Tumor inflamatorio miofibroblástico peritoneal. Respuesta favorable asociada a infliximab: Caso clínico / Peritoneal myofibroblastic tumor successfully treated with infliximab: Report of one case

Myofibroblastic tumor (MIT) is characterized by the infiltration of different organs, most commonly the lungs, with nodular lesions composed of myofibroblasts and inflammatory cells, which can be identified by specific patterns in the immunohistochemical studies. When it involves the peritoneum it is difficult to eradicate, tends to relapse and it has an invasive behavior, requiring its differentiation from peritoneal carcinomatosis. Treatment may be surgical excision, the use of non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids. We report a 30 years old female with an unremarkable medical history, presenting with abdominal pain and progressive abdominal distention. A CT scan revealed multiple peritoneal nodular lesions. A surgical biopsy was reported as a myofibroblast and inflammatory cell infiltrate. Immunohistochemical staining was consistent with MIT. Given the extensive involvement of the peritoneum surgical therapy was not considered appropriate and treatment with NSAID and glucocorticoids was started. No response was observed after 6 months, therefore infliximab therapy was started. After 10 months of follow-up the patient is well, returned to normal life, ascites improved and resolved and CT scan showed partial regression or stabilization of the lesions.

Effect of rosiglitazone on expression of AQP1, VEGF-A and COX-2 in human peritoneal microvascular endothelial cells / 中国病理生理杂志

AIM:To investigate the effect of rosiglitazone on the expression of aquaporin-1 (AQP1), vascular endothelial growth factor-A ( VEGF-A ) and cyclooxygenase-2 ( COX-2 ) in human peritoneal microvascular endothelial cells.METHODS: Cultured peritoneal microvascular endothelial cells were divided into 4 groups.The morphological changes of the cells were observed under inverted microscope .The protein expression of AQP1, VEGF-A and COX-2 in hu-man peritoneal microvascular endothelial cells was determined by Western blotting .The mRNA expression of AQP1, VEGF-A and COX-2 in the cells was measured by real-time PCR.RESULTS:Rosiglitazone stimulated the proliferation of the cells.Rosiglitazone up-regulated the expression of AQP1, and down-regulated the expression of VEGF-2 and COX-2 at mRNA and protein levels in the cells .The PPAR-γantagonist GW9662 partly inhibited the up-regulation of AQP1 expres-sion by rosiglitazone (P0.05).CON-CLUSION:Rosiglitazone up-regulates the expression of AQP 1 and down-regulates the expression of VEGF-A and COX-2 in human peritoneal microvascular endothelial cells , thus promoting water transportation and attenuating peritoneal fibrosis during peritoneal dialysis .

Activation of NF-?B and expression of ICAM-1 and COX-2 genes in rat neointimal formation / 中国病理生理杂志

AIM: To investigate the relationship between NF-?B activation and intimal hyperplasia.METHODS: The protein extract from aorta was used to detect the expression of NF-?B p65,I?B?,ICAM-1 and COX-2 by Western blotting,and detection of threonine phosphorylation of p65 was performed by immunoprecipitation analysis.RESULTS: The level of p65 reached a maximum level at day 7,and then decreased significantly,which was higher than that in the control,in both cellular extract and nuclear extract at day 21 after balloon injury.The p65 level in cytoplasm had no obvious changes at different time points after balloon injury.The threonine phosphorylation of NF-?B p65 was negative correlated with the nuclear translocation of NF-?B.I?B? level showed a 15% decrease at day 1 after balloon injury,compared with control group,then returned at day 14,and reached to normal level at day 21.However,the expression of ICAM-1 and COX-2 was maximal at day 14,and then declined but higher than that in control group at day 21 after balloon injury.CONCLUSION: The activation of NF-?B p65 and the expression of ICAM-1 and COX-2 are parallel to the neointimal thickening after balloon injury.