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1.  Medical Progress 
The New England journal of medicine  1989;321(15):1014-1022.
Advances in the management of both chronic and acute hepatic disease have been made possible and even mandated by the development of liver transplantation. The clinical use of transplantation has proceeded at a rapid pace since a Consensus Development Conference of the National Institutes of Health concluded in June 1983 that liver transplantation had become a service and not simply an experimental procedure.1
The liver can be transplanted as an extra (auxiliary) organ at an ectopic site, or in the orthotopic location after the removal of the host liver (Fig. 1). This article will focus primarily on the orthotopic procedure. However, there has been renewed interest in the auxiliary operation, which will be discussed separately.
doi:10.1056/NEJM198910123211505
PMCID: PMC3091023  PMID: 2674716
3.  Immunosuppressive Therapy and Tolerance of Organ Allografts 
The New England journal of medicine  2008;358(4):407-411.
doi:10.1056/NEJMe0707578
PMCID: PMC2980288  PMID: 18216363
4.  LIVER TRANSPLANTATION TO PROVIDE LOW-DENSITY-LIPOPROTEIN RECEPTORS AND LOWER PLASMA CHOLESTEROL IN A CHILD WITH HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA 
The New England journal of medicine  1984;311(26):1658-1664.
A six-year-old girl with severe hypercholesterolemia and atherosclerosis had two defective genes at the low-density-lipoprotein (LDL) receptor locus, as determined by biochemical studies of cultured fibroblasts. One gene, inherited from the mother, produced no LDL receptors; the other gene, inherited from the father, produced a receptor precursor that was not transported to the cell surface and was unable to bind LDL. The patient degraded intravenously administered 125I-LDL at an extremely low rate, indicating that her high plasma LDL-cholesterol level was caused by defective receptor-mediated removal of LDL from plasma. After transplantation of a liver and a heart from a normal donor, the patient’s plasma LDL-cholesterol level declined by 81 per cent, from 988 to 184 mg per deciliter. The fractional catabolic rate for intravenously administered 125I-LDL, a measure of functional LDL receptors in vivo, increased by 2.5-fold. Thus, the transplanted liver, with its normal complement of LDL receptors, was able to remove LDL cholesterol from plasma at a nearly normal rate.
We conclude that a genetically determined deficiency of LDL receptors can be largely reversed by liver transplantation. These data underscore the importance of hepatic LDL receptors in controlling the plasma level of LDL cholesterol in human beings.
doi:10.1056/NEJM198412273112603
PMCID: PMC2975980  PMID: 6390206
5.  LIVER TRANSPLATATION IN A HEMOPHILIAC 
The New England journal of medicine  1985;312(18):1189-1190.
doi:10.1056/NEJM198505023121812
PMCID: PMC2965446  PMID: 3920523
6.  ANTIGEN LOCALIZATION AND MIGRATION IN IMMUNITY AND TOLERANCE 
The New England journal of medicine  1998;339(26):1905-1913.
doi:10.1056/NEJM199812243392607
PMCID: PMC2963936  PMID: 9862947
8.  CHIMERISM AFTER LIVER TRANSPLANTATION FOR TYPE IV GLYCOGEN STORAGE DISEASE AND TYPE 1 GAUCHER’S DISEASE 
The New England journal of medicine  1993;328(11):745-749.
Background
Liver transplantation for type IV glycogen storage disease (branching-enzyme deficiency) results in the resorption of extrahepatic deposits of amylopectin, but the mechanism of resorption is not known.
Methods
We studied two patients with type IV glycogen storage disease 37 and 91 months after liver transplantation and a third patient with lysosomal glucocerebrosidase deficiency (type 1 Gaucher’s disease), in whom tissue glucocerebroside deposition had decreased 26 months after liver replacement, to determine whether the migration of cells from the allograft (microchimerism) could explain the improved metabolism of enzyme-deficient tissues in the recipient. Samples of blood and biopsy specimens of the skin, lymph nodes, heart, bone marrow, or intestine were examined immunocytochemically with the use of donor-specific monoclonal anti-HLA antibodies and the polymerase chain reaction, with preliminary amplification specific to donor alleles of the gene for the beta chain of HLA-DR molecules, followed by hybridization with allele-specific oligonucleotide probes.
