Total hepatectomy and liver replacement (orthotopic liver transplantation) for primary hepatic malignancy

There has been a high incidence of tumor recurrence after liver transplantation for primary hepatic malignancy. Nevertheless, a small but significant palliation has been possible with this approach, even in patients who eventually died of recurrence. Two patients with incidental malignancies in their excised livers apparently have been cured. Further gains will be possible only with extremely discriminating selection of prospective recipients. © 1982 Société Internationale de Chirurgie

Liver transplantation for biliary atresia

Orthotopic liver transplantation was performed 15 months to 20 years ago in 126 recipients, all of whom were under 18 years of age. Eighty-six of these pediatric recipients were treated before 1980 with azathioprine (or eyclophosphamide) and prednisone, to which antilymphocyte globulin (ALG) usually was added. One-year patient survival was 40%. In the last 40 cases, the new drug cyclosporine has been given with low doses of steroids. The one-year patient survival increased to 65%. Both in the pre-cyclosporine era and more recently, the survival of patients with biliary atresia has been lower than in the next largest category of patients, namely, those with liver-based inborn metabolic errors. The difficulty of operation in patients with biliary atresia has been greater than in recipients with other diagnoses, partly because of previous operations such as portoenterostomy (Kasai procedure). Hepatic portoenterostomy, worthwhile as it is, has posed technical difficulties for eventual liver transplantation, particularly when complicated Roux limb techniques or venting procedures have been applied. In our total experience the longest survival after liver replacement in a child whose original diagnosis was biliary atresia is 132/3 years. © 1984 Société Internationale de Chirurgie

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

IMMUNOPATHOLOGICAL STUDIES OF ORTHOTOPIC HUMAN LIVER ALLOGRAFTS

Twenty-six specimens obtained from twenty human orthotopic liver allografts 10-968 days after transplantation were studied by light microscopy, electron microscopy, and immunofluorescence. The main lesions consisted of mononuclear-cell infiltration around the portal tracts, centrilobular cholestasis, liver-cell atrophy and reticulin collapse, obliterative intimal thickening of hepatic arteries, and fibrosis. Moderate amounts of IgG and/or IgM and complement (β1C/β1A globulin or C'lq) were observed in four of the liver samples and smaller deposits were present in another five. A further three specimens contained IgG without complement. IgA was detected in only one of the samples. The immunoglobulins were found in the walls of the portal and central veins and of the sinusoids in all thirteen positive liver samples, in the walls of branches of the hepatic artery in three, and in the cytoplasm of some of the mononuclear cells infiltrating the portal tracts in nine of the specimens. Fibrinogen was seen in eight of the samples, usually in the spaces of Disse. Accumulations of immunoglobulins and complement were less frequent in liver than in kidney and heart allografts. These findings suggest that in the failure of human liver allografts cell-mediated immunity and non-immunological factors may be more important than humoral antibody. © 1972

Immunohistochemical detection of macrophage migration inhibitory factor in fetal and adult bovine epididymis: Release by the apocrine secretion mode?

Originally defined as a lymphokine inhibiting the random migration of macrophages, the macrophage migration inhibitory factor (MIF) is an important mediator of the host response to infection. Beyond its function as a classical cytokine, MIF is currently portrayed as a multifunctional protein with growth-regulating properties present in organ systems beyond immune cells. In previous studies, we detected substantial amounts of MIF in the rat epididymis and epididymal spermatozoa, where it appears to play a role during post-testicular sperm maturation and the acquisition of fertilization ability. To explore its presence in other species not yet examined in this respect, we extended the range of studies to the bull. Using a polyclonal antibody raised against MIF purified from bovine eye lenses, we detected MIF in the epithelium of the adult bovine epididymis with the basal cells representing a prominently stained cell type. A distinct accumulation of MIF at the apical cell pole of the epithelial cells and in membranous vesicles localized in the lumen of the epididynnal duct was obvious. In the fetal bovine epididymis, we also detected MIF in the epithelium, whereas MIF accumulation was evident at the apical cell surface and in apical protrusions. By immuno-electron microscopy of the adult bovine epididymis, we localized MIF in apical protrusions of the epithelial cells and in luminal membrane-bound vesicles that were found in close proximity to sperm cells. Although the precise origin of the MIF-containing vesicles remains to be delineated, our morphological observations support the hypothesis that they become detached from the apical surface of the epididymal epithelial cells. Additionally, an association of MIF with the outer dense fibers of luminal spermatozoa was demonstrated. Data obtained in this study suggest MIF release by an apocrine secretion mode in the bovine epididymis. Furthermore, MIF localized in the basal cells of the epithelium and in the connective tissue could be responsible for regulating the migration of macrophages in order to avoid contact of immune cells with spermatozoa that carry a wide range of potent antigens. Copyright (c) 2006 S. Karger AG, Basel

Organ transplantation has come of age

10.3184/003685010X12708274571283Science Progress932141-15

The role of research in transplantation

Annals of the Academy of Medicine Singapore384354-358AAMS

Gene therapy for hemophilia A.

Discovery medicine635198-20