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External Genital (external + genital)

Distribution by Scientific Domains
Medical Sciences83%

Selected Abstracts

Evaluation of imiquimod for the therapy of external genital and anal warts in comparison with destructive therapies

BRITISH JOURNAL OF DERMATOLOGY, Issue 2007
H. Schöfer
Summary External genital and anal warts (acuminate condyloma) were the first medical indication the topical immune response modifier imiquimod was approved for in 1997. Since then, many placebo controlled randomized clinical trials have demonstrated the efficacy and safety of this synthetic imidazoquinoline derivate for the treatment of different human papillomavirus infections and tumours. Treatment modalities for genital warts (5% cream, three times weekly, minimum duration 4 weeks, control of side-effects) have been optimized and assured by further clinical trials and meta-analyses. For a few years clinical studies focussed on the long-term efficacy of the immunomodulatory therapy (sustained clearance from warts) and most recent studies compared the efficacy of ablative, destructive and imiquimod monotherapy as well as combination therapies. [source]

Enhanced type I interferon signaling and recruitment of chemokine receptor CXCR3-expressing lymphocytes into the skin following treatment with the TLR7-agonist imiquimod

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 4 2005
Joerg Wenzel
Introduction:, Imiquimod (AldaraÔ) is an immune response modifier approved for the topical treatment of external genital and perianal warts which can mediate regression of several cutaneous malignancies [basal cell carcinoma (BCC), Bowen's disease, actinic keratosis, and metastasis of malignant melanoma]. Recently, it was discovered that imiquimod acts through the toll-like receptor (TLR) 7. We hypothesize that TLR7-signaling strongly induces the production of interferon (IFN) ,, which is able to enhance Th1-mediated cellular antiviral and antitumor immunity. Patients and methods:, In the present study we analyzed the expression of MxA, a protein specifically induced by type I IFNs during topical imiquimod treatment in several patients suffering from different cutaneous malignancies (BCC, cutaneous metastasis of melanoma, and breast cancer), and characterized the inflammatory infiltrate, along with the expression of chemokine receptor CXCR3, by immunohistochemistry. Results:, Treatment with the TLR7-agonist imiquimod induced a significant lesional lymphocytic inflammation, associated with strong expression of MxA, indicating the induction of type I IFN signaling. The extent of lesional MxA staining closely correlated with the number of infiltrating T lymphocytes and the expression of the chemokine receptor CXCR3, characteristic for Th1-biased immune responses. Discussion:, Our in vivo results suggest an important role for TLR7-induced production of type I IFN, which links innate and adaptive immunity and promotes specific Th1-biased cellular immune response capable of eliminating cutaneous malignancies. MxA appears to be a valuable parameter to demonstrate IFN-type I expression in imiquimod therapy. [source]

Imiquimod 5% cream for external genital or perianal warts in human immunodeficiency virus-positive patients treated with highly active antiretroviral therapy: an open-label, noncomparative study

BRITISH JOURNAL OF DERMATOLOGY, Issue 4 2009
P. Saiag
Summary Background, Human immunodeficiency virus (HIV)+ patients have an increased risk of anogenital warts. High-risk (HR) human papillomaviruses (HPVs), especially types 16 and 18, are major risk factors for precancerous and cancerous lesions of the anogenital tract, while low-risk (LR) HPVs are associated with benign lesions. Cure of genital warts with ablative techniques, surgical excision, podophyllotoxin or trichloroacetic acid is frequently difficult. Treatment with imiquimod cream showed a total clearance of external genital or perianal warts in about 50% of immunocompetent subjects. However, total clearance was reduced in HIV+ subjects not treated with highly active antiretroviral therapy (HAART). Objectives, To assess clinically and by monitoring HPV content the efficacy of 5% topical imiquimod to treat anogenital warts in HIV+ subjects with at least partially restored immune functions. Methods, Fifty HIV+ patients successfully treated with HAART (total CD4+ cells , 200 cells mm,3 and plasma HIV RNA load < 104 copies mL,1) with anogenital warts were included. Imiquimod 5% cream was applied on external genital or perianal warts three times weekly for up to 16 weeks. Warts were tested at entry and after treatment for human LR- and HR-HPV DNA. Results, Total wart clearance was observed in 16 of 50 (32%) patients at week 16. At enrolment, HPV DNA was present in more than 90% of lesions with a majority of lesions co-infected by HR- and LR-HPV. At study end, the HPV load decreased or became undetectable in 40% of cases studied. Conclusions, Imiquimod 5% cream did not show safety concerns and is suitable for use in HIV+ subjects with anogenital warts and successful HAART treatment. [source]

Evaluation of imiquimod for the therapy of external genital and anal warts in comparison with destructive therapies

BRITISH JOURNAL OF DERMATOLOGY, Issue 2007
H. Schöfer
Summary External genital and anal warts (acuminate condyloma) were the first medical indication the topical immune response modifier imiquimod was approved for in 1997. Since then, many placebo controlled randomized clinical trials have demonstrated the efficacy and safety of this synthetic imidazoquinoline derivate for the treatment of different human papillomavirus infections and tumours. Treatment modalities for genital warts (5% cream, three times weekly, minimum duration 4 weeks, control of side-effects) have been optimized and assured by further clinical trials and meta-analyses. For a few years clinical studies focussed on the long-term efficacy of the immunomodulatory therapy (sustained clearance from warts) and most recent studies compared the efficacy of ablative, destructive and imiquimod monotherapy as well as combination therapies. [source]

Ror2 knockout mouse as a model for the developmental pathology of autosomal recessive Robinow syndrome

DEVELOPMENTAL DYNAMICS, Issue 2 2004
Georg C. Schwabe
Abstract Robinow syndrome (RS) is a human dwarfism syndrome characterized by mesomelic limb shortening, vertebral and craniofacial malformations and small external genitals. We have analyzed Ror2 -/- mice as a model for the developmental pathology of RS. Our results demonstrate that vertebral malformations in Ror2 -/- mice are due to reductions in the presomitic mesoderm and defects in somitogenesis. Mesomelic limb shortening in Ror2 -/- mice is a consequence of perturbed chondrocyte differentiation. Moreover, we show that the craniofacial phenotype is caused by a midline outgrowth defect. Ror2 expression in the genital tubercle and its reduced size in Ror2 -/- mice makes it likely that Ror2 is involved in genital development. In conclusion, our findings suggest that Ror2 is essential at multiple sites during development. The Ror2 -/- mouse provides a suitable model that may help to explain many of the underlying developmental malformations in individuals with Robinow syndrome. Developmental Dynamics 229:400,410, 2004, © 2004 Wiley-Liss, Inc. [source]