Colin A. Ramsay

The treatment of atopic dermatitis with topical fusidic acid and hydrocortisone acetate

Aim To compare the clinical efficacy of a cream combination containing 2% fusidic acid and 1% hydrocortisone acetate in the treatment of patients with mild to moderate atopic dermatitis. Subject Atopic dermatitis and efficacy of antibacterial and antiinflammatory topical therapy. Methods Randomized, double blind, prospective, parallel group trials. Results Study I, involving 186 patients, compared the combination 2% fusidic acid and 1% hydrocortisone acetate with 1% hydrocortisone cream. Analysis was performed on patients who had pathogens at entry and on the total patient population. Study II, involving 68 patients, compared the combination 2% fusidic acid and 1% hydrocortisone acetate with 2% fusidic acid cream. Analysis was the same as in study I. Results of study I in patients with pathogens at baseline showed a significant difference in favour of the combination (P = 0.04) in terms of the primary efficacy criterion which was a combination of clinical and bacteriological efficacy measures. When all patients in the study were analyzed there was no significant difference between the two groups. The combination was significantly more effective in removing pathogens than 1% hydrocortisone cream (P < 0.0001). Results of study II in all patients showed that the combination was significantly better than 2% fusidic acid cream (P = 0.04) in terms of the primary efficacy criterion. Both preparations were highly successful in eradicating pathogens. Pooled analysis of studies I and II showed a difference with respect to the primary efficacy criterion among the 3 preparations in the order Fucidin 2% plus HC 1% cream > HC 1% cream > Fucidin 2% cream in all patients and in those with pathogens (P = 0.007 for all patients and P = 0.01 for those with pathogens). Similarly, regarding the reduction in sign/symptom score a significant difference among the 3 preparations existed (P = 0.009 for all patients and P = 0.01 for those with pathogens). Adverse events with the combination were minimal. Conclusion 2% fusidic acid and 1% hydrocortisone acetate cream is an effective therapy in patients with mild to moderate degrees of atopic dermatitis.

Dietary fat alters progression of some age-related changes of the immune system

SJL mice develop resistance against tolerance between the 9th and 25th wk of life. This resistance is linked with a loss of suppressor capacity in the thymus. We have shown here that contact photosensitivity (CPS) decreases as a function of age and that this is due to an age-dependent increase in suppressor capacity. Diet fats have a differential effect on age-dependent changes in suppressor activity; a low P/S diet prevents or delays loss of suppressor activity for antibody formation and a high P/S diet prevents or delays the development of suppressor activity in CPS reactions.

Gentamicin: Systemic exposure to a contact allergen

A case is presented of an allergic dermatitis provoked by intravenous gentamicin in a patient previously sensitized by topical medications. Patch tests confirmed hypersensitivity to gentamicin and neomycin. The nature of reactions to contact allergens given systemically and the nature of cross-reactions between aminoglycoside antibiotics are reviewed.

Darier's disease and Kaposi's varicelliform eruption

Kaposs varicelliform eruption usually occurs in persons with active skin disease of various types; however, in atopic dermatitis the condition may occur when the underlying disease is inactive. Two cases of widespread herpes simplex infection associated with Dariers disease are reported. In both cases, infection occurred in the absence of preexisting Darier skin lesions. In one case there was no previous history of Dariers disease. The infection occurred in the third trimester of pregnancy, but it did not appear to affect the infant or the placenta. In the second case, the Dariers disease was in remission at the time of onset of the virus infection.

Ultraviolet a protective sunscreens

Abstract A wide range of topical preparations for protecting the skin against sun exposure is now available. In general, these preparations are cosmetically elegant, and they have been shown to be effective and to conform to standards laid down by various regulatory bodies. Development of these compounds has grown along with acceptance by the general public of potential long-term adverse effects of unprotected sun exposure. It must be stressed, however, that the assessment procedures now used for topical sunscreens essentially measure their protection against the ultraviolet B (UVB, 290–320 nm) content of natural sunlight. Topical sunscreens are usually assessed by means of the sun protection factor (SPF), which compares the minimal erythema dose (MED) of protected normal skin with the MED of unprotected normal skin. 1 The dose of UVB is much lower than the dose of UVA (320–400 nm) for the production of erythema in normal skin. When natural or artificial broad band sources are used to produce erythema, the UVB content will produce an effect before a sufficient dose of UVA can be delivered. If exposure times are prolonged enough to deliver sufficient UVA with these sources, erythema from the UVB content will mask any UVA effect; thus, for practical purposes, the current testing procedures that utilize erythema to develop an SPF provide information concerning protection against UVB. There are two factors that generally limit an individuals exposure to natural sunlight. The first is discomfort from heat, the infrared effect, which induces a person to seek shade. The second is the knowledge that long periods of unprotected exposure will lead a few hours later to a painful sunburn, due mainly to UVB. If the UVB effect of natural sunlight can be obviated and current high-potency topical sunscreens are very successful in this regard, then long exposures become more likely. With these long exposures, greater amounts of UVA are received than would otherwise be possible. UVA is certainly not innocuous. It has a crucial role in some photosensitive skin diseases, especially those produced by drugs and chemicals. 2,3 Studies have also shown the adverse effects of UVA in other situations; eg, this part of the spectrum can produce both epidermal 4 and dermal 5 effects in experimental animals.

