5%咪喹莫特霜治疗结节型基底细胞癌1例及文献复习

报道5%咪喹莫特霜治疗1例结节型基底细胞癌。患者女,57岁,左侧额部斑块20年。病理活检证实为结节型基底细胞癌。以5%咪喹莫特霜外用治疗,每日1次共8周,接着每日2次共4周,总疗程12周。皮损部分消退。停药2周后手术切除肿瘤,组织内仍可见癌巢。免疫组化显示治疗后肿瘤细胞的Bcl-2蛋白表达减少。国外报道5%咪喹莫特乳膏治疗基底细胞癌可收到较好疗效,其机制可能与细胞免疫被激活有关。     

5%咪喹莫特乳膏外用治疗基底细胞癌2例

目的观察5%咪喹莫特乳膏治疗基底细胞癌的疗效。方法 5%咪喹莫特乳膏外用基底细胞癌皮肤破损处,每晚用药1次,每2周复查1次,共观察8周。结果 1例治疗6周达到临床病理治愈,随访15个月无复发。另1例治疗8周达到临床治愈。结论 5%咪喹莫特乳膏治疗非浸袭性基底细胞癌疗效满意,耐受性好。     

反射式共聚焦激光扫描显微镜在基底细胞癌术后随访中的应用

目的：明确反射式共聚焦激光扫描显微镜检测在基底细胞癌术后随访中的应用价值。方法：对22例基底细胞癌患者术后1个月、3个月、6个月、12个月分别进行手术部位的RCM扫描检测，RCM发现肿瘤组织的患者行组织病理学检查。结果：22例患者行RCM规律复查，其中4例于术后1个月复查发现肿瘤细胞，1例术后3个月复查发现肿瘤细胞，1例于术后半年发现肿瘤组织。6例患者均再次病理学检查诊断明确基底细胞癌，其余16例随访12个月于手术部位未见复发。结论：RCM在基底细胞癌术后随访中具有重要的应用价值。     

5%咪喹莫特乳膏治疗眼睑结节型基底细胞癌4例

本组患者采用5％咪喹莫特乳膏治疗眼险结节型基底细胞癌，疗效显著，治疗过程中无明显不良反应，而且通过2年的随访，患者皮损未见复发。     

多发性基底细胞癌6例临床与皮肤镜特征分析

目的 探讨多发性基底细胞癌的临床及皮肤镜特征.方法 回顾性分析经皮肤镜诊断且组织病理确诊为多发性基底细胞癌的6例21处皮损其临床及皮肤镜特征.结果 6例多发性基底细胞癌患者的平均年龄54.2岁,平均病程8.25年,男女比例1∶1.21处皮损中临床分型为结节溃疡型9处、色素型7处、浅表型5处.多发性基底细胞癌皮肤镜特征按...     

基底细胞癌误诊为湿疹1例

患者女,66岁。左小腿皮疹1年半。以"湿疹"予卤米松乳膏治疗无效。皮损组织病理示基底样细胞呈芽蕾状向真皮内侵袭生长,有核异形。诊断:浅表型基底细胞癌。予手术完整切除。患者随访3个月无复发。     

小汗腺汗孔癌1例

 报告1例小汗腺汗孔癌。患者女，56岁，头部结节30余年，破溃、渗液2个月。皮损病理检查示：真皮内可见瘤细胞团呈巢状分布，部分瘤细胞巢与表皮相连，瘤细胞以不典型嗜伊红鳞状细胞样细胞为主，细胞核大，深染，形态不规则，核分裂相增多，瘤细胞巢内可见管腔样结构。诊断为小汗腺汗孔癌。予扩大手术切除，现随访中。     

手术切除与5％咪喹莫特乳膏外用治疗结节性、浅表性基底细胞癌的疗效比较：一项多中心、非劣效性、随机对照性研究北大核心CSCD

2003年6月至2007年2月，Hextall等在英国的12个中心纳入501例结节性或浅表性基底细胞癌患者，随访3年。患者被随机分到咪喹莫特组（254例）和手术组（247例），咪喹莫特组接受5％咪喹莫特乳膏每天2次治疗，浅表性者疗程6周，结节性者疗程12周；手术组接受切除肿瘤及瘤外4mm范围的手术治疗。     

