The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Timothy W Schacker - One of the best experts on this subject based on the ideXlab platform.
-
the immunosuppressive role of il 32 in Lymphatic Tissue during hiv 1 infection
Journal of Immunology, 2011Co-Authors: Anthony J Smith, Timothy W Schacker, Cavan S Reilly, Stephen W Wietgrefe, Chad M Toledo, Lijie Duan, Ashley T HaaseAbstract:One pathological hallmark of HIV-1 infection is chronic activation of the immune system, driven, in part, by increased expression of proinflammatory cytokines. The host attempts to counterbalance this prolonged immune activation through compensatory mediators of immune suppression. We recently identified a gene encoding the proinflammatory cytokine IL-32 in microarray studies of HIV-1 infection in Lymphatic Tissue (LT) and show in this study that increased expression of IL-32 in both gut and LT of HIV-1–infected individuals may have a heretofore unappreciated role as a mediator of immune suppression. We show that: 1) IL-32 expression is increased in CD4+ T cells, B cells, macrophages, dendritic cells, and epithelial cells in vivo; 2) IL-32 induces the expression of immunosuppressive molecules IDO and Ig-like transcript 4 in immune cells in vitro; and 3) in vivo, IL-32-associated IDO/Ig-like transcript 4 expression in LT macrophages and gut epithelial cells decreases immune activation but also may impair host defenses, supporting productive viral replication, thereby accounting for the correlation between IL-32 levels and HIV-1 replication in LT. Thus, during HIV-1 infection, we propose that IL-32 moderates chronic immune activation to avert associated immunopathology but at the same time dampens the antiviral immune response and thus paradoxically supports HIV-1 replication and viral persistence.
-
host genes associated with hiv 1 replication in Lymphatic Tissue
Journal of Immunology, 2010Co-Authors: Anthony J Smith, Timothy W Schacker, Cavan S Reilly, Stephen W Wietgrefe, Ashley T HaaseAbstract:Much effort has been spent recently in identifying host factors required for HIV-1 to effectively replicate in cultured human cells. However, much less is known about the genetic factors in vivo that impact viral replication in Lymphatic Tissue, the primary anatomical site of virus-host interactions where the bulk of viral replication and pathogenesis occurs. To identify genetic determinants in Lymphatic Tissue that critically affect HIV-1 replication, we used microarrays to transcriptionally profile and identify host genes expressed in inguinal lymph nodes that were associated determinants of viral load. Strikingly, ∼95% of the transcripts (558) in this data set (592 transcripts total) were negatively associated with HIV-1 replication. Genes in this subset 1) inhibit cellular activation/proliferation (e.g., TCFL5, SOCS5 and SCOS7, KLF10), 2) promote heterochromatin formation (e.g., HIC2, CREBZF, ZNF148/ZBP-89), 3) increase collagen synthesis (e.g., PLOD2, POSTN, CRTAP), and 4) reduce cellular transcription and translation. Potential anti-HIV-1 restriction factors were also identified (e.g., NR3C1, HNRNPU, PACT). Only ∼5% of the transcripts (34) were positively associated with HIV-1 replication. Paradoxically, nearly all of these genes function in innate and adaptive immunity, particularly highlighting heightened gene expression in the IFN system. We conclude that this conventional host response cannot contain HIV-1 replication and, in fact, could well contribute to increased replication through immune activation. More importantly, genes that have a negative association with virus replication point to target cell availability and potentially new viral restriction factors as principal determinants of viral load.