Results
Histopathological examination revealed that the cardiac deposits of amylopectin in the patients with glycogen storage disease and the lymph-node deposits of glucocerebroside in the patient with Gaucher’s disease were dramatically reduced after transplantation. Immunocytochemical analysis showed cells containing the HLA phenotypes of the donor in the heart and skin of the patients with glycogen storage disease and in the lymph nodes, but not the skin, of the patient with Gaucher’s disease. Polymerase-chain-reaction analysis demonstrated donor HLA-DR DNA in the heart of both patients with glycogen storage disease, in the skin of one of them, and in the skin, intestine, blood, and bone marrow of the patient with Gaucher’s disease.
Conclusions
Systemic microchimerism occurs after liver allotransplantation and can ameliorate pancellular enzyme deficiencies.
doi:10.1056/NEJM199303183281101
PMCID: PMC2963442  PMID: 8437594
9.  EXPRESSION OF EPSTEIN–BARR VIRUS–ENCODED SMALL RNA (BY THE EBER-1 GENE) IN LIVER SPECIMENS FROM TRANSPLANT RECIPIENTS WITH POST-TRANSPLANTATION LYMPHOPROLIFERATIVE DISEASE 
The New England journal of medicine  1992;327(24):1710-1714.
Background
Epstein–Barr virus (EBV)–associated post-transplantation lymphoproliferative disease (PTLD) develops in 1 to 10 percent of transplant recipients, in whom it can be treated by a reduction in the level of immunosuppression. We postulated that the tissue expression of the small RNA transcribed by the EBER-1 gene during latent EBV infection would identify patients at risk for PTLD.
Methods
We studied EBER-1 gene expression in liver specimens obtained from 24 patients 2 days to 22 months before the development of PTLD, using in situ hybridization with an oligonucleotide probe. Control specimens were obtained from 20 recipients of allografts with signs of injury due to organ retrieval, acute graft rejection, or viral hepatitis in whom PTLD had not developed 9 to 71 months after the biopsy.
Results
Of the 24 patients with PTLD, 17 (71 percent) had specimens in which 1 to 40 percent of mononuclear cells were positive for the EBER-1 gene. In addition, 10 of these 17 patients (59 percent) had specimens with histopathological changes suggestive of EBV hepatitis. In every case, EBER-1–positive cells were found within the lymphoproliferative lesions identified at autopsy. Only 2 of the 20 controls (10 percent) had specimens with EBER-1–positive cells (P< 0.001), and such cells were rare.
Conclusions
EBER-1 gene expression in liver tissue precedes the occurrence of clinical and histologic PTLD. The possibility of identifying patients at risk by the method we describe here and preventing the occurrence of PTLD by a timely reduction of immunosuppression needs to be addressed by future prospective studies.
doi:10.1056/NEJM199212103272403
PMCID: PMC2956494  PMID: 1331789
10.  LIVER TRANSPLANTATION FOR ADVANCED LIVER DISEASE WITH ALPHA-1-ANTITRYPSIN DEFICIENCY 
The New England journal of medicine  1980;302(5):272-275.
Alpha-1-antitrypsin deficiency associated with chronic obstructive airway disease was recognized in 1963 by Laurell and Ericksson.1 In 1969, Sharp2 described the first cases of alpha-1-antitrypsin-deficiency disease in children with cirrhosis. Since then, this inborn error has been recognized as one of the more common factors in cirrhosis of infancy and childhood,3 including “neonatal hepatitis.”4 Alpha-1-antitrypsin is a glycoprotein that accounts for a major portion of the alpha-1 globulin fraction of the serum.5 It is responsible for approximately 90 per cent of the antitrypsin activity6 of the serum, and it also inhibits several other plasma enzymes, including plasmin,7 elastase,8 collagenase,9 and chymotrypsin.10
Cirrhosis develops in about 15 per cent of patients with homozygous phenotype PiZZ (Pi = protease inhibitor),11 and there have been a few recent reports of cirrhosis in heterozygous patients.12,13 There has been no effective, specific medical treatment for such patients. This report will examine the place of orthotopic liver transplantation in the treatment of seven white patients who had end-stage liver disease due to alpha-1-antitrypsin deficiency. After transplantation, the phenotypes of the recipients became those of the donors, and alpha-1-antitrypsin levels were restored to normal. Thus, the metabolic basis of the disease was corrected for as long as the patients survived the transplantation procedure. Three of the patients are still alive after 13, 21, and 36 months. The others died between 12 days and 28 months after transplantation.
