.7%) developed an elevated IOP at any point to warrant treatment (28 mmHg). Rebleeding was documented in three patients, one of whom developed a layered hyphema. The incidence of rebleeding was not statistically associated with the use of topical corticosteroids. ConclusionsComplications from traumatic microhyphema treated with standard measures are few. Closeness of follow-up may be determined by IOP on presentation. Secondary hemorrhage seems to be unaffected by the use of topical corticosteroids.

Effects of topical corticosteroid and combined mediator blockade on domiciliary and laboratory measurements of nasal function in seasonal allergic rhinitis

Both domiciliary and laboratory measures of nasal function have been used to evaluate treatment response in allergic airways disease; however, these measures have not been compared. To determine the relationship of domiciliary measures (daily symptoms, peak inspiratory nasal flow, and nasal oral index) and laboratory measures (rhinomanometry, acoustic rhinometry) in assessing treatment response with topical steroids and specific inflammatory mediator blockage. Twenty-one patients with seasonal allergic rhinitis and asthma were enrolled into a single-blind, placebo-controlled, crossover study comparing 2 weeks of 1) 400 microg inhaled plus 200 microg intranasal budesonide once daily and 2) 10 mg montelukast plus 10 mg cetirizine once daily. Before each treatment, patients received 7 to 10 days of placebo period. Laboratory measurements were made of nasal resistance by posterior rhinomanometry, and nasal volume between 0 and 5 cm by acoustic rhinometry after both placebo and active treatment periods. Daily domiciliary recordings were made of allergic rhinitis nasal symptoms scores and peak nasal and oral inspiratory flow rate (enabling the calculation of a nasal/oral index) throughout the study. There were significant (P < 0.05) improvements for all allergic rhinitis symptoms with both therapies, after factoring for pollen count. Spearman's rank correlation for comparison among nasal symptoms and the objective responses were: nasal inspiratory flow rate (R = -0.50, P = 0.02); nasal/oral index (R = -0.55 P = 0.01); rhinomanometry (R = 0.24, P = 0.30); and acoustic rhinometry (R = -0.21, P = 0.36). Both treatments were effective in managing allergic rhinitis symptoms, and patients' symptoms were more closely associated with domiciliary measurements of nasal flow than laboratory measurements of nasal function.

Monocyte chemotactic proteins in allergen-induced inflammation in the nasal mucosa: Effect of topical corticosteroids

Background: Human allergen-induced rhinitis is associated with the recruitment and activation of inflammatory cells, particularly eosinophils and CD4 + T cells, in the nasal mucosa. Chemokines are inflammatory mediators capable of attracting specific inflammatory cell populations. Monocyte chemotactic proteins (MCPs), a subfamily of CC chemokines, have been shown to induce chemotactic activity particularly in eosinophils, T cells, and monocytes under in vitro assay conditions. Objective: To assess the contribution of MCPs in the recruitment of inflammatory cells in vivo, we investigated the allergen-induced late response in subjects with allergic rhinitis. Methods: Patients were randomized to receive a 6-week treatment with either topical corticosteroid (n = 6) or a matched placebo (n = 6). Nasal inferior turbinate biopsy specimens were obtained from all subjects before and during allergen-induced late responses. By using immunocytochemistry, tissue sections were examined for the presence of MCP-1, MCP-3, and MCP-4 and for the phenotype of infiltrating cells within the nasal mucosa. In addition, double sequential immunocytochemistry was used to confirm the phenotype of MCP-immunoreactive positive cells. Furthermore, the effect of topical corticosteroids on the expression of MCPs and on the cellular infiltrate was also examined. Results: MCP-1, MCP-3, and MCP-4 were expressed in all the baseline samples, with prominent staining observed within the nasal epithelium. Biopsy specimens taken after challenge exhibited significant upregulation in the expression of MCP-3 and MCP-4 ( P < .001). On the other hand, this increase in response to allergen was reduced in patients pretreated with topical corticosteroids. Colocalization experiments revealed that the majority of MCP + cells in the subepithelium were macrophages, followed by T cells and eosinophils. Conclusion: Our results demonstrate that allergen-induced rhinitis is associated with an increased expression of MCP-3 and MCP-4, which may be closely related to the influx of inflammatory cells and may thus contribute to the pathogenesis of allergic rhinitis. (J Allergy Clin Immunol 1999;103:1036-44.)