-
microarray analysis of Lymphatic Tissue reveals stage specific gene expression signatures in hiv 1 infection
Journal of Immunology, 2009Co-Authors: Qingsheng Li, Timothy W Schacker, Cavan S Reilly, John V Carlis, Lijie Duan, Adrian Smith, Ashley T HaaseAbstract:Untreated HIV-1 infection progresses through acute and asymptomatic stages to AIDS. Although each of the three stages has well-known clinical, virologic, and immunologic characteristics, much less is known of the molecular mechanisms underlying each stage. In this study, we report Lymphatic Tissue microarray analyses, revealing for the first time stage-specific patterns of gene expression during HIV-1 infection. We show that although there is a common set of key genes with altered expression throughout all stages, each stage has a unique gene expression signature. The acute stage is most notably characterized by increased expression of hundreds of genes involved in immune activation, innate immune defenses (e.g., RIG-1, MDA-5, TLR7 and TLR8, PKR, APOBEC3B, 3F, 3G), adaptive immunity, and in the proapoptotic Fas-Fas ligand pathway. Yet, quite strikingly, the expression of nearly all acute stage genes return to baseline levels in the asymptomatic stage, accompanying partial control of infection. This transition from acute to asymptomatic stage is tied to increased expression of a diverse array of immunosuppressive genes (e.g., CLEC12B, ILT4, galectin-3, CD160, BCMA, FGL2, LAG3, GPNMB). In the AIDS stage, decreased expression of numerous genes involved in T cell signaling identifies genes contributing to T cell dysfunction. These common and stage-specific gene expression signatures identify potential molecular mechanisms underlying the host response and the slow, natural course of HIV-1 infection.
-
the role of secondary Lymphatic Tissue in immune deficiency of hiv infection
AIDS, 2008Co-Authors: Timothy W SchackerAbstract:HIV infection is a disease primarily of Lymphatic Tissues, in which most viral replication occurs in CD4 T cells. The most common measures of the impact of HIV infection are made by counting CD4 T cells in peripheral blood. Peripheral blood, however, contains only 2% of the total CD4 cell population in the body and these are typically effector memory cells in transit; the vast majority of CD4 cells reside in the secondary lymphoid Tissues (e.g. lymph nodes and mucosal Lymphatic Tissues) and the impact of HIV replication is most profound on the population residing within these compartments. Within organized follicular aggregates in mucosal Tissues and the very precise structures of lymph nodes most viral replication occurs in the parafollicular T-cell zone, both in primary infection and throughout the course of the disease, such that by the time the patient presents with symptoms of HIV seroconversion approximately 50% of the population is already depleted. Therefore, if we are to understand the pathophysiology and pathogenesis of HIV and its related complications fully, we need to examine the structure and function of secondary lymphoid Tissues before and during HIV infection and before and during HIV treatment. This may provide valuable insights into the underlying pathogenesis of a range of disorders associated with HIV infection, and potentially aid in the development of therapies aimed at emerging complications of long-term HIV infection.
-
the role of collagen deposition in depleting cd4 t cells and limiting reconstitution in hiv 1 and siv infections through damage to the secondary lymphoid organ niche
Seminars in Immunology, 2008Co-Authors: Jacob D Estes, Ashley T Haase, Timothy W SchackerAbstract:The hallmark of HIV/SIV infections is the progressive depletion of CD4+ T cells that ultimately renders the host incapable of defending against AIDS defining opportunistic infections and malignancies. Although many potential mechanisms have been proposed to explain CD4+ T cell loss, we review here the growing evidence that fibrotic ‘scarring’ and consequent damage to the Lymphatic Tissue niche contributes to CD4+ T cell decline and limits CD4+ T cell re-population with retroviral therapy.
Ashley T Haase - One of the best experts on this subject based on the ideXlab platform.
