Lewis Wd

Improved Survival After Live Donor Adult Liver Transplantation (LDALT) Using Right Lobe Grafts: Program Experience and Lessons Learned

We present our program experience with 85 live donor adult liver transplantation (LDALT) procedures using right lobe grafts with five simultaneous live donor kidney transplants using different donors performed over a 6‐year period. After an ‘early’ 2‐year experience of 25 LDALT procedures, program improvements in donor and recipient selection, preoperative imaging, donor and recipient surgical technique and immunosuppressive management significantly reduced operative mortality (16% vs. 3.3%, p = 0.038) and improved patient and graft 1‐year survival in recipients during our ‘later’ experience with the next 60 cases (January 2001 and March 2005; patient survival: early 70.8% vs. later 92.7%, p = 0.028; graft survival: Early 64% vs. later 91.1%, p = 0.019, respectively). Overall patient and graft survival were 82% and 80%. There was a trend for less postoperative complications (major and minor) with program experience (early 88% vs. later 66.7%; p = 0.054) but overall morbidity remained at 73.8%. Biliary complications (cholangitis, disruption, leak or stricture) were not influenced by program experience (early 32% vs. later 38%). Liver volume adjusted to 100% of standard liver volume (SLV) within 1 month post‐transplant. Despite a high rate of morbidity after LDALT, excellent patient and graft survival can be achieved with program experience.

Native liver xanthogranulomatous cholangiopathy in primary sclerosing cholangitis: Impact on posttransplant outcome

A retrospective analysis of 51 primary sclerosing cholangitis (PSC) patients who underwent liver transplant (LT) identified 16 with xanthogranulomatous cholangiopathy (XGC) at the native liver hilum. Pre‐LT clinical and laboratory data and post‐LT course and outcome of patients with XGC were compared with the 35 PSC patients without XGC. The XGC and non‐XGC groups were similar with respect to age and laboratory data at the time of LT. Pre‐LT cholecystectomy was performed in 44% versus 26% and biliary bypass procedure in 38% versus 26% of patients with and without XGC, respectively (P = NS). Peri‐operative complications resulted in six (38%) deaths or retransplantation within 60 days of LT in the XGC group compared with 4 (11%) in the non‐XGC group (P = .05). Patient survival at 60 and 100 days post‐LT was better in the non‐XGC group (P = .01). The causes of death or retransplantation within 60 days post‐LT in the patients with XGC included primary nongraft function (1), uncontrolled bleeding (3), and sepsis (2), while in the non‐XGC group these were uncontrolled bleeding (2), sepsis (1), and primary nongraft function (1). Mean graft survival ± SD was 1,081 ± 1,584 days in patients with XGC versus 2,149 ± 1,679 days in patients without XGC. The presence of XGC in the native liver hilum of PSC patients undergoing LT was associated with a higher rate of early post‐LT mortality or retransplantation. In conclusion, no pre‐LT clinical features or laboratory tests were identified that predicted the presence of XGC in PSC patients. (Liver Transpl 2004;10:115–122.)

Post-liver transplant cholestatic disorder with biliary strictures: de novo versus recurrent primary sclerosing cholangitis

Cholestatic allograft dysfunction following liver transplantation (LT) can result from many different underlying pathogenetic mechanisms and is a major cause of morbidity and graft loss. Although recurrence of primary sclerosing cholangitis (PSC) is a described entity following LT, the diagnosis is difficult and requires exclusion of common risk factors for stricture formation. There are no reports in the literature of de novo PSC arising in a patient who did not have that disease prior to transplantation. Reported herein is the case of a patient who underwent transplantation for end‐stage cryptogenic cirrhosis and who had no underlying risk factors, but who developed late post‐LT cholestatic disorder with non‐anastomotic biliary strictures. The combined clinical, radiological, and pathological findings resembled those of PSC. Admittedly, it is a challenging proposition but the possibility of a de novo PSC‐like syndrome in this patient is raised. A recurrence in a patient who may have had a burnt‐out, PSC‐like syndrome presenting as cryptogenic cirrhosis, however, cannot be entirely excluded.