tag:blogger.com,1999:blog-83524241420189123892024-02-06T18:22:09.133-08:00Liver TransplantationLiver Transplantation Procedure and ReviewAnonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.comBlogger11125tag:blogger.com,1999:blog-8352424142018912389.post-55559459631208612422010-12-03T09:29:00.000-08:002012-01-25T04:49:14.978-08:00Liver Transplantation ReviewThese results indicate that <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> can cure not only genetic disorders that present in the liver, but also <a href="http://liver-transplantation.blogspot.com/2010/11/inborn-metabolic-disorders-treated-by.html">liver disorders</a> associated with extrahepatic pathology. Furthermore, a genetic defect present in all body cells such as familial hypercholesterolemia can be compensated by the mass of normal cells provided by <b>liver transplantation</b>.<br />
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Moreover, the survising decrease of extrahepatic deposits of amylopectin in glycogen storage disease type IV and of glucocerebroside in Gaucher's disease type I after <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> opens the possibility that the microchimerism due to migration of lymphocytes/macrophages from the donor's liver tothe host's extrahepatic sites result in cell-to-cell enzyme transmission; this may not be true in all instances, however, as shown by some lipid storage diseases, where neurological involvement may not be prevented by <b>liver transplatation</b>.<br />
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In diseases that do not result in severe <a href="http://liver-transplantation.blogspot.com/2010/12/cholesterol-ester-storage-disease.html">liver damage</a>, gene theraphy my provide a less risky solution in the future; auxiliary transplantation leaving the recipient's right lobe in place might prove a satisfactory way of awaiting the availability of gene theraphy.<br />
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</tbody></table>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com11tag:blogger.com,1999:blog-8352424142018912389.post-31818285616667515912010-12-02T07:34:00.000-08:002012-01-25T04:48:56.320-08:00Cholesterol Ester Storage Disease<div style="text-align: justify;"> <a href="http://liver-transplantation.blogspot.com/2010/11/type-iv-glycogen-storage-disease.html">Cirrhosis</a> is a possible complication and was successfully treated by <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> in a 14-year-old child. Neonatal Hemochromatosis. A few infants received <b>liver transplantation</b> with success. The recent availability of medical antioxidant therapy may limit the need for transplantation in the future.<br />
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<i><b><span style="font-size: small;">Gaucher's Disease Type I and Niemann-Pick Disease Type A</span></b></i><br />
<div style="text-align: justify;">Four patients with Gaucher's or Niemann-Pick disease and <a href="http://liver-transplantation.blogspot.com/2010/11/type-iv-glycogen-storage-disease.html">cirrhosis</a> received a successful liver transplant. Reaccumulation of glucocerebroside or sphyngomyelin was not detected or was minimal in the transplanted liver.</div><br />
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<span style="font-size: small;"><i><b> Liver DisordersAssocited with Severe Extrahepatic Complications</b></i><i>.</i></span> <br />
<div style="text-align: justify;">A small number of patients underwent <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> for a genetic disorder of e liver-specific or liver-predominant function that would not result in severe permanent <a href="http://liver-transplantation.blogspot.com/2010/11/inborn-metabolic-disorders-treated-by.html"> liver damage</a> but rather in severe lesions of extrahepatic organs.</div><b><i><br />
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<b><i><span style="font-size: small;">Type I Hyperoxaluria</span></i></b><br />
<div style="text-align: justify;">This is due to a deficiency of liver peroxisomal alanine:glyoxylate aminotransferase and results in renal lithiasis, nephrocalcinosis, ad kidney failure.Current recommendations are that transplantation should be planned as soon as the glomerular filtration rate (GFR) is between 25 and 65ml/mn per 1,73m2. <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">Liver transplantation</a> alone could be considered if the decline in kidney-<b>liver transplantation</b> should be carried out as soon as GFR decreases below 25ml/mn per 1,73m2.</div><b><i><br />
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<b><i><span style="font-size: small;">Crigler-Najjar Disease Type I</span></i></b><br />