-
the immunosuppressive role of il 32 in Lymphatic Tissue during hiv 1 infection
Journal of Immunology, 2011Co-Authors: Anthony J Smith, Timothy W Schacker, Cavan S Reilly, Stephen W Wietgrefe, Chad M Toledo, Lijie Duan, Ashley T HaaseAbstract:One pathological hallmark of HIV-1 infection is chronic activation of the immune system, driven, in part, by increased expression of proinflammatory cytokines. The host attempts to counterbalance this prolonged immune activation through compensatory mediators of immune suppression. We recently identified a gene encoding the proinflammatory cytokine IL-32 in microarray studies of HIV-1 infection in Lymphatic Tissue (LT) and show in this study that increased expression of IL-32 in both gut and LT of HIV-1–infected individuals may have a heretofore unappreciated role as a mediator of immune suppression. We show that: 1) IL-32 expression is increased in CD4+ T cells, B cells, macrophages, dendritic cells, and epithelial cells in vivo; 2) IL-32 induces the expression of immunosuppressive molecules IDO and Ig-like transcript 4 in immune cells in vitro; and 3) in vivo, IL-32-associated IDO/Ig-like transcript 4 expression in LT macrophages and gut epithelial cells decreases immune activation but also may impair host defenses, supporting productive viral replication, thereby accounting for the correlation between IL-32 levels and HIV-1 replication in LT. Thus, during HIV-1 infection, we propose that IL-32 moderates chronic immune activation to avert associated immunopathology but at the same time dampens the antiviral immune response and thus paradoxically supports HIV-1 replication and viral persistence.
-
host genes associated with hiv 1 replication in Lymphatic Tissue
Journal of Immunology, 2010Co-Authors: Anthony J Smith, Timothy W Schacker, Cavan S Reilly, Stephen W Wietgrefe, Ashley T HaaseAbstract:Much effort has been spent recently in identifying host factors required for HIV-1 to effectively replicate in cultured human cells. However, much less is known about the genetic factors in vivo that impact viral replication in Lymphatic Tissue, the primary anatomical site of virus-host interactions where the bulk of viral replication and pathogenesis occurs. To identify genetic determinants in Lymphatic Tissue that critically affect HIV-1 replication, we used microarrays to transcriptionally profile and identify host genes expressed in inguinal lymph nodes that were associated determinants of viral load. Strikingly, ∼95% of the transcripts (558) in this data set (592 transcripts total) were negatively associated with HIV-1 replication. Genes in this subset 1) inhibit cellular activation/proliferation (e.g., TCFL5, SOCS5 and SCOS7, KLF10), 2) promote heterochromatin formation (e.g., HIC2, CREBZF, ZNF148/ZBP-89), 3) increase collagen synthesis (e.g., PLOD2, POSTN, CRTAP), and 4) reduce cellular transcription and translation. Potential anti-HIV-1 restriction factors were also identified (e.g., NR3C1, HNRNPU, PACT). Only ∼5% of the transcripts (34) were positively associated with HIV-1 replication. Paradoxically, nearly all of these genes function in innate and adaptive immunity, particularly highlighting heightened gene expression in the IFN system. We conclude that this conventional host response cannot contain HIV-1 replication and, in fact, could well contribute to increased replication through immune activation. More importantly, genes that have a negative association with virus replication point to target cell availability and potentially new viral restriction factors as principal determinants of viral load.
-
microarray analysis of Lymphatic Tissue reveals stage specific gene expression signatures in hiv 1 infection
Journal of Immunology, 2009Co-Authors: Qingsheng Li, Timothy W Schacker, Cavan S Reilly, John V Carlis, Lijie Duan, Adrian Smith, Ashley T HaaseAbstract:Untreated HIV-1 infection progresses through acute and asymptomatic stages to AIDS. Although each of the three stages has well-known clinical, virologic, and immunologic characteristics, much less is known of the molecular mechanisms underlying each stage. In this study, we report Lymphatic Tissue microarray analyses, revealing for the first time stage-specific patterns of gene expression during HIV-1 infection. We show that although there is a common set of key genes with altered expression throughout all stages, each stage has a unique gene expression signature. The acute stage is most notably characterized by increased expression of hundreds of genes involved in immune activation, innate immune defenses (e.g., RIG-1, MDA-5, TLR7 and TLR8, PKR, APOBEC3B, 3F, 3G), adaptive immunity, and in the proapoptotic Fas-Fas ligand pathway. Yet, quite strikingly, the expression of nearly all acute stage genes return to baseline levels in the asymptomatic stage, accompanying partial control of infection. This transition from acute to asymptomatic stage is tied to increased expression of a diverse array of immunosuppressive genes (e.g., CLEC12B, ILT4, galectin-3, CD160, BCMA, FGL2, LAG3, GPNMB). In the AIDS stage, decreased expression of numerous genes involved in T cell signaling identifies genes contributing to T cell dysfunction. These common and stage-specific gene expression signatures identify potential molecular mechanisms underlying the host response and the slow, natural course of HIV-1 infection.
