| DB ID | MyCo_2729 |
| Title | Soluble HLA-G pre-transplant levels to identify the risk for development of infection in heart transplant recipients |
| Year | 2019 |
| PMID | 31677945 |
| Fungal Diseases involved | Fungal infection |
| Associated Medical Condition | heart transplant |
| Genus | None |
| Species | None |
| Organism | None |
| Ethical Statement | None |
| Site of Infection | Heart |
| Opportunistic invasive | None |
| Sample type | Body fluid |
| Sample source | Serum |
| Host Group | Human |
| Host Common name | Human |
| Host Scientific name | Homo sapiens |
| Biomarker Name | HLA-G molecules |
| Biomarker Full Name | Human Leukocyte antigen-G molecules |
| Biomarker Type | Diagnostic |
| Biomolecule | Protein |
| Geographical Location | Italy |
| Cohort | We enrolled 122 patients who underwent heart transplanted at the Heart and Lung Transplant Centre of the St. Orsola-Malpighi Polyclinic in Bologna, Italy, between May 2009 and February 2014. These patients represent a subgroup of patients enrolled in the randomized study PROTECT (Prevention of Transplant Atherosclerosis with Everolimus and Anti-cytomegalovirus Therapy; ClinicalTrials registration no.NCT00966836). The population consisted of 93 males and 29 females, with a mean age of 55.6 years (range, 19–69 years). The most common indication for heart transplant was dilated cardiomyopathy (n=85; 70%), followed by hypertrophic cardiomyopathy (n=15; 13%), restrictive cardiomyopathy (n=10; 9%), valvular cardiomyopathy (n=4; 4%), and congenital cardiomyopathy (n=2; 2%). Induction therapy using thymoglobulin at a cumulative dose of 1–4 mg/kg of body weight was administered to 103 (85%) patients. In most cases, the postoperative immunosuppressive treatment consisted of a combination of CsA (cyclosporine), mycophenolate mofetil, and prednisone (PRED) (n=63; 52%), followed by a combination of CsA, everolimus, and PRED (n=42; 34%), CsA and PRED (n=13; 11%), and, in one case, PRED and tacrolimus (n=2; 2%). At the time of transplant, all patients were CMV seropositive; the CMV donor/recipient serostatus (D/R) data were as follows: D+/R+ (n=111; 91%) and D−/R+ (n=11; 9%). |
| Cohort No. | 122 Patients |
| Age Group | 19 - 69 |
| P Value | None |
| Sensitivity | None |
| Specificity | None |
| Positive Predictive Value | None |
| MIC | None |
| Fold Change | None |
| Pathway | None |
| Disease Introduction Mechanism | Both solid organ and hematopoietic stem cell transplantation represent life-saving therapies for patients with end stage organ failure or severe haematological malignancies, respectively. However, genetic incompatibilities between donor and recipient, in particular among classical human leukocyte antigen (HLA) class I (HLA-A, -B, -C) and class II (HLA-DR, -DQ, -DP) molecules, lead to a powerful allo-response by the adaptive and/or innate immune system, which has to be controlled by immunosuppressive drugs. Despite the development of modern immunosuppressive strategies, the induction of such reactions cannot always be completely prevented, and acute or chronic rejection remains a major complication in transplantation. The positive effects of the immunosuppressive agents, obligatory for the prevention of organ rejection, have been tempered by the negative effects of these same therapies, leading to various infections that range in both frequency and severity. Newer immune-modulating agents have been developed, increasing the number of therapies that prevent organ rejection, mainly in heart transplanted patients. However, this has simultaneously created newer unwanted opportunities for pathogens to cause infectious complications. These adverse effects are the result of their negative impact on both the cellular and humoral arms of the heart transplanted recipient's immune system. Fortunately, newer diagnostic laboratory methods have also added much-needed capacity to identify the presence and types of pathogens, often early enough in the heart transplanted recipient’s course to prevent or mitigate severe infection. However, it seems important to understand the mechanisms at the basis of a different follow-up of heart transplanted patients in term of infection outcome and transplant survival. |
| Technique | ELISA |
| Analysis Method | ELISA Based |
| ELISA kits | None |
| Assay Data | None |
| Validation Techniques used | ELISA |
| Up Regulation Down Regulation | Increase |
| Sequence Data | None |
| External Link | None |
