Right lobe graft in living donor liver transplantation.

BACKGROUND: For the sake of donor safety in living donor liver transplantation (LDLT), the left lobe is currently being used most often for the graft. However, size mismatch has been a major obstacle for an expansion of the indication for LDLT to larger-size recipients, because a left lobe graft is not safe enough for them. METHODS: In 1998, LDLT using a right lobe graft was introduced and performed on 26 recipients to overcome the small-for-size problem. The right lobe, which does not include the middle hepatic vein of the donor, was used. Initially, indication for right lobe LDLT was basically defined as an estimated left lobe graft volume/recipient body weight ratio (GRWR) of <0.8%, which was later raised to <1.0%. RESULTS: All the donors recovered from the operation without persistent complications. Two donors with transient bile leakage were successfully treated with a conservative approach. A right lobectomy resulted in more blood loss (337+/-175 ml), and a longer operative time (6.67+/-0.85 hr) than a lateral segmentectomy, but not a left lobectomy. Grafts with a GRWR >0.8% were implanted in all recipients, except for two, who received relatively smaller right lobes (GRWR of 0.68% and 0.66%). In one of these two, the right lobe from the donor was used as the orthotopic auxiliary graft. Postoperative transitory increases in total bilirubin and aspartate transaminoferase for right lobe donors were higher than those for the left lateral segmentectomy. Nineteen recipients (73.1%) were successfully treated with this procedure. The causes of death were not specific for right lobe LDLT, except for one patient with a graft that had multiple hepatic venous orifices. These multiple and separate anastomoses of the hepatic veins caused an outflow block as a result of a positional shift of the graft, which finally led to graft loss. CONCLUSION: Our experience suggests that right lobe grafting is a safe and effective procedure, resulting in the expansion of the indication for LDLT to large-size recipients. How to deal with the possible variation in the anatomy of the right lobe graft should be given attention throughout the procedure.

Serotonin as a useful parameter for cold and warm ischemic injury in small bowel transplantation.

We investigated serotonin as a parameter of cold and warm ischemic injury prior to transplantation. Lewis rats were used as both donors and recipients, and the proximal 20 cm of jejunum served as the graft. The grafts were preserved in 4 degrees C lactated Ringer's solution for 0, 6, 12, 18, and 24 hr after harvest for cold ischemia (n=7/group). The superior mesenteric artery was clamped for 0, 15, 30, 60, and 120 min before harvest for warm ischemia (n=7/group). The serotonin concentration was measured in the luminal effluent and the preservation solution before transplantation, and total serotonin was calculated as the sum of these amounts. Finally, transplantation was performed heterotopically. Total serotonin increased significantly with both cold and warm ischemic time (P<0.01 by analysis of variance, Fisher's PLSD); however, between 18 hr and 24 hr of cold ischemic time only, there were no significant changes. Total serotonin levels correlated well with cold and warm ischemic time, as shown by linear regression analysis (cold ischemia: R2=80.2%, P<0.01; warm ischemia: R2=92.8%, P<0.01). We established the cutoff level of total serotonin to predict the graft survival at 2200 ng, and using this critical level, graft survival was predicted by total serotonin with a sensitivity of 71.4% and a specificity of 89.8%. Immunohistochemical staining with the serotonin antibody revealed that the number of serotonin-positive cells decreased with both cold and warm ischemic time. In conclusion, serotonin is a useful parameter of cold and warm ischemic injury before transplantation and can assist in predicting graft survival.

Living related liver transplantation from donors with the left-sided gallbladder/portal vein anomaly.

The presence of a left-sided gallbladder poses a unique challenge for living related liver donation. Associated anomalies include segment IV atrophy, absence of portal vein bifurcation, and abnormal intrahepatic portal branches to segments II and III. The complex is rare, but is more frequent in Japan. Of 379 living related liver transplants from our institution, the complex has been encountered on four occasions (incidence: 1.1%), and we herein review our experience. Anomalies were identified preoperatively (by computed tomography and ultrasound) in all instances. One donor was turned down because there was no common portal trunk to segment II and III branches. Three donors underwent successful retrieval using a modified technique. There were no complications in the donors or recipients relating to the complex. Thus, living related liver retrieval can be achieved safely in the presence of the left-sided gallbladder/portal anomaly complex, but technical modifications are required.