-
the role of collagen deposition in depleting cd4 t cells and limiting reconstitution in hiv 1 and siv infections through damage to the secondary lymphoid organ niche
Seminars in Immunology, 2008Co-Authors: Jacob D Estes, Ashley T Haase, Timothy W SchackerAbstract:The hallmark of HIV/SIV infections is the progressive depletion of CD4+ T cells that ultimately renders the host incapable of defending against AIDS defining opportunistic infections and malignancies. Although many potential mechanisms have been proposed to explain CD4+ T cell loss, we review here the growing evidence that fibrotic ‘scarring’ and consequent damage to the Lymphatic Tissue niche contributes to CD4+ T cell decline and limits CD4+ T cell re-population with retroviral therapy.
-
amount of Lymphatic Tissue fibrosis in hiv infection predicts magnitude of haart associated change in peripheral cd4 cell count
AIDS, 2005Co-Authors: Timothy W Schacker, Cavan S Reilly, Gregory J Beilman, Jodie H Taylor, David E Skarda, David Krason, Matthew Larson, Ashley T HaaseAbstract:The structure of Lymphatic Tissues is an important component of Lymphatic Tissue T-cell homeostasis. Collagen deposition in Lymphatic Tissues (common in HIV infection) disrupts the niche and limits the size of the resident CD4 cell population. In this report we show that a single measurement of Lymphatic Tissue collagen predicts the magnitude of recovery of the peripheral CD4 cell pool with HAART (P < 0.001). This suggests that collagen-targeted therapies might be of benefit.
Cavan S Reilly - One of the best experts on this subject based on the ideXlab platform.
-
the immunosuppressive role of il 32 in Lymphatic Tissue during hiv 1 infection
Journal of Immunology, 2011Co-Authors: Anthony J Smith, Timothy W Schacker, Cavan S Reilly, Stephen W Wietgrefe, Chad M Toledo, Lijie Duan, Ashley T HaaseAbstract:One pathological hallmark of HIV-1 infection is chronic activation of the immune system, driven, in part, by increased expression of proinflammatory cytokines. The host attempts to counterbalance this prolonged immune activation through compensatory mediators of immune suppression. We recently identified a gene encoding the proinflammatory cytokine IL-32 in microarray studies of HIV-1 infection in Lymphatic Tissue (LT) and show in this study that increased expression of IL-32 in both gut and LT of HIV-1–infected individuals may have a heretofore unappreciated role as a mediator of immune suppression. We show that: 1) IL-32 expression is increased in CD4+ T cells, B cells, macrophages, dendritic cells, and epithelial cells in vivo; 2) IL-32 induces the expression of immunosuppressive molecules IDO and Ig-like transcript 4 in immune cells in vitro; and 3) in vivo, IL-32-associated IDO/Ig-like transcript 4 expression in LT macrophages and gut epithelial cells decreases immune activation but also may impair host defenses, supporting productive viral replication, thereby accounting for the correlation between IL-32 levels and HIV-1 replication in LT. Thus, during HIV-1 infection, we propose that IL-32 moderates chronic immune activation to avert associated immunopathology but at the same time dampens the antiviral immune response and thus paradoxically supports HIV-1 replication and viral persistence.