<div style="text-align: justify;">The lack of detectable activity of liver glycuronyltransferase results in a permanently raised serum level of unconjugated bilirubin which is usually maintained at acceptable levels by home phototherapy; <a href="http://liver-transplantation.blogspot.com/2010/11/long-term-follow-up-at-liver.html">serum bilirubin</a> may increase suddenly and unexpectedly with a risk of kernicterus. <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">Liver transplantation</a> is thus recommended before such neurological accidents occur. The treated patients display normal <a href="http://liver-transplantation.blogspot.com/2010/11/long-term-follow-up-at-liver.html">serum bilirubin</a> levels and lead normal lives.</div><b><i><br />
<input name="IL_RELATED_TAGS" type="hidden" value="1" /><span style="font-size: small;">Familial Hypercholesterolemia</span></i></b><br />
<div style="text-align: justify;">This was treated by combined liver-heart transplantation in a few patients. <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">Liver transplantation</a> alone was successfully carried out in a 4-year-old boy with less than 2% low-density lipoprotein (LDL) receptor activity and serum cholesterol levels close to 700mg/dl and resulted in long-term normalization of serum cholesterol and presumably prevention of atheroselerosis.</div><i><b><br />
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<i><b><span style="font-size: small;">Homozigous Protein C Deficiency</span></b></i><br />
<div style="text-align: justify;">A 20-month-old child with severe thromboses was successfully treated by <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a><a href="http://./">.</a></div><i><b><br />
<input name="IL_RELATED_TAGS" type="hidden" value="1" /><span style="font-size: small;">Urea Cycle Disorders </span></b></i><br />
<div style="text-align: justify;">A few patents with partial ornithine carbamyltransferase, carbamoylphosphate synthetase, or origininosuccinate synthetase deficiency were succesfully treated with <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a>. Ammonemia remained normal on a normal diet.</div><br />
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</tbody></table>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com11tag:blogger.com,1999:blog-8352424142018912389.post-29493244598466437642010-11-29T08:13:00.000-08:002012-01-25T04:48:37.728-08:00Type IV Glycogen Storage Disease<a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">Liver transplantation</a> eliminates <a href="http://liver-transplantation.blogspot.com/2010/11/inborn-metabolic-disorders-treated-by.html">cirrhosis</a> and may even improve the degree of amylopectin storage in the heart. Careful follow-up is, however, necessary in this respec. <br />
<a name='more'></a><div style="text-align: justify;"><b><i><span style="font-size: small;">Hemophilia</span></i></b><b><span style="font-size: large;"> </span> </b></div><div style="text-align: justify;">Four patients who had severe post-transfusion hepatitis <a href="http://liver-transplantation.blogspot.com/2010/12/cholesterol-ester-storage-disease.html">cirrhosis</a> underwent <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a>. In yhe three surviving patients, the plasma coagulating activity of factor VIII was normal, confirming that the liver is the main source of factor VIII synthesis and secretion.<i><span style="font-size: large;"><b><span style="font-size: small;"> </span></b></span></i></div><br />
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<i><span style="font-size: large;"><b><span style="font-size: small;">Protoporphyria</span> </b></span></i><br />
<div class="separator" style="clear: both; text-align: center;"></div><div class="separator" style="clear: both; text-align: center;"></div>Five adult and adolescent patients with <a href="http://liver-transplantation.blogspot.com/2010/11/hereditary-tyrosinemia.html">cirrhosis</a> underwent <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a>.<br />
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<div style="text-align: justify;">This resulted in normal liver function and disappearance of or significant improvement in skin photosensitivity. Careful follow-up remains necessary because of the impotant role of erythropoietic tissue in protoporphyrin production in such patients, which may result in relapsing accumulation of protoporphyrin in the transplanted liver.</div><br />
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</tbody></table></div>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-62568986792064999842010-11-29T01:01:00.000-08:002012-01-25T04:48:23.309-08:00Type IA and IB Glycogen Storage DiseasesBeside severe hypoglycemia, growth failure, and acidosis, they also carry a risk of liver adenoma, possibly complicated by intratumoral hemorrhage or liver cell carcinoma.<br />
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<a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">Liver transplantation</a> may be recommended in patients with adenomas or failure of medical therapy; it allows restoration of a normal glucose metabolism and significant improvement in growth. In type IB, polymorphonuclear dysfunction is not corrected by <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> and requires permanent treatment with granulocyte colony-stimulating factor (GCSF).</div><br />
