[Ischemic cholecystitis caused by arterial chemoembolization of hepatocellular carcinoma].
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Carcinoma, Hepatocellular↗
Biomedical subjects
M Salcedo
Publications and source records attributed to M Salcedo.
[The usefulness of transjugular hepatic biopsy in the evaluation of liver disease in candidates for heart transplantation].
Heart transplantation is a universally accepted procedure in the treatment of terminal heart diseases. However, the presence of advanced liver disease in the potential receptors represents a contraindication for heart transplantation. On the other hand, the true diagnosis of liver disease not secondary to heart disease may be difficult requiring confirmatory liver biopsy. Nonetheless, percutaneous liver biopsy may be difficult to perform due to presence of coagulation alterations, marked dilatation of the hepatic veins, etc. The aim of this study was to evaluate the efficacy and safety of transjugular hepatic biopsy in the presence of severe coagulopathy in potential heart transplantation receptors with suspicion of liver disease and contraindication of percutaneous liver biopsy. Over a 9-year period, 350 potential heart transplantation patients were evaluated. In 23 patients (6.7%) transjugular hepatic biopsy was performed with aspiration needle followed by a hemodynamic study in 17 cases. The transjugular hepatic biopsy was completed in 22 cases (95.6%) with adequate material for the diagnosis being obtained in 21 (91.3% of the total cases indicated). Histologic study showed significant inflammatory infiltrates or alteration of the hepatic architecture in 4 patients (18%), all being positive for some viral markers (AgHBs or anti-HCV). The obtaining of a certain histologic diagnosis modified the consideration of liver disease as a definitive contraindication and allowed the performance of heart transplantation in 17 patients (73.9%). No complications were observed in association with the procedure. The transjugular hepatic biopsy is a feasible, effective and safe alternative for obtaining liver tissue in patients under evaluation for heart transplantation with suspicion of severe liver disease. The establishment of a correct histologic diagnosis may modify the clinical decision in an important number of patients.
Biopsy↗
[Primary tuberculous psoas abscess in a patient with HIV infection].
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AIDS-Related Opportunistic Infections↗
[Arterial complications after liver transplantation: early and late forms].
Arterial complications after liver transplantation (OLT) was related with high morbimortality rates, with variable consequences on patient and graft survival. 234 patients who underwent 270 liver transplantation between april of 1990 and december 1996 have been evaluated. Arterial complications were detected in 34 patients (12.5%), hepatic artery stenosis in 10 patients (29.4%), thrombosis in 24 (70.6%) and aneurysm in 2 (5.9%). It was considered early artery complications those diagnosed at the first month after OLT, and late complications the latest ones. Diagnosis was realized by Doppler sonography in all cases, and confirmed by celiac arteriography in those with Doppler abnormal findings. Clinical appearance of early artery complications were as acute liver failure (61.1%) or graft disfunction (38.8%). On the other hand, late complications were diagnosed incidentally in 46% of the patients due a programmed Doppler follow up. Actuarial survival at 24 months was higher in patients with late arterial complication (50 vs 30%; p < 0.01). Therapeutic measures applied were retransplantation, surgical artery reconstruction and angioplasty. Early complications required more frequently retransplantation or surgical reconstruction. Risk factors related with artery complications development were analyzed, but not significant differences between both types of arterial complications were found. It is concluded that programmed follow up by Doppler or arteriography is necessary to make an earlier diagnose and to detect silent arterial complications.
Adult↗
[Diagnostic value of transjugular liver biopsy in liver transplant recipients].
Liver biopsy after hepatic transplantation essential for the correct diagnosis of grant dysfunction. However, seriously imparied coagulation or massive ascites contraindicate percutaneous liver biopsy. In these cases transjugular liver biopsy may be valid alternative. in this study the efficacy, feasibility and safety of 69 transjugular biopsies carried out in 56 liver transplant recipients are evaluated. The suprahepatic veins were catheterized in 100% of the patients and histological samples were obtained in 63 (91.3%). The number of portal tracts was greater than six in 20.6% of the samples, lower than three in 35% and oscillated between four and six in 44%. The specimens obtained were sufficient for diagnosis in 82.5% of the patients, the overall diagnostic efficacy being 75.4%. The most common histological diagnosis (28.8%) was graft damage, while rejection represented 7.7%. Only one patient (1.18%) suffered a serious complication after transjugular biopsy. Transjugular biopsy is feasible and effective in liver transplant recipients with severely imparied coagulation.