Effects of topical corticosteroids on inflammatory mediator–induced eicosanoid release by human airway epithelial cells

Background: Airway epithelial cells are among the first cells to come in contact with aerosolized corticosteroids. However, the relative potencies and time course of action of the several commonly used aerosolized corticosteroids on eicosanoid production by airway epithelial cells are unknown. Objectives: This study compared the effects of fluticasone, budesonide, and triamcinolone on eicosanoid output by human airway epithelial cells in vitro. We also determined the spectrum of eicosanoids affected and the mechanism for corticosteroid action. Methods: Cultured BEAS-2B airway epithelial cells (a transformed cell line) were exposed to corticosteroids (1 nmol/L to 1 μmol/L) for 2 to 48 hours and then assayed for basal- and bradykinin (BK)-stimulated eicosanoid output. The eicosanoid profile was identified by HPLC in tritiated arachidonic acid prelabelled cells, and PGE 2, the major eicosanoid product, was quantitated by RIA. The effect of corticosteroids on the immunoreactivity of key proteins involved in eicosanoid metabolism (ie, cyclooxygenase [COX], phospholipase A2 [PLA 2], and Clara cell protein, a PLA 2 inhibitor) was determined by Western blotting. Results: Eicosanoid output was largely confined to prostaglandins with values of 5 ± 2 and 82 ± 35 ng PGE 2/10 6 cells for basal- and BK stimulation, respectively (n = 8). All 3 corticosteroids inhibited basal- and BK-induced PGE 2 output in a dose- and time-dependent manner. Fluticasone and budesonide completely eliminated PGE 2 output in nanomolar concentrations in contrast to triamcinolone, which required micromolar concentration. The rank order of potency was: fluticasone = budesonide > triamcinolone. The time course of action for PGE 2 inhibition also differed, with budesonide acting more slowly than the other 2 corticosteroids ( P = .04). All 3 corticosteroids markedly reduced COX2 with little effect on COX1, cPLA 2 (Type IV), or iPLA 2 (Type VI) immunoreactivity or their relative distribution in cytosol versus membrane fractions. Clara cell protein immunoreactivity was undetectable in control and corticosteroid-treated cell lysates. Conclusion: These results show that in a human airway epithelial cell line, the 3 inhaled corticosteroids commonly used to treat asthma differ in onsets of action as inhibitors of prostaglandin synthesis and vary considerably in potency. All 3 corticosteroids act mechanistically in similar fashion by inhibiting COX2 synthesis. (J Allergy Clin Immunol 1999;103:1081-91.)

Expression of IL-4, Cϵ RNA, and Iϵ RNA in the nasal mucosa of patients with seasonal rhinitis: Effect of topical corticosteroids

Background: Nasal allergen provocation has demonstrated that allergen-induced rhinitis is associated with an increase in local IL-4 mRNA and IgE heavy chain (Cϵ) and IgE heavy chain promoter (Iϵ) RNA and that pretreatment with topical glucocorticosteroids inhibits the increase in these transcripts. Objective: This study was undertaken to determine whether observations made after acute allergen provocation can be extended to the case of chronic exposure experienced during the pollen season. Methods: Biopsy specimens were obtained from the inferior turbinate of 33 pollen-sensitive subjects with allergic rhinitis before and during pollen season. Patients were randomized in a double-blind fashion and treated with either topical steroids (200 μg fluticasone propionate twice daily; n = 16) or matched placebo nasal spray ( n = 17) before the pollen season. Alkaline phosphatase anti–alkaline phosphatase immunocytochemistry was used to identify B cells (CD20+), and in situ hybridization was used to detect IL-4, Cϵ, and Iϵ RNA+ cells. Results: Baseline examination revealed IL-4 and Cϵ RNA but virtually no Iϵ RNA+ cells in the nasal mucosa. Analysis revealed a significant difference in the expression of Cϵ and Iϵ RNA+ cells ( p < 0.001). Biopsy specimens taken after antigen exposure exhibited highly significant increases in placebo-treated ( p < 0.001) but not steroid-treated patients. In both groups, the number of CD20+ cells was unchanged when preexposure and postexposure biopsy specimens were compared. Conclusions: These results show strong support for the hypothesis that IgE class switching occurs locally within the nasal mucosa of subjects with seasonal allergic rhinitis and that this response can be inhibited through strategies directed against local IgE production. (J Allergy Clin Immunol 1998;101:330-6.)

Effect of topical corticosteroids on the activity of superoxide dismutase in human skin in vitro.

We measured the superoxide dismutase (SOD) activity in human skin from tissue homogenates after topical application of hydrocortisone-21-acetate and clobetasol proprionate, dissolved in propylene glycol. SOD was measured spectrophotometrically. SOD activity was higher in the treated skin than in the control untreated skin. We separated epidermis from the dermis by curettage and measured the level of SOD in each homogenized layer; SOD activity was higher in the epidermis compared to the dermis in untreated skin. After corticoid application, SOD activity was higher in the dermis compared to the epidermis to a degree dependent on corticoid potency. These experiments demonstrate that the epidermis may have a role in the barrier function of the skin by its antioxidant capacity and that the dermis is the major location of the metabolic activity in the skin. On the other hand, our results suggest that these corticosteroids may stimulate SOD production and may release antioxidants. This could be another anti-inflammatory property of corticosteroids.