-
host genes associated with hiv 1 replication in Lymphatic Tissue
Journal of Immunology, 2010Co-Authors: Anthony J Smith, Timothy W Schacker, Cavan S Reilly, Stephen W Wietgrefe, Ashley T HaaseAbstract:Much effort has been spent recently in identifying host factors required for HIV-1 to effectively replicate in cultured human cells. However, much less is known about the genetic factors in vivo that impact viral replication in Lymphatic Tissue, the primary anatomical site of virus-host interactions where the bulk of viral replication and pathogenesis occurs. To identify genetic determinants in Lymphatic Tissue that critically affect HIV-1 replication, we used microarrays to transcriptionally profile and identify host genes expressed in inguinal lymph nodes that were associated determinants of viral load. Strikingly, ∼95% of the transcripts (558) in this data set (592 transcripts total) were negatively associated with HIV-1 replication. Genes in this subset 1) inhibit cellular activation/proliferation (e.g., TCFL5, SOCS5 and SCOS7, KLF10), 2) promote heterochromatin formation (e.g., HIC2, CREBZF, ZNF148/ZBP-89), 3) increase collagen synthesis (e.g., PLOD2, POSTN, CRTAP), and 4) reduce cellular transcription and translation. Potential anti-HIV-1 restriction factors were also identified (e.g., NR3C1, HNRNPU, PACT). Only ∼5% of the transcripts (34) were positively associated with HIV-1 replication. Paradoxically, nearly all of these genes function in innate and adaptive immunity, particularly highlighting heightened gene expression in the IFN system. We conclude that this conventional host response cannot contain HIV-1 replication and, in fact, could well contribute to increased replication through immune activation. More importantly, genes that have a negative association with virus replication point to target cell availability and potentially new viral restriction factors as principal determinants of viral load.
-
microarray analysis of Lymphatic Tissue reveals stage specific gene expression signatures in hiv 1 infection
Journal of Immunology, 2009Co-Authors: Qingsheng Li, Timothy W Schacker, Cavan S Reilly, John V Carlis, Lijie Duan, Adrian Smith, Ashley T HaaseAbstract:Untreated HIV-1 infection progresses through acute and asymptomatic stages to AIDS. Although each of the three stages has well-known clinical, virologic, and immunologic characteristics, much less is known of the molecular mechanisms underlying each stage. In this study, we report Lymphatic Tissue microarray analyses, revealing for the first time stage-specific patterns of gene expression during HIV-1 infection. We show that although there is a common set of key genes with altered expression throughout all stages, each stage has a unique gene expression signature. The acute stage is most notably characterized by increased expression of hundreds of genes involved in immune activation, innate immune defenses (e.g., RIG-1, MDA-5, TLR7 and TLR8, PKR, APOBEC3B, 3F, 3G), adaptive immunity, and in the proapoptotic Fas-Fas ligand pathway. Yet, quite strikingly, the expression of nearly all acute stage genes return to baseline levels in the asymptomatic stage, accompanying partial control of infection. This transition from acute to asymptomatic stage is tied to increased expression of a diverse array of immunosuppressive genes (e.g., CLEC12B, ILT4, galectin-3, CD160, BCMA, FGL2, LAG3, GPNMB). In the AIDS stage, decreased expression of numerous genes involved in T cell signaling identifies genes contributing to T cell dysfunction. These common and stage-specific gene expression signatures identify potential molecular mechanisms underlying the host response and the slow, natural course of HIV-1 infection.
