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==Overview==
==Overview==
==Liver transplantation prognosis==
==Liver transplantation prognosis==
* Prognosis is quite good. 1-year survival (in Finland) is 83%, 5-year survival is 76% and 10-year survival is 66%.
* Majority of deaths happen during the first three months after transplantation.
* Mortality rates in donors are 0.2% in the USA and vary fro, 0.1 to 1.0% worldwide.
* Overall mortality rate is of the order of 0.2–0.5%.
* The risk associated with left-lobe donation may be lower than that with right-lobe donation.
* The incidence of complications in the donor varies from 9 to 67%.<ref name="pmid18505689">{{cite journal| author=Ghobrial RM, Freise CE, Trotter JF, Tong L, Ojo AO, Fair JH et al.| title=Donor morbidity after living donation for liver transplantation. | journal=Gastroenterology | year= 2008 | volume= 135 | issue= 2 | pages= 468-76 | pmid=18505689 | doi=10.1053/j.gastro.2008.04.018 | pmc=3731061 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18505689  }}</ref>
* The modified Clavien classification is commonly used to describe, report, and compare donor morbidity:<ref name="pmid11932469">{{cite journal| author=Surman OS| title=The ethics of partial-liver donation. | journal=N Engl J Med | year= 2002 | volume= 346 | issue= 14 | pages= 1038 | pmid=11932469 | doi=10.1056/NEJM200204043461402 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11932469  }}</ref>
Grade I—a complication that is not life-threatening, does not result in residual disability, and does not require a therapeutic invasive intervention


Living-donor recipients have been noted to have a higher incidence of surgical complications post-transplant compared with whole-liver recipients.
Grade II—a complication that is potentially life-threatening and that requires the use of drug therapy or foreign blood units


Early data suggested that outcomes (graft survival) might be inferior to those in whole-liver transplants, especially if the patients were matched for severity of liver disease [39].
Grade III—a complication that is potentially lifethreatening and that requires a therapeutic invasive intervention


Partial grafts have smaller vessels, more complicated biliary reconstructions, and a cut surface, all of which make for
Grade IV—a complication with residual or lasting disability or which leads to Living-donor Liver Transplantation death.<ref name="pmid15201680">{{cite journal| author=Salvalaggio PR, Baker TB, Koffron AJ, Fryer JP, Clark L, Superina RA et al.| title=Comparative analysis of live liver donation risk using a comprehensive grading system for severity. | journal=Transplantation | year= 2004 | volume= 77 | issue= 11 | pages= 1765-7 | pmid=15201680 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15201680  }}</ref>
a technically more challenging procedure and a higher incidence of surgical complications.
 
Maluf et al. and Fan et al. reported that despite smaller graft
size and higher technical complexity, the graft and patient survival rates of patients with right-liverLDLTare not different from those of patients receiving whole-graft DDLT [40,41].
 
The only difference is a higher incidence of biliary complications in the LDLT patients (25.8 versus 7.1%) [40].
 
Most centers have reported a 15–46% incidence of biliary complications, including early bile leaks, after transplant, and a 15–20% incidence of late biliary strictures.
 
These figures are significantly higher than are generally
reported for whole-liver recipients (9–15%) [40]. The possible factors associated with an increased risk of postoperative biliary complications include having multiple bile ducts to reconstruct and an inadequate arterial perfusion in patients with a high preoperative MELD score [42,43].
 
With advances in microsurgical techniques, the incidence of vascular complications such as hepatic artery thrombosis has decreased and is now not significantly different from that in deceased-liver transplants [44–47].
Certain subgroups of recipients may do worse after living-donor transplants. Critically ill adult recipients with advanced liver failure, high MELD scores, and numerous secondary complications have generally been reported to have worse outcomes with this procedure. Such recipients have minimal
functional reserve and are probably ill equipped to manage the lower hepatocyte mass and the higher complication rate associated with partial transplants. However, in parts of the world where DDLTs are uncommon, living donors have been used for critically ill patients, with good results [40].


== Recurrence ==
== Recurrence ==
The disorders most commonly associated with recurrence include hepatitis B virus (HBV) and hepatitis C virus (HCV).


Recurrence of HBV after liver transplantation can be prevented by administering hepatitis B immune globulin at the time of transplantation and at regular intervals thereafter in combination with antivirals such as tenofovir or entecavir.  
==== Hepatitis B virus ====
* Recurrence of HBV after liver transplantation can be prevented by administering hepatitis B immune globulin at the time of transplantation and at regular intervals thereafter in combination with antivirals such as tenofovir or entecavir.  


