ABSTRACT
Thalidomide has been shown to selectively inhibit TNF-alpha production in vitro by lipopolysaccharide (LPS)-stimulated monocytes. TNF-alpha has been shown to play a pivotal role in the pathophysiology of endototoxic shock. Using a mouse model of LPS-induced shock, we investigated the effects of thalidomide on the introduction of TNF-alpha and other cytokines and on animal survival. After injecton of 100-350 mug LPS into mice, cytokines including TNF-alpha, IL-6, IL-10, IL-1beta, GM-CSF and IFN-gamma were measured in the serum. Administration of 200 mg/kg thalidomide to mice before LPS challenge modified the profile of LPS-induced cytokine secretion. Serum TNF-alpha levels were reduced by 93 percent, in a dose-dependent manner, and TNF-alpha mRNA expression in the spleens of mice was reduced by 70 percent. Serum IL-6 levels were also inhibited by 50 percent. Thalidomide induced a two-fold increase in serum IL-10 levels. Thalidomide treatment did not interfere with the production of GM-CSF, IL-1beta or IFN-gamma. The LD50 of LPS in this model was increased by thalidomide pre-treatment from 150 mug to 300 mug in 72 h. Thus, at otherwise lethal doses of LPS, thalidomide treatment was found to protect animals from death.
Subject(s)
Mice , Animals , Female , Disease Models, Animal , Lipopolysaccharides , Shock, Septic/drug therapy , Thalidomide/pharmacologyABSTRACT
E apresentado um caso de fistula uretrorretal com estenose de uretra, como complicacoes de prostatectomia transvesical, onde a enucleacao foi dificultada por aderencias fibrosas. Por acesso perineal, a fistula foi corrigida cirurgicamente,assim como a estenose uretral. Obteve-se sucesso com o procedimento empregado