Four cases of human herpesvirus 6 variant B infection after pediatric liver transplantation.

BACKGROUND: Little is known about human herpesvirus (HHV)-6 infection after liver transplantation. We present our experiences with four cases of HHV-6 infection after liver transplantation from living related donors. METHODS: Peripheral blood was collected from four donor and recipient pairs at the time of transplantation and biweekly from the recipients after transplantation. We attempted to isolate HHV-6 and measure antibody titers to HHV-6 and HHV-7. RESULTS: HHV-6 was isolated from four recipients approximately 2 weeks after transplantation. A significant rise in HHV-6 antibody titers was observed in four recipients at some point in their course, whereas HHV-7 antibody titers were increased in one recipient. Four isolates were variant B. When HHV-6 was isolated, all recipients had an unexplained fever. CONCLUSIONS: HHV-6 variant B infection after pediatric liver transplantation was confirmed. HHV-6 infection occurred approximately 2 weeks after transplantation. Moreover, there appears to be an association between HHV-6 infection and unexplained fever.

The clinical significance of the arterial ketone body ratio as an early indicator of graft viability in human liver transplantation.

Arterial ketone body ratio (AKBR) was measured sequentially in 84 liver transplantations (OLTx). These transplantation procedures were classified into 3 groups with respect to graft survival and patient condition at the end of the first month (Group A, the grafts survived longer than 1 month with satisfactory patient condition; Group B, the grafts survived longer than 1 month but the patients were ICU-bound; Group C, the grafts were lost and the patients died or underwent re-OLTx). In Group A, the AKBR was elevated to above 1.0 by the second postoperative day. In Group B, the AKBR was elevated to above 0.7 but stayed below 1.0 during this period. In Group C, the AKBR remained below 0.7 longer than 2 days after operation. Although conventional liver function tests showed significant increases in Groups B and C as compared with Group A, they were less specific in predicting ultimate graft survival.

Effects of hypoxemia on early postoperative course of liver transplantation in pediatric patients with intrapulmonary shunting.

Nine pediatric patients (mean age, 10 years) with biliary atresia, who had hypoxemia related to intrapulmonary shunting, underwent living related liver transplantation. The effects of hypoxemia during the early postoperative period after liver transplantation on cardiopulmonary and renal function, as well as on transplanted liver, were analyzed. Based on the degree of shunt ratio calculated by technetium-99m macroaggregated albumin scintigraphy, the nine patients were included in the moderate group (shunt ratio under 40%, n=4) or the severe group (shunt ratio over 40%, n=5). Partial pressure of arterial oxygen was maintained at normal range in the moderate group, while that in the severe group persistently had very low values (<50 mmHg), in spite of a high degree of oxygen supply. However, all patients in the severe group maintained stable cardiopulmonary vital signs, including systemic blood pressure, heart rate, respiratory rate, and cardiac index. They also demonstrated stable renal function. None of the patients died of cardiopulmonary or renal insufficiency after transplantation, but three patients died of portal vein thrombosis, sepsis, and intracranial hemorrhage (one each). The minimal adverse effect of hypoxemia on the transplanted liver was confirmed by a rapid increase of arterial ketone body ratio, low peak values (under 200 IU/L) of aspartate aminotransferase, and a steady decrease of serum total bilirubin. Four patients encountered surgical complications, including two bile leaks from the cut liver surface, two leaks from bilioenteric anastomosis, and one intestinal perforation. Six patients suffered from bacterial infections, including four wound infections, three right subphrenic abscesses, one cholangitis, and two systemic sepses. All patients in the moderate group recovered from hypoxemia, but four of five patients in the severe group have not recovered during the follow-up period between 4 and 9 months. It was concluded that the adverse effects of hypoxemia on cardiopulmonary and renal function and transplanted liver were minimal, so that patients with severe hypoxemia could tolerate the stress of liver transplantation without special management. However, the high incidence of surgical complication and infection suggested the adverse effects of hypoxemia on wound healing and resistance to bacteria infection.

Living-related liver transplantation and neurological outcome in children with fulminant hepatic failure.

