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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.

Background: Desonide, a class 6 nonfluorinated topical corticosteroid, has been available for more than two decades. Hydrocortisone is widely used in the treatment of dermatoses in children. Objective: Our purpose was to compare the safety and efficacy of desonide ointment and 1.0% hydrocortisone ointment in children with atopic dermatitis. Methods: One hundred thirteen children (mean age, 4.8 years) with mild to moderate atopic dermatitis were enrolled in a multicenter, randomized, investigator-masked, parallel-group study. Treatments were applied twice daily for 5 weeks and extended to 6 months in 36 of the patients. Signs of atrophy were evaluated. Efficacy was determined by measuring global improvement, erythema, lichenification, excoriations, oozing or crusting, pruritus, and induration. Results: No differences in safety were observed between hydrocortisone and desonide. The investigator's global assessment of improvement significantly favored desonide over hydrocortisone during 3 months of treatment ( p Conclusion: Desonide ointment showed greater efficacy, produced more rapid improvement, and demonstrated an equivalent cutaneous safety profile when compared with 1% hydrocortisone ointment for up to 6 months.

Background Subacute cutaneous lupus erythematosus (SCLE) is characterized by annular, nonscarring, photodistributed, or papulosquamous lesions. The disease may be idiopathic, drug induced, or drug exacerbated. Observations A 66-year-old woman with a history of hypertension, parkinsonism, rheumatoid arthritis, anxiety and depression, and symptoms of Sjogren syndrome was seen with a 1-month history of an eruption on her upper extremities and upper trunk. The eruption had begun 2 to 3 weeks after subcutaneous injection of golimumab for rheumatoid arthritis. She had developed SCLE 2 years previously due to furosemide use and 10 years previously due to hydrochlorothiazide use. Physical examination revealed scaly, annular, erythematous plaques photodistributed on the arms, legs, and upper trunk. A punch biopsy specimen demonstrated vacuolar interface dermatitis and lymphohistiocytic perivascular inflammation. Serological abnormalities included a positive antinuclear antibody, an elevated anti-La/SS-B antibody level, and an elevated anti-Ro/SS-A antibody level. She was diagnosed as having SCLE and was initially treated with desonide lotion, photoprotection, prednisone (40 mg/d) tapered over 6 weeks, and hydroxychloroquine sulfate (200 mg twice daily). Because of persistent disease, methotrexate sodium (12.5 mg/wk) was subsequently added to the regimen, and her eruption cleared completely. Conclusions Golimumab should be added to the list of medications capable of inducing or exacerbating SCLE. Our patient demonstrated variable times to the resolution of SCLE, possibly attributable in part to the different half-lives of the agents administered.

A study of an HPLC method for the analysis of related substances in triamcinolone acetonide is described. Several systems of solvents and samples of different lots and preparative origins were examined and a rapid-scanning diode array UV detector (DAD) was particularly useful. With the proposed technique it was possible to identify 9 alpha-bromo desonide as a principal impurity, which was present in all examined samples of triamcinolone acetonide. This identification was rendered possible by the investigation of the second derivative of the UV spectra and by means of study of the mass spectrum. Furthermore, it was possible, primarily on the basis of the spectrophotometric data, to formulate reliable hypotheses on the possible identification of 9 beta, 11 beta-epoxide of the desonide which was present at very low levels and to exclude the presence of 11-deoxy-9(11)-unsaturated desonide. The presence of the above-mentioned related substances was explained considering the scheme of synthesis described in the literature. The spectrophotometric characteristics of the studied compounds and the limits of applicability of the present procedure are discussed.

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.

Case 1 A 46-year-old white woman presented with a new-onset facial eruption that had developed soon after she had started to use a beclomethasone dipropionate nasal spray for the treatment of allergic rhinitis. The patient did not complain of a history of facial flushing. On examination, she had inflammatory papules and pustules on a background of erythema localized around the mouth and paranasal area, extending onto both cheeks with sparing of the vermilion of the lips ( Fig. 1). The patient had no clinical evidence of conjunctivitis. She stopped the steroid spray and started to use desonide cream topically twice daily and minocycline 100 mg a day. After 8 weeks of therapy and stopping the steroid spray, the patient’s eruption had resolved completely without recurrence. Figure 1. Patient 1 with inflammatory papules and pustules localized around the nose and mouth Download figure to PowerPoint Case 2 A 42-year-old white woman presented with a history of flushing, facial erythema, and perinasal inflammatory papules. These symptoms had worsened after she had started to use a beclomethasone dipropionate nasal spray for the treatment of allergic rhinitis. On examination, she had facial erythema and telangiectasia with inflammatory papules on her nose. The patient stopped using the steroid spray and began applying metronidazole 0.75% cream twice a day with resolution of the inflammatory lesions and diminution of facial flushing.