Biopsy, Needle↗
MHC class I mosaic mice reveal insights into control of Ly49C inhibitory receptor expression in NK cells.
We have analyzed lymphocyte development in natural MHC class I chimeric mice, generated through a transgenic approach in beta2-microglobulin (beta2m)-/- mice. In these mice, MHC class I+ cells coexist with an equal proportion of MHC class I-deficient cells. These MHC class I mosaic mice had normal numbers of CD8+ T cells, which had a target cell specificity similar to that of wild-type mice. Consequently, the mice did not develop any signs of autoimmunity. They also had normal numbers of NK cells. This allowed an examination of the MHC class I influence on the expression of the Ly49C inhibitory receptor on NK cells. This receptor binds to H-2Kb. It is expressed at low levels on NK cells in wild-type mice of the H-2b haplotype, but at markedly higher levels on NK cells in beta2m-/- mice and other strains of mice lacking expression of H-2Kb. Relatively little is known about how MHC class I molecules affect expression of the Ly49 receptors. Through the analysis of the present MHC class I mosaic mice, we demonstrate that the expression levels of Ly49C on NK cells is a consequence not only of MHC class I expression in the environment, but also of the expression of MHC class I molecules by the NK cells themselves. These findings are discussed in relation to the biological role of the calibration of the Ly49 inhibitory receptor expression in relation to self-MHC class I.
Animals↗
Fine tuning of natural killer cell specificity and maintenance of self tolerance in MHC class I-deficient mice.
TAP1-/-, beta2-microglobulin (beta2m)-/- and TAP1/beta2m-/- mice all express low but quantitatively different levels of MHC class I molecules. Using these mice, we have addressed questions relating to the fine tuning of natural killer (NK) cell specificity and maintenance of self tolerance in the NK cell system. NK cells from B6 wild-type mice killed target cells from TAP1-/-, beta2m-/- and TAP1/beta2m-/- mice in vivo and rejected bone marrow grafts from the same mice in vivo at equivalent levels. NK cells from TAP1-/-, beta2m-/- mice did not kill target cells or reject bone marrow grafts from TAP1/beta2m-/- mice. NK cells in all MHC class I-deficient mice were tolerant to autologous MHC class I-deficient cells, as revealed by in vitro cytotoxicity assays using NK cell effectors activated with the interferon-inducing agent Tilorone, or by in vivo bone marrow graft experiments. However, the self-tolerant state of MHC class I-deficient NK cells was broken by in vitro stimulation with IL-2 for 4 days. Under these conditions, NK cells from the MHC class I-deficient mice killed autologous MHC class I-deficient cells while MHC class I-positive targets were spared. The C-type lectin inhibitory receptor Ly49C has a specificity for H-2Kb and is expressed on a subset of NK1.1+ cells in B6 mice. Wild-type and all MHC class I-deficient mice had similar numbers of Ly49C-positive NK1.1+ cells. However, Ly49C expression was markedly down-regulated on NK1.1+ cells from B6 mice, as compared to TAP1-/-, beta2m-/- and TAP1/beta2m-/- mice. In vitro stimulation of NK cells with IL-2 for 4 days did not significantly change this pattern. The present results are discussed in relation to the role of MHC class I molecules and Ly49 receptors in shaping the NK cell repertoire and raise new questions about maintenance of self tolerance in the NK cell system.
Animals↗
The Qa-1b molecule binds to a large subpopulation of murine NK cells.
