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This research aimed to develop a novel drug delivery system to improve treatment of skin disorders. The system is comprised of a Carbopol 980-based nanoemulgel (NE-gel) containing a desonide (DES; 0.05%, w/w) nanoemulsion (NE), which has a small particle size, high encapsulation efficiency, good thermodynamic stability, good permeation ability, and high skin retention. DES-loaded NE (DES-NE) was prepared by high-pressure homogenization. The developed formulation was characterized by differential scanning calorimetry (DSC), X-ray diffraction, drug release, skin permeation, and drug retention. DES in vitro release and skin permeation studies with different formulations of artificial membrane and rat abdominal skin were performed with the Franz diffusion cell system. Confocal laser scanning microscopy (CLSM) was used to detect the localization and permeation pathways of drugs in the skin. Compared with commercially available gel (CA-gel) and NE, the NE-gel release process conformed to the Higuchi release model (R2 = 0.9813). NE-gel prolonged the drug release time and allowed for reduced administration dose and frequency. The unit cumulative permeation of NE and NE-gel through the skin for 12 h was 63.13 ± 2.78 and 42.53 ± 2.06 μg/cm2, respectively, values significantly higher (p < 0.01) than that of the CA-gel (30.65 ± 1.25 μg/cm2) and CA-cream (15.21 ± 0.97 μg/cm2). The DES-NE and DES NE-gel skin drug retention was significantly higher than commercially available formulations (p < 0.01). Hence, the prepared NE-gel is a potential vehicle for improved topical DES delivery for better treatment of skin disorders.

This cohort study uses data from a medical record review of a dermatogynecology practice to describe the association between reduced recurrence of vulvar squamous cell carcinoma and use of topical corticosteroids in the treatment of vulvar lichen sclerosus.

Idiopathic granulomatous mastitis (IGM) is a benign disorder of the breast, for which the optimal treatment modality remains missing. A total of 124 patients with a histopathologically proven diagnosis of IGM were enrolled in a prospective, randomized parallel arm study. Patients were treated with topical steroids in Group T (n: 42), systemic steroids (0.8 mg/kg/day peroral) in Group S (n: 42), and combined steroids (0.4 mg/kg/day peroral + topical) in Group C (n: 40). Compliance with the therapy, response to the therapy, the duration of therapy, side effects and the recurrence rates were compared. Sixteen patients did not comply with the treatment, and the highest ratio of compliance with therapy was seen in Group T (p

The differences between topical corticosteroids are based mainly on their potency, safety and patient acceptability. The aim of this study was to evaluate a mild- to mid-potent topical corticosteroid, desonide 0.05%, on these three parameters in an Australian cohort of patients with facial seborrhoeic or atopic dermatitis. Eighty-one adult patients were randomized to receive desonide 0.05% lotion or its vehicle, applied twice daily for 3 weeks under double-blind conditions. In the active treatment group, 88% of patients had their skin condition cleared or almost cleared and only two patients experienced cutaneous adverse events (rash and pruritus). The acceptability of the lotion was high; 95% of patients stated they would use this topical corticosteroid again. These data support the short-term use of desonide 0.05% lotion as a suitable agent for the short-term treatment of facial dermatitis.

A case of cutaneous rhabdomyomatous mesenchymal hamartoma in a 6-year-old Afro-Caribbean girl is reported with review of the literature. The lesions were fine, located on the central face and became inapparent after six months. Spontaneous regression of these lesions has not been previously reported. Although rare, continued reporting will facilitate the elucidation of the clinical features and natural history of these lesions and the relationship to disordered embryogenesis.

The treatment of seborrheic dermatitis includes topical antifungal agents to eradicate Malassezia spp, corticosteroids, which treat the inflammatory component of the disease and keratolytics which remove scale and crust. This study compared the efficacy of a nonsteroidal topical cream and a low-potency topical corticosteroid for the treatment of mild to moderate seborrheic dermatitis of the face in 77 volunteers randomized to twice-daily treatment with nonsteroidal cream or corticosteroid cream for up to 28 days. If the individual was rated clear by day 14, the study drug was collected and the participant was told not to use any topical products on the previously treated areas until after the 28-day follow-up visit. Both treatments were similarly effective in reducing disease severity, with approximately 90% of participants clearing or almost clear during the study. Both treatments demonstrated significant reductions in erythema, scaling, and pruritus (P < .0001). Safety in both groups was rated as excellent in more than 90%. Those using the nonsteroidal cream who cleared after 14 days of treatment were more likely to remain clear than were participants using the corticosteroid cream (P = .0173). Investigator global assessments of improvement found both study agents were essentially the same, and participants in both groups achieved clinically important improvement.

