56 research outputs found
Traitement de la maladie de Vogt-Koyanagi-Harada : Une revue narrative de la littérature: Treatment of Vogt-Koyanagi-Harada disease: A narrative literature review
Non-traumatic, exudative, bilateral panuveitis associated with extraocular manifestations, Vogt-Koyanagi-Harada disease (VKH) is an autoimmune disease mediated by Th1 lymphocytes reacting against melanocytes. It is a rare disease with female predominance. VKH disease is a diagnostic and therapeutic emergency. Treatment is based mainly on early and aggressive corticosteroid therapy to shorten the duration of the disease, prevent progression to chronicity, and reduce the incidence of extraocular manifestations. It is a corticosteroid-responsive disease, but unfortunately, relapses in the form of anterior uveitis are not rare, mainly at the time or at the end of tapering of corticosteroids. In these situations, or in case of intolerance to prolonged corticosteroid therapy, the use of conventional immunosuppressive agents or immunomodulatory drugs able to suppress the lymphocyte response is recommended. Intravenous immunoglobulins may also be used in patients with relapse or attack of the disease. In the present study, we performed a narrative literature review to summarize the different therapeutic aspects of VKH in the form of treatment algorithm.
PanuvĂ©ite bilatĂ©rale non traumatique, exsudative, associĂ©e Ă des manifestations extraoculaires, la maladie de Vogt-Koyanagi-Harada (VKH) est une maladie auto-immune mĂ©diĂ©e par les lymphocytes Th1 rĂ©agissant contre les mĂ©lanocytes. Câest une maladie rare Ă prĂ©dominance fĂ©minine. La maladie de VKH est une urgence diagnostique et thĂ©rapeutique. Le traitement repose essentiellement sur une corticothĂ©rapie prĂ©coce et agressive avec possibilitĂ© de dĂ©gression progressive lente sur plusieurs mois, afin deraccourcir la durĂ©e de la maladie, dâempĂȘcher la progression vers la chronicitĂ©, et de rĂ©duire lâincidence des manifestations extraoculaires. Câest une maladie corticosensible, mais malheureusement des rechutes sous forme dâuvĂ©ite antĂ©rieure ne sont pas rares, principalement au moment ou en fin de dĂ©gression de la corticothĂ©rapie. Dans ces situations ou en cas dâintolĂ©rance Ă la corticothĂ©rapie prolongĂ©e, le recours aux immunosuppresseurs conventionnels ou mĂ©dicaments immunomodulateurs capables de supprimer la rĂ©ponse lymphocytaire est de rĂšgle. Les immunoglobulines intraveineuses peuvent Ă©galement ĂȘtre proposĂ©es chez les patients prĂ©sentant une rechute ou une poussĂ©e de la maladie. Dans la prĂ©sente Ă©tude, nous rĂ©alisons une revue narrative de la littĂ©rature en dĂ©crivant les diffĂ©rents aspects thĂ©rapeutiques de la maladie de VKH afin de les rĂ©sumer sous forme dâun algorithme thĂ©rapeutique
Cyclic Naphthalene Diimide with a Ferrocene Moiety as a Redox-Active Tetraplex-DNA Ligand
Cyclic naphthalene diimides (cNDIs), with a ferrocene moiety (cFNDs) and different linker lengths between the ferrocene and cNDI moieties, were designed and synthesized as redoxâactive, tetraplexâDNA ligands. Intramolecular stacking was observed between ferrocene and the NDI planes, which could affect the binding properties for Gâquadruplexes. Interestingly, the circular dichroism spectrum of one of these compounds clearly shows new Cotton effects around 320â380 and 240 nm, which can be considered a direct evidence of intramolecular stacking of ferrocene and the NDI. Regarding recognition of hybrid Gâquadruplexes, the less rigid structures (longer linkers) show higher binding affinity (106âMâ1 order of magnitude). All new compounds show higher selectivity for G4 during electrochemical detection than noncyclic FND derivatives, which further identifies the redoxâactive potentiality of the cFNDs. Two of the three compounds tested even show preferential inhibition of cell growth in cancer cells over normal cells in a low concentration range, highlighting the potential for bioapplications of these cFNDs
K-ras mutation in the endometrium of tamoxifen-treated breast cancer patients, with a comparison of tamoxifen and toremifene
The putative presence of a mutation in codon 12 of the K-ras gene was investigated in the endometrium of tamoxifen (TAM) and toremifene (TOR)-treated breast cancer patients. DNA was extracted from fresh cytologic samples of the endometrium in 86 TAM and 21 TOR-treated breast cancer patients. Mutations were detected by enriched PCR and an enzyme-linked mini-sequence assay (ELMA). K-ras mutation was found in 35 TAM-treated endometrial samples, and in only one TOR-treated endometrium (P<0.003). In 24 premenopausal patients, K-ras mutation was found in seven (43.8%) of 16 patients with less than 47 months of TAM treatment, while none was found in eight patients with more than 48 months of TAM treatment (P<0.03). In 62 postmenopausal-amenorrheic patients, K-ras mutation was found in three (15.8%) of 19 patients with less than 23 months of TAM treatment, while it was found in 16 (61.5%) of 26 patients with 24â47 months of TAM treatment and nine (52.9%) of 17 patients with more than 48 months of TAM treatment (P=0.002). The presence of K-ras mutation is significantly influenced by the duration of TAM treatment and menstrual status of the patients. TOR may have a lower potential genotoxicity than TAM
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