Recent studies on human NK cells have demonstrated that the NK cell CD94/NKG2 receptors bind to the nonclassical MHC class I molecule HLA-E. A functional CD94/NKG2 complex has not yet been identified in rodents, but cDNA encoding rat and mouse CD94 and NKG2 have recently been cloned, suggesting that CD94/NKG2 receptors may exist in species other than man. The mouse nonclassical MHC class I molecule Qa-1 shares several features with HLA-E. This suggests that Qa-1 may be similarly recognized by murine NK cells. To study the ability of Qa-1 to bind to murine NK cells, we have produced a soluble tetrameric form of Qa-1b. In the present study, we demonstrate that Qa-1b tetramers distinctly bind to a large subset of fresh or IL-2-activated NK1.1+/CD3- splenocytes independently of the expression of Ly49 inhibitory receptors. Binding occurs whether NK cells have evolved in an MHC class I-expressing or in an MHC class I-deficient environment. Our data suggest the existence of a Qa-1-recognizing structure on a large subpopulation of murine NK cells that may be similar to the human CD94/NKG2 heterodimeric complex.
Animals↗
Triggering of natural killer cell mediated cytotoxicity by costimulatory molecules.
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Animals↗
Pulmonary complications following orthotopic liver transplant.
Pulmonary complications after orthotopic liver transplant (OLT) are frequent, involving high morbidity and mortality. We have determined the pulmonary complication incidence in 187 patients submitted to OLT at the General University Hospital "Gregorio Marañón" in the last 4 years, analyzing the type of infection, evolution, diagnostic and therapeutic measures and their influence on OLT mortality. A total of 120 patients had pulmonary complications, the most frequent being pleural effusion (61.94%), pneumonia (43.36%), and pneumothorax (11.5%). Serious pulmonary hypertension was diagnosed by invasive methods in two patients at the time of surgery (unidentified before OLT); both died at early post postoperative times. Pleural effusion was noted in 70 patients, 31.42% of them requiring thoracic tube drainage, complications developing in 22.72%. Thirteen patients were diagnosed of pneumothorax, the most frequent etiologies being percutaneous liver biopsy, thoracic tube drainage for pleural effusion, and postoperative complications in 41.6, 33.3, and 23.3%, respectively. Pneumonia was diagnosed in the 1st month after OLT in 45 patients. Tests to diagnose and identify the etiological agent were made in 71.1% of diagnosed pneumonia patients, identification being obtained in 62.5%. Telescope catheter culture identified the agent in 48%, fiber optic bronchoscopy in 50%, and lung or pleural biopsy in 100%. Respiratory insufficiency was noted in 64 patients (34.22% of transplanted patients). Factors involved in their development were pneumonia (42.18%), graft dysfunction (39.06%, pleural effusion (34.37%), sepsis (28.18%), and poor nutritional status (7.81%). Fifty patients (41.66%) died, pulmonary pathology being the determinant factor in 28.8%. Patient mortality with respiratory insufficiency was greater, especially in those with three factors involved the development of respiratory insufficiency.
Adult↗
Presence of the 918 mutation in the RET proto-oncogene in a Mexican patient with multiple endocrine neoplasia type 2B.
The dominantly inherited Multiple Endocrine Neoplasia cancer syndrome type 2B (MEN2B) is characterized by the presence of medullary thyroid carcinoma (MTC), phaechromocytoma (PHAEO), mucosal neuromas, ganglioneuromas of the intestinal tract, skeletal and ophthalmic abnormalities. MEN2B has been associated with a specific point mutation in the tyrosine kinase domain of the RET proto-oncogene (918RET mutation). We investigated a Mexican patient MEN2B for the presence of the 918RET mutation using the polymerase chain reaction followed by restriction endonuclease digestion. We have detected this mutation in DNA from the patient's MTC, PHAEO, and peripheral blood cells, but not in DNA from the patient's mother, suggesting that this mutation arose de novo. Our results are in agreement with the suggestion that the 918RET mutation is present in a vast majority of MEN2B cases around the world.
Adult↗
NK cell receptor calibration: effects of MHC class I induction on killing by Ly49Ahigh and Ly49Alow NK cells.