氩气刀联合5%咪喹莫特乳膏治疗Bowen病疗效观察

目的观察氩气刀联合5%咪喹莫特乳膏治疗Bowen病临床疗效和安全性。方法将入选的52例患者按随机数字表法分成治疗组和对照组,治疗组患者26例,皮损26处,采用氩气刀于真皮乳头层浅面气化肿瘤后,创面外用5%咪喹莫特乳膏,隔日1次,连续1个月;对照组患者26例,皮损26处,采用传统手术刀外科扩大切除皮损,酌情闭合创面。结果治疗组痊愈率92.13%和复发率7.69%与对照组的痊愈率80.77%和复发率19.23%比较,差异有统计学意义(P<0.05)。结论氩气刀结合5%咪喹莫特治疗Bowen病比传统手术刀外科治疗Bowen病疗效高,且手术时间短,操作简单,安全性更高。     

71例基底细胞癌皮肤镜下特征分析

目的：明确基底细胞癌在皮肤镜下的特征,为临床皮肤镜鉴别色素性皮损提供参考。方法：分析71例（71 lesions)经组织病理确诊为基底细胞癌的皮损皮肤镜图像。结果：最主要的皮肤镜指征按出现频率由高到低分别为：蓝灰色卵圆形巢（78.9%）、血管模式（74.6%）、多发性蓝灰色小球（60.6%）、溃疡（57.7%）、叶状结构（21.1%）。单纯临床诊断符合率为55%,加用皮肤镜后临床准断符合率为95%,提高了40%。结论：皮肤镜可提高临床诊断基底细胞癌的符合率。     

Topical imiquimod therapy for basal and squamous cell carcinomas: a clinical experience

Basal cell carcinomas (BCCs) and cutaneous squamous cell carcinomas (SCCs) are the most common malignancies in humans. Together, they constitute approximately 95% of nonmelanoma skin cancers (NMSCs). Surgical excision remains the mainstay of therapy of low-risk NMSC, though Mohs micrographic surgery is the gold standard for high-risk NMSC. Both methods produce high cure rates, but they may not be appropriate treatments for elderly patients who are either not surgical candidates or refuse to undergo surgery for their skin cancers. Imiquimod cream 5% is a topical immune response modifier that targets the toll-like receptors 7 and 8 and up-regulates inflammatory pathways targeting diseased tissue. This noninvasive topical therapy may be more appropriate for some patients. Herein, we describe our 5-month clinical experience in mostly elderly subjects with BCC (n=21) or SCC (n= 19) who were not candidates for surgical excision and were treated with topical imiquimod. Most subjects had a history of skin cancer, and the median age of the subjects was 78 years and 79 years in the BCC and SCC groups, respectively. After biopsy alone or biopsy followed by curettage, subjects received imiquimod cream 5% once daily 5 times weekly for 6 weeks. Twenty-three BCC lesions and 22 SCC lesions were included in the analysis. Most of the 45 lesions treated were located on the head and most were in high-risk areas. Approximately 3 months after imiquimod therapy, repeat biopsies showed that only 3 (2 BCCs and 1 SCC) lesion sites had residual tumor. After a median follow-up of 26 months, there was only one additional SCC recurrence. We also present a selection of representative case studies. Imiquimod cream 5% as adjunctive therapy to curettage was safe and well-tolerated in this mostly elderly population. The improved residual tumor and recurrence rates compared with historical rates for electrodesiccation and curettage (ED&C) alone suggest that adjunctive imiquimod therapy may be an appropriate treatment option for patients who desire or require less invasive treatment for NMSCs.     