BACKGROUND: Fulminant hepatic failure (FHF) in children is associated with high mortality under medical management. Living-related liver transplantation (LRLT) is an accepted measure to treat the children with end-stage liver disease. Reversibility of hepatic encephalopathy is crucial for the quality of life among the survivors after transplantation. METHODS: A retrospective review was made of the records of children undergoing LRLT at this hospital between May 1992 and November 1996. RESULTS: Eleven children with FHF underwent emergency LRLT. The mean age was 5 years (range, 2 months to 15 years). The indication for transplantation was persistent or worsening hepatic encephalopathy and severe coagulopathy, despite repeated plasma exchanges or exchange transfusions. The cause of FHF was non-A, non-B hepatitis in seven children, hepatitis B in two children, herpes simplex virus hepatitis in one child, and fulminant Wilson's disease with intravascular hemolysis in one child. The grade of hepatic encephalopathy was II in four children, III in two, and IV in five. The actuarial survival rate was 73% after a mean follow-up of 28 months (range, 13-67 months). Short-term neurological morbidity was present in two children with grade IV encephalopathy who also showed brain edema on cranial computed tomography. Eight survivors exhibited no long-term neurological deficit; the mean intelligence or developmental quotient was 97 (range, 86-110) at the end of the follow-up period. CONCLUSIONS: LRLT is an effective option for the treatment of FHF in children. The long-term neurological status is satisfactory among survivors.

Hepatic artery thrombosis in living related liver transplantation.

BACKGROUND: Hepatic artery thrombosis (HAT) after orthotopic liver transplantation remains a significant cause of graft loss in pediatric patients. We previously reported that the microsurgical techniques for arterial anastomosis can reduce the incidence of HAT in living related liver transplantation (LRLT). The purpose of this study is to analyze the risk factors for HAT after LRLT. A total of 245 patients received 250 liver transplants. METHODS: Eight arteries in eight patients, reconstructed with the use of loupe magnification (HAT; 1/8, 12.5%), were excluded from this study. We observed HAT in 4 patients of the 242 transplants (1.7%, HAT group). Seventeen factors were compared between the HAT and the control group (those without HAT). RESULTS: HAT occurred in 3 of 33 grafts (9%) from ABO-incompatible donors, whereas it occurred in 1 of 209 grafts (0.5%) from identical or compatible donors (P=0.008). The corrected volume of fresh-frozen plasma intraoperatively transfused in the HAT group (46.9+/-30.3 ml/kg) was significantly (P=0.015) different from that in the control group (10.2+/-1.9 ml/mg). In all four patients with HAT, emergent revisions of the anastomosis were performed. Two patients with ABO-incompatible grafts died of hepatic failure and sepsis. CONCLUSIONS: Although microsurgical techniques can minimize the surgical risk factors for HAT, overtransfusion of fresh-frozen plasma in high-risk patients (ABO incompatible) may be a critical factor in the development of HAT in LRLT.

Postoperative flow cytometry crossmatch in living donor liver transplantation: clinical significance of humoral immunity in acute rejection.

BACKGROUND: The role of humoral immunity in acute rejection in solid organ transplantation remains controversial, although it is known that the presence of antidonor antibodies may precipitate graft rejection. We investigated the clinical relevance of antidonor humoral immunity for living donor liver transplantation (LDLT) by means of flow cytometry crossmatch (FCXM). METHODS: T cell FCXM using fresh donor peripheral lymphocytes was performed before and up to 1 month after LDLT in 58 patients. Ten patients received ABO-incompatible grafts. IgM and IgG antidonor antibodies were analyzed in relation to clinical acute rejection as defined by liver function tests with or without histological evidence. RESULTS: Pretransplantation FCXM was positive for five patients (8.6%), resulting in two cases of positive posttransplantation FCXM and two rejection episodes. Twelve patients (20.7%) showed positive posttransplantation FCXM. The incidence of acute rejection within 1 month was 100% in FCXM-positive patients and 17.4% in FCXM-negative patients (P<0.001). Thirteen (76.5%) of 17 rejection episodes in ABO-compatible cases were associated with concomitant antidonor IgM antibody. IgG antibody was also identified in six of these episodes. Antidonor antibodies disappeared after rejection treatments in all cases, but with some delay in clinical improvement. On the other hand, no antidonor antibodies were detected in any of the four rejection episodes in ABO-incompatible cases. CONCLUSIONS: Early acute rejection in LDLT is significantly associated with antidonor T cell antibody formation in ABO-compatible cases. This suggests a definite role for donor-specific humoral immunity in acute rejection. Rejection episodes without antidonor antibodies may suggest graft injury by pure cellular immunity, or possibly the presence of humoral immunity triggered by antigens not present on donor T cells.