A model for distributions and correlation structure of multivariate polytomous data from a two-stage cluster sample

A generalization of the methods for analyzing bivariate dichotomous data from a stratified two-stage cluster sample (Marques and Koch, 1992) is presented in this paper. This development includes the joint estimation of means for marginal distributions and a set of correlation measures for intra-cluster association for the respective outcomes of each response criterion and for correlation among response criteria for units sharing the same cluster in a multivariate polytomous data setting. The methodology is illustrated with a medical example of clinical effects of topical corticosteroids on healthy skin.

Systemic side effects of topical corticosteroids: how to recognise them in time. How to limit or avoid them

Systemic side effects of topical corticosteroids: how to recognise them in time. How to limit or avoid them

Effect of topical corticosteroids on the antiviral inhibitory activity of topical (S)-HPMPC in the AD5/NZ rabbit ocular model: YJ Gordon, EG Romanowski, & T Araullo-Cruz, University of Pittsburgh, Pittsburgh PA., USA

Effect of topical corticosteroids on the antiviral inhibitory activity of topical (S)-HPMPC in the AD5/NZ rabbit ocular model: YJ Gordon, EG Romanowski, & T Araullo-Cruz, University of Pittsburgh, Pittsburgh PA., USA

Basophils and eosinophils in allergic rhinitis

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Type 1 procollagen as a marker of severity of scarring after sternotomy: effects of topical corticosteroids.

To determine whether the abundance of newly formed collagen in healing surgical wounds correlated with scar severity, and whether topical application of steroid cream reduced new collagen formation in patients who have undergone median sternotomy. Thirty three patients six weeks after sternotomy, and 12 controls were studied. Scars were photographed, and biopsy specimens from scars at sites treated or untreated with topical corticosteroids (clobetasol proprionate 0.5%) were examined using immunohistochemical staining for type 1 procollagen (PCP 1) and transforming growth factor beta (TGF-beta), and in situ hybridisation for type 1 procollagen messenger RNA (mRNA). The degree of hypertrophy of the scar and the abundance of PCP 1 immunostaining were ranked independently, blind, and a correlation between these two variables was observed (r = 0.604, p < 0.001). The PCP 1 immunostaining was accompanied by a great abundance of PCP 1 mRNA and only a slight increase in TGF-beta immunostaining, when compared with normal skin or mature scars. Following the application of topical corticosteroids, for either 48 hours or twice daily for seven days, there was no reduction in PCP 1 immunostaining nor the abundance of PCP 1 mRNA. These data suggest that the extent of new collagen formation as assessed by PCP 1 immunohistochemistry may be a useful marker of the exuberance of the scarring process following sternotomy, and that topical corticosteroids are ineffective in reducing this component of the fibrotic response.

The Effects of Topical Corticosteroids and Plasmin Inhibitors on Refractive Outcome, Haze, and Visual Performance after Photorefractive Keratectomy: A Prospective, Randomized, Observer-masked Study

This study of 86 patients with 12 months of follow-up was designed to determine whether topical corticosteroids or plasmin inhibitors have an effect on the outcome of photorefractive keratectomy. Patients were allocated randomly to either steroid (0.1% fluorometholone for 6 months), plasmin-inhibitor (aprotinin 40 IU/ml for 3 weeks), or control (no treatment) groups and underwent either -3.00- or -6.00-diopter (D) corrections. With -3.00-D corrections, the mean refractive change was significantly greater at 3 and 6 months (P < 0.05) in the steroid group compared with the control group. When steroids were discontinued, the difference became insignificant within 3 months. Similarly, with -6.00-D procedures the mean refractive change was greater at 6 weeks and 3 and 6 months (P < 0.01), but the refractive change again became insignificant 3 months after stopping steroid treatment. Four patients treated with steroids had a hyperopic shift greater than +2.00 D of that intended at 12 months. Similar overcorrections were not noted in the other treatment groups. There were no differences in refractive outcome between the aprotinin and control groups at any stage. With -6.00-D procedures, objective measurements of haze were significantly greater in the aprotinin group compared with the control group at 9 and 12 months (P < 0.05). With this exception, there were no differences in haze, forward or backward scatter of light, best-corrected visual acuity, or halo measurements between the groups. Corticosteroids can maintain a hyperopic shift during their administration, but this effect is reversed on cessation of treatment. Objective tests have shown that steroids have no effect on corneal haze or visual performance after PRK. There is no justification for routinely submitting all patients to long-term steroid regimens and their associated side effects. Treatment with aprotinin produced no beneficial effect on refractive outcome, and haze was greater in the -6.00-D procedures. The concept of modulating the plasminogen activator/plasmin system to regulate wound healing after PRK is discussed.

Effects of Topical Corticosteroids and Nonsteroidal Anti-Inflammatory Agents on Corneal Wound Healing After Myopic Photorefractive Keratectomy in Rabbits

Effects of Topical Corticosteroids and Nonsteroidal Anti-Inflammatory Agents on Corneal Wound Healing After Myopic Photorefractive Keratectomy in Rabbits