==== Hepatitis C virus ====
==== Hepatitis C virus ====
* Early treatment post-transplantation with interferon-based regimens has not been shown to improve patient and graft outcomes, and currently there is no established role for prophylactic or preemptive therapy following transplantation [2].  
* There is no established role for prophylactic or preemptive therapy following transplantation.<ref name="pmid4976215">{{cite journal| author=Smith B| title=Segmental liver transplantation from a living donor. | journal=J Pediatr Surg | year= 1969 | volume= 4 | issue= 1 | pages= 126-32 | pmid=4976215 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4976215  }}</ref>
* No effective immunoglobulin prophylaxis exists for HCV.
* No effective immunoglobulin prophylaxis exists for HCV.
* Combination therapy (peginterferon or standard interferon and ribavirin), monotherapy (peginterferon, standard interferon, or ribavirin), and anti-HCV immune globulin.
* Treatment is initiated within six weeks of the transplantation. Theapy may be combined or monotherapy.
* Treatment was initiated within six weeks of the transplantation.
* Combination therapy may be peginterferon or standard interferon and ribavirin, monotherapy may be peginterferon, standard interferon, or ribavirin, and anti-HCV immune globulin.
* Interferon-based treatment is no longer recommended in liver transplant recipients.  
* '''Direct-acting antiviral agents''' 
* '''Direct-acting antiviral agents''' 
* Studies are now emerging showing efficacy of direct-acting antiviral agents for the treatment of HCV recurrence following liver transplantation.
* Sofosbuvir is an NS5B nucleotide analog used for the treatment of HCV.<ref name="pmid25304641">{{cite journal| author=Charlton M, Gane E, Manns MP, Brown RS, Curry MP, Kwo PY et al.| title=Sofosbuvir and ribavirin for treatment of compensated recurrent hepatitis C virus infection after liver transplantation. | journal=Gastroenterology | year= 2015 | volume= 148 | issue= 1 | pages= 108-17 | pmid=25304641 | doi=10.1053/j.gastro.2014.10.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25304641  }}</ref>
* '''Sofosbuvir'''
* Treatment resulted in persistently undetectable HCV ribonucleic acid (RNA) 12 weeks after stopping treatment in 28 of 40 patients (70 percent).  
* Sofosbuvir is an NS5B nucleotide analog used for the treatment of HCV. [83].  
* All of the cases of virologic failure were due to relapse. As a result, sofosbuvir is usually now given in combination with one of several additional direct-acting antivirals (ledipasvir, simeprevir, and daclatasvir), with or without ribavirin.<ref name="pmid23593993">{{cite journal| author=Fontana RJ, Hughes EA, Bifano M, Appelman H, Dimitrova D, Hindes R et al.| title=Sofosbuvir and daclatasvir combination therapy in a liver transplant recipient with severe recurrent cholestatic hepatitis C. | journal=Am J Transplant | year= 2013 | volume= 13 | issue= 6 | pages= 1601-5 | pmid=23593993 | doi=10.1111/ajt.12209 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23593993  }}</ref>
* Treatment resulted in persistently undetectable HCV ribonucleic acid (RNA) 12 weeks after stopping treatment in 28 of 40 patients (70 percent). All of the cases of virologic failure were due to relapse. As a result, sofosbuvir is usually now given in combination with one of several additional direct-acting antivirals (ledipasvir, simeprevir, and daclatasvir), with or without ribavirin [83-90].
 
==== Non-alcoholic fatty liver ====
* Recurrence of NAFLD has been reported following liver transplantation [42-44]. In a series of 622 liver transplants, eight patients, all female, had features consistent with NASH pre-transplantation [44]. At a median follow-up of 15 months, six developed persistent fatty infiltration, three of whom had hepatic degeneration consistent with NASH. In two of the patients, the histologic progression from mild steatosis to steatohepatitis occurred within two years.
 
==== Carcinoma ====
* No large randomized trials have directly compared OLT with other forms of therapy for early HCC. Retrospective studies that included adjustment for disease severity suggest that survival following OLT is as good or better than after alternative treatments in carefully selected patients. For patients with anatomically resectable HCC and adequate hepatic reserve, resection remains the standard with which alternative treatment methods must be compared.
* Observational series suggest that long-term results after transplantation are at least as good and may be superior to those of resection in some groups [4,14-16]:
* An important caveat is that the results of transplantation cited above include only patients who actually received a transplant. Not included are patients with HCC who were listed for transplant but ultimately did not receive a liver transplant because their tumor progressed and exceeded transplant eligibility criteria before the transplant could be performed. Accordingly, intent-to-treat analyses of liver transplantation for HCC consistently demonstrate lower survival rates.
* Ultimately, despite the demonstrated benefit of transplantation, particularly in cirrhotic patients with small tumors, the group of patients with HCC who are candidates for OLT and who actually receive a graft is very small. Worldwide, the majority of patients with early stage HCC (often detected in the setting of formal surveillance programs) are treated in the Far East and Asian countries, where OLT is not a wide-spread option because of religious beliefs, lack of living-donor transplant programs, and its prohibitive cost. Without screening (ie, in most of the West), few patients who have cirrhosis and early stage HCC are identified as candidates for OLT.