PMCID: PMC2777525  PMID: 6985708
11.  RECOVERY FROM “HEPATORENAL SYNDROME” AFTER ORTHOTOPIC LIVER TRANSPLANTATION 
The New England journal of medicine  1973;289(22):1155-1159.
Three patients with progressive renal failure and advanced hepatic insufficiency due to cirrhosis of the liver underwent orthotopic liver transplantation. All three patients had immediate improvement in hepatic function and within two weeks after liver replacement regained nearly normal kidney function. However, the renal recovery was delayed in each case, and its course was not uniform. Plasma renin activity was high, and renin substrate was low before transplantation in one case in which these measurements were obtained; both returned to normal soon after liver replacement.
PMCID: PMC2772065  PMID: 4585359
12.  INFECTIONS IN RECIPIENTS OF LIVER HOMOGRAFTS* 
The New England journal of medicine  1968;279(12):619-626.
Seventeen patients received liver homografts between 1963 and May, 1968. The eight treated before July, 1967, died within 34 days; seven had progressive infections with gram-negative bacilli, Candida albicans and cytomegalovirus. The infections were similar to but more fulminating than those after renal homotransplantation.
In nine later cases, there was more discriminating donor selection, improved immunosuppression, and better organ preservation. In the first five of these nine patients, all infants, lobar hepatic gangrene apparently secondary to delayed right hepatic arterial thrombosis developed. Two died within a few days, two and three and a half months after transplantation. The three who did not die immediately subsequently had multiple bacteremias, fungemias and cytomegalovirus pulmonary infections. One of these children is alive twelve months after transplantation; the others died after four and a half and six months. In contrast, the last four patients, in whom septic liver infarctions were avoided, have been free of serious infections for two to five and a half months.
PMCID: PMC2772060  PMID: 4299208
14.  SHWARTZMAN REACTION AFTER HUMAN RENAL HOMOTRANSPLANTATION* 
The New England journal of medicine  1968;278(12):642-648.
In three human recipients, five renal homografts were destroyed within a few minutes to hours after their revascularization in the new host. The kidneys, removed one to 54 days later, had cortical necrosis. The major vessels were patent, but the arterioles and glomeruli were the site of fibrin deposition. There was little or no fixation of host immunoglobulins in the homografts. The findings were characteristic of a generalized Shwartzman reaction.
Although the cause (or causes) of the Shwartzman reaction in our patients is not known, they may have been conditioned by the bacterial contamination and hemolysis that often attend hemodialysis, by immunosuppression and by the transplantation itself. Some of the patients have preformed lymphocytotoxic antibodies. Thus, certain patients may be predisposed. High-risk patients should be recognized and treated prophylactically with anticoagulants.
PMCID: PMC2765870  PMID: 4866352
16.  CLOTTING CHANGES, INCLUDING DISSEMINATED INTRAVASCULAR COAGULATION, DURING RAPID RENAL-HOMOGRAFT REJECTION* 
The New England journal of medicine  1970;283(8):383-390.
One of two patients in whom early homograft rejection developed after renal transplantation had many antidonor antibodies before operation. By the measurement of gradients across intracorporeal and extracorporeal homografts in this patient, the new kidneys were shown to sequester host immunoglobulins, platelets, white cells and clotting factors. Moreover, the renal venous blood then contained fibrinolytic activity. This presensitized recipient, as well as a second patient who did not have detectable preformed humoral antibodies, gave evidence from clinical observation and from the various clotting tests of disseminated intravascular coagulation with fibrinolysis and a severe bleeding, diathesis. Immunofluorescent and histologic studies revealed a laying down of fibrin in the homograft vessels that continued in some cases to cortical necrosis of the transplanted kidneys or, alternatively, receded at the time fibrinolysis occurred. The variety of rejection seen in these patients has been characterized as an immunologically induced coagulopathy.
PMCID: PMC2757738  PMID: 4193841

Results 1-16 (16)