(P-TS-87) Passenger Lymphocyte and Autoimmune-Mediated Thrombocytopenia Following Liver Transplantation

Background/Case Studies: A 64-year-old male with decompensated hepatic cirrhosis received a liver transplant on 5/13/2024. The patient received significant transfusions intraoperatively and through postoperative day (POD) 4. The patient’s platelet (plt) count was < 10,000/µL. A STAT workup was conducted, including HLA Class I antibody (Ab) identification (ID) and low-resolution HLA typing for HLA-A and HLA-B.

Study

Design/Methods: HLA class I A and B typing was performed using Luminex based genotyping. The patient was antigen-typed as HLA-A1, -A24, and -B35. HLA Class I Ab ID was performed using Luminex based Single Antigen beads. Short tandem repeat (STR) analysis was performed on three different patient post-transplant DNA samples. The patient was highly sensitized, with 100% cPRA , which includes Abs to all three self-HLA antigens measured by mean fluorescence intensity (MFI): anti-HLA-A1 (MFI: 11715), anti-HLA-A24 (MFI: 5044), and anti-HLA-B35 (MFI: 2967) (Figure 1A). The HLA-A, B typing of the liver donor was HLA-A2, -A68, and -B7. Donor-specific antibodies (DSAs) were not present.

Confirmatory samples were drawn and received on 5/23/2024 (POD 10) and testing was repeated. The patient’s HLA typing was concordant with original testing, and he remained sensitized to self-antigens though MFIs decreased slightly. Weak DSAs to HLA-A2 (MFI: 1795) were now presenting, but lower than all HLA self-antigen Abs. The patient continued receiving RBC and plt units, and plt counts remained between 10,000 and 20,000 with very poor corrected count increments (CCI).

Results/Findings: On 5/24/2024, the team decided to trial plt units that were HLA-matched to the liver donor’s HLA type rather than the patient’s, due to moderate to strong self-HLA antibodies. A unit of single donor plts expressing HLA-A2, -B7, and -B65 was transfused. Plt count increased from 28,000/µL to 70,000/µL (CCI of 25,000), 23 minutes post-transfusion. Subsequently, his plt count increased naturally to ~120,000/µL by 5/29/2024 (POD 16).

A final follow-up sample was drawn on 6/11/2024 (POD 29). All self-Abs to HLA-A1, -A24, and -B35 reduced to MFIs below 300, and the DSAs to HLA-A2, -A68, and -B7 were not detected (Figure 1B). The POD 4 sample demonstrated a weakly mixed STR profile at multiple loci, supporting a diagnosis of passenger lymphocyte thrombocytopenia as the likely cause of observed self-antibody mediated thrombocytopenia. Subsequent POD 10 and POD 29 samples showed a single, consistent STR profile, indicating resolution of the mixed micro-chimerism seen previously.

Conclusions: This case highlights the complex interplay between donor-derived immune cells and recipient platelet transfusion responsiveness. Clinicians should be aware of the potential role of passenger lymphocyte thrombocytopenia when managing platelet refractoriness in transplant recipients.