Efficacy of topical 5% imiquimod cream for the treatment of nodular basal cell carcinoma: comparison of dosing regimens

OBJECTIVE: To establish a safe and efficacious dosing regimen for the treatment of primary nodular basal cell carcinoma (BCC) using 5% imiquimod cream. DESIGN: Two phase 2 studies were conducted: a 6-week, randomized, open-label, dose-response study evaluating 4 dosing regimens and a 12-week, randomized, vehicle-controlled, double-blind, dose-response study evaluating 4 dosing regimens. SETTING: Twenty-four public and private dermatology clinics in Australia and New Zealand (6-week study) and the United States (12-week study) participated. PATIENTS: The study populations comprised 99 patients enrolled in the 6-week study and 92 patients in the 12-week study. Patients were at least 18 years old and had a biopsy-confirmed diagnosis of nodular BCC. INTERVENTIONS: In the 6-week study, imiquimod was applied once daily for 3 or 7 days per week or twice daily for 3 or 7 days per week. In the 12-week study, imiquimod or placebo cream (vehicle) was applied once daily for 3, 5, or 7 days per week, or twice daily for 7 days per week. The entire tumor area was excised 6 weeks after treatment and examined histologically for evidence of remaining BCC. MAIN OUTCOME MEASURE: The proportion of patients having no histologic evidence of BCC in the posttreatment excision specimen. RESULTS: Dosing once daily for 7 days per week resulted in the highest clearance rate, with 25 (71%) of 35 and 16 (76%) of 21 patients showing clearance of their tumor in the 6- and 12-week studies, respectively. CONCLUSIONS: Topical 5% imiquimod cream is well tolerated and most effective in treating nodular BCC when applied once daily for 7 days per week for either 12 or 6 weeks.     

Imiquimod: in superficial basal cell carcinoma

Imiquimod, available as a 5% cream, is a new topical treatment for adults with superficial basal cell carcinoma (BCC). The exact mechanism of action of imiquimod in superficial BCC is unknown. Imiquimod may act as a toll-like receptor-7 agonist, and is thought to exert its anti-tumor effect via modification of the immune response and stimulation of apoptosis in BCC cells. Topical imiquimod 5% cream effectively increased clinical and histologic clearance of single superficial BCC lesions compared with vehicle in patients enrolled in two large, well designed trials. Patients applied imiquimod five or seven times per week or vehicle for 6 weeks, and the composite clearance rates at 12 weeks post-treatment for the corresponding treatment groups were 75%, 73%, and 2%, respectively. In a trial investigating the long-term efficacy of imiquimod 5% cream following application five times per week for 6 weeks, a clinical clearance rate of 90% was reported at the initial 12-week post-treatment examination. The estimated rate of clinical clearance at the 1-year follow-up visit was 84%. Application site and local skin reactions were the most common adverse events reported by imiquimod recipients. The severity of erythema, erosion, and scabbing/crusting correlated positively with the composite and histologic response rates.     

Therapeutic response of basal cell carcinoma to the immune response modifier imiquimod 5% cream

BACKGROUND: Basal cell carcinoma (BCC) responds to interferon therapy. Imiquimod is a cytokine and interferon inducer. OBJECTIVE: This randomized, double-blind pilot trial evaluated the safety and efficacy of imiquimod 5% cream versus vehicle in the treatment of BCC. METHODS: In this population of 35 patients with BCC, 24 received imiquimod 5% cream and 11 received vehicle cream in 1 of 5 dosing regimens for up to 16 weeks. Six weeks after treatment, an excisional biopsy of the target site was performed. RESULTS: BCC cleared (on the basis of histologic examination) in all 15 patients (100%) dosed twice daily, once daily, and 3 times weekly; in 3 of 5 (60%) patients dosed twice weekly; 2 of 4 (50%) dosed once weekly; and in 1 of 11 (9%) treated with vehicle. Adverse events were predominantly local reactions at the target tumor site, with the incidence and severity of local skin reactions declining in groups dosed less frequently. CONCLUSION: Imiquimod 5% cream shows clinical efficacy in the treatment of BCC.     

Imiquimod

? Imiquimod, available as a 5% cream, is a new topical treatment for adults with superficial basal cell carcinoma (BCC). The exact mechanism of action of imiquimod in superficial BCC is unknown. Imiquimod may act as a toll-like receptor-7 agonist, and is thought to exert its anti-tumor effect via modification of the immune response and stimulation of apoptosis in BCC cells. ? Topical imiquimod 5% cream effectively increased clinical and histologic clearance of single superficial BCC lesions compared with vehicle in patients enrolled in two large, well designed trials. Patients applied imiquimod five or seven times per week or vehicle for 6 weeks, and the composite clearance rates at 12 weeks post-treatment for the corresponding treatment groups were 75%, 73%, and 2%, respectively. ? In a trial investigating the long-term efficacy of imiquimod 5% cream following application five times per week for 6 weeks, a clinical clearance rate of 90% was reported at the initial 12-week post-treatment examination. The estimated rate of clinical clearance at the 1-year follow-up visit was 84%. ? Application site and local skin reactions were the most common adverse events reported by imiquimod recipients. The severity of erythema, erosion, and scabbing/crusting correlated positively with the composite and histologic response rates.     