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</tbody></table>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-58124288543682617762010-11-29T00:10:00.000-08:002012-01-25T04:48:05.893-08:00Wilson's DiseaseThis is usually treated successfully with copper-chelating agents; in a few cases, howover (e.g., acure liver failure with or without hemolysis, acute relapse after discontinuation of therapy),<br />
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<a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> is necessary and results not only in the elimination of liver pathology and normalization of copper metabolism, but also in the regression of the neurological signs if already present.<br />
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</tbody></table>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-4440900551461925642010-11-28T21:10:00.000-08:002012-01-25T04:47:48.446-08:00Hereditary TyrosinemiaFor several years,<a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html"> liver transplantation</a> has proven extremely useful in children with this otherwise lethal disease. The recenr introduction of the enzyme inhibitor NTBC (see chapter by Kvitington, Clayton, and Leonard, this volume), may diminish the need for <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation.</a><br />
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So far, however, <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> remains indicated in children with <a href="http://liver-transplantation.blogspot.com/2010/11/type-iv-glycogen-storage-disease.html">cirrhosis</a> above the age of 2 because of the high risk of <a href="http://liver-transplantation.blogspot.com/2010/11/inborn-metabolic-disorders-treated-by.html">hepatocellular carcinoma</a> after this age and of the lack of data concerning the afficacy of NTBC for its prevention.<br />
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</tbody></table>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-18844561141251825392010-11-28T20:29:00.000-08:002012-01-25T04:47:30.622-08:00Inborn Metabolic Disorders Treated by Liver TransplantationIn the European Liver Transplant Registry issued in October 1993 a metabolic disorder was recorder as a indication for transplantation in 18% of 1248 children treated by <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation </a>from May 1988 to June 1993. Two groups can be distinguished, as discussed below.<br />
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<a href="http://liver-transplantation.blogspot.com/2010/12/liver-transplantation-review.html">Liver disorders</a> associated with severe <a href="http://liver-transplantation.blogspot.com/2010/11/long-term-follow-up-at-liver.html">liver damage</a>.The majority of <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantations</a> reported in the literature were performed in children with hereditary liver diseases resulting in <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html">liver cell failure</a>, <br />
<div style="text-align: justify;"><a href="http://liver-transplantation.blogspot.com/2010/12/cholesterol-ester-storage-disease.html">cirrhosis</a>, or a risk of <a href="http://liver-transplantation.blogspot.com/2010/11/hereditary-tyrosinemia.html">hepatocellular carcinoma</a> and for which there was no other effective treatment avaliable.<br />
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Alpha-1-Antiterypsin Defictency. <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">Liver transplantation</a> is the only effective therapy for<a href="http://www.blogger.com/goog_273340208"> </a>children with <a href="http://liver-transplantation.blogspot.com/2010/11/hereditary-tyrosinemia.html">cirrhosis</a> and the protein inhibitor (PI) Z phenotype. Serum levels of alpha-1-antitrypsin (AAT) return to normal; the PI phenotype of the donor's liver becomes detectable in the recipient's serum within 24h of transplantation. It may be hoped that this will prevent pulmonary emphisema during adulthood.<br />
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</tbody></table>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-86419210180684756872010-11-28T08:59:00.000-08:002012-01-25T04:47:04.447-08:00Long-Term Follow-Up at Liver TransplantationIn the majority of cases the children can resume a life close to normal when they leave the hospital and can atted school within 2-3 months of surgery. Clinical and biochemical monitorings are carried out in outpatient clinics; a salt-restricted diet is recommended, at least initially, because of the hipertensive effect of <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html">cyclosporine</a>. Since the risk of rejection persists, immunosuppression must be pursued indefinitely, with the goal of reaching the lowest possible doses compatible with normal liver function tests in order to lower the risk of kidney damage due to <b>cyclosporin</b>. Prednisone is given on an alternate day basis, allowing normal growth and a significant increase in height velocity in most children who displayed growth retardation prior to tranplantation.<i> <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html">Complications</a></i> at this stage include late biliary stenosis, opportunistic infections, anemia and gastrointestinal bleeding due to portal vein stenosis, and Epstein Barr Virus (EBV) related lymphoproliferative syndrom. The latter seems in part related to the cumulative degree of immunosuppression, with early diagnosis, lowering or interruption of immunosupression, resection of the proliferative zones when limited and solitary, and careful supervision, regression may occur, but retransplantation may later be necessary because of chronic rejection.<br />
