Andrew C. Satchell

Treatment of interdigital tinea pedis with 25% and 50% tea tree oil solution: a randomized, placebo-controlled, blinded study

Tea tree oil has been shown to have activity against dermatophytes in vitro. We have conducted a randomized, controlled, double‐blinded study to determine the efficacy and safety of 25% and 50% tea tree oil in the treatment of interdigital tinea pedis. One hundred and fifty‐eight patients with tinea pedis clinically and microscopy suggestive of a dermatophyte infection were randomized to receive either placebo, 25% or 50% tea tree oil solution. Patients applied the solution twice daily to affected areas for 4 weeks and were reviewed after 2 and 4 weeks of treatment. There was a marked clinical response seen in 68% of the 50% tea tree oil group and 72% of the 25% tea tree oil group, compared to 39% in the placebo group. Mycological cure was assessed by culture of skin scrapings taken at baseline and after 4 weeks of treatment. The mycological cure rate was 64% in the 50% tea tree oil group, compared to 31% in the placebo group. Four (3.8%) patients applying tea tree oil developed moderate to severe dermatitis that improved quickly on stopping the study medication.

Imiquimod induced regression of clinically diagnosed superficial basal cell carcinoma is associated with early infiltration by CD4 T cells and dendritic cells

Imiquimod is presumed to clear basal cell carcinoma (BCC) through apoptosis mediated by cytokines and lymphocytes, with erosion often observed correlating with complete clearance. The objective was to determine the cellular immune response early in the course of treatment in order to examine whether cell mediated immunity could be responsible for imiquimod mediated regression of BCC. Sixteen adults with clinically diagnosed BCC were openly assigned to 5 days per week of drug (1, 2 or 4 weeks) or placebo (2 weeks) in groups of four. No baseline biopsy was performed. Post‐treatment excision specimens were examined by routine and immunohistochemical staining. Treatment was associated with the early appearance of CD4 cells, activated dendritic cells and macrophages, with later infiltration by CD8 T cells. Dendritic cells continually increased with time, while macrophages reached a maximum at 1 week and then declined slightly. There were comparatively few neutrophils or γδ T cells. Early infiltrates were most prominent in the tumour and upper dermis. The results are consistent with a cell mediated immune response being responsible for the clearance of the BCC. Several immune‐mediated tumour destruction mechanisms are likely to be involved.

Reactive perforating collagenosis: A condition that may be underdiagnosed

Reactive perforating collagenosis is a perforating disorder developing in adults, usually in association with diabetes mellitus or renal failure. We present three cases diagnosed at the Royal Prince Alfred Hospital in a 5 month period. All three patients had long‐standing diabetes mellitus, hypertension, hypercholesterolaemia and ischaemic heart disease. Each patient presented with generalized pruritus and a papular eruption across the trunk and limbs. More than one biopsy or multiple levels were needed before the diagnostic histological features were seen. The first patient responded to 0.5% phenol with 10% glycerine in sorbolene cream. The second patient did not respond to topical betamethasone diproprionate 0.5 mg/g cream and antihistamines (hydroxyzine 25 mg nocte) and required narrow‐band ultraviolet (UV) B. The third patient, having failed to respond to topical betamethasone diproprionate 0.5 mg/g cream and wet dressings, antihistamines (hydroxyzine 25 mg tds and doxepin 50 mg nocte) and UVB required acitretin 25 mg orally per day. Because reactive perforating collagenosis responds to treatment, we believe this condition should be considered in patients with diabetes mellitus or renal failure presenting with pruritus and that biopsy of intact lesions may need multiple levels to help establish the diagnosis.

Increased Fas ligand expression by T cells and tumour cells in the progression of actinic keratosis to squamous cell carcinoma

Background  In the counterattack model of tumorigenesis, it has been proposed that tumours develop resistance to attack from Fas ligand (FasL)‐expressing cytotoxic T cells by downregulating Fas (immune escape), while at the same time upregulating FasL expression to induce apoptosis in Fas‐expressing T cells (counterattack).