Impact of graft size mismatching on graft prognosis in liver transplantation from living donors.

BACKGROUND: Although living donor liver transplantation for small pediatric patients is increasingly accepted, its expansion to older/larger patients is still in question because of the lack of sufficient information on the impact of graft size mismatching. METHODS: A total of 276 cases of living donor liver transplantation, excluding ABO-incompatible, auxiliary, or secondary transplants, were reviewed from graft size matching. Forty-three cases were highly urgent cases receiving intensive care preoperatively. Cases were categorized into five groups by graft-to-recipient weight ratio (GRWR): extra-small-for-size (XS; GRWR<0.8%, 17 elective and 4 urgent cases), small (S; 0.8< or =GRWR< 1.0%, 21 and 7), medium (M; 1.0< or =GRWR<3.0%, 119 and 19), large (L; 3.0< or =GRWR<5.0%, 67 and 10), and extra-large (XL; GRWR> or =5.0%, 9 and 3). RESULTS: Smaller-for-size grafts were associated not only with larger and older recipients, but also with rather older donors. Posttransplant bilirubin clearance was delayed and aspartate aminotransferase corrected by relative graft size was higher in XS and S. Posttransplant hemorrhage and intestinal perforation were more frequent in XS and S, and vascular complications and acute rejection were more frequent in larger-for-size grafts. Consequently, graft survival in XS (cumulative 58% and actuarial 42% at 1 year) and S (76% and 74%) was significantly lower compared with that in M (93% and 92%) in elective cases. Graft survival in L (83% and 82%) and XL (75% and 71%) did not reach statistical significance. CONCLUSIONS: The use of small-for-size grafts (less than 1% of recipient body weight) leads to lower graft survival, probably through enhanced parenchymal cell injury and reduced metabolic and synthetic capacity. Although large-for-size grafts are associated with some anatomical and immunological disadvantages, the negative impact is less pronounced.

Transmission of hepatitis B virus from hepatitis B core antibody-positive donors in living related liver transplants.

BACKGROUND: In order to clarify the risk of hepatitis B virus (HBV) transmission from hepatitis B core antibody-positive (HBcAb(+)) donors and to evolve a new strategy to counter such a risk, we undertook a retrospective (1990-1995) and prospective (1995-1996) analysis of our experience with living related liver transplantation involving HBcAb(+) donors. METHODS: Between June 15, 1990, and June 30, 1995, HBcAb(+) individuals were not excluded as donor candidates at our institutions. For 171 liver transplants, 16 donors were HBcAb(+). Between July 1, 1995, and June 30, 1996, HBcAb(+) individuals were generally excluded as donor candidates; however, three recipients were given liver grafts from HBcAb(+) donors because other donor candidates presented even higher risks. In the latter period, recipients with transplants from HBcAb(+) donors underwent prophylactic passive immunization with hyperimmune hepatitis B immunoglobulin (HBIG). The serum of 10 HBcAb(+) donors was examined by nested polymerase chain reaction for the presence of HBV-DNA, but it was not detected in any of them. However, the same examination of the liver tissue of five such donors yielded positive results in all cases. RESULTS: In the first 5-year period, out of 16 recipients with HBcAb(+) donors, 15 became hepatitis B surface antigen-positive after transplant. The three recipients with HBcAb(+) donors during the second 1-year period, who were treated by prophylactic passive immunization with HBIG, remained hepatitis B surface antigen-negative and negative for serum HBV-DNA after transplant. CONCLUSIONS: HBV exists in the liver of healthy HBcAb(+) individuals, but not in the blood. Therefore, HBV is thought to be transmitted to recipients by liver grafts from the HBcAb(+) donors at a significantly high rate. The prevention of viral activation and clinical disease development by means of passive immunization with HBIG seems promising, although the follow-up period in our study may be too short for any definitive conclusions.