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Medium-range follow-up studies indicate that 80% of surviving children have normal <a href="http://liver-transplantation.blogspot.com/2010/12/cholesterol-ester-storage-disease.html">serum bilirubin</a> levels and serum transaminase activity below twice normal. Eighty percent of surviving children attend a school level normal for their ages or only 1 year below normal. A significant prognostic factor is the condition of the child before transplantation, both in term of nutrition and liver cell function. For instance among 284 children treated in our group between 1986 and 1993, survival was 57% in the children whose pretransplant prothrombin time was below 50%, and 93% in the children whose prothrombin time was equal to or above 50%. In particular all children transplanted for an inborn error of metabolism without severe <a href="http://liver-transplantation.blogspot.com/2010/11/inborn-metabolic-disorders-treated-by.html">liver damage</a> are currently alive.Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-64191716376808897912010-11-28T06:55:00.000-08:002012-01-25T04:41:52.095-08:00Intermediary Folllow-Up at Liver TransplantationThe second period of follow-up takes place in conventional hospital settings and lasts an average of 6 weeks, Monitoring of liver and kidney function tests and blood <a href="http://liver-transplantation.blogspot.com/2010/11/long-term-follow-up-at-liver.html">cyclosporine</a> trough levels is carried out daily. Prednisone is given orally and its dosage diminished to 0,5mg/kg per day at 1 month, cyclosperine is progressively switched from i.v. to oral.Three main <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html"><i>complications</i></a> are observed in this period :<br />
<div style="text-align: justify;">1. Rejections is always possible and is managed as described above.</div><div style="text-align: justify;">2. CMV infection must be searched for by repeated blood and urine cultures; the combination of prevention with specific immunoglobulins, early detection, and DHPG (dehydrosyphenylguanine, Gancyclovir) treatment of the symptomatic forms has made the severe forms of CMV infections vey rare.<br />
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3.Biliary <a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html">complications</a> occur in 10%-15% of cases and may be of two types: either stenosis at the level of the anastomosis, unrrelated to <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html">hepatic artery thrombosis</a> and cured by endoluminal dilation or surgical repair, or as a delayed consequence of <b>hepatic artery thrombosis</b>; treatment of the latter is difficult, using various types of interventional radiology techniques, reoperation on the bile ducts, and sometimes <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html">retransplantion</a>.</div>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-990178933558950042010-11-27T09:29:00.000-08:002012-01-25T04:41:35.279-08:00Early Postoperative Period at Liver TransplantationThis lasts an average of 10 days and takes place in the intensive care unit. Supportive measures are taken as after any major surgical procedure; it is especially important to monitor adequate diuresis, as a good renal function will ease the use of <a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html">cyclosporine</a>. An attempt at lowering the incidence or severity of cytomegalovirus {CMV} infections is made by specific anti-CMV immunoglobulin infusions or with acyclovir. In high-risk situations, heparin is used to prevent <a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html">hepatic artery thrombosis.</a> Immunosuppression is started with i.v. methylprednisolone {10 mg/kg} and azathioprine {2 mg/kg} during the operation; i.v. cyclosporine is started postoperatively at increasing doses as soon as the hemodynamics and diuresis are satisfactory; azathioprine is discontinued when stable blood levels of <a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html">cyclosporine</a> are reached; methylprednisolone is progressively decreased down to 1 mg/kg per day at the end of the first week.<br />
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A rise in serum transaminases is normally observed on days 1-3, followed by a rapid decrease to normal or near-normal values. Prothrombin time, often somewhat prolonged on day 1, also decreases regularly, a proaccelerin level above 50% is an carly indicator of good liver function.Four major <a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html"><i>complications</i></a> may be observed during this period :<br />
