1,721,090 research outputs found

    SENTINEL NODE IN DIFFERENTIATED THYROID CANCER: COMPARISON BETWEEN VITAL-DYE PATENT BLUE, LYMPHOSCINTIGRAPHY AND COMBINED TECHNIQUE

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    Obiettivo dello studio : aim of the study is to evaluate the role of sentinel node (SN) identification in the treatment of differentiated thyroid cancer (DTC). We also aim to assess feasibility and reproducibility of the SN techniques with vital-dye patent blue, radiotracer and combined technique Materiali e metodi : the study is multicentric, prospective, randomized three arms open. We expect to enroll 120 patients in 2 years. Patients have to be preoperative diagnosis of DTC. Exclusion criteria are previous cervical surgery, medullary cancer, nodes metastasis and multifocal tumor. All patients undergo total thyroidectomy, SN identification and central compartment (CC) dissection: in Arm A SN identification is obtained with vital-dye Patent blue technique, in Arm B with lymphoscintigraphy and in Arm C with combined technique. Specimen histopathology provides information about the characteristics of primary tumor, SN and the remaining nodes with specific immuno-histochemistry protocols Principali risultati : so far we enrolled 42 patients Arm A (26 pts): 18 patients (69.2%) had negative SN and nonSN; 1 (3.8%) with negative SN had micrometastasis in 2 nodes of CC; 2 (7.6%) with macrometastasis in the SN had metastatic nodes in the CC and 1 (3.8%) had macrometastasis in the SN with no other positive nodes. In 4 (15.2%) patients identification of the SN wasn't possible and there was no evidence of metastasis in all nodes removed Arm B: 2 patients (100%) had negative SN and nonSN Arm C (14 pts): 4 patients (28.6%) had negative SN and nonSN; 1 (7.1%) with negative SN had macrometastasis in 2 nodes; 4 (28.6%) with macrometastasis in the SN had metastatic nodes in the CC and 1 (7.1%) had macrometastasis in the SN with no other positive nodes. In 4 (28.6%) patients identification of the SN wasn't possible and in 3 of them there was no evidence of metastasis Conclusioni : so far the data we gathered are too few to make statistic significant conclusions. Once adequate scientific evidence is available, detection of the SN could become a routine procedure in DTC treatment, avoiding central compartment dissection in patients with negative SN. The achievement of a standard protocol of SN detection remains an important issue to solve, although both techniques had shown a good rate of detection of the SN, several studies report that the combined method could reduce false negatives and increase detection rates of SN metastase

    Infrahepatic terminolateral cavo-cavostomy as rescue technique in complicated "modified" piggyback liver transplantation

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    Infrahepatic terminolateral cavo-cavostomy as a rescue technique in complicated "modified" piggyback liver transplantation

    NITRIC OXIDE GENERATION IS ASSOCIATED WITH AN UNBALANCE OF PROTEIN TYROSINE PHOSPHATASES DURING LIVER TRANSPLANTATION

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    Organ dysfunction secondary to ischemia-reperfusion (I/R) injury still represents a major problem in liver transplantation. Apoptosis has been observed in hepatocytes and sinusoidal endothelial cell, following I/R injury and it has been postulated as a contributing factor in ischemia-reperfusion graft dysfunction, involving a complex series of events, as changes of protein tyrosine-kinase phosphorylation. We evaluated hepatic purine metabolites, protein tyrosine phosphatases (PTPs), nitrate plus nitrite levels (NOx), caspase-3 (C-3) activity and DNA fragmentation in the time course of twelve pig orthotopic liver transplantation. Biopsies were taken before explantation (t0), after cold ischemic storage (t1) and 30 min from reperfusion (t2). During the ischemic period we observed a reduction of high energy phosphates and an increase of purine bases; PTP activity was largely increased. At t2 high energy phosphates showed a tendency to increase with respect to t1, with a partial restoration of phosphorylation potential, measured as ATP/ADT ratio. PTP activity was significantly reduced, with a concomitant increase of NOx production and C-3 activity; in a considerable number of cases we observed a sustained DNA fragmentation. We speculate that NOx production could be related to nitrosative stress, which in turn leads to dynamic alteration in PTP balance and cell signalling, regulating the activity of a number of proteins implicated in apoptotic cell death. These findings could be of interest in new potential strategy to prevent and treat I/R injury

