The incidence of hepatitis B (HB) recurrence after a liver transplantation has been reduced by prophylaxis with hepatitis B immunoglobulin (HBIG) and lamivudine. However, the long-term incidence of recurrence is Ͻ10%, and the factors associated with HB recurrence are unclear. This study analyzed the factors associated with HB recurrence in 203 recipients who underwent liver transplantation for HB in 3 major centers in Korea over 4 years. Eighty-five patients (41.9%) had a hepatocellular carcinoma (HCC). Preoperative active virus replicators with the HBeAg(ϩ) (46.8%) and/or hepatitis B virus DNA(ϩ) (39.4%) were observed in 136 patients (67.0%). The HB prophylaxis consisted of either HBIG monotherapy (n ϭ 95, HBIG group) or combination therapy with lamivudine (n ϭ 108, combination group). HB recurrence was defined as the appearance of the HBsAg. The follow-up period was 28.3 Ϯ 13.1 months (mean Ϯ SD). HB recurred in 21 patients (10.3%) after transplantation. The time from transplantation to recurrence was 16.3 Ϯ 9.4 months. Pre-LT DNA positivity was more prevalent in HBIG group (55.8%) than in the combination group (39.8%) (P ϭ 0.015). However, the incidence of HB recurrence was similar in the HBIG (6.3%) and combination group (13.8%), as well as between the active replicators (12.5%) and nonreplicators (4.1%) (P Ͻ 0.05). There was a far higher incidence of HB recurrence in patients receiving corticosteroid pulse therapy (21.0% vs. 7.9%), patients who experienced HCC recurrence (31.3% vs. 8.6%), and patients receiving chemotherapy to prevent HCC recurrence (25.0% vs. 4.4%) (P Ͻ 0.05). The cumulative corticosteroid dose was higher in patients who experienced recurrence of HB (P ϭ 0.002). Multivariable analysis confirmed the effect of the cumulative corticosteroid dose and chemotherapy to be risk factors. Liver transplantation for HB is safe, with low recurrence rates if adequate prophylaxis is used. However, the cumulative corticosteroid dose and the chemotherapy used for HCC were risk factors for HB recurrence, so careful monitoring for HB recurrence is needed in these patients. Liver Transpl 13:451-458, 2007. © 2007 AASLD. Received December 19, 2005 accepted October 18, 2006.The outcome of liver transplantation (LT) for hepatitis B virus (HBV)-related liver diseases was dismal before the advent of an effective means for preventing the virtually universal reinfection of the graft. Reinfection was followed by progressive destruction by recurrent hepatitis. This led to quick graft failure. HBV-related liver disease was once considered to be a contraindication for LT. However, over the last 15 years, there have been major advances in the management of transplant candidates with hepatitis B (HB). The long-term use of

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OBJECTIVE -The aim of this study was to assess the incidence of posttransplantation diabetes mellitus (PTDM) in renal allograft recipients and to investigate factors contributing to the onset and progression of PTDM and its underlying pathogenic mechanism(s).RESEARCH DESIGN AND METHODS -A total of 77 patients with normal glucose tolerance (NGT) were enrolled in this study. An oral glucose tolerance test was performed 1 week before transplantation and repeated at 1 and 7 years after transplantation.RESULTS -The overall incidence of PTDM was 39% at 1 year and 35.1% at 7 years posttransplantation. The incidence for each category of PTDM was as follows: persistent PTDM (P-PTDM) (patients who developed diabetes mellitus within 1 year of transplantation and remained diabetic during 7 years), 23.4%; transient PTDM (T-PTDM) (patients who developed diabetes mellitus during the 1st year after transplantation but eventually recovered to have NGT), 15.6%; late PTDM (L-PTDM) (patients who developed diabetes mellitus later than 1 year after transplantation), 11.7%; and non-PTDM during 7 years (N-PTDM 7 ) (patients who did not develop diabetes mellitus during 7 years), 49.3%. Older age (Ն40 years) at transplantation was a higher risk factor for P-PTDM, whereas a high BMI (Ն25 kg/m 2 ) and impaired fasting glucose (IFG) at 1 year posttransplantation were higher risk factors for L-PTDM. Impaired insulin secretion rather than insulin resistance was significantly associated with the development of Pand L-PTDM.CONCLUSIONS -Impaired insulin secretion may be the main mechanism for the development of PTDM. Older age at transplantation seems to be associated with P-PTDM, whereas a high BMI and IFG at 1 year after transplantation were associated with L-PTDM. Diabetes Care 30:609 -615, 2007P osttransplantation diabetes mellitus (PTDM) is a major complication after kidney transplantation and can lead to a wide range of complications including graft loss, increased mortality, increased number of rejections, and increased risk of cardiovascular disease (1-4). A recent meta-analysis of observational studies and randomized, controlled trials showed that the incidence of PTDM during the 1st year after transplantation varied from 2 to 50% (5). There have been several previous reports on PTDM in Korean patients, albeit for a short period of observation. We reported previously that the incidence of PTDM was 23.7% in 114 patients treated with cyclosporine A (CsA) at 9 -12 months after transplantation (6), whereas Cho et al. (7) reported that it was 57.1% in 21 patients treated with tacrolimus at 6 months after transplantation in Korea.PTDM and type 2 diabetes are similar in many ways. One example is that the onset of both can be insidious (8); individuals may experience glucose intolerance and remain asymptomatic for years before symptoms manifest clinically (9,10). Furthermore, PTDM is not always permanent and may resolve within weeks or months, sometimes without treatment (11). Although several recent reports on a consensus definition of PTDM ha...