REPORT OF A CASE A 17-year-old boy presented with a 12-month history of an intensely pruritic eruption on his back and neck. Previous treatment with acyclovir, nafcillin, hydroxyzine, and cimetidine orally did not affect the pruritus or alter the eruption; neither did topical fluocinonide, desonide, and hydrocortisone. He felt well, had no significant medical history, and was taking no medications except hydroxyzine at the time of presentation. His family had no history of a similar eruption. On physical examination, the patient had excoriated erythematous and hyperpigmented keratotic papules distributed in a reticulate pattern covering most of the midback (Fig 1) and scattered on the lateral aspect on his neck. His physical examination was otherwise unremarkable. Histopathologic examination of lesional skin showed elongation of epidermal rete ridges, focal spongiosis, exocytosis, liquefaction degeneration of the basal cell layer, and an edematous papillary dermis (Fig 2). Direct immunofluorescence was performed on a skin

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.

Summary Theoretically two corticosteroid preparations should show the same clinical activity even though they possess different medicament concentrations, provided that both preparations are at or above saturation e.g. they are suspensions. To test this theory, the non-fluorinated corticosteroid desonide prepared as two suspensions in the same cream formulation (Apolar Cream 0.1% and 0.05%) were evaluated for vasoconstriction using an occluded blanching test. Included in the vasoconstriction test were also another desonide 0.05% preparation (Tridesilon Cream®) and Betnovate Cream® (betamethasone 17-valerate 0.1%). The study was extended into patients by comparing the effects of Apolar Cream 0.1% and 0.05, in a double-blind, randomized, right-left comparative study including 40 patients with bilateral, non-infected hand eczemas, No significant difference could be demonstrated between the blanching responses of the four preparations tested in the vasoconstriction study. Betnovate Cream provided the lowest blanching response. Thirty-eight patients completed the clinical trial. All patients improved after 11 days of treatment with Apolar Cream 0.1%. With the 0.05% cream, 37 improved and, in one, the condition remained unchanged. No statistically significant difference could be demonstrated between treatments. It is concluded that, for practical therapeutic purposes, Apolar Cream 0.05% will equate with the corresponding 0.1% preparation.

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.

The effect of structural alterations on the biotransformation rate of glucocorticosteroids (GCS) by rat- and human-liver 9000 g supernatant fraction was studied. Insertion of a 16 alpha-hydroxy group in the prednisolone molecule (16 alpha-hydroxyprednisolone) was found to decrease the rate of biotransformation. Substitution of the 16 alpha,17 alpha-hydroxy groups with a symmetric acetal (in, for example, desonide) or especially a non-symmetric acetal (in, for example, budesonide), enhanced the biotransformation rate several-fold, particularly in human liver. Differences in the rates of metabolism in rat and human liver were observed. Hydrogenation of the 1,2-double bond in prednisolone and budesonide (hydrocortisone and 1,2-dihydrobudesonide) enhanced the biotransformation rate nine-fold in rat liver but only two-fold in human liver. Fluorination of the steroid nucleus in 6 alpha- and 9 alpha-positions enhanced the biotransformation rate several-fold in human liver, but in rat liver fluorination marginally decreased the rate of biotransformation. These in vitro results correlate well with available data on the first-pass liver metabolism of the studied GCS. This indicates that in vitro data can be useful in predicting oral bioavailability of GCS.

The major degradation product of desonide in a pharmaceutical ointment formulation has been shown to be identical with the C-17-carboxylic acid obtained on oxidative cleavage of the alpha-ketol group of desonide with alkaline hydrogen peroxide. The pKa value of this acid has been estimated from chromatographic data.

Selected glucocorticoids have been demonstrated to increase the growth rate of human skin fibroblasts in culture, over a physiologically significant concentration range. At the same concentrations and identical conditions, the glucocorticoid compounds tested inhibited the growth rate of mouse L-929 cells. We have discussed currently acceptable theories of glucocorticoid mechanism of action that permit this dichotomous effect, the main point being that inhibition can no longer be regarded as the only response of fibroblasts to glucocorticoids. Conclusions drawn from observations of cell cultures affected by addition of glucocorticoids must have considered the source of the cells, as response may vary with source and biologic state of the cells in culture.

We have used intradermal injections of corticosteroids into normal and ultraviolet light (UVL)-induced inflamed human skin to evaluate the inherent atrophy producing potential as well as the vasoconstrictor potency of selected compounds. Two corticosteroids, desonide and triamcinolone acetonide, which differ only by the presence of a fluorine atom, exhibited similar vasoconstrictor potency but only the fluorine containing steroid produced severe persistent atrophy. Hydrocortisone 17-valerate and desonide produced a mild, transient atrophy while hydrocortisone produced none. Triamcinolone acetonide and desonide were more effective than hydrocortisone and hydrocortisone 17-valerate in producing vasocontriction in this model system of inflammation. The production of atrophy always greater in the UVL-induced inflamed skin than in normal control skin.