Auxiliary partial orthotopic living donor liver transplantation as an aid for small-for-size grafts in larger recipients.

BACKGROUND: In countries where living donors are the only source of liver grafts, restrictions on graft size are a serious obstacle for the expansion of indications for adult recipients. To overcome this problem, auxiliary partial orthotopic liver transplants (APOLT*) was performed on the basis of the concept that the residual native liver would support the graft function until the graft had grown enough to function by itself. METHODS: APOLT as an aid for small-for-size (SFS) grafts was reviewed retrospectively to evaluate its feasibility. Between April 1995 and March 1998, 20 recipients underwent APOLT, which was indicated because of a SFS graft in 15 of them. The indication was based on the estimated graft/recipient's body weight ratio (GRWR). If the ratio was <0.8%, APOLT was performed. The other 5 patients had a graft with a GRWR >0.8% and underwent APOLT on the basis of the residual native liver supporting the graft function temporarily, 4 for supplementation of the defective enzyme in metabolic liver diseases and one for leaving the potential of the regeneration of the native liver in fulminant hepatic failure. The recipients who underwent APOLT because of a SFS graft were categorized as the SFS group, and the others were the second group. RESULTS: In the SFS group, the age of the recipients ranged from 13 to 48 (median 23). The original indications of this group were fulminant hepatic failure in 2 recipients, acute deterioration of chronic liver diseases in 3, Wilson's disease in 2, biliary atresia in 4, primary biliary cirrhosis in 3, and primary sclerosing cholangitis (PSC) in one. The actual GRWR ranged from 0.45 to 0.72 (median 0.55). The graft was implanted after resection of the left lateral segment of the native liver. Except in the first two patients, the portal vein to the residual native liver was completely transected so that all of the portal blood drained into the graft liver. This procedure was successful in 9 patients. The cause of death in the other 6 was mainly infection. The mortality rate among the recipients with signs of advanced liver failure, such as massive ascites or hepatic coma, was higher, even though APOLT was used to support the SFS graft. In the second group, in the other five recipients who underwent APOLT for other indications, one recipient with fulminant hepatic failure died of sepsis caused by the dehiscence of bilio-enteric anastomosis. CONCLUSIONS: APOLT as an aid for a SFS graft is technically viable. This procedure can thus expand the indication of living donor liver transplants for adult recipients when the native liver retains some functional capability to support the grafted liver during the immediate postoperative period.

Auxiliary partial orthotopic liver transplantation from living donors: significance of portal blood flow.

BACKGROUND: Auxiliary liver transplantation has several advantages over standard orthotopic liver transplantation. However, functional competition has been reported even in auxiliary partial orthotopic liver transplantation (APOLT). We evaluated herein the interaction in APOLT between the native liver and the graft in terms of portal blood flow and regeneration. The need for diversion of the portal blood flow to the graft was also assessed. METHODS: A total of 15 patients received APOLT from living donors. Portal blood flow to the native liver was preserved in 6 patients, and the portal vein to the native liver was preemptively transected at the time of transplantation in 9 patients. RESULTS: Of the patients with preservation of the portal blood flow to the native liver, two showed inadequate graft portal blood flow just after operation, and in the other three patients the graft portal blood flow decreased or the graft atrophied after deterioration of the graft function. In the patients with preemptive transection of the portal vein to the native liver, optimal graft portal blood flow was obtained, and the native liver, supplied only by arterial inflow, supported a small-for-size graft until the graft regenerated. The damage to the native liver was minimal. CONCLUSIONS: Functional competition may occur in APOLT with preservation of the portal blood flow to the native liver, whereas preemptive transection of the native liver portal vein is a safe procedure and effectively prevents the portal steal phenomenon.

Living-related liver transplantation for type II citrullinemia using a graft from heterozygote donor.