-
simian immunodeficiency virus induced Lymphatic Tissue fibrosis is mediated by transforming growth factor β1 positive regulatory t cells and begins in early infection
The Journal of Infectious Diseases, 2007Co-Authors: Jacob D Estes, Timothy W Schacker, Cavan S Reilly, Gregory J Beilman, Stephen W Wietgrefe, Peter J Southern, Jeffrey M Milush, Jeffrey D Lifson, Donald L Sodora, John V CarlisAbstract:In human immunodeficiency virus (HIV) infection, collagen deposition and fibrosis within the T cell zone disrupt the Lymphatic Tissue architecture, contributing to depletion of CD4(+) T cells and limiting immune reconstitution. We used relevant animal and in vitro models to investigate the kinetics and possible underlying mechanism(s) of this process. In the Lymphatic Tissue of simian immunodeficiency virus (SIV)-infected rhesus macaques, we observed parallel increases in immune activation, transforming growth factor (TGF) beta 1-positive regulatory T (T(reg)) cells, and collagen type I deposition by 7 days after inoculation, consistent with the hypothesis that early immune activation elicits a countering T(reg) cell response associated with TGF beta 1 expression and collagen deposition. In support of this hypothesis and the possible role of fibrosis in viral pathogenesis, we show (1) spatial colocalization and temporal concordance in levels of TGF beta 1(+) T(reg) cells and collagen deposition; (2) TGF beta 1(+) inducible T(reg) cell stimulation of primary Lymphatic Tissue fibroblasts to produce collagen type I in vitro; and (3) high levels of immune activation, TGF beta 1(+) T(reg) cells, and collagen deposition in pathogenic SIV infection of macaques, in contrast to apathogenic SIV infection in sooty mangabeys in which levels of immune activation, TGF beta 1(+) T(reg) cells, and collagen deposition were low. We thus conclude that the response of TGF beta 1(+) T(reg) cells to immune activation in early SIV/HIV infection is a double-edged sword: TGF beta 1(+) T(reg) cells normally have a positive effect by limiting immunopathological and autoreactive immune responses, but they also have a negative effect by dampening the antiviral immune response and, as we show here, causing deleterious effects on CD4(+) T cell homeostasis by inducing collagen deposition in Lymphatic Tissues.
-
amount of Lymphatic Tissue fibrosis in hiv infection predicts magnitude of haart associated change in peripheral cd4 cell count
AIDS, 2005Co-Authors: Timothy W Schacker, Cavan S Reilly, Gregory J Beilman, Jodie H Taylor, David E Skarda, David Krason, Matthew Larson, Ashley T HaaseAbstract:The structure of Lymphatic Tissues is an important component of Lymphatic Tissue T-cell homeostasis. Collagen deposition in Lymphatic Tissues (common in HIV infection) disrupts the niche and limits the size of the resident CD4 cell population. In this report we show that a single measurement of Lymphatic Tissue collagen predicts the magnitude of recovery of the peripheral CD4 cell pool with HAART (P < 0.001). This suggests that collagen-targeted therapies might be of benefit.
David Krason - One of the best experts on this subject based on the ideXlab platform.
-
amount of Lymphatic Tissue fibrosis in hiv infection predicts magnitude of haart associated change in peripheral cd4 cell count
AIDS, 2005Co-Authors: Timothy W Schacker, Cavan S Reilly, Gregory J Beilman, Jodie H Taylor, David E Skarda, David Krason, Matthew Larson, Ashley T HaaseAbstract:The structure of Lymphatic Tissues is an important component of Lymphatic Tissue T-cell homeostasis. Collagen deposition in Lymphatic Tissues (common in HIV infection) disrupts the niche and limits the size of the resident CD4 cell population. In this report we show that a single measurement of Lymphatic Tissue collagen predicts the magnitude of recovery of the peripheral CD4 cell pool with HAART (P < 0.001). This suggests that collagen-targeted therapies might be of benefit.
-
the clustering of infected siv cells in Lymphatic Tissue
Journal of the American Statistical Association, 2002Co-Authors: Cavan S Reilly, Timothy W Schacker, Ashley T Haase, Steve Wietgrefe, David KrasonAbstract:Here we investigate the clustering of simian immunodeficiency virus (SIV)–infected cells in a Lymphatic Tissue sample taken from a rhesus macaque to test a spatial proximity model of the spread of infection. We see that standard methods for analysis of the clustering of point processes are not entirely satisfactory for this application, so we define a novel statistic to understand the clustering in the data. This statistic examines how events spread out from certain points deemed cluster centers. Using this statistic, we can demonstrate the statistical significance of the clustering and examine over what distances this clustering is witnessed. We use Bayesian methods to fully assess the uncertainty in the estimation of this statistic by positing a model for the process. (We assume the process is a nonhomogeneous Poisson process with an intensity that is a linear combination of Gaussian densities.) We see that the distances at which clustering is present are consistent with a simple model of SIV spread wit...
