Limits...
Antibody-mediated rejection after adult living-donor liver transplantation triggered by positive lymphocyte cross-match combination.

Hori T, Egawa H, Uemoto S - Ann Gastroenterol (2012)

Bottom Line: Flow cytometry initially showed that immunoreactivity against Class I antigens was down-regulated immediately after LDLT, but further testing showed that it had increased again.We diagnosed humoral rejection based on clinical, immunological and histopathological findings and suggest that this was mediated by an immune response to donor-specific antigens.The patient experienced multi-organ failure and died on post-operative Day 9.

View Article: PubMed Central - PubMed

Affiliation: Divisions of Hepato-Biliary-Pancreatic, Transplant and Pediatric Surgery, Department of Surgery, Kyoto University Hospital, Sakyo-ku, Kyoto, 606-8507, Japan.

ABSTRACT
A 46-year-old female suffering from liver cirrhosis was referred to us for living-donor liver transplantation (LDLT). Pre-transplant lymphocyte cross-match tests were positive. The recipient showed immunoreactivity against donor human leukocyte antigen (HLA) Class I antigens, a finding confirmed by flow cytometry. Additional tests confirmed donor-specific lymphocyte immunoreactivity against HLA B 55. As no other suitable donor was available, we performed LDLT coupled with splenectomy, despite the positive cross-match. Tacrolimus, methylprednisolone and mycophenolate mofetil were used postoperatively for immunosuppression. The postoperative course was uneventful until Day 3 when blood tests showed disorders in liver function and the patient's condition suddenly worsened. Although intensive care (including plasma exchange) was given, her condition continued to deteriorate. Flow cytometry initially showed that immunoreactivity against Class I antigens was down-regulated immediately after LDLT, but further testing showed that it had increased again. We diagnosed humoral rejection based on clinical, immunological and histopathological findings and suggest that this was mediated by an immune response to donor-specific antigens. The patient experienced multi-organ failure and died on post-operative Day 9.

No MeSH data available.


Related in: MedlinePlus

Changes in the patient’s blood biochemistry after LDLT. Temporal changes in each of the variables are represented as follows: closed square, AST; closed circle, LDH; open circle, T-Bil; open square, PT-INR; closed triangle, lactate.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3959345&req=5

Figure 4: Changes in the patient’s blood biochemistry after LDLT. Temporal changes in each of the variables are represented as follows: closed square, AST; closed circle, LDH; open circle, T-Bil; open square, PT-INR; closed triangle, lactate.

Mentions: Post-operative splanchnic in-flow and out-flow were excellent as assessed by Doppler ultrasound studies. The post-operative course was uneventful until POD 3 when the patient experienced a sudden elevation of serum lactate dehydrogenase (LDH) levels, a decrease in the platelet count and severe fragmentation of red blood cells. Serum total bilirubin (T-Bil) levels were increased after POD 3 leading to a prolonged case of jaundice. On POD 4 a chest X-ray was taken and showed an acute respiratory distress syndrome-like condition. Blood gas analysis revealed significant respiratory insufficiency. The patient’s respiratory function worsened to a point where she required mechanical ventilation. Plasma exchange (PE) (80 mL/kg/d) was performed daily after POD 4 (Fig. 4) and she received steroid pulse therapy (methylprednisolone at 10 mg/kg, i.v.) from POD 5. The gated area represented immunoreactivity against Class I antigens, and the percentages were calculated as the counts in the gated area/the whole counts. The percentages at pre-LDLT, PODs 2, 5, 6, 8 and 9 were 71.7, 1.7, 1.9, 11.2, 7.3 and 25.8 %, respectively. Although immunoreactivity against HLA Class I antigen was down-regulated during the early period after LDLT it increased again from POD 6. Note that this immunoreactivity was down-regulated on POD 5 even though graft dysfunction began on POD 3 and that this immunoreactivity remained from POD 6 even after repeated PE. On POD 8, peripheral blood examination showed evidence of hemolysis and that haptoglobin levels had fallen (<5.0 mg/dL). Percutaneous microecchymosis was noted and coagulation profiles were consistent with disseminated intravascular coagulation (DIC). The patient’s condition worsened and she did not respond to further treatment, including daily PE. On POD 9 we performed a liver needle biopsy under US guidance. Histopathological examination clearly showed severe graft damage (Fig. 5). We diagnosed HR mediated by an antigen-specific immune response to the donor tissue based on the clinical, immunological and histopathological findings. The patient experienced multi-organ failure accompanied by DIC and died at POD 9 despite intensive treatment.


