Blood use in liver transplantation

Lewis, JH; Bontempo, F A; Cornell, F.W.; Kiss, J; Larson, P.; Ragni, MV; Rice, Eo O.; Spero, JA; Starzl, TE

doi:10.1046/j.1537-2995.1987.27387235624.x

Cited by 71 publications

(41 citation statements)

References 7 publications

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“…The plasma samples were obtained 2 h after a fat-rich meal (see Methods). Liver transplant recipients 1-4 in this table are identical to recipients [1][2][3][4] in Table V. * The MBI9 phenotype of the apoB100 and apoB48 bands of the postoperative liver transplant recipients' chylomicrons are shown in parentheses.…”

Section: Resultsmentioning

confidence: 99%

“…Postoperatively, the patient had increased hepatic clearance of LDL and only moderate hypercholesterolemia, indicating that the metabolic defect had been partially corrected by the liver transplantation (2). A patient with tyrosinemia had nearly complete correction ofthat defect with liver transplantation (1,3), and both hemophilia A and hemophilia B are correctable by liver transplantation (1,4,5). The extent to which inborn errors of metabolism are corrected after this procedure has frequently yielded fresh insights into the extent of the liver's role in the development of disease (1).…”

Section: Introductionmentioning

confidence: 99%

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Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

Linton¹,

Gish²,

Hubl³

et al. 1991

J. Clin. Invest.

316

214

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IntroductionApolipoprotein (apo) E and the two B apolipoproteins, apoB48 and apoB100, are important proteins in human lipoprotein metabolism. Commonly occurring polymorphisms in the genes for apoE and apoB result in amino acid substitutions that produce readily detectable phenotypic differences in these proteins. We studied changes in apoE and apoB phenotypes before and after liver transplantation to gain new insights into apolipoprotein physiology. In all 29 patients that we studied, the postoperative serum apoE phenotype of the recipient, as assessed by isoelectric focusing, converted virtually completely to that of the donor, providing evidence that > 90% of the apoE in the plasma is synthesized by the liver. In contrast, the cerebrospinal fluid apoE phenotype did not change to the donor's phenotype after liver transplantation, indicating that most of the apoE in CSF cannot be derived from the plasma pool and therefore must be synthesized locally. The apoB100 phenotype (assessed with immunoassays using monoclonal antibody MB19, an antibody that detects a two-allele polymorphism in apoB) invariably converted to the phenotype of the donor. In four normolipidemic patients, we determined the MB19 phenotype of both the apoB100 and apoB48 in the "chylomicron fraction" isolated from plasma 3 h after a fat-rich meal. Interestingly, the apoB100 in the chylomicron fraction invariably had the phenotype of the donor, indicating that the vast majority of the large, triglyceride-rich apoB100-containing lipoproteins that appear in the plasma after a fat-rich meal are actually VLDL of hepatic origin. The MB19 phenotype of the apoB48 in the plasma chylomicron fraction did not change after liver transplantation, indicating that almost all of the apoB48 in plasma chylomicrons is derived from the intestine. These results were consistent with our immunocytochemical studies on intestinal biopsy specimens of organ donors; using apoB-specific monoclonal antibodies, we found evidence for apoB48, but not apoB100, in donor intestinal biopsy specimens. (J. Clin. Invest. 1991.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

Linton¹,

Gish²,

Hubl³

et al. 1991

J. Clin. Invest.

316

214

View full text Add to dashboard Cite

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“…Another 37 adults (7.5%) and 15 children (5.2%) developed such antibodies after their first transplant; blood usage in these transplants averaged 9 units of RBCs in children and 19 in adults, which was no different than usual. 4 Posttransplant antibodies were all found 1 to 5 weeks later, except for three patients in whom antibodies (anti-K [n = 3] and -E [n = 1]) were found at 7 weeks to 4.5 months after transplant. Eleven percent of retransplants were preceded by potentially significant RBC antibodies in both adults (13/120) and children (11/98); these totals include third transplants in 20 adults and 14 children and fourth transplants in 1 adult and 1 child.…”

