Oltean M, Herlenius G, Gäbel M, Friman V, Olausson M
Departments of Transplantation and Liver Surgery, Sahlgrenska University Hospital, Göteborg, Sweden.
Transplant Proc. 2006 Oct;38(8):2683-5. doi: 10.1016/j.transproceed.2006.07.035.
It is thought that multivisceral transplantation requires high levels of immunosuppression and therefore, patients run an increased risk of infection. We retrospectively reviewed our center's experience with clinically relevant infectious complications.
Between 2000 and 2005, 10 adult patients underwent multivisceral transplantation. Two immunosuppression protocols were used: between 2000 and 2003, a high immunosupression protocol (six patients; daclizumab induction, tacrolimus trough levels >20 ng/mL and steroids) and an immunomodulatory, low imunosuppression scheme from 2003 onward (four patients; ATG induction, tacrolimus levels 5 to 10 ng/mL, no steroids). Standard antimicrobial prophylaxis consisted of vancomycin, meropenem, and amphotericin B. Cytomegalovirus (CMV) prophylaxis was used in all but first two cases. Donor and recipient CMV status were D+/R+ (n = 7), D+/R- (n = 2), D-/R+ (n = 1).
The median follow-up period was 627 days (range, 19 to 2207 days). A total of 47 infectious episodes were recorded in all patients (range 1 to 14 per patient). The etiology was bacterial in 32 (69%), viral in 8 (17%), and fungal in 7 (14%) cases. The most frequent were catheter related (n = 13) followed by respiratory (n = 7), intraabdominal (n = 6), and wound infections (n = 5). Symptomatic viral infection of the graft (CMV gastritis or enteritis, adenoviral enteritis) was also encountered. Epstein-Barr virus was transiently detected in the serum of nine patients, one of whom later developed posttransplant lymphoproliferative disorder (PTLD). Three deaths all among patients receiving high immunosuppression were owing to infectious complications: pulmonary PTLD at 4 months posttransplantation, ruptured mycotic aneurysm after 8 weeks, and sepsis after 3 weeks.
Infections accounted for a high morbidity after multivisceral transplantation, representing the leading cause of mortality. Exhaustive monitoring, early antimicrobial intervention, and lower immunosuppression may improve the outcome.
人们认为多脏器移植需要高水平的免疫抑制，因此患者感染风险增加。我们回顾性分析了本中心临床相关感染并发症的经验。
2000年至2005年间，10例成年患者接受了多脏器移植。采用了两种免疫抑制方案：2000年至2003年，采用高免疫抑制方案（6例患者；使用达利珠单抗诱导，他克莫司谷浓度>20 ng/mL并使用类固醇）；2003年起采用免疫调节性低免疫抑制方案（4例患者；使用抗胸腺细胞球蛋白诱导，他克莫司浓度为5至10 ng/mL，不使用类固醇）。标准抗菌预防措施包括万古霉素、美罗培南和两性霉素B。除前两例患者外，所有患者均采用了巨细胞病毒（CMV）预防措施。供体和受体的CMV状态分别为D+/R+（7例）、D+/R-（2例）、D-/R+（1例）。
中位随访期为627天（范围19至2207天）。所有患者共记录到47次感染发作（每位患者1至14次）。病因包括细菌感染32例（69%）、病毒感染8例（17%）、真菌感染7例（14%）。最常见的是与导管相关的感染（13例），其次是呼吸道感染（7例）、腹腔内感染（6例）和伤口感染（5例）。还出现了移植物的有症状病毒感染（CMV胃炎或肠炎、腺病毒肠炎）。9例患者血清中短暂检测到爱泼斯坦-巴尔病毒，其中1例后来发生了移植后淋巴细胞增生性疾病（PTLD）。3例死亡患者均为接受高免疫抑制治疗的患者，死因均为感染并发症：移植后4个月发生肺部PTLD，8周后发生霉菌性动脉瘤破裂，3周后发生败血症。
感染是多脏器移植后高发病率的原因，也是主要死亡原因。全面监测、早期抗菌干预和降低免疫抑制可能改善预后。