Open study of the efficacy and mechanism of action of topical imiquimod in basal cell carcinoma

Imiquimod is an immune-response modifier that has been shown to be effective in the treatment of superficial and nodular basal cell carcinoma (BCC). The objective of this open-label study was to investigate the effectiveness of imiquimod 5% cream in superficial, nodular, and infiltrative BCC. Fifty-five Caucasian patients with primary BCC measuring 8 mm or more in diameter with a superficial, nodular, or infiltrative histological pattern were included in the study. Four groups of BCC (A, B, C, and D) and two dosing regimens were studied: 35 BCCs (groups A, B, and C) were treated with imiquimod three times weekly and 20 BCCs (group D) were treated with imiquimod five times weekly. Histological samples were obtained before treatment, during treatment (on day 22 in group A, day 15 in group B, and day 8 in groups C and D), and 6 weeks after treatment. All patients were followed-up for a minimum of 2 years. In the biopsy specimens obtained, the expression of Bcl-2, p53, and Ki-67, apoptotic index (Tunel technique), and the number of CD3+, CD8+, CD20+, CD56+, CD68+, granzyme B+, and S-100+ cells in the peritumoural inflammatory infiltrate, were determined and quantified. Of the 55 BCCs treated with imiquimod 41 (74%) were in complete remission after 2 years of follow-up. These comprised 4/4 superficial BCCs, 7/8 (88%) nodular BCCs, and 30/43 (70%) infiltrative BCCs. Multi-variate analysis demonstrated that baseline tumour size was the most powerful independent prognostic variable (P < 0.05). Treatment with imiquimod increased the apoptotic index (P < 0.05), reduced Bcl-2 expression (P < 0.05), and increased the number of CD3+, CD8+, CD20+, CD68+, granzyme B+, and S-100+ cells in the inflammatory infiltrate of the BCC (P < 0.05). In conclusion, imiquimod induced an antitumour immune response mediated by lymphocytes and macrophages, reduced Bcl-2 expression and increased the apoptotic index of BCC, and was clinically effective in 74% of BCCs after a 2-year follow-up period.     

First case series on the use of imiquimod for morphoea

BACKGROUND: Morphoea is characterized by fibrosis, which is mediated by cytokines including transforming growth factor (TGF)-beta. OBJECTIVE: Our objective was to use imiquimod 5% cream (Aldara), an inducer of interferon-gamma, known to inhibit TGF-beta, to treat morphoea. METHODS: Patients with morphoea were treated with imiquimod and evaluated during their follow-up visits to 6 months. RESULTS: The dyspigmentation, induration and erythema of 12 patients with morphoea lesions improved. The histology of the skin also showed a decrease in dermal thickness. CONCLUSION: This is the first case series describing the successful application of imiquimod in the management of morphoea.     

Randomized, comparative trial on the sustained efficacy of topical imiquimod 5% cream versus conventional ablative methods in external anogenital warts

Conventional ablative treatments for external anogenital warts are affected by high recurrence rates. This study compared sustained clearance after ablation vs. treatment with imiquimod 5% cream vs. the combination of both methods. This was a 3-arm, open-label, randomized clinical study comparing ablation alone (Group A), imiquimod 5% cream monotherapy (Group B), or combined ablation followed by topical imiquimod (Group C). Subjects whose anogenital warts were completely cleared entered a 6-month follow-up to evaluate sustained clearance.After 3 months follow-up, 83.9% (73/87), 93.8% (90/96) and 91.7% (66/72) of subjects in Groups A, B, C, respectively, remained free of recurrent anogenital warts. After 6-months follow-up, 73.6% (64/87), 93.7% (89/95) and 91.5% (65/71) of subjects presented free of recurrence (Group A vs. B & C p-values each p < 0.004 in favour of the imiquimod-treated groups).Imiquimod 5% cream, as monotherapy or in combination with ablation, was superior to ablation alone in reducing the recurrence of successfully treated anogenital warts.     