1. Primary graft nonfunction is rare, but of such severity that it requires emergency <a href="http://retransplantation./">retransplantation.</a><br />
2. Infections, mostly bacterial, are very frequent, but usually controlled by antibiotics.<br />
<div class="separator" style="clear: both; text-align: center;"></div><div style="text-align: justify;">3. Rejection is also frequent and usually occurs at the end of the first week. Liver needle biopsy is carried out as carried out as soon as rejection is suspected on clinical or biochemical grounds, histological signs of rejection include portal tract inflammatory infiltrates, endotheliitis of the portal and centrilobular, veins, and/or periductular infiltrate with interlobular bile duct damage. Urgent therapy is needed, usually using three i.v. injections of methylprednisolone. Whenever this fails to control rejection, OKT3 monoclonal antilymphocyte preparation or FK-506 is given after checking the signs of persisting rejection by a repeat biopsy. Refractory rejection can lead to rapid or progressive <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver cell failure</a> and/or to a vanishing bile duct syndrome, which ultimately requires <a href="http://retransplantation./">retransplantation.</a></div><div class="separator" style="clear: both; text-align: center;"></div><div style="text-align: justify;">4..<a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html">Hepatic artery thrombosis</a> is a major risk in children; it occurs in 10%-15% of cases with a much higher incidence when both donor and recipient are very young. Thrombosis is looked for daily by Duplex ultrasound and confirmed by arteriography. Emergency surgery may make it possible to remove the obstruction of the artery and to prevent necrosis of the liver or biliary complications secondary to ischemia of the biliary epithelium.</div>Anonymoushttp://www.blogger.com/profile/10758928560724982405noreply@blogger.com0tag:blogger.com,1999:blog-8352424142018912389.post-69609906838879844242010-11-27T08:07:00.000-08:002012-01-25T04:40:03.362-08:00Liver TransplantationCurrent results of <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> indicate that 70%-80% of children treated are alive, most of them leading normal. <b>Liver transplantation </b>is carried out for liver diseases {inborn or acquired} wich result in death through l<a href="http://www.blogger.com/posts.g?blogID=8352424142018912389">iver cell failure</a> and for inherited disorders exclusively or mostly in the liver without the risk of <b>liver cell failure</b>, but with the risk of severe extrahepatic damage.This chapter reviews briefly the main surgical and postsurgical aspects of <a href="http://liver-transplantation.blogspot.com/2010/11/liver-transplantation.html">liver transplantation</a> performed so far in patients with inborn errors of metabolism.<br />
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</div><b><span style="font-size: small;">Procedure</span></b></div><span style="font-size: large;"><b> </b></span></div><div style="text-align: justify;"><div class="separator" style="clear: both; text-align: center;"></div>The development of <b>liver transplantation</b> and the extension of the indications in adults and in children have resulted, over the past few years, in a shortage of donors for children. This has been partially overcome by the use of liver splitting, in brain dead patients as well as by the use of the left lobe of related living donors. <br />
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with results similar to those of whole liver transplantation. Excspt for emergency situations, ABO blood group identity or compatibility is necessary.</div><div style="text-align: justify;">Orthotopic liver transplantatiun is a major procedure, comprising hepatectomy in the donor, hepatectomy in the recipient, and engraftment of the donor's liver with vascular and biliary anastomoses. With the UW {University of Wisconsin} preservation solution, cold ischemia time may be extended to 10-15h. A first impression of the graft function is provided by its early production of bile</div><div style="text-align: justify;">The postoperative follow-up can be separated into three periods :</div><div style="text-align: justify;"><br />
1. <a href="http://liver-transplantation.blogspot.com/2010/11/early-postoperative-period-at-liver.html">Early Postoperative Period.</a></div><div style="text-align: justify;">2. <a href="http://liver-transplantation.blogspot.com/2010/11/intermediary-folllow-up-at-liver.html">Intermediary Follow-Up</a></div><div style="text-align: justify;">3. <a href="http://liver-transplantation.blogspot.com/2010/11/long-term-follow-up-at-liver.html">Long-Term Follow-Up</a></div><table border="1" bordercolor="#e4e4e4" cellpadding="0" cellspacing="0" style="font-size: 11px; margin: 0pt auto; width: 95%;"><tbody>
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