Roxithromycin reduces cyclosporine-induced gingival hyperplasia in renal transplant patients
被引:12
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作者:
Conde, S. A. P.
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UFJF, Postgrad Program Brazilian Hlth, BR-36036900 Juiz De Fora, MG, BrazilUFJF, Postgrad Program Brazilian Hlth, BR-36036900 Juiz De Fora, MG, Brazil
Conde, S. A. P.
[1
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Aarestrup, F. M.
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UFJF, Lab Immunopathol & Expt Pathol, BR-36036900 Juiz De Fora, MG, BrazilUFJF, Postgrad Program Brazilian Hlth, BR-36036900 Juiz De Fora, MG, Brazil
Aarestrup, F. M.
[2
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Vieira, B. J.
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UFJF, Lab Immunopathol & Expt Pathol, BR-36036900 Juiz De Fora, MG, BrazilUFJF, Postgrad Program Brazilian Hlth, BR-36036900 Juiz De Fora, MG, Brazil
Vieira, B. J.
[2
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Bastos, M. G.
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UFJF, IMEPEN Fdn, NIEPEN Inst, Dept Nefrol, BR-36036900 Juiz De Fora, MG, BrazilUFJF, Postgrad Program Brazilian Hlth, BR-36036900 Juiz De Fora, MG, Brazil
Bastos, M. G.
[3
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机构:
[1] UFJF, Postgrad Program Brazilian Hlth, BR-36036900 Juiz De Fora, MG, Brazil
[2] UFJF, Lab Immunopathol & Expt Pathol, BR-36036900 Juiz De Fora, MG, Brazil
[3] UFJF, IMEPEN Fdn, NIEPEN Inst, Dept Nefrol, BR-36036900 Juiz De Fora, MG, Brazil
Gingival overgrowth (GO) is a common side effect of chronic cyclosporine use. The average prevalence of GO is about 30%, ranging from 10% to 85% in various series, due to diverse aggravating risk factors: drug interactions with calcium channel blockers, age, cyclosporine dose, bacterial plaque, and genetic predisposition. Recent studies have demonstrated elevated levels of specific cytokines particularly transforming growth factor-beta (TGF-beta) in hyperplastic gingival tissue, suggesting that this growth factor plays a role in the accumulation of the extracellular matrix. Until recently treatment for this complication was only surgical. Nowadays, several studies have been performed to evaluate the effects of antibiotic treatment on the regression of GO. In the present study, we used roxithromycin, a macrolide antibiotic that has inhibitory effect on TGF-beta production by inflammatory cells. The results suggested that roxithromycin may be an important therapeutic tool to reduce cyclosporine-induced GO.