Section: Resultsmentioning

confidence: 99%

Red cell antibody problems in 1000 liver transplants

et al. 1989

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Liver transplant patients frequently require large amounts of blood. The frequency and nature of their red cell (RBC) antibody problems were examined. Records were reviewed in 496 adults and 286 children undergoing 1000 consecutive transplants. Twenty-two percent of adults and 14 percent of children had RBC alloantibodies. Antibodies of potential clinical significance were found before transplant in 6.3 percent of adults and 1.0 percent of children; despite immunosuppression, they appeared 1 to 5 weeks after transplant in an additional 7.5 and 5.2 percent respectively. These antibodies probably represented secondary immune responses. Of 58 transplant patients with prior potentially significant antibodies, 8 required 7 to 110 units of antigen-untyped blood after 8 to 28 units of antigen-negative blood; of these patients, one had subsequent hemolysis. Positive direct antiglobulin tests in 24 percent of adults and 10 percent of children were most often thought to be due to nonspecific adsorption of IgG. Anti-recipient ABO antibodies developed in 22 of 60 (37%) evaluable ABO-unmatched grafts; 13 cases had associated hemolysis. In all, 36 percent of adults and 20 percent of children had diverse RBC antibody problems. Resolution of these problems is an important part of the laboratory support necessary for a liver transplantation program.The Blood Bank plays an important role in the supportive care of liver transplant patients before, during, and after surgery. Before transplant for end-stage liver disease, patients are often transfused for bleeding due to portal hypertension, esophageal varices, deficient coagulation factors, thrombocytopenia, or other surgery. After transplant, many patients need further transfusions and some require retransplantation. The liver transplant program at the University of Pittsburgh has the world's largest such experience, and since the program's inception in 1981, its overall perioperative and postoperative blood use has been carefully documented.1 -5 These patients have ample opportunity for red cell (RBC) alloimmunization.The purpose of this study was to examine all RBC antibody problems encountered in 1000 consecutive liver transplants performed in our center from February 1981 to February 1987. Previously, as part of an examination of the relationship of the HLA system to RBC alloimmunization, 6 we reported a 9.5 percent frequency of potentially significant RBC alloantibodies in 263 adults. We present here our cumulative experience in both adults and children with regard to 1) the overall frequencies of RBC antibodies; 2) the onset and duration of significant RBC antibodies relative to transplant immunosuppression; 3) the cases in which insufficient compatible blood was available for surgery; and 4) the frequencies and causes of © J. B. Lippincott Co.

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“…Hepatocytes and liver sinusoidal endothelial cells, but not Kupffer cells, produce factor VIII in the mouse liver (5). The role of the liver in factor VIII synthesis has been supported by liver transplantation studies in both hemophilic animals and humans, after which increasing factor VIII levels were detected (6)(7)(8)(9)(10). Early transplantation studies in the canine model (11,12) led, in the early 1960s, to the first human spleen transplants in four patients with malignancies and one with agammaglobulinemia (13).…”

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confidence: 99%

Correction of hemophilia as a proof of concept for treatment of monogenic diseases by fetal spleen transplantation

Aronovich

Tchorsh

Katchman

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Previous clinical attempts to correct genetic deficiencies such as hemophilia or Gaucher disease by transplantation of allogeneic spleen were associated with aggressive graft versus host disease, mediated by mature T cells derived from the donor spleen. We show that a fetal pig spleen harvested at the embryonic day 42 stage, before the appearance of T cells, exhibited optimal growth potential upon transplantation into SCID mice, and the growing tissue expressed factor VIII. Transplantation of embryonic day 42 spleen tissue into hemophilic SCID mice led to complete alleviation of hemophilia within 2–3 months after transplant, as demonstrated by tail bleeding and by assays for factor VIII blood levels. These results provide a proof of principle to the concept that transplantation of a fetal spleen, obtained from a developmental stage before the appearance of T cells, could provide a novel treatment modality for genetic deficiencies of an enzyme or a factor that can be replaced by the growing spleen tissue.

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Blood use in liver transplantation

Cited by 71 publications

References 7 publications

Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

Phenotypes of apolipoprotein B and apolipoprotein E after liver transplantation.

Red cell antibody problems in 1000 liver transplants

Correction of hemophilia as a proof of concept for treatment of monogenic diseases by fetal spleen transplantation

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