NK cells from C57BL/6 (B6) mice and H-2Dd transgenic B6 (D8) mice express different levels of the inhibitory receptor Ly49A, and they also differ in their target cell specificity. Here, we examined this differential specificity with respect to the role of the Ly49A receptor expression on effector cells and levels of H-2Dd inhibitory ligands on target cells. NK cells from D8 mice express low levels of Ly49A receptor (Ly49Alow), and are able to kill SP2/0 tumor cells in spite of their expression of H-2Dd. H-2Dd is expressed at reduced levels on SP2/0 cells; when these were increased three- to fivefold after IFN-gamma treatment, the killing by Ly49Alow NK cells from D8 mice was markedly reduced. Efficient killing was restored when the effectors were preincubated with anti-Ly49A F(ab')2 Abs. A separate experimental system was based on D8 TAP1-deficient Con A blasts exogenously loaded with H-2Dd-specific peptides. In this system, higher levels of cell surface H-2Dd had to be induced by peptide to inhibit D8 Ly49Alow NK cells to an extent similar to that of B6 Ly49Ahigh NK cells. Ly49A receptors on NK cells from H-2Dd transgenic mice are thus functional, although they require high levels of ligand to inhibit progression of the NK-target cell interaction. The data are in favor of the "receptor-calibration" model, which suggests that down-regulation of inhibitory receptors on NK cells may be useful in order for NK cells to discriminate between normal and reduced levels of MHC class I molecules.
Animals↗
Altered expression of Ly49 inhibitory receptors on natural killer cells from MHC class I-deficient mice.
MHC class I molecules in the host affect the specificity of NK cells. Previous work has suggested that this specificity is conferred by the expression of products encoded by the Ly49 gene family. This gene family encodes receptors that upon specific recognition of MHC class I ligands mediate an inhibitory signal that prevents killing by NK cells. The pattern of expression of the Ly49 MHC class I binding inhibitory receptors on NK cells is thought to be adapted to the host to ensure the generation of a self-tolerant, yet functional, NK cell repertoire. In the present study we have examined the expression of inhibitory receptors (Ly49A, Ly49C, and Ly49G2) on NK1.1+ cells from B6 (H-2b) and D8 (B6 mice transgenic for H-2Dd) mice as well as corresponding TAP1 -/-, beta2m -/-, and TAP1/beta2m -/- mutants of these mice. We demonstrate that receptor expression on NK1.1+ cells can be specifically modulated by host MHC class I molecules in at least two different ways: alteration of numbers of cells expressing a given receptor and modulation of the levels of expression of a given receptor at the cell surface. The degree of this modulation varies significantly among the various receptors studied and may depend upon the nature of their MHC class I ligands. The results are discussed in relation to the influence of MHC class I molecules on the development of an NK cell repertoire.
Animals↗
Major histocompatibility complex class I-independent killing of xenogeneic targets by rat allospecific natural killer cells.
Major histocompatibility complex class I molecules can inhibit mouse as well as human natural killer (NK) cell cytotoxicity. In contrast, antigens encoded in the RT1.C region of the rat MHC gene complex have been suggested to trigger, rather than inhibit, rat NK cells. In an attempt to analyze rat NK cell specificity, with respect to the cross-species difference that may exist in NK cell-mediated cytotoxicity, we investigated the ability of interleukin 2-activated, allospecific rat NK cells to recognize MHC class I-positive and -deficient target cells of mouse and human origins. Recognition of xenogeneic target cells by rat allospecific NK cells was found to be MHC class I independent; target cell MHC class I was not required for killing, and expression of different sets of mouse and human MHC class I molecules did not influence the cytotoxic response. These results indicate that rat NK cells can recognize xenogeneic nontransformed cells by mechanisms not related to target cell MHC class I expression, and that mouse and human MHC class I molecules, at least among those tested in this study, are unable to confer inhibition of rat NK cells.
Animals↗
Immunohistochemical evidence of immunopathogenetic mechanisms in chronic hepatitis C recurrence after liver transplantation.
