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81.
Practical aspects of management of recurrent aphthous stomatitis 总被引:2,自引:0,他引:2
A Altenburg†¶ MB Abdel-Naser†‡¶ H Seeber§ M Abdallah‡ CC Zouboulis† 《Journal of the European Academy of Dermatology and Venereology》2007,21(8):1019-1026
Treatment of recurrent aphthous stomatitis (RAS) remains, to date, empirical and non-specific. The main goals of therapy are to minimize pain and functional disabilities as well as decrease inflammatory reactions and frequency of recurrences. Locally, symptomatically acting modalities are the standard treatment in simple cases of RAS. Examples include topical anaesthetics and analgesics, antiseptic and anti-phlogistic preparations, topical steroids as cream, paste or lotions, antacids like sucralfate, chemically stable tetracycline suspension, medicated toothpaste containing the enzymes amyloglucosidase and glucoseoxidase in addition to the well-known silver nitrate application. Dietary management supports the treatment. In more severe cases, topical therapies are again very useful in decreasing the healing time but fail to decrease the interval between attacks. Systemic immunomodulatory agents, like colchicine, pentoxifylline, prednisolone, dapsone, levamisol, thalidomide, azathioprine, methotrexate, cyclosporin A, interferon alpha and tumour necrosis factor (TNF) antagonists, are helpful in resistant cases of major RAS or aphthosis with systemic involvement. 相似文献
82.
A Kalayciyan†‡ CC Zouboulis†§ 《Journal of the European Academy of Dermatology and Venereology》2007,21(1):1-10
Behçet's disease (Adamantiades‐Behçet's disease, ABD) is a multisystemic inflammatory disease, the pathogenesis of which is still a mystery. Many questions are still to be answered and the available diverse data need to be brought together to be compared and analysed. There is at least consensus on the effect of possible, but currently unknown, environmental triggering factor(s) against a background of genetic susceptibility. The possible aetiological factors form a broad spectrum, with infectious agents being the most probable ones. Whatever the stimulus is, the target tissue seems to be the small blood vessels, with various consequences of either vasculitis and/or thrombosis in many organ systems. The endothelium seems to be the primary target in this disease; however, it may just be the subject of the bizarre behaviour of the immune system. The diverse existing data could be interpreted in favour of either explanation. A similar confusion exists about the thrombotic tendency in Adamantiades‐Behçet's disease, in terms of whether a primary hypercoagulability is present or whether it is secondary to inflammation. Recent interesting immunological data promise a way out of the existing dilemma. These findings will be outlined within the context of possible hypotheses and attention will be paid to further investigations that are needed. 相似文献
83.
Cyclosporin inhibits nitric oxide production in medullary ascending limb cultured cells 总被引:1,自引:1,他引:0
Wu M; Yang C; Bens M; Yu H; Huang J; Wu C; Huang C; Vandewalle A 《Nephrology, dialysis, transplantation》1998,13(11):2814-2820
Background: Nitric oxide (NO) has been shown to play a
role in cyclosporin (CsA) nephrotoxicity, but its mechanism of action is
still unclear. As inducible NO synthase (iNOS) mRNA
has been found to be expressed in rat medullary thick ascending limb (mTAL)
cells, we investigated the effects of CsA on NO production in a model of
mouse cultured mTAL cells. Materials and methods: The
experiments were carried out on sub-cultured cells derived from isolated
mTAL microdissected from the kidney of C57BL/6 mice. The identification of
the iNOS mRNA in mTAL microdissected segment and
cultured cell was confirmed by RT-PCR and RsaI
digestion. Nitrite (NO2-) released by mTAL cells was
determined using the modified Griess reagent method and taken as an index
of nitric oxide production. The cultured cells were treated with various
concentrations of CsA and different signal transduction regulators to
assess the effect and possible pathway(s) of action of CsA on NO production
in mTAL cells. Results: The basal production of NO by
mTAL cells increased by 1.8-fold following incubation with bacterial
lipopolysaccharide (LPS). Both aminoguanidine and
L-NAME inhibited NO production. CsA (10-300 ng/ml)
also inhibited NO production in a dose-dependent manner and prevented its
increase induced by LPS. Phorbol 12-myristate 13-acetate (PMA), a PKC
stimulator, enhanced slightly the production of NO under basal conditions
and prevented the inhibitory action of CsA on NO production. These results
suggest that the NO secreted by mouse cultured mTAL cells is dependent on
the PKC pathway. Conclusion: These results show that
CsA may downregulate the production of NO by cultured mTAL cells expressing
iNOS mRNA and that the PKC pathway is involved in this
process. 相似文献
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