==== Hepatocellular Carcinoma ====
* Resection remains the standard with which alternative treatment methods must be compared. [4,14-16]:
*
==== Alcoholic liver disease ====
==== Alcoholic liver disease ====
* Patient survival rates following liver transplantation for alcoholic liver disease are similar to rates following transplantation for non-alcohol related diagnoses [51-53]. In a study of 123 patients with alcoholic liver disease, one-, five-, and seven-year patient and graft survival rates were 84 and 81 percent (one year), 72 and 66 percent (five years), and 63 and 59 percent (seven years), respectively [51]. In comparison, five-year survival without liver transplantation is as low as 23 percent.
* Patient survival rates following liver transplantation for alcoholic liver disease are similar to rates following transplantation for non-alcohol related diagnoses.
* Five-year patient and graft survival rates 72 and 66 percent. Five-year survival without liver transplantation is 23 percent.


==== Primary biliary cirrhosis ====
==== Primary biliary cirrhosis ====
* A precise estimate of the recurrence rate is uncertain since not all studies have used uniform criteria for defining recurrent PBC, and studies have had variable follow-up.   [9,13-19].
* A precise estimate of the recurrence rate is uncertain.<ref name="pmid11124816">{{cite journal| author=Liermann Garcia RF, Evangelista Garcia C, McMaster P, Neuberger J| title=Transplantation for primary biliary cirrhosis: retrospective analysis of 400 patients in a single center. | journal=Hepatology | year= 2001 | volume= 33 | issue= 1 | pages= 22-7 | pmid=11124816 | doi=10.1053/jhep.2001.20894 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11124816  }}</ref>
* Two of the largest series with the longest follow-up (in which the diagnosis of recurrent PBC was based upon histologic features) probably represent the best available estimates [9,13].
* Methods to prevent recurrence may include immunosuppression using cyclosporine rather than tacrolimus and giving ursodeoxycholic acid (UDCA) following liver transplantation.  
* Methods to prevent recurrence may include immunosuppression using cyclosporine rather than tacrolimus and giving ursodeoxycholic acid (UDCA) following liver transplantation.  


==== Primary sclerosing cholangitis ====
==== Primary sclerosing cholangitis (PSC) ====
* Recurrent PSC following liver transplantation in 14 to 20 percent of patients [83,86-96].  
* Recurrent PSC following liver transplantation in 14 to 20 percent of patients.<ref name="pmid8045496">{{cite journal| author=Harrison RF, Davies MH, Neuberger JM, Hubscher SG| title=Fibrous and obliterative cholangitis in liver allografts: evidence of recurrent primary sclerosing cholangitis? | journal=Hepatology | year= 1994 | volume= 20 | issue= 2 | pages= 356-61 | pmid=8045496 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8045496  }}</ref>
* Only approximately one-third of patients with recurrence develop progressive disease leading to retransplantation or death.  
* Risk factors for recurrence include age, sex mismatch, male sex, coexistent IBD, presence of an intact colon after transplantation, cytomegalovirus (CMV) infection, recurrent acute cellular rejection, steroid-resistant cellular rejection, use of OKT3.
* Risk factors for recurrence include age, sex mismatch, male sex, coexistent IBD, presence of an intact colon after transplantation, cytomegalovirus (CMV) infection, recurrent acute cellular rejection, steroid-resistant cellular rejection, use of OKT3.

Revision as of 23:42, 17 December 2017


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]

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Prognosis

Overview

Liver transplantation prognosis

  • Prognosis is quite good. 1-year survival (in Finland) is 83%, 5-year survival is 76% and 10-year survival is 66%.
  • Majority of deaths happen during the first three months after transplantation.
  • Mortality rates in donors are 0.2% in the USA and vary fro, 0.1 to 1.0% worldwide.
  • Overall mortality rate is of the order of 0.2–0.5%.
  • The risk associated with left-lobe donation may be lower than that with right-lobe donation.
  • The incidence of complications in the donor varies from 9 to 67%.[1]
  • The modified Clavien classification is commonly used to describe, report, and compare donor morbidity:[2]

Grade I—a complication that is not life-threatening, does not result in residual disability, and does not require a therapeutic invasive intervention

Grade II—a complication that is potentially life-threatening and that requires the use of drug therapy or foreign blood units

Grade III—a complication that is potentially lifethreatening and that requires a therapeutic invasive intervention

Grade IV—a complication with residual or lasting disability or which leads to Living-donor Liver Transplantation death.[3]

Recurrence

Hepatitis B virus

  • Recurrence of HBV after liver transplantation can be prevented by administering hepatitis B immune globulin at the time of transplantation and at regular intervals thereafter in combination with antivirals such as tenofovir or entecavir.