PURPOSE OF REVIEW The goal of this article is to evaluate developments in the knowledge of inflammatory mechanisms and treatments of ocular allergy. RECENT FINDINGS Research developments in ocular allergy summarized in this article include the following findings: (1) ocular epithelial cells play a role in inflammation; (2) respiratory syncytial virus is a pathogen in allergic conjunctivitis; (3) transglutaminase inhibitors reverse allergic related inflammation; (4) eosinophils and neutrophils both play a role in ocular allergy; (5) eotaxin-1 and eotaxin-2 play a role in eosinophilic recruitment; and (6) loteprednol etabonate, desonide phosphate, and cyclosporine have been shown to be effective and safe in the treatment of ocular allergy. SUMMARY This article summarizes the research conducted for each of the above recent findings and outlines their clinical applications.

Glucocorticoids can boost some Malassezia-driven dermatoses. However, both antifungals and topical corticosteroids improve lesions of seborrheic dermatitis.To revisit the topical activity of the antifungal ketoconazole and the corticosteroid desonide on Malassezia growth on human stratum corneum.The computer-assisted corneofungimetry bioassay was used to compare the growth of M. furfur, M. globosa and M. restricta on human stratum corneum coated with olive oil. Four blinded gel formulations were tested. They contained either 2% ketoconazole, 0.05% desonide or a combination of 2% ketoconazole and 0.05% desonide; one gel was unmedicated. Untreated stratum corneum and specimens coated with a 2% ketoconazole cream were used as negative and positive comparators, respectively. A total of 45 samples (15 M. furfur, 15 M. globosa, and 15 M. restricta) were used for each test formulation in this randomized, double-blind study.The 2% ketoconazole gel and cream and the combination of 2% ketoconazole and 0.05% desonide formulation abated similarly and significantly the M. furfur, M. globosa and M. restricta growth. The 3 species were similarly sensitive to these formulations. By contrast, no significant inhibitory effect was yielded by the 0.05% desonide gel and the vehicle.The presence of 0.05% desonide does not impair or improve the Malassezia susceptibility to 2% ketoconazole when growing on lipid-enriched human stratum corneum.

Systemic side effects of local corticosteroid therapy may occur when treating chronic inflammatory dermatoses in children. We compared the effect of micronized desonide cream 0.1 p.100 versus betamethasone dipropionate cream 0.5 p.100.A randomized double-blind trial was conducted to assess the efficacy of micronized desonide cream 0.1 p.100 (group 1) versus bethamethasone cream dipropionate 0.05 p.100 (group 2) in children treated for atopic dermatitis and to compare their effects on serum cortisol levels 8 hours after administration. Twenty-nine patients, mean age 13.8 months were included (15 in group 1 and 14 in group 2). The creams were applied twice a day from day 1 to 5 then once a day from day 6 to 7 and finally once every two days to day 15.The two treatments were effective with a decrease in body surface area involved and an improvement in lesion score from day 5 to day 20. Cortisolemia fell off significantly for both treatments between day 0 and day 5 (group 1: Deltad5=-4.74 mg/ml, p=0.01; group 2: Deltad5=-13.06 mg/ml, p0.0001), only for group 2 between day 0 and day 20 (Deltad20=-7.38 mg/ml, p=0.02) and to a lesser degree between day 0 and day 30 (Deltad30=-3.18 mg/ml, p=0.06). The decrease was greater in group 2 than in group 1 on day 5 (p=0.01) and to a lesser degree at day 20 (p=0.06).Micronized desonide cream 0.1 p.100 has less potential for suppressing the adrenal cortisol axis than betamethasone dipropionate cream 0.05 p.100 while the therapeutic effect on childhood atopic dermatitis is the same.