BACKGROUND: Type II citrullinemia (CTLN2) characterized by a liver-specific argininosuccinate synthetase deficiency is an adult onset genetical disorder caused by the mutation of SLC25A13 gene, which results in fulminant hyperammonemia often with poor prognosis. METHODS: A 16-year-old Japanese boy presented fulminant hyperammonemia and encephalopathy and recovered after aggressive medical treatment. The patient was diagnosed as CTLN2 by plasma amino acid pattern and detection of the mutated SLC25A13 gene. We performed living-related liver transplantation (LRLT) using a graft from the genetically proven heterozygote father. RESULTS: Serum amino acid concentration was normalized within a day after transplantation without protein restriction and medication. The patient's postoperative course was natural. The patient is back in school 6 months after surgery. CONCLUSIONS: Living-related liver transplantation using a graft from genetically proven heterozygote donors might be a permissible treatment modality for CTLN2. Long-term observation may be necessary to make a definite conclusion possible.

Coexistence of a graft with the preserved native liver in auxiliary partial orthotopic liver transplantation from a living donor for ornithine transcarbamylase deficiency.

BACKGROUND: Auxiliary partial orthotopic liver transplantation (APOLT) has recently been performed in patients with noncirrhotic metabolic liver diseases. However, long-term outcomes for the preserved native liver and the transplanted liver graft have not been clearly established yet. METHODS: The recipient was a 36-month-old girl with ornithine transcarbamylase deficiency. She underwent APOLT, using her father's left lateral segment. RESULTS: Liver function was normalized soon after APOLT and the patient was able to ingest a normal diet without medication. Coexistence of the well-functioning native liver and graft was demonstrated in a computed tomography scan, Doppler ultrasonography, scintigraphy, and histological examination, during a relatively long-term follow-up period. CONCLUSIONS: APOLT seems to be most useful for the treatment of noncirrhotic metabolic liver diseases.

Selective portal blood flow diversion in auxiliary partial orthotopic liver transplantation to induce regeneration of the graft.

Experience with auxiliary partial orthotopic liver transplantation (APOLT) is still very limited and many questions remain to be solved. In this article, we present the case of a 5-year-old girl with ornithine transcarbamylase deficiency who initially did well after APOLT. During a severe rejection episode 16 months after transplantation, she developed encephalopathy and hyperammonemia. Despite a good clinical and histopathological response to antirejection therapy, the graft had become smaller and the native liver had undergone compensatory hypertrophy. After we surgically ligated the right portal branch, the graft recovered and the patient was able to stop her medication 1 month after surgery. We have estimated that the minimum volume of normal liver required to correct the metabolic defect in ornithine transcarbamylase deficiency is 8 cm3/kg. The ligation of the right portal branch was a safe and effective method of inducing a gradual and progressive involution of the hypertrophic native liver and regeneration of the atrophic graft.

Long-term outcome of living related liver transplantation for patients with intrapulmonary shunting and strategy for complications.

BACKGROUND: In 320 living related liver transplantation performed between June 1990 and September 1997, there were 21 living related liver transplantation for patients with intrapulmonary shunting, manifested by digital clubbing, cyanosis, and dyspnea. We report the long-term outcome for more 6 months and our strategy to overcome complications in these recipients. PATIENTS: A total of 21 patients (age range 2-33 years, 19 children and 2 adults, 6 males and 15 females) were classified into three grades according to shunt ratio calculated by TcMAA pulmonary scintigraphy; 5 in mild group (shunt ratio: less than 20%), 6 in moderated group (20%-40%), and 10 in severe group (more than 40%). The original underlying liver disease was biliary atresia in all patients. RESULTS: Spearmen's correlation coefficient rank test revealed that shunt ratio correlated significantly with PaO2 in room air (P=0.0001), PaO2 in 100% oxygen (P=0.0004), hematocrit (P=0.0276), and period of dyspnea before transplantation (P=0.023). COMPLICATIONS: Wound infection occurred in 80, 66, and 80%, and bile leakage in 20, 0, 40% in mild, moderate, and severe group, respectively. Patients who had portal vein thrombosis, and intracranial complication were classified as severe group and the incidence was 20 and 20%, respectively. The patient actuarial one year survival was 80, 66.7, and 48%, in mild, moderate, and severe group, respectively, although there was no significant difference. All patients who survived improved hepatopulmonary syndrome and the length of period required for the resolution was significantly correlated to the preoperative shunt ratio (P=0.023). COMMENTS: Patients with severe shunting are susceptible to wound infection and bile leak. The trend of higher incidence of portal thrombosis and intracranial complications in the severe group was closely related high hematocrit. Secure surgical technique to reduce bile leak and delayed primary wound closure to reduce wound infection were found to be effective. Anticoagulant therapy by infusing heparin through the portal vein followed by coumadin could prevent fatal portal vein thrombosis without counter risk of fatal cerebral hemorrhage.