Hepatitis C virus

  • There is no established role for prophylactic or preemptive therapy following transplantation.[4]
  • No effective immunoglobulin prophylaxis exists for HCV.
  • Treatment is initiated within six weeks of the transplantation. Theapy may be combined or monotherapy.
  • Combination therapy may be peginterferon or standard interferon and ribavirin, monotherapy may be peginterferon, standard interferon, or ribavirin, and anti-HCV immune globulin.
  • Direct-acting antiviral agents 
  • Sofosbuvir is an NS5B nucleotide analog used for the treatment of HCV.[5]
  • Treatment resulted in persistently undetectable HCV ribonucleic acid (RNA) 12 weeks after stopping treatment in 28 of 40 patients (70 percent).
  • All of the cases of virologic failure were due to relapse. As a result, sofosbuvir is usually now given in combination with one of several additional direct-acting antivirals (ledipasvir, simeprevir, and daclatasvir), with or without ribavirin.[6]

Hepatocellular Carcinoma

  • Resection remains the standard with which alternative treatment methods must be compared. [4,14-16]:

Alcoholic liver disease

  • Patient survival rates following liver transplantation for alcoholic liver disease are similar to rates following transplantation for non-alcohol related diagnoses.
  • Five-year patient and graft survival rates 72 and 66 percent. Five-year survival without liver transplantation is 23 percent.

Primary biliary cirrhosis

  • A precise estimate of the recurrence rate is uncertain.[7]
  • Methods to prevent recurrence may include immunosuppression using cyclosporine rather than tacrolimus and giving ursodeoxycholic acid (UDCA) following liver transplantation.

Primary sclerosing cholangitis (PSC)

  • Recurrent PSC following liver transplantation in 14 to 20 percent of patients.[8]
  • Risk factors for recurrence include age, sex mismatch, male sex, coexistent IBD, presence of an intact colon after transplantation, cytomegalovirus (CMV) infection, recurrent acute cellular rejection, steroid-resistant cellular rejection, use of OKT3.
  1. ↑ Ghobrial RM, Freise CE, Trotter JF, Tong L, Ojo AO, Fair JH; et al. (2008). "Donor morbidity after living donation for liver transplantation". Gastroenterology. 135 (2): 468–76. doi:10.1053/j.gastro.2008.04.018. PMC 3731061. PMID 18505689.
  2. ↑ Surman OS (2002). "The ethics of partial-liver donation". N Engl J Med. 346 (14): 1038. doi:10.1056/NEJM200204043461402. PMID 11932469.
  3. ↑ Salvalaggio PR, Baker TB, Koffron AJ, Fryer JP, Clark L, Superina RA; et al. (2004). "Comparative analysis of live liver donation risk using a comprehensive grading system for severity". Transplantation. 77 (11): 1765–7. PMID 15201680.
  4. ↑ Smith B (1969). "Segmental liver transplantation from a living donor". J Pediatr Surg. 4 (1): 126–32. PMID 4976215.
  5. ↑ Charlton M, Gane E, Manns MP, Brown RS, Curry MP, Kwo PY; et al. (2015). "Sofosbuvir and ribavirin for treatment of compensated recurrent hepatitis C virus infection after liver transplantation". Gastroenterology. 148 (1): 108–17. doi:10.1053/j.gastro.2014.10.001. PMID 25304641.
  6. ↑ Fontana RJ, Hughes EA, Bifano M, Appelman H, Dimitrova D, Hindes R; et al. (2013). "Sofosbuvir and daclatasvir combination therapy in a liver transplant recipient with severe recurrent cholestatic hepatitis C." Am J Transplant. 13 (6): 1601–5. doi:10.1111/ajt.12209. PMID 23593993.
  7. ↑ Liermann Garcia RF, Evangelista Garcia C, McMaster P, Neuberger J (2001). "Transplantation for primary biliary cirrhosis: retrospective analysis of 400 patients in a single center". Hepatology. 33 (1): 22–7. doi:10.1053/jhep.2001.20894. PMID 11124816.
  8. ↑ Harrison RF, Davies MH, Neuberger JM, Hubscher SG (1994). "Fibrous and obliterative cholangitis in liver allografts: evidence of recurrent primary sclerosing cholangitis?". Hepatology. 20 (2): 356–61. PMID 8045496.
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