A randomized,double-blind,vehicle-controlled study to assess 5% imiquimod cream for the treatment of multiple actinic keratoses

BACKGROUND: Actinic keratoses (AKs) are precancerous epidermal lesions found most frequently on areas of the skin exposed to the sun. Several case studies published recently have indicated that 5% imiquimod cream, currently licensed for the treatment of genital warts, may be an effective treatment for AK. OBJECTIVE: To assess the efficacy and safety of imiquimod for the treatment of AK. DESIGN: Patients in this randomized, double-blind, vehicle-controlled study applied 5% imiquimod cream or vehicle to AK lesions 3 times per week for a maximum of 12 weeks or until lesions had resolved. In the event of an adverse reaction, application of imiquimod was reduced to 1 or 2 times per week. Rest periods were also allowed if necessary. SETTING: A specialized outpatient dermatology clinic within a state-funded hospital in Germany. PATIENTS: The study population was aged 45 to 85 years. Of 52 patients screened, 36 men and women with AK confirmed by histological diagnosis were enrolled. Patients were excluded from the study if they did not have a histological diagnosis for AK, if they were older than 85 years, or if they did not comply with the protocol. All patients had responded to a notice asking for volunteers. MAIN OUTCOME MEASURES: The number and appearance of lesions were evaluated before, during, and after treatment. All adverse effects were recorded. RESULTS: Lesions treated with 5% imiquimod cream were clinically cleared in 21 (84%) of 25 patients and partially cleared in 2 (8%). Clearance was histologically confirmed 2 weeks after the last application of imiquimod in all patients clinically diagnosed as lesion free. Only 10% of patients treated with imiquimod were clinically diagnosed with recurrence 1 year after treatment. No reduction in the size or number of AK lesions was observed in vehicle-treated patients. Adverse effects reported by patients treated with imiquimod included erythema, edema, induration, vesicles, erosion, ulceration, excoriation, and scabbing. However, imiquimod was well tolerated since all patients completed the 12-week treatment. Only a few, mild adverse reactions to the vehicle cream were reported. CONCLUSION: Application of 5% imiquimod cream for 12 weeks is an effective and well-tolerated treatment for AK.     

Efficacy of imiquimod for the expression of Bcl-2, Ki67, p53 and basal cell carcinoma apoptosis

BACKGROUND: Imiquimod is a modifier of the immune response that has been proven to be an effective treatment for basal cell carcinoma (BCC). However, its mechanism of action is still unknown. OBJECTIVES: To determine whether imiquimod modifies the expression of proteins such as Bcl-2, Ki67, p53 and the BCC apoptotic index. PATIENTS AND METHODS: Thirty caucasian patients with primary BCCs larger than 8 mm in diameter were included in a double-blind randomized clinical and immunohistochemical study which was designed in a reference university hospital. The 30 BCCs were randomized in two treatment arms between September 2001 and February 2002. Twenty-four BCCs were treated with imiquimod 5% cream and six BCCs with Aldara (3M Pharmaceuticals) excipient. Histological samples were obtained before treatment and on days 8 and 15 during the course of treatment. The BCC expression of Bcl-2, Ki67 and p53 was determined in paraffin samples and the apoptotic index of the BCC was studied using the TUNEL technique (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labelling) in frozen samples. All variables were evaluated quantitatively in fields with a magnification x 400. RESULTS: The BCCs treated with imiquimod showed a decrease in the expression of Bcl-2 (88.7% before treatment, 61.4% day 15, P = 0.01) and an increase in the apoptotic index (0.53% before treatment, 1.66% day 15, P = 0.002), which were not observed in the BCCs treated with the excipient. Ki67 and p53 did not show significant changes in any group. CONCLUSIONS: Imiquimod reduces the expression of Bcl-2 in the BCC cells and increases the BCC apoptotic index.