OBJECTIVE—Posttransplantation diabetes mellitus (PTDM) is a major metabolic complication in renal transplant recipients, and insulin secretory defects play an important role in the pathogenesis of PTDM. The R325W (rs13266634) nonsynonymous polymorphism in the islet-specific zinc transporter protein gene, SLC30A8, has been reported to be associated with type 2 diabetes and possibly with a defect in insulin secretion. This study investigated the association between genetic variations in the SLC30A8 gene and PTDM in renal allograft recipients. RESEARCH DESIGN AND METHODS—A total of 624 unrelated renal allograft recipients without previously diagnosed diabetes were enrolled. Rs13266634 was genotyped in the cohort, which consisted of 174 posttransplantation diabetic patients and 450 non-posttransplantation diabetic subjects. The genotyping of the SLC30A8 polymorphism was performed using real-time PCR. RESULTS—The prevalence of PTDM was 33.8% in patients carrying the R/R genotype, 26.8% in patients with the R/W genotype, and 19.8% in patients with the W/W genotype. There was a strong association between the number of W-alleles and PTDM risk reduction (P for trend = 0.007). Patients with at least one T-allele showed a decreased risk of PTDM compared with those with the R/R genotype (R/W, risk ratio [RR] 0.78, P = 0.126; W/W, RR 0.52, P = 0.007). The effect of the SLC30A8 genotype remained significant after adjustments for age, sex, body weight gain, and type of immunosuppressant (R/W, hazard ratio [HR] 0.77, P = 0.114; W/W, HR 0.58, P = 0.026). CONCLUSIONS—These data provide evidence that the SLC30A8 rs13266634 gene variation is associated with protection from the development of PTDM in renal allograft recipients.

The clinical outcomes of 2,054 renal recipients were examined retrospectively based on pre-transplant hepatitis B surface antigen (HBsAg) status to investigate the efficacy of lamivudine treatment in HBsAg positive recipients. Pre-transplant HBsAg positivity was documented in 66 recipients. The 10-year patient and graft survival rates in Ag positive group were significantly lower than those of Ag negative group (64.4/36.6% vs. 88.2/70.5%, respectively, P < 0.0001). Since 1997, lamivudine was used when hepatitis B virus polymerase chain reaction (HBV PCR) was positive or when the level of post-transplant viral load rose. Lamivudine given to 27 recipients markedly improved both 10-year patient and graft survivals compared to Ag positive renal recipients who did not take lamivudine (85.3/59.2% vs. 49.9/22.7%, respectively, P < 0.0001). Overall, 13 viral breakthroughs among 24 lamivudine-responsive patients were observed. The cumulative incidence of viral breakthrough at 60 months was 53.3%. Adefovir rescue in three viral breakthroughs patients induces virological response and restoration of liver function. In 10 patients who did not changed to adefovir, 6 patients are alive with elevated liver enzymes. In conclusion, in the era of lamivudine and adefovir, renal transplantation in HBsAg positive end-stage renal disease patients should not be abandoned.