Desonide ointment has demonstrated a good safety and efficacy profile during the many years it has been used in treating dermatoses. However, there have been no controlled clinical trials to evaluate its systemic safety when used in treating children. Suppression of the hypothalamic-pituitary-adrenal (HPA) axis can occur after repeated application of topical corticosteroids. In general, the degree of suppression of the HPA axis function is related to the daily dosage of steroid given, the duration of its administration, the extent of body surface covered, and the potency of the corticosteroid. This study sought to determine the comparative effects of 0.05 percent desonide and 2.5 percent hydrocortisone ointments on the HPA axis of children with atopic dermatitis. There was no suppression of early morning cortisol in either treatment group. The ACTH-stimulated mean cortisol values after four weeks of treatment were not significantly different from the baseline values for either treatment group. We conclude that neither 0.05 percent desonide ointment nor 2.5 percent hydrocortisone ointment compromised the HPA axis of children with atopic dermatitis treated topically for four weeks.

HPLC methods were developed for the analysis of pharmaceutical creams containing binary drug mixtures (betamethasone valerate-chlorocresol; hydrocortisone-miconazole nitrate; desonide pivalate-chlorhexidine; dexamethasone-clotrimazole; triamcinolone acetonide-econazole nitrate). The chromatographic separations were performed on C-18 and cyano columns under reversed-phase conditions. A post-column on-line photochemical reactor (irradiation at 254 nm) was arranged between the analytical column and the diode-array detector to enhance the performance of the method. Two UV spectra (photoreactor on and off) were obtained for each analyte and these additional sources of information proved to be useful for the unambiguous identification of the various analytes. The method was applied to the quality control of commercial creams using a solid-phase extraction procedure for the sample clean-up.

The Minolta tri-stimulus colorimeter CR-200 was used to quantify the blanching effect of topical corticosteroids in a non-occluded vasoconstriction test. To investigate the influence of time on variations in colorimetric parameters, an initial series of measurements was performed on Day 1 on six predetermined sites on the ventral surface of the forearm of six healthy volunteers every 2 h over a 12-h period. The colorimetric values were shown to be site related but hourly variations occurred with similar profiles for all the sites. On Day 2, four topical corticosteroid creams, representative of their potency groups, as well as a base were applied in a randomized double-blind manner on five of the predetermined sites. Visual gradings and colorimetric measurements were carried out every 2 h over the following 12-h diurnal period and were continued on Day 3. The colorimetric parameters L* (luminance) and a* (colour hue ranging from green(-) to red(+] gave a rank order correlated to corticosteroid potency that showed superior discrimination compared to simple visual grading. In this study, L* was more discriminative parameter than a*. The Minolta Chroma Meter CR-200 appears to be a simple and accurate device for objectively measuring the blanching effects of topical corticosteroids.

Desonide foam is a newly approved topical corticosteroid preparation of 0.05% desonide. It has been shown effective compared with vehicle placebo in the treatment of mild-to-moderate atopic dermatitis in both pediatric and adult populations. Given the favorable safety profile of all other desonide preparations and their utility as a low potency corticosteroid, desonide foam promises to be a useful addition to the armamentarium, when other desonide vehicles might be less acceptable.

Six groups of children suffering from widespread atopic dermatitis were treated once daily with six topical steroids of different potency. Systemic effects were measured by the morning estimation of plasma cortisol. A clear relationship was demonstrated between clinical efficacy of the steroid treatment and degree of reduced adrenal function. This study demonstrated that a rapid and marked therapeutic effect can be obtained with potent topical steroids applied once daily without occlusion, but in children is accompanied by a fall in plasma cortisol.

