Search

[Evaluation of Chimerism in Patients with Graft Hematopoietic Progenitor Cells in Panama from 2000­2018]

Aim The first heart transplant in Panama, made in March 2016, involved two hospitals, the Metropolitan Panama Complex and Punta Pacifica Hospital. The National Transplant Laboratory algorithm included all aspects of immunological compatibility in order to minimize one of the most common complications of transplantation: rejection such as acute heart donor. This paper presents the algorithm developed in the Laboratory in this first heart transplant. Methods The patient is female, 52 years old, blood type “A”. Molecular HLA typing use amplified DNA with specific HLA primer and hybridized with a panel of sequence specific oligonucleotide probes (SSOP) (LIFECODES HLA-SSO-Typing kits) The results of HLA recipient are: A ∗ 02, A ∗ 24, B ∗ 51, B ∗ 58, DRB1 ∗ 04, DRB1 ∗ 13, C ∗ 05, Cw ∗ 15, DQB1 ∗ 03(08), DQB1 ∗ 03(07), DPB1 ∗ 04, DPB1 ∗ 05. The studies to establish the presence of anti-HLA preformed antibodies included LIFECODES Antibody Screen, identification of anti-HLA Class I, II using LIFECODES Class I, II ID, and LIFECODES LSA Class I, II. The patient has in his serum anti-A ∗ 36,anti-B ∗ 14(B64) and anti DQB1 ∗ 02 with PRA Class I and Class II, 4%, 30%. The deceased donor was male, 24 years old, blood “A”, and HLA: A ∗ 02, A ∗ 24, B ∗ 58, B ∗ 63, DRB1 ∗ 13, DRB1 ∗ 13, Cw ∗ 07, C w ∗ 07, DQB1 ∗ 06, DQB ∗ 01. DPB1 01, DPB1 ∗ 02. The virtual Crossmatch was negative and actual crossmatching Test (DSA) was negative (LIFE CODES Donor Specific antibodies). In the Bank Laboratory we keep historical sera of the recipient and the pre-transplant serum and preserve HLA glycoproteins of the deceased donor for future humoral antibody-mediated rejection. Conclusion The time used by the laboratory to complete the algorithm was 4 h and the patient was successfully transplanted. Subsequent studies at 15, 30, 45 days have shown the absence of donor specific antibodies. The Laboratory has developed an algorithm that includes all high-tech procedures that avoid the risk of acute antibody-mediated rejection and guarantee further studies to monitor AMR presence. Final del formulario. Download high-res image (95KB) Download full-size image

Aim The Contribution of MICA antibodies to AMR and poor transplant outcomes have been described by multiple reports. In order to evaluate the prevalence of these antibodies in allosensitized kidney transplant candidates on our deceased donor waiting list, we tested patients that were positive for the presence of HLA Class I and/or Class II for the presence of MICA antibodies. Methods A total of 200 patients were tested for the presence of Class I and Class II HLA antibodies using Screen De Luxe Life Codes. The patients that tested positive for HLA antibodies Class I and/or Class II were tested for the presence of MICA antibodies using LifeCodes LSA-MIC. Results Of the 200 patients on the waiting list for deceased kidney donors, 55 (28%) were positive for anti HLA Class I and /or Class II antibodies, 25 (45%) were positive for HLA Class I and II antibodies; 21 (38%) patients were positive for HLA Class I antibodies only; 9 (16%) patients were positive for Class II antibodies only. We tested the presence of MICA antibodies in the 55 sera positive for HLA antibodies, of these 11 (20%) were positive for MICA antibodies. 7/55 (13%) patients were positive for MICA and HLA Class I and Class II antibodies. The most frequency MICA antibodies is MICA∗041 (5/11= 45%). Conclusions Our results indicate that MICA antibodies are present in a significant proportion of HLA allosensitized patients. These findings are clinically relevant to both donor selection and post-transplant monitoring strategies and warrants further investigation.

Aim Published reports have described KIR gene frequency distributions in more than 120 populations. Besides the classical HLA matching, KIR genes form an independent diverse immunogenetic system that implicated in influencing the clinical outcomes of allogeneic HSCT. KIRs are NK cell surface protein, and are encoded by the Leukocyte Receptor Complex (LCR) on chromosome 19 (19q13.4) and expressed on NK cell and subset of T cells. They play important role in the prevention of autoreactivity and elimination of viral-infected cells, tumor cells and anti-leukemia effect. The Aim of this study is to study the distribution of KIR gene polymorphisms in the Panamanian population for future consideration of incorporation in our Laboratory evaluation of donors as an additional selection criterion. Methods Stored genomic DNA (86 oC) of a total of 84 hematopoietic stem cell transplant (HSCT) donors evaluated between 2000-2012, from Instituto Oncologico, Hospital del Nino, Complejo Metropolitano of Panama, were tested for KIR genotyping using LIFECODES KIR TYPING KIT (Gen-Probe) and PCR-SSO. Results 22 patients (26%) were homozygous for haplotype A whereas 62 patients had at least one haplotype B (Bx, 74%). The most frequently seen KIR genotypes in Bx haplotypes in this cohort are: 3DL3, 2DL3, DL5, 2DS5, 2DP1, 2DL1, 3DP1, 2DL4, 3DL1, 3DS1, 2DS1, 2DS4, 3DL2 (13 patients, 15%); 3DL3, 2DS2; 2DL2, 2DL3, 2DL5, 2DS5, 2DP1, 2DL1, 3DP1, 2DL4, 3DL1, 3DS1, 2DS1, 2DS4, 3DL2 (6 patients, 7%); 3DL3, 2DS2, 2DL2, 2DL3, 2DL5, 2DS3, 2DP1, 2DL1, 3DP1, 2DL4, 3DL1 (6 patients, 7%). Conclusions This is the first report to describe KIR haplotypes and genotypes in the Panamanian population.