Viremia and genotype are implicated in a rapid course of posttransplant hepatitis C virus (HCV) infection recurrence, but the role played by host immune reactions has not yet been evaluated. We correlated the degree of liver injury with the intrahepatic expression of molecules involved in immune response. The study included 32 biopsies of 30 liver transplant recipients. Recurrence of viremia was detected by Amplicor assay. Genotype was tested by Inno-Lipa. Cryostat sections were assessed by immunohistochemistry, using a wide panel of monoclonal antibodies. Correlations between histological-immunohistochemical semiquantitative evaluation and levels of viremia were performed. In severe hepatic inflammation, high numbers of activated cytotoxic T cells were found, along with marked hepatocellular expression of beta 2-microglobulin (beta 2-MG) and intercellular adhesion molecules. Likewise, a strong vascular adhesion molecule expression was observed mainly in those areas that were more inflamed. A striking endoglin reactivity was detected in enlarged portal tracts, and the presence of neoformed microvessels was also noteworthy. By contrast, in mild hepatic inflammation only a few activated T cells were detected, together with a weaker reactivity for all molecules studied. The level of viremia did not correlate with the degree of liver damage. The severe forms of post-transplant HCV infection recurrence are associated with a marked and aberrant intrahepatic expression of molecules involved in antigen recognition, and intercellular and vascular adhesion, decisive in regulating the recruitment and activation of cytotoxic T lymphocytes.
Adult↗
Host MHC class I gene control of NK-cell specificity in the mouse.
The missing self model predicts that NK cells adapt somatically to the type as well as levels of MHC class I products expressed by their host. Transgenic and gene knock-out mice have provided conclusive evidence that MHC class I genes control specificity and tolerance of NK cells. The article describes this control and discusses the possible mechanisms behind it, starting from a genetic model to study how natural resistance to tumors is influenced by MHC class I expression in the host as well as in the target cells. Data on host gene regulation of NK-cell functional specificity as well as Ly49 receptor expression are reviewed, leading up to the central question: how does the system develop and maintain "useful" NK cells, while avoiding "harmful" and "useless" ones? The available data can be fitted within each of two mutually none-exclusive models: cellular adaptation and clonal selection. Recent studies supporting cellular adaptation bring the focus on different possibilities within this general mechanism, such as anergy, receptor calibration and, most importantly, whether the specificity of each NK cell is permanently fixed or subject to continuous regulation.
Animals↗
Bacteremia following liver biopsy in transplant recipients with Roux-en-Y choledochojejunostomy.
Between 1990 and 1995, 666 percutaneous liver biopsies were performed in 196 patients at Gregorio Marañón General Hospital (mean 3.4 biopsies/patient); 533 biopsies (80.03%) were carried out in patients with choledochostomy biliary anastomosis and 133 (19.97%) in patients with choledochojejunostomy. Infectious complications, in the form of sepsis, occurred in two patients, who recovered favorably with antibiotic therapy. These two patients had undergone Roux-en-Y choledochojejunostomy (1.5%, not significant). Our findings suggest that the incidence of infectious complications after liver biopsy in transplant recipients is very low. Antibiotic prophylaxis at the time of liver biopsy in patients with Roux-en-Y choledochojejunostomy may decrease the frequency of infectious complications.
Adult↗
[Famciclovir plus interferon in the treatment of a patient with chronic hepatitis B and severe liver failure].
The natural history of liver disease caused by persistent infection with hepatitis B virus (HBV) can be quite variable. The wide range of liver injury suggests a great degree of variability in the interaction between the replicating virus and possible immune responses. At the current time, Interferon is the most extensively studied antiviral agent for chronic hepatitis B, but because of the substantial number of nonresponders, relapses and side events, it continues the search of alternative therapies. Many nucleoside analogues agents have been found to have antiviral activity in vitro or in vivo. The second generation nucleoside analogues with the most promising potential at present include Famciclovir. We report the case of a patient with HBV infection in whom a reactivation of his disease lead to hepatic failure, analysing the possible pathogenic mechanisms implied and calling attention upon the excellent results achieved with a combine regimen of Interferon and Famciclovir.
2-Aminopurine↗