    Epstein-Barr virus associated PTLD of donor origin in liver transplant recipients

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    BACKGROUND/AIMS: Post-transplant lymphoproliferative disease, a potential complication of solid organ transplantation, occurs in about 3% of orthotopic liver transplant recipients. We report the genetic and virological characterization of two cases of post-transplant lymphoproliferative disease that occurred early (4 and 6 months) after orthotopic liver transplant as large-cell non-Hodgkin's lymphomas located at the hepatic hilum. METHODS: Lymphomatous tissues were analyzed for clonality and presence of Epstein-Barr virus (EBV) sequences by Southern blot, polymerase chain reaction, and in situ hybridization techniques. RESULTS: The tumors in both cases were sustained by a clonal proliferation of B lymphocytes containing type A EBV DNA. Moreover, in situ hybridization with a digoxigenin-labeled EBV-specific probe evidenced a strong nuclear signal in most of the neoplastic cells. DNA microsatellite analysis at three different loci detected alleles of donor origin in both tumor samples, suggesting that the neoplastic B cells were of donor origin. CONCLUSIONS: EBV-infected donor B lymphocytes might be responsible for intragraft post-transplant lymphoproliferative disease in orthotopic liver transplant recipients. As 20 to 30% of post-transplant lymphomas involve the graft itself, donor-derived post-transplant lymphoproliferative disease might be more frequent than presently appreciated. Prospective studies are needed to assess its real incidence and identify possible risk factors

    Long term persistence of low bone density in orthotopic liver transplantation

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    We determined bone density and metabolism in 46 patients (35 males, 11 females) who had undergone liver transplantation 1-48 months previously. Twenty-one patients were then followed for the next 24 months. At each visit, blood and urine samples for bone and liver metabolism parameters, as well as spinal and femoral dual-energy X-ray absorptiometry (DXA) scans, were obtained. Basal spinal and femoral density was low (p < 0.001). Patients with pre-transplant cholestatic diseases had lower spinal density than all the other subjects (p <0.05) and the cumulative methylprednisolone intake was an independent negative predictor of total hip density (p < 0.02). At baseline, urinary hydroxyproline and N-telopeptide were at the upper normal level and decreased only after 24 months of follow-up (p < 0.05). During the first year of follow-up, femoral density decreased (p < 0.05) and a partial recovery was observed for both spine and femur after 24 months. After 12 months, femoral bone density was negatively associated with serum cyclosporin A levels (p < 0.005) and cumulative methylprednisolone intake (p < 0.05), while the percent decrease in spinal density after the first 12 months was negatively predicted by mean daily methylprednisolone intake (p < 0.05). In patients with pre-transplant cholestatic diseases, femoral and spinal density increased after the first (p < 0.05) and second year (p < 0.05), respectively. In patients with previous post-necrotic cirrhosis, femoral density decreased after 12 months (p<0.05) and was still lower than baseline after 24 months (p < 0.05). However, at the end of the study the cumulative percentage of femoral neck osteoporosis was 43%. In conclusion, an elevated prevalence of spinal and femoral osteoporosis is present even many years after liver transplantation, with immunosuppressive treatment and pre-transplant liver disease being the most important pathogenetic factors

    LIVER TRANSPLANT: ADENOSINE METABOLISM AND APOPTOSIS

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    Apoptosis and necrosis coexist in ischemia-reperfusion (I/R) injury following organ transplant. During experimental liver transplant we evidenced a deep alteration in energy and antioxidant status. The activity of purine catabolic enzymes was also altered. Caspase-3 (C-3), protein tyrosine phosphatase (PTP) showed significative alterations that lead to DNA fragmentation. These findings could be of interest in new potential strategy to prevent and treat I/R injury
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