Experiments were conducted to: (a) compare the bioavailability of betamethasone benzoate in a quick-break aerosol foam and semisolid dosage forms, (b) compare the activity of betamethasone benzoate, betamethasone valerate, clobetasol propionate, triamcinolone acetonide, desonide, flumethasoid reservoir formation in skin, and (d) assess the effect of a natural moisturizer. Efficacy was determined by a graded response 6-hr occluded vasoconstriction test with subsequent reocclusion for reservoir demonstration. Moisturizer effect was assessed by a nonoccluded vasoconstriction test using "plain" and sodium 2-pyrrolidone-5-carboxylate-containing concentrates on arms pretreated with water or moisturizer. The activities of betamethasone benzoate concentrate, collapsed foam, ointment, and gel were similar and significantly better than the activity of the cream. Clobetasol propionate was significantly better than the other medicated concentrates, which were equivalent. Steroid-induced blanching decreased in the presence of a moisturizer.

Cantharidin applied to the Swiss mouse ear induced a clearly observable inflammatory reaction after 6 hr, maximal after 24 hr, and persisting several days. Desonide and hydrocortisone strongly inhibited the acute (6 hr) and delayed (24 hr) phases after their local application, while, after oral treatment, a reduction in the acute edema was obtained only when using high doses. The cutaneous application of high doses of mepyramine, disodium cromoglycate, methysergide, and (at a quite lower level) cimetidine reduced the 6-hr inflammation. Phenylbutazone and acetylsalicylic acid showed little activity on the same phase after their cutaneous administration. All the nonsteroid compounds produced little or no effect on the 24-hr inflammation after their cutaneous application and were quite inactive on both phases after their systemic treatment. The cantharidin-induced inflammatory reaction in Swiss mouse seems thus to be characterized by two phases. The chronic delayed phase is an example of chronic inflammation without the involvement of immunological processes. Histamine and serotonin might be involved in the acute inflammation.

Corticosteroid-induced dermal atrophy has been studied in the rat using daily application of ethanolic solutions to small areas of flank skin. After 12 days of treatment, the degree of atrophy was determined by comparing the weights of skin plugs (16 mm diameter) taken from the treated areas with contralaterally paired control areas. Doses can be adjusted so that systemic effects are minimized and only local effects are observed. Hydrocortisone, hydrocortisone butyrate, dexamethasone, betamethasone, desonide and triamcinolone acetonide all produce atrophy in the rat, and the degree of thinning is dose dependent. Potencies in the dermal atrophy assay compare directly with topical anti-inflammatory potencies in the rat, and the presence of fluorine in the steroid molecule is not a determining factor in the production of atrophy.

Although there is a variety of animal models available, neither a single assay system nor the results of the various assays permit absolute protection of relative anti-inflammatory potency. Equally, current clinical dose titration studies, although more reliable, provide only gross estimates of therapeutic potency when conducted in certain clinical situations in a double-blind randomized fashion. This paper delineated clinical means to titrate more objectively and accurately therapeutic potency in the patient. Moreover, it has submitted considerations as to how to assess therapeutic anti-inflammatory activity in the complex multi-component process of inflammation accompanying most dermatologic diseases that eventually may permit titration of specific anti-inflammatory compounds on certain tissue components of the inflammatory process.

Summary Forty patients with perioral dermatitis were assessed with particular reference to factors which might be incriminated in the aetiology of this condition. Many previously implicated features could not, in fact, be substantiated. We believe that perioral dermatitis is a distinct entity but that the abuse of topical corticosteroids aggravates the disease.

The ratios of antiinflammatory activity after oral administration (oral ED50/cutaneous ED50) for desonide (Locapred) and hydrocortisone (hydrocortisone acetate) were compared in various nonimmunological and immunological experimental models on mouse ears: edema induced by croton oil; primary irritation due to picryl chloride; the acute phase (6 h) and the beginning of the chronic phase (24 h) of inflammation due to cantharidin; delayed contact hypersensitivity to picryl chloride; and the semi-delayed (6 h) and delayed (24 h) phases of contact hypersensitivity to oxazolone. These investigations showed that, besides having a better antiinflammatory effect, desonide had a better ratio of local activity to systemic effect in all the models. In addition, by contrast with orally active doses, locally active doses did not induce any thymolytic effect. Such results were confirmed in rats in which desonide reduced 24 h carrageenin abscess after cutaneous application without any significant thymolytic effect. Hydrocortisone was inactive.

