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The objective of the study was to determine the long-term stricture rate of hepaticojejunostiomy (HJ) performed for benign disease, to compare stricture rates for transplant patients and non-transplant patients, and to compare the success rates of procedural and surgical treatment options. Hospital charts of 135 consecutive patients undergoing HJ between 1998 and 2016 were analyzed retrospectively. The primary outcome was stricture formation. Secondary outcomes were time to stricture diagnosis and success rates of various interventions. The anastomotic stricture rate was 13.3 per cent (18). The mean follow-up period was 4.3 years. The mean time to stricture diagnosis was 2.3 years. Stricture rates were similar between the transplant (19.2%) and nontransplant, non-Whipple group (13%). Strictures were treated with radiological intervention with a 44.4 per cent success rate; each required multiple interventions. Mortality from liver disease after failure of nonoperative management of HJ strictures reached 30 per cent (3). Five of ten patients who failed radiological intervention underwent HJ revision; the success rate was 80 per cent. Anastomotic strictures of HJ performed for benign disease occur in 13 per cent of patients and typically develop within 2.5 years postoperatively. Yet, given the dangerous sequelae of chronic biliary obstruction and potential delay in presentation, a follow-up is recommended for up to 10 years. When strictures occur, HJ revision should be considered early, after two failed radiological interventions.

Rates of transmission of hepatitis B virus (HBV) infection from organ donors with HBV markers to recipients along with reactivation of HBV during immunosuppression following transplantation have fallen significantly with the advent of hepatitis B immune globulin (HBIg) and effective antiviral therapy. Although the availability of potent antiviral agents and HBIg has highly impacted the survival rate of HBV-infected patients after transplantation, the high cost associated with this practice represents a major financial burden. The availability of potent antivirals with high genetic barrier to resistance and minimal side effects have made it possible to recommend an HBIg-free prophylactic regimen in selected patients with low viral burden prior to transplant. Significant developments over the last two decades in the understanding and treatment of HBV infection necessitate a re-appraisal of the guidelines for prophylaxis of HBV infection in solid organ transplant recipients.

Elimination of galactose-α( 1 , 3 )galactose (Gal) expression in pig organs has been previously shown to prevent hyperacute xenograft rejection. However, naturally present antibodies to non-Gal epitopes activate endothelial cells, leading to acute humoral xenograft rejection. Still, it is unknown whether xenogeneic pig liver sinusoidal endothelial cells (LSECs) from α( 1 , 3 )galactosyltransferase (GalT)-deficient pigs are damaged by antibody and complement-mediated mechanisms. The present study examined the xeno-antibody response of LSECs from GalT-deficient and wild pigs. Isolated LSEC from wild-type and GalT pigs were expose to human and baboon sera; IgM and IgG binding was analyzed by flow cytometry. Complement activation (C3a and CH50) was quantified in vitro from serum-exposed LSEC cultures using Enzyme-Linked ImmunoSorbent assay (ELISA). Levels of complement-activated cytotoxicity (CAC) were also determined by a fluorescent Live-Dead Assay and by the quantification of LDH release. IgM binding to GalT knockout (KO) LSECs was significantly lower (80% human and 87% baboon) compare to wild-type pig LSEC. IgG binding was low in all groups. Moreover, complement activation (C3a and CH50) levels released following exposure to human or baboon sera were importantly reduced (42% human and 52% baboon), CAC in GalT KO LSECs was reduced by 60% in human serum and by 72% in baboon serum when compared to wild-type LSECs, and LDH release levels were reduced by 37% and 57%, respectively. LSECs from GalT KO pigs exhibit a significant protection to humoral-induced cell damage compared to LSECs from wild pigs when exposed to human serum. Although insufficient to inhibit xenogeneic reactivity completely, transgenic GalT KO expression on pig livers might contribute to a successful application of clinical xenotransplantation in combination with other protective strategies.