Aim: To evaluate whether a significant difference exists between the initial and final mean central corneal thickness that might affect Goldmann applanation tonometer recordings of patients with allergic conjunctivitis treated with desonide 0.25% ophthalmic solution, and to determine the effect of desonide on intraocular pressure by using adjusted intraocular pressure values.Methods: This double-blind randomised placebo-controlled trial enrolled 30 patients (60 eyes) with allergic conjunctivitis. Patients were randomly assigned to receive desonide to 1 eye (study eye) and preservative-free tear supplement (Tears Naturale Free®) to the other eye (control eye) 3 times daily for 3 weeks. Goldmann applanation tonometry and central corneal thickness of both eyes were recorded on the day of presentation and 3 weeks later.Results: Regression of itching, tearing, conjunctival hyperaemia, and tarsal conjunctival papillary reaction were noted in the study eyes after 3 weeks of treatment. The control eyes showed mild regression of pruritis, tearing, conjunctival hyperaemia, and tarsal conjunctival papillary reaction after 3 weeks. There was a significant difference between the initial and final mean central corneal thickness values for the study eyes (p = 0.003). There were no statistically significant differences between the initial and final mean values of Goldmann applanation tonometry and adjusted intraocular pressure for the study eyes. No statistically significant differences were found between the initial and final mean values of any of the parameters for the control eyes.Conclusion: Inflammation-induced increase in central corneal thickness of patients with allergic conjunctivitis treated with desonide showed statistically significant regression. However, this regression did not significantly affect Goldmann applanation tonometry and adjusted intraocular pressure values of the treated eyes.

Phenylbutazone, cyclophosphamide and prednacinolone acetonide, administered around the period of challenge reduced the exudate of pleurisy due to Bordetella pertussis hypersensitivity in the rat. The results on the leukocytes of the exudate are different depending on the class of product studied. Phenylbutazone only slightly reduced the number of mononuclears cells. Both the immunosuppressive and the corticoid induced a clear decrease in the total leukocyte number. But, while prednacinolone effects were nearly equally distributed among mononuclears and polynuclears, cyclophosphamide was mainly active on mononuclears.

The effects of a non-steroidal anti-inflammatory agent, phenylbutazone, a corticosteroid, desonide, an immunosuppressive, cyclophosphamide and an immunomodulator, levamisole on a number of experimental inflammatory models were compared. Compounds were first tested in carrageenin-induced pleurisy as a non-immune acute inflammation, then in passive skin anaphylaxis and reversed passive Arthus oedema in the rat as models of humoral immunity. Finally the compounds were investigated in various delayed hypersensitivity tests: reaction to sheep red cells and to oxazolone in the mouse, skin reaction to purified protein derivative (P.P.D.) in the rat and guinea-pig, P.P.D. induced pleurisy in the guinea-pig.

The major degradation product of desonide in a pharmaceutical ointment formulation has been shown to be identical with the C-17-carboxylic acid obtained on oxidative cleavage of the alpha-ketol group of desonide with alkaline hydrogen peroxide. The pKa value of this acid has been estimated from chromatographic data.

The authors studied various drugs with anti-inflammatory or antirheumatic properties on pleurisy due to Bordetella pertussis hypersensitivity in the rat. The following compounds were studies according to various methods of treatment: indomethacin, phenylbutazone, cyclophosphamide, desonide, chloroquine, levamisole, D-penicillamine and sodium aurothiopropanol sulphonate. The action on the volume of pleural exudate and on cell events depended on the compounds and the conditions of treatment. Only gold salt produced no reduction in the pleural volume under all methods of treatment. All the compounds studied produced various degrees of significant modifications at the level of the cell events.

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.

A 58-year-old female patient with recurrent ulcus cruris in connection with chronic venous insufficiency, as well as a known allergy to neomycin sulfate, benzocaine (Anesthesin), formalin, and (possibly) penicillin, developed severe eczema through treatment with triamcinolone acetonide (Volon A) shaking mix. Tests indicated an extensive eczematous cross-sensitivity to acetonide-substituted corticoids, such as triamcinolone acetonide, fluocinonide, fluocinolone acetonide, flurandrenolone, desonide, and halcinonide; in addition, allergies to adjuvants such as benzyl alcohol and sodium disulfite were diagnosed. Such cases of ulcus cruris often result in epidermal sensitization, which can also include topically applied corticoids. It is suspected that the lability of the acetonide group allows for the development of a common antigen determinant.

The action of phenylbutazone, a non-steroid anti-inflammatory drug, desonide, a corticosteroid, and cyclophosphamide, an immunosuppressant agent, was studied on four types of experimental pleurisy: carrageenan-pleurisy in rats; passive reversed Arthus pleurisy in rats; Bordetella pertussis- delayed hypersensitivity pleurisy in rats and PPD (purified protein derivative)—delayed hypersensitivity pleurisy in guinea-pigs. For each compound, the action on the exudate and on the number of the different categories of leucocytes in the inflammation focus was evaluated. In carrageenan-inflammation, phenylbutazone reduced the oedema and the number of neutrophils and macrophages. Its favourable effect on exudative events in Arthus—and B. pertussis—reactions was not accompanied by high modifications at the cellular level. With the exception of PPD-pleurisy, desonide reduced the three other reactions. Its action related to the exudate and the various leucocyte types, except in the Arthus reaction in which only the number of neutrophils was decreased. The effect of cyclophosphamide was mainly in B. pertussis pleurisy in which it resulted in a decrease of oedema and a reduction in the number of mononuclears. For each compound, correlations between the effect on exudative and cellular phenomena are discussed.

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.