Elmar Fritsche - One of the best experts on this subject based on the ideXlab platform.
-
combined pedicled superficial circumflex iliac artery perforator scip flap with Lymphatic Tissue preservation and lymphovenous anastomosis lva for defect reconstruction and lymphedema lymphocele prevention in thigh sarcoma surgery preliminary results
Journal of Surgical Oncology, 2021Co-Authors: Mario F Scaglioni, Matteo Meroni, Elmar Fritsche, Bruno FuchsAbstract:Background Sarcoma surgery often requires large Tissue resection to be treated safely. When the tumor is localized in the groin and/or medial thigh, lymphocele and lymphedema are common complications because of the rich Lymphatic network present there. The aim of this study is to share the outcome of seven patients who received defect reconstruction in this area with combined pedicled superficial circumflex artery perforator (SCIP) flap with Lymphatic Tissue preservation and lymphovenous anastomosis (LVA) for prevention of Lymphatic complications. Patients and methods Seven patients who underwent surgical resection of sarcoma in the groin and/or adductors compartment received defect reconstruction with pedicled SCIP flap combined with LVA. For a better dead space obliteration, four of them also received an additional Tissue flap: two pedicled deep inferior epigastric perforator flaps and two free anterolateral thigh flaps. Indocyanine green lymphography was performed in all cases to identify the Lymphatic pathway, make the preoperative marking and check the patency of the anastomoses. Results All seven patients were successfully treated reaching a good aesthetic result and a full range of motion. No immediate nor delayed complications such as lymphocele or lymphorrhea and early extremity lymphedema were observed during the follow up (range: 6-9 months; mean: 7.3) and no secondary procedures were required. Conclusions The combination of the pedicle SCIP Lymphatic Tissue transfer with LVA seems to be effective in preventing the development of Lymphatic sequelae after large resections in the medial thigh.
-
combined lymphovenous anastomosis and deep inferior epigastric perforator flap with Lymphatic Tissue preservation for defect reconstruction and lymphedema lymphocele prevention after medial thigh sarcoma resection a case report
Microsurgery, 2020Co-Authors: Mario F Scaglioni, Matteo Meroni, Alberto Franchi, Elmar FritscheAbstract:: Soft Tissue sarcomas are a rare group of malignant tumors that often require an extensive surgical resection to be safely treated. When they are localized in the upper medial thigh, this treatment inevitably leads to large defects frequently causing a series of early and late postoperative complications. Among these, lymphocele and lymphedema are rather common and should try to be avoided. Many solutions with a demonstrated efficacy have been described for this purpose after groin dissection procedure, ranging from lymphovenous anastomosis to pedicled or free flaps. Anyway, there is much less information regarding the medial thigh. Here we present a case of resected sarcoma involving the adductors compartment reconstructed using a pedicled deep inferior epigastric (DIEP) flap with Lymphatic Tissue transfer, combined with preventive lymphovenous anastomosis (LVA) performed at the superior-edge-of-the-knee incision (SEKI) point. A 58-year-old patient presented a 10 cm × 12 cm soft Tissue defect after margin free sarcoma removal. To fill this defect, we harvest a 24 × 9 cm pedicled DIEP flap conserving its Lymphatic vessels running from the upper margin to the right groin lymphnodes. Then we rotated it maintaining the lymphnodes in their original site and moved it through an inguinal tunnel in the area of the defect. The distal part was de-epithelized and folded down to cover the deeper region. The postoperative course was uneventful and at the 6 months follow up the patient showed a good outcome with no swelling and no signs of tumor relapse. This result therefore may suggest that this kind of combined treatment might be an effective technique to prevent all those complications linked to the impairment of Lymphatic system drainage in the proximal medial thigh.
