Lentigo maligna (LM) is an in situ melanoma which usually occurs in sun-damaged skin on the head and neck of elderly patients. Depending on the anatomical site and its size treatment of LM can be problematic and usually includes surgical excision or radiotherapy. Recent reports indicate that topical imiquimod may be an effective treatment. However, no data on the underlying immune response in the skin during treatment of LM with topical imiquimod are available so far. We report a 62-year-old caucasian woman with a histologically verified LM which was successfully treated with topical imiquimod 5% cream. Skin biopsy specimens were obtained before, during (at week 10) and 4 weeks after cessation of topical treatment with imiquimod 5% cream. Histological and immunohistochemical examination was performed in order to detect residual atypical melanocytes and to characterize the inflammatory infiltrate. A complete clinical and histological clearance of the skin lesion was achieved, with no recurrence up to 9 months after the end of treatment. During topical application of imiquimod 5% cream a depletion of epidermal and dermal CD1a+ dendritic cells was observed. The inflammatory infiltrate consisted of CD68+ macrophages and mainly of CD3+ T cells with a slight predominance of CD8+ T cells. An enhanced expression of granzyme B and TIA-1 was also noted particularly in the epidermis and near the dermoepidermal junction. In conclusion, our data indicate that imiquimod 5% cream induces a cytotoxic T-cell-mediated immune response in situ which may account for the complete destruction of the malignant melanocytes in LM. Further clinical trials and longer follow-up periods on the use of imiquimod for LM are warranted.
We evaluated the management of cardiovascular risk factors focusing on the treatment of hypercholesterolaemia in 245 patients who had had their first coronary revascularisation in a university hospital 1 year earlier. Subjects, methods, and resultsThe patients had had bypass grafting or angioplasty as a first coronary revascularisation procedure. Neither they nor their doctors were informed about the study until 1 year later, when the patients were asked to complete a questionnaire. Serum lipid concentrations were measured, and the modification of cardiovascular risk factors since coronary revascularisation noted.Data are presented as medians (90% confidence interval) unless indicated otherwise. Clinical data were analysed either by one way analysis of variance or the Mann-Whitney U test. Categorical variables were compared between groups by a 2 test. The degree of linear association between variables was evaluated by Pearson's correlation coefficient. Log transformation was used when necessary to normalise distribution. Values of P < 0.05 were considered significant.Overall, 186 (76%) of the 245 patients participated in the study; 98 had had angioplasty and 88 bypass grafting. Of the remainder, 37 refused to participate, 15 were lost to follow up, and 7 had died. Baseline concentrations were total cholesterol 6.1 mmol/l (5.9 to 6.2), high density lipoprotein cholesterol 1.1 mmol/l (1.1 to 1.2), low density lipoprotein cholesterol 4.1 mmol/l (3.9 to 4.2), triglyceride 2.0 mmol/l (1.9 to 2.1), and body mass index 26.6 kg/m 2 (26.1 to 27.1). Serum lipid concentrations were the same 1 year after revascularisation. Ninety four patients had stopped smoking before revascularisation, 29 of the 55 smokers at revascularisation were smoking one year later (P < 0.005); only six of the 26 heavy smokers continued to smoke > 20 cigarettes daily (P < 0.001). Of all the patients, 180 (97%) were receiving antiplatelet or warfarin treatment, or both, whereas only 37 (25%) of the 148 with a serum cholesterol concentration > 5.2 mmol/l were receiving lipid lowering treatment. After patients over 65 years were excluded, 29 of the 97 (30%) with a serum cholesterol concentration > 5.2 mmol/l were receiving lipid lowering treatment (figure). Fifty two patients had maintained a low fat diet. Multivariate analysis showed no correlation between adherence to a low fat diet or lipid lowering treatment and either surgical revascularisation-rather than angioplasty-inpatient rehabilitation (89 patients), previous myocardial infarction, low ejection fraction, the presence of symptoms, closer follow up, or satisfaction with treatment. CommentDespite guidelines on the treatment of hypercholesterolaemia in coronary heart disease and recent evidence of the benefit and safety of this treatment, the management of patients after coronary revascularisation in a Swiss university centre was inadequate.1-4 Only a few patients with hypercholesterolaemia received adequate lipid lowering treatment and ate a suitable diet 1 year after revascularisation despit...
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