The actions of F 1865 (ethyl 4' methoxy 4 phenyl thiazolyl 2 oxamate), an inhibitor of the release of histamine from mast cell, desonide, a corticosteroid, mepyramine maleate, an anti-H1 antihistaminic, and disodium cromoglycate were compared after cutaneous application in various experimental models of allergy and inflammation. F 1865 decreased IgE- and IgG-dependent passive cutaneous anaphylaxis in rats at doses having no effect on histamine- and serotonin-induced capillary permeability. Disodium cromoglycate showed the same activity spectrum, but its action was only found after intradermal application. The reduction of cutaneous anaphylaxis by desonide was found parallel to its inhibition of histamine effects, and to a lesser extent of serotonin effects. In the case of mepyramine, the antiallergic effect may be explained by its antihistaminic action. Desonide was highly active on cantharidin-induced non-immune inflammation and on non-immune and delayed hypersensitivity reactions induced by picryl chloride in mouse ear. Although far less active than the corticosteroid, F 1865, mepyramine and disodium cromoglycate did reduce the three types of reactions in mice. This evidenced a part played by histamine in such inflammations. Then it is likely that the inhibition of histamine release by F 1865 plays an important part in the effect of the compound observed in the various inflammations studied. However we cannot exclude actions against other mediators involved in these reactions.

The human blanching assay was used to assess the potency of two new proprietary corticosteroid creams. The blanching abilities of 0.1% desonide cream and 0.05% halometasone cream were evaluated relative to the blanching elicited by 0.05% clobetasol 17-propionate cream, 0.1% betamethasone 17-valerate cream and 0.05% clobetasone 17-butyrate cream. The results of the trial indicated that the 0.1% desonide cream falls into the potent group of topical corticosteroid preparations and the 0.05% halometasone cream falls into the moderately potent group.

A randomized, double-blind, left-right study to compare the therapeutic efficacy and the cosmetic acceptability of the new hydrocortisone 17-butyrate (Locoid®) 0·1% fatty cream application form with desonide (Apolar®) 0·1% ointment was performed in thirty patients suffering from moderate to severe atopic dermatitis. The medications were applied to symmetrical, bilateral skin lesions twice daily for 4 weeks. Both treatments effected highly significant reductions of the score values for the severity of all clinical skin parameters assessed. Score reductions were, however, more pronounced on Locoid-treated sides than on Apolar-treated sides both after 2 and 4 weeks of therapy. It appeared further that clinical efficacy of treatment at completion of the study was also in favour of Locoid-treated sides, indicating that Locoid fatty cream is more effective than Apolar ointment. No serious side-effects were reported during the study. The expressed patient preferences with respect to cosmetic acceptability of treatments were significantly in favour of Locoid fatty cream, indicating that patients preferred the use of this new galenic formulation over an ointment formulation. It is concluded that the new application form of Locoid, a fatty cream, is a useful and beneficial addition to topical corticosteroid therapy, which will promote patient compliance in a wide range of corticosteroid-responsive skin diseases.

Desonide, 16α-hydroxyprednisolone-16,17-acetonide, is a nonhalogenated steroid possessing physical properties predictive of potent topical antiinflammatory activity. Based on assay findings in 4 animal models (liver glycogen deposition, cotton pellet granuloma, ear edema, and ocular inflammation), desonide showed an average potency about 60 times that of hydrocortisone, which suggested that desonide should exhibit, on topical use, considerable antiinflammatory activity. Subsequently, desonide proved to be about as active as fluocinolone acetonide in human dose titration studies, having a more rapid onset than the reference steroid during the early phase of treatment. The absorption of desonide from a cream formulation applied to the skin of rabbits averaged 54% greater than that of triamcinolone acetonide (as predicted by the physical properties of desonide), an observation that may partially explain the apparently greater clinical activity of desonide. In view of the apparently greater clinical activity of desonide, this finding indicates that somewhat less steroid will be absorbed from clinically effective doses of desonide than from equieffective doses of triamcinolone acetonide. Desonide was only 6 times as toxic as hydrocortisone and one-fifteenth as toxic as triamcinolone acetonide on acute sc administration to rats. A cream formulation of desonide was virtually nontoxic on po administration to rats and dogs, and it elicited a low order of toxicity when administered topically in large doses to rabbits.