[The pilot study of the effect of paclitaxel by local slow delivery on intimal hyperplasia of vascular anastomosis after vascular graft bypass].

OBJECTIVE: To develop a new way to prevent restenosis in the anastomotic site due to intimal hyperplasia after vascular graft bypass (VGB) in peripheral arteries. METHODS: Five mongrel dogs received bilateral iliac-femoral VGB and their arteries between the graft were ligated and cut off under general anaesthesia. The mixture of the paclitaxel and fibrin gel (FG) were randomly sprayed onto one side of grafts including distal and proximal anastomotic site, and the fibrin gel served as control were sprayed onto the other one. The bilateral grafts including distal and proximal anastomotic site were harvested four weeks postoperationally and the anastomotic sites were observed grossly, pathologically and by electron microscopy. The intimal thickness and area of each anastomotic site were measured, then the data were analysed statistically. RESULTS: The bilateral grafts of all dogs were patent and the neointima of all anastomotic sites have been seen grossly. The neointimal thickness and area of the experimental side were significantly reduced compared with the control side (P < 0.05). Scanning electron microscopy showed that the anastomotic intima of the experimental side was covered with one layer of intact and regular endothelium cells with deposition of little blood components, but the anastomotic intima of the control side was covered with irregular endothelium cells and deposited with a lot of blood cells and fibrins. Transmission electron microscopy showed the anastomotic intima of the control side that rich in vascular smooth muscle cells and the matrix of the intima was composed of regular collagenous fibers, and that of the experimental side consisted of several types of cells with a lot of foreign particles in the matrix. CONCLUSION: It is safe and effective to locally use low dose of paclitaxel carried by FG in the prevention of vascular anastomotic site intimal hyperplasia. Paclitaxel molecules can penetrate the graft wall and stay in the anastomotic intima more than four weeks postoperationally.

[HSC transplantation-associated intestinal thrombotic microangiopathy: clinical pathological features, diagnosis criteria and treatment].

Thrombotic microangiopathy (TMA) is a lethal transplantation-associated complication which exactly likes acute intestinal graft-versus-host disease (GVHD) in the clinical manifestation. 373 consecutive patients with hematological diseases received family HLA matched or mismatched HCT from May, 2002 to July, 2004. To analyse the clinical and pathological characteristics of TMA, 30 patients who suffered from severe diarrhea and received colonoscopic examination and gut biopsy were retrospectively analyzed. The results indicated that 7 patients originally diagnosed as gut GVHD showed the pathological evidence of enteric TMA. The incidence of TMA was 7 out of 30 specimen (23.3%). Pathological evidence of enteric TMA shown microvascular disorder characterized by thrombus in the capillary without infiltration of lymphocytes and perivascular hemorrhages in the mucosa, swelling and focal denudation of epithelial cells. All patients with TMA were associated with cytomegalovirus (CMV) antigenemia/disease. Among these patients, 4 cases, who only showed TMA without the evidence of gut GVHD pathologically, displayed treatment-resistant bloody diarrhea, renal failure, veno-occlusive disease, hemorrhagic cystitis, hemolytic anemia as well as thrombocytopenia. But the other 3 cases, with co-existence of both TMA and GVHD pathological characteristics had better treatment response. Survival analysis indicated that 3 patients with TMA-GVHD survived for 461 to 536 days but three out of four TMA patients died from VOD with liver failure as well as multiple organ failure during 101 to 254 days after HCT. In conclusion, to better diagnose those patients with severe and refractory diarrhea following HCT, pathological examination may indicate crux evidence to identify intestinal TMA from gut GVHD. Furthermore, this primary report has first evidenced that TMA and TMA-GVHD are two pathologically well-recognized subtypes with the difference between the pathological characteristics, treatment response and clinical outcomes.