Anthralin and tar with UVB increase epidermal cell proliferation in asebia mice

The asebia mouse has chronic epidermal cell hyperproliferation. The epidermal labelling index (LI) for asebia was more than double that for BALB/cJ mice (7.3%vs. 2.7%). Using the asebia model of chronic epidermal hyperproliferation we examined the changes in epidermal LI and epidermal thickness after 3 weeks of treatment with certain treatments used for psoriasis. Changes in LI were generally paralleled by changes in thickness. UVB alone did not significantly increase the LI. UVB plus 0.1% anthralin in propylene glycol (PG) significantly increased the LI to 13.7% but this increase was largely due to the UVB plus PG. Crude coal tar (1%) increased the LI to 15.2%. The combination of UVB and 1% crude coal tar increased the LI even further to 26.2%. The LI did not show an additional increase when the concentration of crude coal tar was increased to 2% or 4%, These findings of increased epidermal cell proliferation in a model of chronic epidermal hyperproliferation are similar to published findings of increased epidermal cell proliferation in the normal skin of humans and hairless mice after multiple applications of these treatments whereas psoriatic lesions respond to these treatments with a reduction in epidermal cell proliferation.

Photosensitivity in children.

When photosensitivity presents in children, it frequently signifies a serious or potentially serious condition. Both disorders with genetic bases and idiopathic disorders are discussed.

Epidermolysis bullosa simplex with keratoderma of the palms and soles

A family is described who had epidermolysis bullosa (EB) simplex (Koebner) associated with keratoderma of the palms and soles. This association has been infrequently reported in the literature. The keratoderma appears to have a protective effect as these patients developed few palmar and plantar blisters in the area of the keratoderma. EB simplex (Koebner) with keratoderma appears to be a distinct syndrome, but the simultaneous occurrence of two dominantly inherited traits cannot be excluded.

Age-related changes in contact photsensitivity differ among mouse strains

There are differences among mouse strains in the age-related changes in reactivity to the contact photosensitizer tetrachlorosalicylanilide (TCSA). We found a tendency to lower reactions in older mice, with some strains showing declines from an early age (BALB/cJ, MRL/MpJ +/+, MRL/MpJ lpr/lpr and SJL/J). Others had increasing reactions until about 30-50 weeks of age before declining (DBA/1J, C3H/HeJ, and A/J) and one strain (C57BL/6J) had increased reactivity with age. There are also differences in the role of cyclophosphamide-sensitive T-suppressor cells in these age-related changes. In some mouse strains, BALB/cJ, C57BL/6J, A/J, DBA/1J and C3H/HeJ, age-related changes in reactivity to TCSA are independent of changes in cyclophosphamide-sensitive suppressor cells. In other strains, MRL/MpJ +/+, MRL/MpJ lpr/lpr and SJL/J, the development of cyclophosphamide-sensitive suppressor cells is responsible for the initial, though not later, stages of the age-related decline in reactivity.

Epidermolysis bullosa: assessment of a treatment regimen

Abstract: Nineteen patients with a variety of types of epidermolysis bullosa were initially assessed in an open study of a treatment regime for the genetic type of epidermolysis bullosa. Nine of the ten patients admitted to the hospital for treatment showed definite objective improvement with decreased number of blisters and increased rate of healing of blisters. The mean percentage decrease in blister numbers from the time of admission until discharge from hospital was 76%. Sixteen patients were followed as outpatients for 5–11 months. Two patients continued to show objective improvement, while eight reported more rapid healing of their blisters. Six patients failed to improve. This treatment has a beneficial effect in inpatients with epidermolysis bullosa. The improvement may be due to the intense topical treatment rather than to a specific item of the therapy. In the long term, this treatment has little effect on the formation of new blisters, but an accelerated healing of blisters is reported by 50% of the patients.