Human herpesvirus 6 latently infects mononuclear cells but not liver tissue.

AIM: To investigate whether human herpesvirus 6 (HHV-6) can cause latent infection of liver tissue. METHODS: Peripheral blood and liver tissue were collected from 25 living related liver transplant recipients at the time of transplantation. An avidin-biotin complex peroxidase method was used to identify HHV-6 antigen in the liver tissue. A nested polymerase chain reaction (PCR) was used to detect HHV-6 DNA in the liver tissue and mononuclear cells. Variant of HHV-6 was determined by the presence of the Hind III site in a second PCR product. RESULTS: Immunohistochemical analysis for HHV-6 antigen was negative in all the liver specimens. HHV-6 DNA was not detected in liver tissue. Virus DNA was detected in peripheral blood mononuclear cells in nine of 25 recipients. All nine HHV-6 identified in the mononuclear cells were variant B. CONCLUSIONS: HHV-6 variant B latently infects mononuclear cells but not liver tissue.

Hepatic vein reconstruction in 152 living-related donor liver transplantation patients.

BACKGROUND: Hepatic vein (HV) reconstruction is crucial in partial liver transplantation in which the inferior vena cava (IVC) is preserved. METHODS: We reviewed the medical records of 152 living-related donor liver transplantations (LRDLTs) in 150 children (45 left lobe grafts, 106 lateral segment grafts, and 1 right lobe graft) monitored for 12 months or longer. RESULTS: A standard technique was a wide end-to-side anastomosis between the donor HV and cuffs, consisting of the recipient middle and left HV and an incision to the IVC. In 15 of 22 partial grafts with two separated HVs the two vessels were reformed by back table surgery to have a common anastomotic orifice, and two separate anastomoses of the individual vessels were made for the remaining seven grafts. Four patients with an absence of infrahepatic IVCs and two with completely obstructed IVCs had end-to-end anastomoses with recipient IVCs. Four patients with stenotic IVCs had end-to-side anastomoses with new orifices on the IVCs. Two patients had acute HV obstruction caused by twisting of the HV that required laparotomy, and six had late-onset HV obstruction that required radiologic intervention. A tissue expander was placed prophylactically in the right subphrenic space in 10 patients to prevent the dislocation of the graft into the right subphrenic space. CONCLUSIONS: It is important in HV reconstruction in partial liver transplantation to make wide orifices and to adapt each graft to its orthotopic place, taking into consideration graft shape, size of the abdominal cavity of the recipient, and anatomic variations in vessels.

Biliary complications in pediatric living related liver transplantation.

BACKGROUND: The goal of this study was to evaluate cause and outcome of biliary complications occurring after pediatric living related liver transplantation (LRLT). METHODS: A database of 205 pediatric patients (71 male and 134 female) undergoing 208 LRLT from June 1990 to April 1996 was reviewed. RESULTS: The overall incidence of bile duct complications was 13.9% (29 patients). There were 19 bile leaks, 7 anastomotic strictures, 8 intrahepatic biliary complications, and the bile duct was ligated inadvertently in 2 cases. Logistic regression analysis revealed hepatic artery thrombosis, ABO incompatible transplantation, intrapulmonary shunting in recipients, mode of artery reconstruction, and cytomegalovirus infection were all significant risk factors for biliary complications. CONCLUSIONS: Avoidance of ABO incompatible transplantation where possible, routine use of microvascular techniques for hepatic artery reconstruction to minimize the risk of artery thrombosis, earlier transplantation for patients with intrapulmonary shunt, and prophylaxis against cytomegalovirus infection should all reduce the rate of biliary complications after LRLT in pediatric recipients.