Antibody-mediated rejection after adult living-donor liver transplantation triggered by positive lymphocyte cross-match combination.

Hori T, Egawa H, Uemoto S - Ann Gastroenterol (2012)

Changes in the patient’s blood biochemistry after LDLT. Temporal changes in each of the variables are represented as follows: closed square, AST; closed circle, LDH; open circle, T-Bil; open square, PT-INR; closed triangle, lactate.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3959345&req=5

Figure 4: Changes in the patient’s blood biochemistry after LDLT. Temporal changes in each of the variables are represented as follows: closed square, AST; closed circle, LDH; open circle, T-Bil; open square, PT-INR; closed triangle, lactate.
Mentions: Post-operative splanchnic in-flow and out-flow were excellent as assessed by Doppler ultrasound studies. The post-operative course was uneventful until POD 3 when the patient experienced a sudden elevation of serum lactate dehydrogenase (LDH) levels, a decrease in the platelet count and severe fragmentation of red blood cells. Serum total bilirubin (T-Bil) levels were increased after POD 3 leading to a prolonged case of jaundice. On POD 4 a chest X-ray was taken and showed an acute respiratory distress syndrome-like condition. Blood gas analysis revealed significant respiratory insufficiency. The patient’s respiratory function worsened to a point where she required mechanical ventilation. Plasma exchange (PE) (80 mL/kg/d) was performed daily after POD 4 (Fig. 4) and she received steroid pulse therapy (methylprednisolone at 10 mg/kg, i.v.) from POD 5. The gated area represented immunoreactivity against Class I antigens, and the percentages were calculated as the counts in the gated area/the whole counts. The percentages at pre-LDLT, PODs 2, 5, 6, 8 and 9 were 71.7, 1.7, 1.9, 11.2, 7.3 and 25.8 %, respectively. Although immunoreactivity against HLA Class I antigen was down-regulated during the early period after LDLT it increased again from POD 6. Note that this immunoreactivity was down-regulated on POD 5 even though graft dysfunction began on POD 3 and that this immunoreactivity remained from POD 6 even after repeated PE. On POD 8, peripheral blood examination showed evidence of hemolysis and that haptoglobin levels had fallen (<5.0 mg/dL). Percutaneous microecchymosis was noted and coagulation profiles were consistent with disseminated intravascular coagulation (DIC). The patient’s condition worsened and she did not respond to further treatment, including daily PE. On POD 9 we performed a liver needle biopsy under US guidance. Histopathological examination clearly showed severe graft damage (Fig. 5). We diagnosed HR mediated by an antigen-specific immune response to the donor tissue based on the clinical, immunological and histopathological findings. The patient experienced multi-organ failure accompanied by DIC and died at POD 9 despite intensive treatment.

Bottom Line: Flow cytometry initially showed that immunoreactivity against Class I antigens was down-regulated immediately after LDLT, but further testing showed that it had increased again.We diagnosed humoral rejection based on clinical, immunological and histopathological findings and suggest that this was mediated by an immune response to donor-specific antigens.The patient experienced multi-organ failure and died on post-operative Day 9.

View Article: PubMed Central - PubMed

Affiliation: Divisions of Hepato-Biliary-Pancreatic, Transplant and Pediatric Surgery, Department of Surgery, Kyoto University Hospital, Sakyo-ku, Kyoto, 606-8507, Japan.

ABSTRACT
A 46-year-old female suffering from liver cirrhosis was referred to us for living-donor liver transplantation (LDLT). Pre-transplant lymphocyte cross-match tests were positive. The recipient showed immunoreactivity against donor human leukocyte antigen (HLA) Class I antigens, a finding confirmed by flow cytometry. Additional tests confirmed donor-specific lymphocyte immunoreactivity against HLA B 55. As no other suitable donor was available, we performed LDLT coupled with splenectomy, despite the positive cross-match. Tacrolimus, methylprednisolone and mycophenolate mofetil were used postoperatively for immunosuppression. The postoperative course was uneventful until Day 3 when blood tests showed disorders in liver function and the patient's condition suddenly worsened. Although intensive care (including plasma exchange) was given, her condition continued to deteriorate. Flow cytometry initially showed that immunoreactivity against Class I antigens was down-regulated immediately after LDLT, but further testing showed that it had increased again. We diagnosed humoral rejection based on clinical, immunological and histopathological findings and suggest that this was mediated by an immune response to donor-specific antigens. The patient experienced multi-organ failure and died on post-operative Day 9.

No MeSH data available.


Related in: MedlinePlus